american heart association basic life support cpr card

American heart association basic life support cpr card

This class format is OSHA, Government, and Workplace Compliant with the same certification as an in-person classroom.

This course is also known as "BLS for Healthcare Providers"

Steps for the class:

1. Register and choose a date and time for your live zoom hands-on skills portion.

2. We email you a link to complete the online HeartCode portion of this class.

3. We ship class supplies and a prepaid return label to you before the zoom meeting.

4. We connect over zoom to complete the hands-on skills portion of the class on the day and time you select below.

5. You will receive a full AHA BLS Provider certification valid for two years.

Location: Your Location - Home or Business via ZOOM Meeting

Price Includes: HeartCode BLS online portion, online student manual, Zoom skills check, and your AHA BLS card.

Who should take this course?

This BLS course is a full course designed toward those who work in the healthcare field, such as nurses or nursing students, dentists, pharmacists, and EMTs. Although, anyone may take this course. Topics covered will be geared toward those in a healthcare environment and includes situations for adults, children and infants which include the following:

• Chain of survival

• BLS for adults

• The framework for CPR

• High-Performance Rescue Teams

• Main Components of CPR

• Adult BLS Algorithm for Healthcare Providers

• CPR techniques, including how to use a pocket mask and bag-mask device

• 2 rescuer BLS

• Team dynamics

• BLS for children and infants

• AED use for adults, children and infants

• Opioid treatment

• Choking relief for adults, children and infants

The BLS Course focuses on what you need to know to perform high-quality CPR in a wide variety of settings. You will also learn how to respond to choking and other types of life-threatening emergencies.

After successfully completing the BLS Provider Course, you should be able to:

• Describe the importance of high-quality CPR and its impact on survival.

• Describe all the steps in the Chains of Survival.

• Apply the BLS concepts of the Chains of Survival.

• Recognize the signs of someone needing CPR.

• Perform high-quality CPR for an adult, a child, and an infant.

• Describe the importance of early use of an automated external defibrillator (AED).

• Demonstrate the appropriate use of an AED.

• Provide effective ventilation by using a barrier device.

• Describe the importance of teams in multirescuer resuscitation.

• Perform as an effective team member during multirescuer CPR.

• Describe the technique for relief of foreign-body airway obstruction for an adult, a child, and an infant.

You will receive an American Heart Association certification valid for two years. You will receive an email from the American Heart Association with your certificate.

To register for the Skills Check Only go to:
American Heart Association (AHA) BLS Provider Skills Check Only

Become an AHA Instructor:

Top 10 Take-Home Messages for Adult Cardiovascular Life Support

On recognition of a cardiac arrest event, a layperson should simultaneously and promptly activate the emergency response system and initiate cardiopulmonary resuscitation (CPR).
Performance of high-quality CPR includes adequate compression depth and rate while minimizing pauses in compressions,
Early defibrillation with concurrent high-quality CPR is critical to survival when sudden cardiac arrest is caused by ventricular fibrillation or pulseless ventricular tachycardia.
Administration of epinephrine with concurrent high-quality CPR improves survival, particularly in patients with nonshockable rhythms.
Recognition that all cardiac arrest events are not identical is critical for optimal patient outcome, and specialized management is necessary for many conditions (eg, electrolyte abnormalities, pregnancy, after cardiac surgery).
The opioid epidemic has resulted in an increase in opioid-associated out-of-hospital cardiac arrest, with the mainstay of care remaining the activation of the emergency response systems and performance of high-quality CPR.
Post–cardiac arrest care is a critical component of the Chain of Survival and demands a comprehensive, structured, multidisciplinary system that requires consistent implementation for optimal patient outcomes.
Prompt initiation of targeted temperature management is necessary for all patients who do not follow commands after return of spontaneous circulation to ensure optimal functional and neurological outcome.
Accurate neurological prognostication in brain-injured cardiac arrest survivors is critically important to ensure that patients with significant potential for recovery are not destined for certain poor outcomes due to care withdrawal.
Recovery expectations and survivorship plans that address treatment, surveillance, and rehabilitation need to be provided to cardiac arrest survivors and their caregivers at hospital discharge to optimize transitions of care to home and to the outpatient setting.

Preamble

In 2015, approximately 350 000 adults in the United States experienced nontraumatic out-of-hospital cardiac arrest (OHCA) attended by emergency medical services (EMS) personnel.1 Approximately 10.4% of patients with OHCA survive their initial hospitalization, and 8.2% survive with good functional status. The key drivers of successful resuscitation from OHCA are lay rescuer cardiopulmonary resuscitation (CPR) and public use of an automated external defibrillator (AED). Despite recent gains, only 39.2% of adults receive layperson-initiated CPR, and the general public applied an AED in only 11.9% of cases.1 Survival rates from OHCA vary dramatically between US regions and EMS agencies.2,3 After significant improvements, survival from OHCA has plateaued since 2012.

Approximately 1.2% of adults admitted to US hospitals suffer in-hospital cardiac arrest (IHCA).1 Of these patients, 25.8% were discharged from the hospital alive, and 82% of survivors have good functional status at the time of discharge. Despite steady improvement in the rate of survival from IHCA, much opportunity remains.

The International Liaison Committee on Resuscitation (ILCOR) Formula for Survival emphasizes 3 essential components for good resuscitation outcomes: guidelines based on sound resuscitation science, effective education of the lay public and resuscitation providers, and implementation of a well-functioning Chain of Survival.4

These guidelines contain recommendations for basic life support (BLS) and advanced life support (ALS) for adult patients and are based on the best available resuscitation science. The Chain of Survival, introduced in Major Concepts, is now expanded to emphasize the important component of survivorship during recovery from cardiac arrest, requires coordinated efforts from medical professionals in a variety of disciplines and, in the case of OHCA, from lay rescuers, emergency dispatchers, and first responders. In addition, specific recommendations about the training of resuscitation providers are provided in “Part 6: Resuscitation Education Science,” and recommendations about systems of care are provided in “Part 7: Systems of Care.”

Introduction

Scope of the Guidelines

These guidelines are designed primarily for North American healthcare providers who are looking for an up-to-date summary for BLS and ALS for adults as well as for those who are seeking more in-depth information on resuscitation science and gaps in current knowledge. The BLS care of adolescents follows adult guidelines. This Part of the 2020 American Heart Association (AHA) Guidelines for CPR and Emergency Cardiovascular Care includes recommendations for clinical care of adults with cardiac arrest, including those with life-threatening conditions in whom cardiac arrest is imminent, and after successful resuscitation from cardiac arrest.

Some recommendations are directly relevant to lay rescuers who may or may not have received CPR training and who have little or no access to resuscitation equipment. Other recommendations are relevant to persons with more advanced resuscitation training, functioning either with or without access to resuscitation drugs and devices, working either within or outside of a hospital. Some treatment recommendations involve medical care and decision-making after return of spontaneous circulation (ROSC) or when resuscitation has been unsuccessful. Importantly, recommendations are provided related to team debriefing and systematic feedback to increase future resuscitation success.

Organization of the Writing Group

The Adult Cardiovascular Life Support Writing Group included a diverse group of experts with backgrounds in emergency medicine, critical care, cardiology, toxicology, neurology, EMS, education, research, and public health, along with content experts, AHA staff, and the AHA senior science editors. Each recommendation was developed and formally approved by the writing group.

The AHA has rigorous conflict of interest policies and procedures to minimize the risk of bias or improper influence during the development of guidelines. Before appointment, writing group members disclosed all commercial relationships and other potential (including intellectual) conflicts. These procedures are described more fully in “Part 2: Evidence Evaluation and Guidelines Development.” Disclosure information for writing group members is listed in Appendix 1.

Methodology and Evidence Review

These guidelines are based on the extensive evidence evaluation performed in conjunction with the ILCOR and affiliated ILCOR member councils. Three different types of evidence reviews (systematic reviews, scoping reviews, and evidence updates) were used in the 2020 process. Each of these resulted in a description of the literature that facilitated guideline development. A more comprehensive description of these methods is provided in “Part 2: Evidence Evaluation and Guidelines Development.”

Class of Recommendation and Level of Evidence

As with all AHA guidelines, each 2020 recommendation is assigned a Class of Recommendation (COR) based on the strength and consistency of the evidence, alternative treatment options, and the impact on patients and society (Table 1). The Level of Evidence (LOE) is based on the quality, quantity, relevance, and consistency of the available evidence. For each recommendation, the writing group discussed and approved specific recommendation wording and the COR and LOE assignments. In determining the COR, the writing group considered the LOE and other factors, including systems issues, economic factors, and ethical factors such as equity, acceptability, and feasibility. These evidence-review methods, including specific criteria used to determine COR and LOE, are described more fully in “Part 2: Evidence Evaluation and Guidelines Development.” The Adult Basic and Advanced Life Support Writing Group members had final authority over and formally approved these recommendations.

Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care (Updated May 2019)*

This table defines the Classes of Recommendation (COR) and Levels of Evidence (LOE). COR indicates the strength the writing group assigns the recommendation, and the LOE is assigned based on the quality of the scientific evidence. The outcome or result of the intervention should be specified (an improved clinical outcome or increased diagnostic accuracy or incremental prognostic information).Classes of RecommendationCOR designations include Class 1, a strong recommendation for which the potential benefit greatly outweighs the risk; Class 2a, a moderate recommendation for which benefit most likely outweighs the risk; Class 2b, a weak recommendation for which it’s unknown whether benefit will outweigh the risk; Class 3: No Benefit, a moderate recommendation signifying that there is equal likelihood of benefit and risk; and Class 3: Harm, a strong recommendation for which the risk outweighs the potential benefit.Suggested phrases for writing Class 1 recommendations includeIs recommendedIs indicated/useful/effective/beneficialShould be performed/administered/otherComparative-effectiveness phrases include treatment/strategy A is recommended/indicated in preference to treatment B, and treatment A should be chosen over treatment B.Suggested phrases for writing Class 2a recommendations includeIs reasonableCan be useful/effective/beneficialComparative-effectiveness phrases include treatment/strategy A is probably recommended/indicated in preference to treatment B, and it is reasonable to choose treatment A over treatment B.For comparative-effectiveness recommendations (COR 1 and 2a; LOE A and B only), studies that support the use of comparator verbs should involve direct comparisons of the treatments or strategies being evaluated.Suggested phrases for writing Class 2b recommendations includeMay/might be reasonableMay/might be consideredUsefulness/effectiveness is unknown/unclear/uncertain or not well-establishedSuggested phrases for writing Class 3: No Benefit recommendations (generally, LOE A or B use only) includeIs not recommendedIs not indicated/useful/effective/beneficialShould not be performed/administered/otherSuggested phrases for writing Class 3: Harm recommendations includePotentially harmfulCauses harmAssociated with excess morbidity/mortalityShould not be performed/administered/otherLevels of EvidenceFor LOEs, the method of assessing quality is evolving, including the application of standardized, widely-used, and preferably validated evidence grading tools; and for systematic reviews, the incorporation of an Evidence Review Committee. LOE designations include Level A, Level B-R, Level B-NR, Level C-LD, and Level C-EO.Those categorized as Level A are derived fromHigh-quality evidence from more than 1 randomized clinical trial, or RCTMeta-analyses of high-quality RCTsOne or more RCTs corroborated by high-quality registry studiesThose categorized as Level B-R (randomized) are derived fromModerate-quality evidence from 1 or more RCTsMeta-analyses of moderate-quality RCTsThose categorized as Level B-NR (nonrandomized) are derived fromModerate-quality evidence from 1 or more well-designed, well-executed nonrandomized studies, observational studies, or registry studiesMeta-analyses of such studiesThose categorized as Level C-LD (limited data) are derived fromRandomized or nonrandomized observational or registry studies with limitations of design or executionMeta-analyses of such studiesPhysiological or mechanistic studies in human subjectsThose categorized as Level C-EO (expert opinion) are derived fromConsensus of expert opinion based on clinical experienceCOR and LOE are determined independently (any COR may be paired with any LOE).A recommendation with LOE C does not imply that the recommendation is weak. Many important clinical questions addressed in guidelines do not lend themselves to clinical trials. Although RCTs are unavailable, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.

Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care (Updated May 2019)*

Unfortunately, despite improvements in the design and funding support for resuscitation research, the overall certainty of the evidence base for resuscitation science is low. Of the 250 recommendations in these guidelines, only 2 recommendations are supported by Level A evidence (high-quality evidence from more than 1 randomized controlled trial [RCT], or 1 or more RCT corroborated by high-quality registry studies.) Thirty-seven recommendations are supported by Level B-Randomized Evidence (moderate evidence from 1 or more RCTs) and 57 by Level B-Nonrandomized evidence. The majority of recommendations are based on Level C evidence, including those based on limited data (123 recommendations) and expert opinion (31 recommendations). Accordingly, the strength of recommendations is weaker than optimal: 78 Class 1 (strong) recommendations, 57 Class 2a (moderate) recommendations, and 89 Class 2b (weak) recommendations are included in these guidelines. In addition, 15 recommendations are designated Class 3: No Benefit, and 11 recommendations are Class 3: Harm. Clinical trials in resuscitation are sorely needed.

Guideline Structure

The 2020 Guidelines are organized into knowledge chunks, grouped into discrete modules of information on specific topics or management issues.5 Each modular knowledge chunk includes a table of recommendations that uses standard AHA nomenclature of COR and LOE. A brief introduction or short synopsis is provided to put the recommendations into context with important background information and overarching management or treatment concepts. Recommendation-specific text clarifies the rationale and key study data supporting the recommendations. When appropriate, flow diagrams or additional tables are included. Hyperlinked references are provided to facilitate quick access and review.

Document Review and Approval

Each of the 2020 Guidelines documents was submitted for blinded peer review to 5 subject-matter experts nominated by the AHA. Before appointment, all peer reviewers were required to disclose relationships with industry and any other conflicts of interest, and all disclosures were reviewed by AHA staff. Peer reviewer feedback was provided for guidelines in draft format and again in final format. All guidelines were reviewed and approved for publication by the AHA Science Advisory and Coordinating Committee and the AHA Executive Committee. Disclosure information for peer reviewers is listed in Appendix 2.

References

1. Virani SS, Alonso A, Benjamin EJ, Bittencourt MS, Callaway CW, Carson AP, Chamberlain AM, Chang AR, Cheng S, Delling FN, et al.; on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2020 update: a report from the American Heart Association.Circulation. 2020; 141:e139–e596. doi: 10.1161/CIR.0000000000000757LinkGoogle Scholar
2. Okubo M, Schmicker RH, Wallace DJ, Idris AH, Nichol G, Austin MA, Grunau B, Wittwer LK, Richmond N, Morrison LJ, Kurz MC, Cheskes S, Kudenchuk PJ, Zive DM, Aufderheide TP, Wang HE, Herren H, Vaillancourt C, Davis DP, Vilke GM, Scheuermeyer FX, Weisfeldt ML, Elmer J, Colella R, Callaway CWResuscitation Outcomes Consortium Investigators. Variation in Survival After Out-of-Hospital Cardiac Arrest Between Emergency Medical Services Agencies.JAMA Cardiol. 2018; 3:989–999. doi: 10.1001/jamacardio.2018.3037CrossrefMedlineGoogle Scholar
3. Zive DM, Schmicker R, Daya M, Kudenchuk P, Nichol G, Rittenberger JC, Aufderheide T, Vilke GM, Christenson J, Buick JE, Kaila K, May S, Rea T, Morrison LJROC Investigators. Survival and variability over time from out of hospital cardiac arrest across large geographically diverse communities participating in the Resuscitation Outcomes Consortium.Resuscitation. 2018; 131:74–82. doi: 10.1016/j.resuscitation.2018.07.023CrossrefMedlineGoogle Scholar
4. Søreide E, Morrison L, Hillman K, Monsieurs K, Sunde K, Zideman D, Eisenberg M, Sterz F, Nadkarni VM, Soar J, Nolan JPUtstein Formula for Survival Collaborators. The formula for survival in resuscitation.Resuscitation. 2013; 84:1487–1493. doi: 10.1016/j.resuscitation.2013.07.020CrossrefMedlineGoogle Scholar
5. Levine GN, O’Gara PT, Beckman JA, Al-Khatib SM, Birtcher KK, Cigarroa JE, de Las Fuentes L, Deswal A, Fleisher LA, Gentile F, Goldberger ZD, Hlatky MA, Joglar JA, Piano MR, Wijeysundera DN. Recent Innovations, Modifications, and Evolution of ACC/AHA Clinical Practice Guidelines: An Update for Our Constituencies: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines.Circulation. 2019; 139:e879–e886. doi: 10.1161/CIR.0000000000000651LinkGoogle Scholar

Abbreviations

ACD	active compression-decompression
ACLS	advanced cardiovascular life support
ADC	apparent diffusion coefficient
AED	automated external defibrillator
AHA	American Heart Association
ALS	advanced life support
aOR	adjusted odds ratio
AV	atrioventricular
BLS	basic life support
COR	Class of Recommendation
CoSTR	International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations
CPR	cardiopulmonary resuscitation
CT	computed tomography
DWI	diffusion-weighted imaging
ECG	electrocardiogram
ECPR	extracorporeal cardiopulmonary resuscitation
EEG	electroencephalogram
EMS	emergency medical services
ETCO2	(partial pressure of) end-tidal carbon dioxide
ETI	endotracheal intubation
GWR	gray-white ratio
ICU	intensive care unit
IHCA	in-hospital cardiac arrest
ILCOR	International Liaison Committee on Resuscitation
IO	intraosseous
ITD	impedance threshold device
IV	intravenous
LAST	local anesthetic systemic toxicity
LOE	Level of Evidence
MAP	mean arterial pressure
MRI	magnetic resonance imaging
NSE	neuron-specific enolase
OHCA	out-of-hospital cardiac arrest
Paco2	arterial partial pressure of carbon dioxide
PCI	percutaneous coronary intervention
PE	pulmonary embolism
PMCD	perimortem cesarean delivery
pVT	pulseless ventricular tachycardia
RCT	randomized controlled trial
ROSC	return of spontaneous circulation
S100B	S100 calcium binding protein
SGA	supraglottic airway
SSEP	somatosensory evoked potential
STEMI	ST-segment elevation myocardial infarction
SVT	supraventricular tachycardia
TCA	tricyclic antidepressant
TOR	termination of resuscitation
TTM	targeted temperature management
VF	ventricular fibrillation
VT	ventricular tachycardia

Major Concepts

Overview Concepts of Adult Cardiac Arrest

Survival and recovery from adult cardiac arrest depend on a complex system working together to secure the best outcome for the victim. The main focus in adult cardiac arrest events includes rapid recognition, prompt provision of CPR, defibrillation of malignant shockable rhythms, and post-ROSC supportive care and treatment of underlying causes. This approach recognizes that most sudden cardiac arrest in adults is of cardiac cause, particularly myocardial infarction and electric disturbances. Arrests without a primary cardiac origin (eg, from respiratory failure, toxic ingestion, pulmonary embolism [PE], or drowning) are also common, however, and in such cases, treatment for reversible underlying causes is important for the rescuer to consider.1 Some noncardiac etiologies may be particularly common in the in-hospital setting. Others, such as opioid overdose, are sharply on the rise in the out-of-hospital setting.2 For any cardiac arrest, rescuers are instructed to call for help, perform CPR to restore coronary and cerebral blood flow, and apply an AED to directly treat ventricular fibrillation (VF) or ventricular tachycardia (VT), if present. Although the majority of resuscitation success is achieved by provision of high-quality CPR and defibrillation, other specific treatments for likely underlying causes may be helpful in some cases.

Adult Chain of Survival

The primary focus of cardiac arrest management for providers is the optimization of all critical steps required to improve outcomes. These include activation of the emergency response, provision of high-quality CPR and early defibrillation, ALS interventions, effective post-ROSC care including careful prognostication, and support during recovery and survivorship. All of these activities require organizational infrastructures to support the education, training, equipment, supplies, and communication that enable each survival. Thus, we recognize that each of these diverse aspects of care contributes to the ultimate functional survival of the cardiac arrest victim.

Resuscitation causes, processes, and outcomes are very different for OHCA and IHCA, which are reflected in their respective Chains of Survival (Figure 1). In OHCA, the care of the victim depends on community engagement and response. It is critical for community members to recognize cardiac arrest, phone 9-1-1 (or the local emergency response number), perform CPR (including, for untrained lay rescuers, compression-only CPR), and use an AED.3,4 Emergency medical personnel are then called to the scene, continue resuscitation, and transport the patient for stabilization and definitive management. In comparison, surveillance and prevention are critical aspects of IHCA. When an arrest occurs in the hospital, a strong multidisciplinary approach includes teams of medical professionals who respond, provide CPR, promptly defibrillate, begin ALS measures, and continue post-ROSC care. Outcomes from IHCA are overall superior to those from OHCA,5 likely because of reduced delays in initiation of effective resuscitation.

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Figure 1. 2020 American Heart Association Chains of Survival for IHCA and OHCA. CPR indicates cardiopulmonary resuscitation; IHCA, in-hospital cardiac arrest; and OHCA, out-of-hospital cardiac arrest.

The Adult OHCA and IHCA Chains of Survival have been updated to better highlight the evolution of systems of care and the critical role of recovery and survivorship with the addition of a new link. This Recovery link highlights the enormous recovery and survivorship journey, from the end of acute treatment for critical illness through multimodal rehabilitation (both short- and long-term), for both survivors and families after cardiac arrest. This new link acknowledges the need for the system of care to support recovery, discuss expectations, and provide plans that address treatment, surveillance, and rehabilitation for cardiac arrest survivors and their caregivers as they transition care from the hospital to home and return to role and social function.

References

1. Lavonas EJ, Drennan IR, Gabrielli A, Heffner AC, Hoyte CO, Orkin AM, Sawyer KN, Donnino MW. Part 10: special circumstances of resuscitation: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S501–S518. doi: 10.1161/CIR.0000000000000264LinkGoogle Scholar
2. Dezfulian C, Orkin AM, Maron BA, Elmer J, Girota S, Gladwin MT, Merchant RM, Panchal AR, Perman SM, Starks M, van Diepen S, Lavonas EJon behalf of the American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular and Stroke Nursing; and Council on Clinical Cardiology. Opioid-associated out-of-hospital cardiac arrest: distinctive clinical features and implications for healthcare and public responses: a scientific statement from the American Heart Association.Circulation. In press.Google Scholar
3. Sayre MR, Berg RA, Cave DM, Page RL, Potts J, White RDAmerican Heart Association Emergency Cardiovascular Care Committee. Hands-only (compression-only) cardiopulmonary resuscitation: a call to action for bystander response to adults who experience out-of-hospital sudden cardiac arrest: a science advisory for the public from the American Heart Association Emergency Cardiovascular Care Committee.Circulation. 2008; 117:2162–2167. doi: 10.1161/CIRCULATIONAHA.107.189380LinkGoogle Scholar
4. Kleinman ME, Brennan EE, Goldberger ZD, Swor RA, Terry M, Bobrow BJ, Gazmuri RJ, Travers AH, Rea T. Part 5: adult basic life support and cardiopulmonary resuscitation quality: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S414–S435. doi: 10.1161/CIR.0000000000000259LinkGoogle Scholar
5. Virani SS, Alonso A, Benjamin EJ, Bittencourt MS, Callaway CW, Carson AP, Chamberlain AM, Chang AR, Cheng S, Delling FN, et al.; on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2020 update: a report from the American Heart Association.Circulation. 2020; 141:e139–e596. doi: 10.1161/CIR.0000000000000757LinkGoogle Scholar

Sequence of Resuscitation

Recognition of Cardiac Arrest

Synopsis

Lay rescuer CPR improves survival from cardiac arrest by 2- to 3-fold.1 The benefit of providing CPR to a patient in cardiac arrest outweighs any potential risk of providing chest compressions to someone who is unconscious but not in cardiac arrest. It has been shown that the risk of injury from CPR is low in these patients.2

It has been shown previously that all rescuers may have difficulty detecting a pulse, leading to delays in CPR, or in some cases CPR not being performed at all for patients in cardiac arrest.3 Recognition of cardiac arrest by lay rescuers, therefore, is determined on the basis of level of consciousness and the respiratory effort of the victim. Recognition of cardiac arrest by healthcare providers includes a pulse check, but the importance of not prolonging efforts to detect a pulse is emphasized.

Recommendation-Specific Supportive Text

Agonal breathing is characterized by slow, irregular gasping respirations that are ineffective for ventilation. Agonal breathing is described by lay rescuers with a variety of terms including, abnormal breathing, snoring respirations, and gasping.4 Agonal breathing is common, reported as being present in up to 40% to 60% of victims of OHCA.5 The presence of agonal breathing is cited as a common reason for lay rescuers to misdiagnose a patient as not being in cardiac arrest.6 In patients who are unresponsive, with absent or abnormal breathing, lay rescuers should assume the patient is in cardiac arrest, call for help, and promptly initiate CPR. These 2 criteria (patient responsiveness and assessment of breathing) have been shown to rapidly identify a significant proportion of patients who are in cardiac arrest, allowing for immediate initiation of lay rescuer CPR. Further, initiation of chest compressions in patients who are unconscious but not in cardiac arrest is associated with low rates of significant adverse events.2 The adverse events noted included pain in the area of chest compressions (8.7%), bone fracture (ribs and clavicle) (1.7%), and rhabdomyolysis (0.3%), with no visceral injuries described.2
Protracted delays in CPR can occur when checking for a pulse at the outset of resuscitation efforts as well as between successive cycles of CPR. Healthcare providers often take too long to check for a pulse7,8 and have difficulty determining if a pulse is present or absent.7–9 There is no evidence, however, that checking for breathing, coughing, or movement is superior to a pulse check for detection of circulation.10 Thus, healthcare providers are directed to quickly check for a pulse and to promptly start compressions when a pulse is not definitively palpated.9,11

This topic last received formal evidence review in 2010.3

References

1. Sasson C, Rogers MA, Dahl J, Kellermann AL. Predictors of survival from out-of-hospital cardiac arrest: a systematic review and meta-analysis.Circ Cardiovasc Qual Outcomes. 2010; 3:63–81. doi: 10.1161/CIRCOUTCOMES.109.889576LinkGoogle Scholar
2. Olasveengen TM, Mancini ME, Perkins GD, Avis S, Brooks S, Castrén M, Chung SP, Considine J, Couper K, Escalante R, et al.; on behalf of the Adult Basic Life Support Collaborators. Adult basic life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S41–S91. doi: 10.1161/CIR.0000000000000892LinkGoogle Scholar
3. Berg RA, Hemphill R, Abella BS, Aufderheide TP, Cave DM, Hazinski MF, Lerner EB, Rea TD, Sayre MR, Swor RA. Part 5: adult basic life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S685–S705. doi: 10.1161/CIRCULATIONAHA.110.970939LinkGoogle Scholar
4. Riou M, Ball S, Williams TA, Whiteside A, Cameron P, Fatovich DM, Perkins GD, Smith K, Bray J, Inoue M, O’Halloran KL, Bailey P, Brink D, Finn J. ‘She’s sort of breathing’: What linguistic factors determine call-taker recognition of agonal breathing in emergency calls for cardiac arrest?Resuscitation. 2018; 122:92–98. doi: 10.1016/j.resuscitation.2017.11.058CrossrefMedlineGoogle Scholar
5. Fukushima H, Imanishi M, Iwami T, Seki T, Kawai Y, Norimoto K, Urisono Y, Hata M, Nishio K, Saeki K, Kurumatani N, Okuchi K. Abnormal breathing of sudden cardiac arrest victims described by laypersons and its association with emergency medical service dispatcher-assisted cardiopulmonary resuscitation instruction.Emerg Med J. 2015; 32:314–317. doi: 10.1136/emermed-2013-203112CrossrefMedlineGoogle Scholar
6. Brinkrolf P, Metelmann B, Scharte C, Zarbock A, Hahnenkamp K, Bohn A. Bystander-witnessed cardiac arrest is associated with reported agonal breathing and leads to less frequent bystander CPR.Resuscitation. 2018; 127:114–118. doi: 10.1016/j.resuscitation.2018.04.017CrossrefMedlineGoogle Scholar
7. Eberle B, Dick WF, Schneider T, Wisser G, Doetsch S, Tzanova I. Checking the carotid pulse check: diagnostic accuracy of first responders in patients with and without a pulse.Resuscitation. 1996; 33:107–116. doi: 10.1016/s0300-9572(96)01016-7CrossrefMedlineGoogle Scholar
8. Moule P. Checking the carotid pulse: diagnostic accuracy in students of the healthcare professions.Resuscitation. 2000; 44:195–201. doi: 10.1016/s0300-9572(00)00139-8CrossrefMedlineGoogle Scholar
9. Ochoa FJ, Ramalle-Gómara E, Carpintero JM, García A, Saralegui I. Competence of health professionals to check the carotid pulse.Resuscitation. 1998; 37:173–175. doi: 10.1016/s0300-9572(98)00055-0CrossrefMedlineGoogle Scholar
10. Perkins GD, Stephenson B, Hulme J, Monsieurs KG. Birmingham assessment of breathing study (BABS).Resuscitation. 2005; 64:109–113. doi: 10.1016/j.resuscitation.2004.09.007CrossrefMedlineGoogle Scholar
11. Mather C, O’Kelly S. The palpation of pulses.Anaesthesia. 1996; 51:189–191. doi: 10.1111/j.1365-2044.1996.tb07713.xCrossrefMedlineGoogle Scholar

Initiation of Resuscitation

Synopsis

After cardiac arrest is recognized, the Chain of Survival continues with activation of the emergency response system and initiation of CPR. The prompt initiation of CPR is perhaps the most important intervention to improve survival and neurological outcomes. Ideally, activation of the emergency response system and initiation of CPR occur simultaneously. In the current era of widespread mobile device usage and accessibility, a lone responder can activate the emergency response system simultaneously with starting CPR by dialing for help, placing the phone on speaker mode to continue communication, and immediately commencing CPR. In the rare situation when a lone rescuer must leave the victim to dial EMS, the priority should be on prompt EMS activation followed by immediate return to the victim to initiate CPR.

Existing evidence suggests that the potential harm from CPR in a patient who has been incorrectly identified as having cardiac arrest is low.1 Overall, the benefits of initiation of CPR in cardiac arrest outweigh the relatively low risk of injury for patients not in cardiac arrest. The initial phases of resuscitation once cardiac arrest is recognized are similar between lay responders and healthcare providers, with early CPR representing the priority. Lay rescuers may provide chest compression–only CPR to simplify the process and encourage CPR initiation, whereas healthcare providers may provide chest compressions and ventilation (Figures 2–4).

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Figure 2. Adult BLS Algorithm for Healthcare Providers. AED indicates automated external defibrillator; ALS, advanced life support; BLS, basic life support; and CPR, cardiopulmonary resuscitation.

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Figure 3. Adult Cardiac Arrest Algorithm. CPR indicates cardiopulmonary resuscitation; ET, endotracheal; IO, intraosseous; IV, intravenous; PEA, pulseless electrical activity; pVT, pulseless ventricular tachycardia; and VF, ventricular fibrillation.

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Figure 4. Adult Cardiac Arrest Circular Algorithm. CPR indicates cardiopulmonary resuscitation; ET, endotracheal; IO, intraosseous; IV, intravenous; pVT, pulseless ventricular tachycardia; and VF, ventricular fibrillation.

Recommendation-Specific Supportive Text

CPR is the single-most important intervention for a patient in cardiac arrest, and chest compressions should be provided promptly. Chest compressions are the most critical component of CPR, and a chest compression–only approach is appropriate if lay rescuers are untrained or unwilling to provide respirations. Beginning the CPR sequence with compressions minimized time to first chest compression.2–4 Nationwide dissemination of chest compression–only CPR for lay rescuers was associated with an increase in the incidence of survival with favorable neurological outcome after OHCAs in Japan, likely due to an increase in lay rescuers providing CPR.5 Chest compressions should be provided as soon as possible, without the need to remove the victim’s clothing first.
The optimal timing of CPR initiation and emergency response system activation was evaluated by an ILCOR systematic review in 2020.1 An observational study of over 17 000 OHCA events reported similar results from either a “call-first” strategy or a “CPR-first” strategy.6 In the current era of ubiquitous mobile devices, ideally both the call to activate EMS and the initiation of CPR can occur simultaneously.
Four observational studies7–10 reported outcomes from patients who were not in cardiac arrest and received CPR by lay rescuers. No serious harm from CPR was found in patients when they were later determined not to have been in cardiac arrest.1 This is in contrast to the significant risk of withholding CPR when a patient is in cardiac arrest, making the risk:benefit ratio strongly in favor of providing CPR for presumed cardiac arrest.
In some observational studies, improved outcomes have been noted in victims of cardiac arrest who received conventional CPR (compressions and ventilation) compared with those who received chest compressions only.5,11,12 Other studies have reported no difference in outcomes for patients receiving conventional versus compression-only CPR.11,13–21 Given the potential benefit of conventional CPR, if lay rescuers are appropriately trained, they should be encouraged to concurrently deliver ventilation with compressions. A thorough review of the data concerning the ratio of compressions to ventilation when performing conventional CPR is discussed in Ventilation and Compression-to-Ventilation Ratio.

These recommendations are supported by the 2020 ILCOR Consensus on CPR and Emergency Cardiovascular Care Science With Treatment Recommendations (CoSTR).1

Recommendation-Specific Supportive Text

The 2010 Guidelines for CPR and Emergency Cardiovascular Care included a major change for trained rescuers, who were instructed to begin the CPR sequence with chest compressions rather than with breaths (circulation, airway, and breathing versus airway, breathing, and circulation) to minimize the time to initiation of chest compressions. This approach is resupported by new literature, summarized in a 2020 ILCOR systematic review (Table 2).1–4 In the recommended sequence, once chest compressions have been started, a single trained rescuer delivers rescue breaths by mouth to mask or by bag-mask device to provide oxygenation and ventilation. Manikin studies demonstrate that starting with chest compressions rather than with ventilation is associated with faster times to chest compressions,3,23 rescue breaths,4 and completion of the first CPR cycle.4
Healthcare providers are trained to deliver both compressions and ventilation. Delivery of chest compressions without assisted ventilation for prolonged periods could be less effective than conventional CPR (compressions plus ventilation) because arterial oxygen content decreases as CPR duration increases. This concern is especially pertinent in the setting of asphyxial cardiac arrest.11 Healthcare providers, with their training and understanding, can realistically tailor the sequence of subsequent rescue actions to the most likely cause of arrest.

Table 2. Adult BLS Sequence22

StepLay Rescuer Not TrainedLay Rescuer TrainedHealthcare Provider

1	Ensure scene safety.	Ensure scene safety.	Ensure scene safety.
2	Check for response.	Check for response.	Check for response.
3	Shout for nearby help. Phone or ask someone to phone 9-1-1 (the phone or caller with the phone remains at the victim’s side, with the phone on speaker mode).	Shout for nearby help and activate the emergency response system (9-1-1, emergency response). If someone responds, ensure that the phone is at the side of the victim if at all possible.	Shout for nearby help/activate the resuscitation team; the provider can activate the resuscitation team at this time or after checking for breathing and pulse.
4	Follow the telecommunicator’s* instructions.	Check for no breathing or only gasping; if none, begin CPR with compressions.	Check for no breathing or only gasping and check pulse (ideally simultaneously). Activation and retrieval of the AED/emergency equipment by the lone healthcare provider or by the second person sent by the rescuer must occur no later than immediately after the check for no normal breathing and no pulse identifies cardiac arrest.
5	Look for no breathing or only gasping, at the direction of the telecommunicator.	Answer the telecommunicator’s questions, and follow the telecommunicator’s instructions.	Immediately begin CPR, and use the AED/defibrillator when available.
6	Follow the telecommunicator’s instructions.	Send the second person to retrieve an AED, if one is available.	When the second rescuer arrives, provide 2-rescuer CPR and use the AED/defibrillator.

These recommendations are supported by the 2020 CoSTR for BLS.1

References

1. Olasveengen TM, Mancini ME, Perkins GD, Avis S, Brooks S, Castrén M, Chung SP, Considine J, Couper K, Escalante R, et al.; on behalf of the Adult Basic Life Support Collaborators. Adult basic life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S41–S91. doi: 10.1161/CIR.0000000000000892LinkGoogle Scholar
2. Lubrano R, Cecchetti C, Bellelli E, Gentile I, Loayza Levano H, Orsini F, Bertazzoni G, Messi G, Rugolotto S, Pirozzi N, Elli M. Comparison of times of intervention during pediatric CPR maneuvers using ABC and CAB sequences: a randomized trial.Resuscitation. 2012; 83:1473–1477. doi: 10.1016/j.resuscitation.2012.04.011CrossrefMedlineGoogle Scholar
3. Sekiguchi H, Kondo Y, Kukita I. Verification of changes in the time taken to initiate chest compressions according to modified basic life support guidelines.Am J Emerg Med. 2013; 31:1248–1250. doi: 10.1016/j.ajem.2013.02.047CrossrefMedlineGoogle Scholar
4. Marsch S, Tschan F, Semmer NK, Zobrist R, Hunziker PR, Hunziker S. ABC versus CAB for cardiopulmonary resuscitation: a prospective, randomized simulator-based trial.Swiss Med Wkly. 2013; 143:w13856. doi: 10.4414/smw.2013.13856MedlineGoogle Scholar
5. Iwami T, Kitamura T, Kiyohara K, Kawamura T. Dissemination of Chest Compression-Only Cardiopulmonary Resuscitation and Survival After Out-of-Hospital Cardiac Arrest.Circulation. 2015; 132:415–422. doi: 10.1161/CIRCULATIONAHA.114.014905LinkGoogle Scholar
6. Kamikura T, Iwasaki H, Myojo Y, Sakagami S, Takei Y, Inaba H. Advantage of CPR-first over call-first actions for out-of-hospital cardiac arrests in nonelderly patients and of noncardiac aetiology.Resuscitation. 2015; 96:37–45. doi: 10.1016/j.resuscitation.2015.06.027CrossrefMedlineGoogle Scholar
7. White L, Rogers J, Bloomingdale M, Fahrenbruch C, Culley L, Subido C, Eisenberg M, Rea T. Dispatcher-assisted cardiopulmonary resuscitation: risks for patients not in cardiac arrest.Circulation. 2010; 121:91–97. doi: 10.1161/CIRCULATIONAHA.109.872366LinkGoogle Scholar
8. Haley KB, Lerner EB, Pirrallo RG, Croft H, Johnson A, Uihlein M. The frequency and consequences of cardiopulmonary resuscitation performed by bystanders on patients who are not in cardiac arrest.Prehosp Emerg Care. 2011; 15:282–287. doi: 10.3109/10903127.2010.541981CrossrefMedlineGoogle Scholar
9. Moriwaki Y, Sugiyama M, Tahara Y, Iwashita M, Kosuge T, Harunari N, Arata S, Suzuki N. Complications of bystander cardiopulmonary resuscitation for unconscious patients without cardiopulmonary arrest.J Emerg Trauma Shock. 2012; 5:3–6. doi: 10.4103/0974-2700.93094CrossrefMedlineGoogle Scholar
10. Tanaka Y, Nishi T, Takase K, Yoshita Y, Wato Y, Taniguchi J, Hamada Y, Inaba H. Survey of a protocol to increase appropriate implementation of dispatcher-assisted cardiopulmonary resuscitation for out-of-hospital cardiac arrest.Circulation. 2014; 129:1751–1760. doi: 10.1161/CIRCULATIONAHA.113.004409LinkGoogle Scholar
11. Kitamura T, Iwami T, Kawamura T, Nagao K, Tanaka H, Hiraide AImplementation Working Group for All-Japan Utstein Registry of the Fire and Disaster Management Agency. Bystander-initiated rescue breathing for out-of-hospital cardiac arrests of noncardiac origin.Circulation. 2010; 122:293–299. doi: 10.1161/CIRCULATIONAHA.109.926816LinkGoogle Scholar
12. Ogawa T, Akahane M, Koike S, Tanabe S, Mizoguchi T, Imamura T. Outcomes of chest compression only CPR versus conventional CPR conducted by lay people in patients with out of hospital cardiopulmonary arrest witnessed by bystanders: nationwide population based observational study.BMJ. 2011; 342:c7106. doi: 10.1136/bmj.c7106CrossrefMedlineGoogle Scholar
13. Svensson L, Bohm K, Castrèn M, Pettersson H, Engerström L, Herlitz J, Rosenqvist M. Compression-only CPR or standard CPR in out-of-hospital cardiac arrest.N Engl J Med. 2010; 363:434–442. doi: 10.1056/NEJMoa0908991CrossrefMedlineGoogle Scholar
14. Rea TD, Fahrenbruch C, Culley L, Donohoe RT, Hambly C, Innes J, Bloomingdale M, Subido C, Romines S, Eisenberg MS. CPR with chest compression alone or with rescue breathing.N Engl J Med. 2010; 363:423–433. doi: 10.1056/NEJMoa0908993CrossrefMedlineGoogle Scholar
15. Iwami T, Kawamura T, Hiraide A, Berg RA, Hayashi Y, Nishiuchi T, Kajino K, Yonemoto N, Yukioka H, Sugimoto H, Kakuchi H, Sase K, Yokoyama H, Nonogi H. Effectiveness of bystander-initiated cardiac-only resuscitation for patients with out-of-hospital cardiac arrest.Circulation. 2007; 116:2900–2907. doi: 10.1161/CIRCULATIONAHA.107.723411LinkGoogle Scholar
16. Kitamura T, Iwami T, Kawamura T, Nagao K, Tanaka H, Berg RA, Hiraide AImplementation Working Group for All-Japan Utstein Registry of the Fire and Disaster Management Agency. Time-dependent effectiveness of chest compression-only and conventional cardiopulmonary resuscitation for out-of-hospital cardiac arrest of cardiac origin.Resuscitation. 2011; 82:3–9. doi: 10.1016/j.resuscitation.2010.09.468CrossrefMedlineGoogle Scholar
17. Ong ME, Ng FS, Anushia P, Tham LP, Leong BS, Ong VY, Tiah L, Lim SH, Anantharaman V. Comparison of chest compression only and standard cardiopulmonary resuscitation for out-of-hospital cardiac arrest in Singapore.Resuscitation. 2008; 78:119–126. doi: 10.1016/j.resuscitation.2008.03.012CrossrefMedlineGoogle Scholar
18. SOS-KANTO Study Group. Cardiopulmonary resuscitation by bystanders with chest compression only (SOS-KANTO): an observational study.Lancet. 2007; 369:920–926. doi: 10.1016/S0140-6736(07)60451–6CrossrefMedlineGoogle Scholar
19. Bobrow BJ, Spaite DW, Berg RA, Stolz U, Sanders AB, Kern KB, Vadeboncoeur TF, Clark LL, Gallagher JV, Stapczynski JS, LoVecchio F, Mullins TJ, Humble WO, Ewy GA. Chest compression-only CPR by lay rescuers and survival from out-of-hospital cardiac arrest.JAMA. 2010; 304:1447–1454. doi: 10.1001/jama.2010.1392CrossrefMedlineGoogle Scholar
20. Olasveengen TM, Wik L, Steen PA. Standard basic life support vs. continuous chest compressions only in out-of-hospital cardiac arrest.Acta Anaesthesiol Scand. 2008; 52:914–919. doi: 10.1111/j.1399-6576.2008.01723.xCrossrefMedlineGoogle Scholar
21. Panchal AR, Bobrow BJ, Spaite DW, Berg RA, Stolz U, Vadeboncoeur TF, Sanders AB, Kern KB, Ewy GA. Chest compression-only cardiopulmonary resuscitation performed by lay rescuers for adult out-of-hospital cardiac arrest due to non-cardiac aetiologies.Resuscitation. 2013; 84:435–439. doi: 10.1016/j.resuscitation.2012.07.038CrossrefMedlineGoogle Scholar
22. Kleinman ME, Brennan EE, Goldberger ZD, Swor RA, Terry M, Bobrow BJ, Gazmuri RJ, Travers AH, Rea T. Part 5: adult basic life support and cardiopulmonary resuscitation quality: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S414–S435. doi: 10.1161/CIR.0000000000000259LinkGoogle Scholar
23. Kobayashi M, Fujiwara A, Morita H, Nishimoto Y, Mishima T, Nitta M, Hayashi T, Hotta T, Hayashi Y, Hachisuka E, Sato K. A manikin-based observational study on cardiopulmonary resuscitation skills at the Osaka Senri medical rally.Resuscitation. 2008; 78:333–339. doi: 10.1016/j.resuscitation.2008.03.230CrossrefMedlineGoogle Scholar

Opening the Airway

Introduction

A patent airway is essential to facilitate proper ventilation and oxygenation. Although there is no high-quality evidence favoring one technique over another for establishment and maintenance of a patient’s airway, rescuers should be aware of the advantages and disadvantages and maintain proficiency in the skills required for each technique. Rescuers should recognize that multiple approaches may be required to establish an adequate airway. Patients should be monitored constantly to verify airway patency and adequate ventilation and oxygenation. There are no studies comparing different strategies of opening the airway in cardiac arrest patients. Much of the evidence examining the effectiveness of airway strategies comes from radiographic and cadaver studies.

Recommendation-Specific Supportive Text

1 and 2. The head tilt–chin lift has been shown to be effective in establishing an airway in noncardiac arrest and radiological studies.2–5 No studies have compared head tilt–chin lift with other airway maneuvers to establish an airway during cardiac arrest.
3. Although there is no evidence examining the effectiveness of their use during cardiac arrest, oropharyngeal and nasopharyngeal airways can be used to maintain a patent airway and facilitate appropriate ventilation by preventing the tongue from occluding the airway. Incorrect placement, however, can cause an airway obstruction by displacing the tongue to the back of the oropharynx.6,7
4. The benefit of an oropharyngeal compared with a nasopharyngeal airway in the presence of a known or suspected basilar skull fracture or severe coagulopathy has not been assessed in clinical trials. However, an oral airway is preferred because of the risk of trauma with a nasopharyngeal airway. Multiple case reports have observed intracranial placement of nasopharyngeal airways in patients with basilar skull fractures.8,9
5. There is no evidence that cricoid pressure facilitates ventilation or reduces the risk of aspiration in cardiac arrest patients. There is some evidence that in non–cardiac arrest patients, cricoid pressure may protect against aspiration and gastric insufflation during bag-mask ventilation.10–13 However, cricoid pressure may also impede ventilation and the placement of a supraglottic airway (SGA) or intubation,14–20 and increase the risk of airway trauma during intubation.21

This topic last received formal evidence review in 2010.22

Recommendation-Specific Supportive Text

Healthcare providers should consider the possibility of a spinal injury before opening the airway. If a spinal injury is suspected or cannot be ruled out, providers should open the airway by using a jaw thrust instead of head tilt–chin lift.2
Maintaining a patent airway and providing adequate ventilation and oxygenation are priorities during CPR. If a jaw thrust and/or insertion of an airway adjunct are ineffective in opening the airway and allowing ventilation to occur, a head tilt–chin lift may be the only way to open the airway. In these cases, this maneuver should be used even in cases of potential spinal injury because the need to open the airway outweighs the risk of further spinal damage in the cardiac arrest patient.
When spinal injury is suspected or cannot be ruled out, rescuers should maintain manual spinal motion restriction and not use immobilization devices. Manual stabilization can decrease movement of the cervical spine during patient care while allowing for proper ventilation and airway control.23,24 Spinal immobilization devices may make it more difficult to maintain airway patency25,26 and provide adequate ventilation.

This topic last received formal evidence review in 2010.22

References

1. Deleted in proof.Google Scholar
2. Elam JO, Greene DG, Schneider MA, Ruben HM, Gordon AS, Hustead RF, Benson DW, Clements JA, Ruben A. Head-tilt method of oral resuscitation.JAMA. 1960; 172:812–815. doi: 10.1001/jama.1960.03020080042011CrossrefMedlineGoogle Scholar
3. Guildner CW. Resuscitation—opening the airway: a comparative study of techniques for opening an airway obstructed by the tongue.JACEP. 1976; 5:588–590. doi: 10.1016/s0361-1124(76)80217-1MedlineGoogle Scholar
4. Greene DG, Elam JO, Dobkin AB, Studley CL. Cinefluorographic study of hyperextension of the neck and upper airway patency.JAMA. 1961; 176:570–573. doi: 10.1001/jama.1961.03040200006002CrossrefMedlineGoogle Scholar
5. Ruben HM, Elam JO, Ruben AM, Greene DG. Investigation of upper airway problems in resuscitation. 1. Studies of pharyngeal x-rays and performance by laymen.Anesthesiology. 1961; 22:271–279. doi: 10.1097/00000542-196103000-00017CrossrefMedlineGoogle Scholar
6. Kim HJ, Kim SH, Min JY, Park WK. Determination of the appropriate oropharyngeal airway size in adults: Assessment using ventilation and an endoscopic view.Am J Emerg Med. 2017; 35:1430–1434. doi: 10.1016/j.ajem.2017.04.029CrossrefMedlineGoogle Scholar
7. Kim HJ, Kim SH, Min NH, Park WK. Determination of the appropriate sizes of oropharyngeal airways in adults: correlation with external facial measurements: A randomised crossover study.Eur J Anaesthesiol. 2016; 33:936–942. doi: 10.1097/EJA.0000000000000439CrossrefMedlineGoogle Scholar
8. Schade K, Borzotta A, Michaels A. Intracranial malposition of nasopharyngeal airway.J Trauma. 2000; 49:967–968. doi: 10.1097/00005373-200011000-00032CrossrefMedlineGoogle Scholar
9. Muzzi DA, Losasso TJ, Cucchiara RF. Complication from a nasopharyngeal airway in a patient with a basilar skull fracture.Anesthesiology. 1991; 74:366–368. doi: 10.1097/00000542-199102000-00026CrossrefMedlineGoogle Scholar
10. Salem MR, Wong AY, Mani M, Sellick BA. Efficacy of cricoid pressure in preventing gastric inflation during bag-mask ventilation in pediatric patients.Anesthesiology. 1974; 40:96–98. doi: 10.1097/00000542-197401000-00026CrossrefMedlineGoogle Scholar
11. Lawes EG, Campbell I, Mercer D. Inflation pressure, gastric insufflation and rapid sequence induction.Br J Anaesth. 1987; 59:315–318. doi: 10.1093/bja/59.3.315CrossrefMedlineGoogle Scholar
12. Petito SP, Russell WJ. The prevention of gastric inflation–a neglected benefit of cricoid pressure.Anaesth Intensive Care. 1988; 16:139–143. doi: 10.1177/0310057X8801600202CrossrefMedlineGoogle Scholar
13. Moynihan RJ, Brock-Utne JG, Archer JH, Feld LH, Kreitzman TR. The effect of cricoid pressure on preventing gastric insufflation in infants and children.Anesthesiology. 1993; 78:652–656. doi: 10.1097/00000542-199304000-00007CrossrefMedlineGoogle Scholar
14. Brimacombe J, White A, Berry A. Effect of cricoid pressure on ease of insertion of the laryngeal mask airway.Br J Anaesth. 1993; 71:800–802. doi: 10.1093/bja/71.6.800CrossrefMedlineGoogle Scholar
15. Allman KG. The effect of cricoid pressure application on airway patency.J Clin Anesth. 1995; 7:197–199. doi: 10.1016/0952-8180(94)00048-9CrossrefMedlineGoogle Scholar
16. Hartsilver EL, Vanner RG. Airway obstruction with cricoid pressure.Anaesthesia. 2000; 55:208–211. doi: 10.1046/j.1365-2044.2000.01205.xCrossrefMedlineGoogle Scholar
17. Hocking G, Roberts FL, Thew ME. Airway obstruction with cricoid pressure and lateral tilt.Anaesthesia. 2001; 56:825–828. doi: 10.1046/j.1365-2044.2001.02133.xCrossrefMedlineGoogle Scholar
18. Turgeon AF, Nicole PC, Trépanier CA, Marcoux S, Lessard MR. Cricoid pressure does not increase the rate of failed intubation by direct laryngoscopy in adults.Anesthesiology. 2005; 102:315–319. doi: 10.1097/00000542-200502000-00012CrossrefMedlineGoogle Scholar
19. Asai T, Goy RW, Liu EH. Cricoid pressure prevents placement of the laryngeal tube and laryngeal tube-suction II.Br J Anaesth. 2007; 99:282–285. doi: 10.1093/bja/aem159CrossrefMedlineGoogle Scholar
20. McNelis U, Syndercombe A, Harper I, Duggan J. The effect of cricoid pressure on intubation facilitated by the gum elastic bougie.Anaesthesia. 2007; 62:456–459. doi: 10.1111/j.1365-2044.2007.05019.xCrossrefMedlineGoogle Scholar
21. Carauna E, Chevret S, Pirracchio R. Effect of cricoid pressure on laryngeal view during prehospital tracheal intubation: a propensity-based analysis.Emerg Med J. 2017132–137. doi: 10.1136/emermed-2016–205715CrossrefMedlineGoogle Scholar
22. Berg RA, Hemphill R, Abella BS, Aufderheide TP, Cave DM, Hazinski MF, Lerner EB, Rea TD, Sayre MR, Swor RA. Part 5: adult basic life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S685–S705. doi: 10.1161/CIRCULATIONAHA.110.970939LinkGoogle Scholar
23. Majernick TG, Bieniek R, Houston JB, Hughes HG. Cervical spine movement during orotracheal intubation.Ann Emerg Med. 1986; 15:417–420. doi: 10.1016/s0196-0644(86)80178-0CrossrefMedlineGoogle Scholar
24. Lennarson PJ, Smith DW, Sawin PD, Todd MM, Sato Y, Traynelis VC. Cervical spinal motion during intubation: efficacy of stabilization maneuvers in the setting of complete segmental instability.J Neurosurg. 2001; 94(suppl):265–270. doi: 10.3171/spi.2001.94.2.0265CrossrefMedlineGoogle Scholar
25. Hastings RH, Wood PR. Head extension and laryngeal view during laryngoscopy with cervical spine stabilization maneuvers.Anesthesiology. 1994; 80:825–831. doi: 10.1097/00000542-199404000-00015CrossrefMedlineGoogle Scholar
26. Gerling MC, Davis DP, Hamilton RS, Morris GF, Vilke GM, Garfin SR, Hayden SR. Effects of cervical spine immobilization technique and laryngoscope blade selection on an unstable cervical spine in a cadaver model of intubation.Ann Emerg Med. 2000; 36:293–300. doi: 10.1067/mem.2000.109442CrossrefMedlineGoogle Scholar

Metrics for High-Quality CPR

Introduction

High-quality CPR is, along with defibrillation for those with shockable rhythms, the most important lifesaving intervention for a patient in cardiac arrest. The evidence for what constitutes optimal CPR continues to evolve as research emerges. A number of key components have been defined for high-quality CPR, including minimizing interruptions in chest compressions, providing compressions of adequate rate and depth, avoiding leaning on the chest between compressions, and avoiding excessive ventilation.1 However, controlled studies are relatively lacking, and observational evidence is at times conflicting. The effect of individual CPR quality metrics or interventions is difficult to evaluate because so many happen concurrently and may interact with each other in their effect. Compression rate and compression depth, for example, have both been associated with better outcomes, yet these variables have been found to be inversely correlated with each other so that improving one may worsen the other.1–3 CPR quality interventions are often applied in “bundles,” making the benefit of any one specific measure difficult to ascertain. As more and more centers and EMS systems are using feedback devices and collecting data on CPR measures such as compression depth and chest compression fraction, these data will enable ongoing updates to these recommendations.

Recommendation-Specific Supportive Text

A 2020 ILCOR systematic review identified 3 studies involving 57 total patients that investigated the effect of hand positioning on resuscitation process and outcomes.4 Although no difference in resuscitation outcomes was noted, 2 studies found better physiological parameters (peak arterial pressure, mean arterial pressure [MAP], end-tidal carbon dioxide [ETCO2]) when compression was performed over the lower third of the sternum compared with the middle of the sternum.5,6 A third study found no difference.7 Radiographic studies show the left ventricle is typically located inferior to the internipple line, corresponding with the lower half of the sternum.8 However, hand placement inferior to the internipple line may result in compression over the xiphoid.9 Although data from manikin studies conflict, it does not appear to matter whether the dominant or nondominant hand is placed in contact with the sternum.10,11
The primary considerations when determining if a victim needs to be moved before starting resuscitation are feasibility and safety of providing high-quality CPR in the location and position in which the victim is found. This is a separate question from the decision of if or when to transport a patient to the hospital with resuscitation ongoing.
The effectiveness of CPR appears to be maximized with the victim in a supine position and the rescuer kneeling beside the victim’s chest (eg, out-of-hospital) or standing beside the bed (eg, in-hospital).12 It is thought that optimal chest compressions are best delivered with the victim on a firm surface.13,14 Manikin studies show generally acceptable thoracic compression with CPR performed on a hospital mattress.
An older systematic review identified 22 case reports of CPR being performed in the prone position (21 in the operating room, 1 in the intensive care unit [ICU]), with 10/22 patients surviving.15 In a small case series of 6 patients with refractory IHCA, prone positioning with the use of a board with sandbag to compress the sternum improved hemodynamics during CPR but did not result in ROSC.16 The efficacy of CPR in the prone position is not established, but the very limited evidence suggests it may be better than providing no CPR, when a patient cannot be placed in supine position, or until this can be done safely.

Recommendations 1, 2, and 3 are supported by the 2020 CoSTR for BLS.4 Recommendation 4 last received formal evidence review in 2010.17

Recommendation-Specific Supportive Text

Observational evidence suggests improved outcomes with increased chest compression fraction in patients with shockable rhythms.18,19 Specifically, studies have also reported increased ROSC with shorter perishock pauses.20–22
This recommendation is based on the overall principle of minimizing interruptions to CPR and maintaining a chest compression fraction of at least 60%, which studies have reported to be associated with better outcome.18,19,23
Chest compression depth begins to decrease after 90 to 120 seconds of CPR, although compression rates do not decrease significantly over that time window.24 A randomized trial using manikins found no difference in the percentage of high-quality compressions when rotating every 1 minute compared with every 2 minutes.25 Rotating the designated chest compressor every 2 minutes is sensible because this approach maintains chest compression quality and takes advantage of when CPR would ordinarily be paused for rhythm analysis.
Two RCTs enrolling more than 1000 patients did not find any increase in survival when pausing CPR to analyze rhythm after defibrillation.26,27 Observational studies show decreased ROSC when chest compressions are not resumed immediately after shock.28,29
Because chest compression fraction of at least 60% is associated with better resuscitation outcomes, compression pauses for ventilation should be as short as possible.18,19,23
A 2015 systematic review reported significant heterogeneity among studies, with some studies, but not all, reporting better rates of survival to hospital discharge associated with higher chest compression fractions.18,19,23 In 2 studies, higher chest compression fraction was associated with lower odds of survival.2,30 Compression rate and depth and cointerventions such as defibrillation, airway management, and medications, are also important and may interact with chest compression fraction. High-performing EMS systems target at least 60%, with 80% or higher being a frequent goal.

Recommendations 1 and 4 are supported by the 2020 CoSTR for BLS.4 Recommendations 2, 3, 5, and 6 last received formal evidence review in 2015.31

Recommendation-Specific Supportive Text

A 2020 ILCOR scoping review32 identified 12 studies, including over 12 500 patients, looking at chest compression components. Several studies found better outcomes, including survival to hospital discharge and defibrillation success, when compression depth was at least 5 cm compared with less than 4 cm.3,20,33,34
The same review32 identified 13 studies, involving 15 000 patients, that looked at compression rate. Results were somewhat inconsistent across studies, with only 3 observational studies in adults showing an association between higher compression rate and outcomes.1,35,36 The only RCT identified included 292 patients and compared a rate of 100 to a rate of 120, finding no difference in outcomes.37 There is no evidence to suggest altering the suggested compression rate of 100 to 120/min in adults. Three studies have reported that depth decreases as rate increases, highlighting the pitfalls of evaluating a single CPR quality metric in isolation.1–3
The ILCOR review32 identified 2 observational studies that provided inconsistent results on the association between chest compression release velocity and survival, with 1 study finding no association and the other finding that faster release velocity was associated with increased survival.38,39 Not allowing complete chest wall recoil has been associated with increased intrathoracic pressure and decreased coronary perfusion.40,41
CPR duty cycle refers to the proportion of time spent in compression relative to the total time of the compression plus decompression cycle. The 2010 Guidelines recommended a 50% duty cycle, in which the time spent in compression and decompression was equal, mainly on the basis of its perceived ease of being achieved in practice. Notably, in a clinical study in adults with out-of-hospital VF arrest (of whom 43% survived to hospital discharge), the mean duty cycle observed during resuscitation was 39%.42 A study in children also found the mean duty cycle was 40%, suggesting that shorter duty cycles may be the norm in clinical practice.43 Although many animal studies have observed higher blood flows and better outcomes when the duty cycle was less than 50%, the optimal duty cycle is not known. Currently, there is insufficient evidence to warrant a change from the existing recommendation, which remains a knowledge gap that requires further investigation.

Recommendations 1, 2, and 3 are supported by the 2020 CoSTR for BLS.4 Recommendation 4 last received formal evidence review in 2010.44

Recommendation-Specific Supportive Text

A 2020 ILCOR systematic review found that most studies did not find a significant association between real-time feedback and improved patient outcomes.4 However, no studies identified significant harm, and some demonstrated clinically important improvement in survival. One recent RCT reported a 25.6% increase in survival to hospital discharge from IHCA with audio feedback on compression depth and recoil (54% versus 28.4%; P<0.001).45
An analysis of data from the AHA’s Get With The Guidelines-Resuscitation registry showed higher likelihood of ROSC (odds ratio, 1.22; 95% CI, 1.04–1.34; P=0.017) when CPR quality was monitored using either ETCO2 or diastolic blood pressure.46 An observational study in adult patients (IHCA and OHCA) reported that for every 10 mm compression depth increase, ETCO2 increased 1.4 mm Hg.47 A 2018 systematic review of ETCO2 as a prognostic indicator for ROSC48 found variability in cutoff values, but less than 10 mm Hg was generally associated with poor outcome and greater than 20 mm Hg had a stronger association with ROSC than a value of greater than 10 mm Hg. The combination of the association of higher ETCO2 with ROSC and the finding that increased chest compression depth can increase ETCO2 suggests that targeting compressions to a value of at least 10 mm Hg, and ideally 20 mm Hg or greater, may be useful. The validity and reliability of ETCO2 in nonintubated patients is not well established. When available, invasive arterial blood pressure monitoring may also help assess and guide CPR efforts. The use of diastolic blood pressure monitoring during cardiac arrest was associated with higher ROSC,46 but there are inadequate human data to suggest any specific pressure.

These recommendations are supported by the 2020 CoSTRs for BLS and ALS.4,49

References

1. Idris AH, Guffey D, Pepe PE, Brown SP, Brooks SC, Callaway CW, Christenson J, Davis DP, Daya MR, Gray R, Kudenchuk PJ, Larsen J, Lin S, Menegazzi JJ, Sheehan K, Sopko G, Stiell I, Nichol G, Aufderheide TPResuscitation Outcomes Consortium Investigators. Chest compression rates and survival following out-of-hospital cardiac arrest.Crit Care Med. 2015; 43:840–848. doi: 10.1097/CCM.0000000000000824CrossrefMedlineGoogle Scholar
2. Vadeboncoeur T, Stolz U, Panchal A, Silver A, Venuti M, Tobin J, Smith G, Nunez M, Karamooz M, Spaite D, Bobrow B. Chest compression depth and survival in out-of-hospital cardiac arrest.Resuscitation. 2014; 85:182–188. doi: 10.1016/j.resuscitation.2013.10.002CrossrefMedlineGoogle Scholar
3. Stiell IG, Brown SP, Christenson J, Cheskes S, Nichol G, Powell J, Bigham B, Morrison LJ, Larsen J, Hess E, Vaillancourt C, Davis DP, Callaway CWResuscitation Outcomes Consortium (ROC) Investigators. What is the role of chest compression depth during out-of-hospital cardiac arrest resuscitation?Crit Care Med. 2012; 40:1192–1198. doi: 10.1097/CCM.0b013e31823bc8bbCrossrefMedlineGoogle Scholar
4. Olasveengen TM, Mancini ME, Perkins GD, Avis S, Brooks S, Castrén M, Chung SP, Considine J, Couper K, Escalante R, et al.; on behalf of the Adult Basic Life Support Collaborators. Adult basic life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S41–S91. doi: 10.1161/CIR.0000000000000892LinkGoogle Scholar
5. Cha KC, Kim HJ, Shin HJ, Kim H, Lee KH, Hwang SO. Hemodynamic effect of external chest compressions at the lower end of the sternum in cardiac arrest patients.J Emerg Med. 2013; 44:691–697. doi: 10.1016/j.jemermed.2012.09.026CrossrefMedlineGoogle Scholar
6. Orlowski JP. Optimum position for external cardiac compression in infants and young children.Ann Emerg Med. 1986; 15:667–673. doi: 10.1016/s0196-0644(86)80423-1CrossrefMedlineGoogle Scholar
7. Qvigstad E, Kramer-Johansen J, Tømte Ø, Skålhegg T, Sørensen Ø, Sunde K, Olasveengen TM. Clinical pilot study of different hand positions during manual chest compressions monitored with capnography.Resuscitation. 2013; 84:1203–1207. doi: 10.1016/j.resuscitation.2013.03.010CrossrefMedlineGoogle Scholar
8. Shin J, Rhee JE, Kim K. Is the inter-nipple line the correct hand position for effective chest compression in adult cardiopulmonary resuscitation?Resuscitation. 2007; 75:305–310. doi: 10.1016/j.resuscitation.2007.05.003CrossrefMedlineGoogle Scholar
9. Kusunoki S, Tanigawa K, Kondo T, Kawamoto M, Yuge O. Safety of the inter-nipple line hand position landmark for chest compression.Resuscitation. 2009; 80:1175–1180. doi: 10.1016/j.resuscitation.2009.06.030CrossrefMedlineGoogle Scholar
10. Nikandish R, Shahbazi S, Golabi S, Beygi N. Role of dominant versus non-dominant hand position during uninterrupted chest compression CPR by novice rescuers: a randomized double-blind crossover study.Resuscitation. 2008; 76:256–260. doi: 10.1016/j.resuscitation.2007.07.032CrossrefMedlineGoogle Scholar
11. Kundra P, Dey S, Ravishankar M. Role of dominant hand position during external cardiac compression.Br J Anaesth. 2000; 84:491–493. doi: 10.1093/oxfordjournals.bja.a013475CrossrefMedlineGoogle Scholar
12. Handley AJ, Handley JA. Performing chest compressions in a confined space.Resuscitation. 2004; 61:55–61. doi: 10.1016/j.resuscitation.2003.11.012CrossrefMedlineGoogle Scholar
13. Nishisaki A, Nysaether J, Sutton R, Maltese M, Niles D, Donoghue A, Bishnoi R, Helfaer M, Perkins GD, Berg R, Arbogast K, Nadkarni V. Effect of mattress deflection on CPR quality assessment for older children and adolescents.Resuscitation. 2009; 80:540–545. doi: 10.1016/j.resuscitation.2009.02.006CrossrefMedlineGoogle Scholar
14. Noordergraaf GJ, Paulussen IW, Venema A, van Berkom PF, Woerlee PH, Scheffer GJ, Noordergraaf A. The impact of compliant surfaces on in-hospital chest compressions: effects of common mattresses and a backboard.Resuscitation. 2009; 80:546–552. doi: 10.1016/j.resuscitation.2009.03.023CrossrefMedlineGoogle Scholar
15. Brown J, Rogers J, Soar J. Cardiac arrest during surgery and ventilation in the prone position: a case report and systematic review.Resuscitation. 2001; 50:233–238. doi: 10.1016/s0300-9572(01)00362-8CrossrefMedlineGoogle Scholar
16. Mazer SP, Weisfeldt M, Bai D, Cardinale C, Arora R, Ma C, Sciacca RR, Chong D, Rabbani LE. Reverse CPR: a pilot study of CPR in the prone position.Resuscitation. 2003; 57:279–285. doi: 10.1016/s0300-9572(03)00037-6CrossrefMedlineGoogle Scholar
17. Cave DM, Gazmuri RJ, Otto CW, Nadkarni VM, Cheng A, Brooks SC, Daya M, Sutton RM, Branson R, Hazinski MF. Part 7: CPR techniques and devices: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122:S720–728. doi: 10.1161/CIRCULATIONAHA.110.970970LinkGoogle Scholar
18. Talikowska M, Tohira H, Finn J. Cardiopulmonary resuscitation quality and patient survival outcome in cardiac arrest: A systematic review and meta-analysis.Resuscitation. 2015; 96:66–77. doi: 10.1016/j.resuscitation.2015.07.036CrossrefMedlineGoogle Scholar
19. Christenson J, Andrusiek D, Everson-Stewart S, Kudenchuk P, Hostler D, Powell J, Callaway CW, Bishop D, Vaillancourt C, Davis D, Aufderheide TP, Idris A, Stouffer JA, Stiell I, Berg RResuscitation Outcomes Consortium Investigators. Chest compression fraction determines survival in patients with out-of-hospital ventricular fibrillation.Circulation. 2009; 120:1241–1247. doi: 10.1161/CIRCULATIONAHA.109.852202LinkGoogle Scholar
20. Edelson DP, Abella BS, Kramer-Johansen J, Wik L, Myklebust H, Barry AM, Merchant RM, Hoek TL, Steen PA, Becker LB. Effects of compression depth and pre-shock pauses predict defibrillation failure during cardiac arrest.Resuscitation. 2006; 71:137–145. doi: 10.1016/j.resuscitation.2006.04.008CrossrefMedlineGoogle Scholar
21. Eftestøl T, Sunde K, Steen PA. Effects of interrupting precordial compressions on the calculated probability of defibrillation success during out-of-hospital cardiac arrest.Circulation. 2002; 105:2270–2273. doi: 10.1161/01.cir.0000016362.42586.feLinkGoogle Scholar
22. Cheskes S, Schmicker RH, Christenson J, Salcido DD, Rea T, Powell J, Edelson DP, Sell R, May S, Menegazzi JJ, Van Ottingham L, Olsufka M, Pennington S, Simonini J, Berg RA, Stiell I, Idris A, Bigham B, Morrison LResuscitation Outcomes Consortium (ROC) Investigators. Perishock pause: an independent predictor of survival from out-of-hospital shockable cardiac arrest.Circulation. 2011; 124:58–66. doi: 10.1161/CIRCULATIONAHA.110.010736LinkGoogle Scholar
23. Vaillancourt C, Everson-Stewart S, Christenson J, Andrusiek D, Powell J, Nichol G, Cheskes S, Aufderheide TP, Berg R, Stiell IGResuscitation Outcomes Consortium Investigators. The impact of increased chest compression fraction on return of spontaneous circulation for out-of-hospital cardiac arrest patients not in ventricular fibrillation.Resuscitation. 2011; 82:1501–1507. doi: 10.1016/j.resuscitation.2011.07.011CrossrefMedlineGoogle Scholar
24. Sugerman NT, Edelson DP, Leary M, Weidman EK, Herzberg DL, Vanden Hoek TL, Becker LB, Abella BS. Rescuer fatigue during actual in-hospital cardiopulmonary resuscitation with audiovisual feedback: a prospective multicenter study.Resuscitation. 2009; 80:981–984. doi: 10.1016/j.resuscitation.2009.06.002CrossrefMedlineGoogle Scholar
25. Manders S, Geijsel FE. Alternating providers during continuous chest compressions for cardiac arrest: every minute or every two minutes?Resuscitation. 2009; 80:1015–1018. doi: 10.1016/j.resuscitation.2009.05.014CrossrefMedlineGoogle Scholar
26. Jost D, Degrange H, Verret C, Hersan O, Banville IL, Chapman FW, Lank P, Petit JL, Fuilla C, Migliani R, et al.; and the DEFI 2005 Work Group. DEFI 2005: a randomized controlled trial of the effect of automated external defibrillator cardiopulmonary resuscitation protocol on outcome from out-of-hospital cardiac arrest.Circulation. 2010; 121:1614–1622. doi: 10.1161/CIRCULATIONAHA.109.878389LinkGoogle Scholar
27. Beesems SG, Berdowski J, Hulleman M, Blom MT, Tijssen JG, Koster RW. Minimizing pre- and post-shock pauses during the use of an automatic external defibrillator by two different voice prompt protocols. A randomized controlled trial of a bundle of measures.Resuscitation. 2016; 106:1–6. doi: 10.1016/j.resuscitation.2016.06.009CrossrefMedlineGoogle Scholar
28. Rea TD, Helbock M, Perry S, Garcia M, Cloyd D, Becker L, Eisenberg M. Increasing use of cardiopulmonary resuscitation during out-of-hospital ventricular fibrillation arrest: survival implications of guideline changes.Circulation. 2006; 114:2760–2765. doi: 10.1161/CIRCULATIONAHA.106.654715LinkGoogle Scholar
29. Bobrow BJ, Clark LL, Ewy GA, Chikani V, Sanders AB, Berg RA, Richman PB, Kern KB. Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest.JAMA. 2008; 299:1158–1165. doi: 10.1001/jama.299.10.1158CrossrefMedlineGoogle Scholar
30. Cheskes S, Schmicker RH, Rea T, Powell J, Drennan IR, Kudenchuk P, Vaillancourt C, Conway W, Stiell I, Stub D, Davis D, Alexander N, Christenson JResuscitation Outcomes Consortium investigators. Chest compression fraction: A time dependent variable of survival in shockable out-of-hospital cardiac arrest.Resuscitation. 2015; 97:129–135. doi: 10.1016/j.resuscitation.2015.07.003CrossrefMedlineGoogle Scholar
31. Kleinman ME, Brennan EE, Goldberger ZD, Swor RA, Terry M, Bobrow BJ, Gazmuri RJ, Travers AH, Rea T. Part 5: adult basic life support and cardiopulmonary resuscitation quality: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S414–S435. doi: 10.1161/CIR.0000000000000259LinkGoogle Scholar
32. Considine J, Gazmuri RJ, Perkins GD, Kudenchuk PJ, Olasveengen TM, Vaillancourt C, Nishiyama C, Hatanaka T, Mancini ME, Chung SP, Escalante-Kanashiro R, Morley P. Chest compression components (rate, depth, chest wall recoil and leaning): A scoping review.Resuscitation. 2020; 146:188–202. doi: 10.1016/j.resuscitation.2019.08.042CrossrefMedlineGoogle Scholar
33. Stiell IG, Brown SP, Nichol G, Cheskes S, Vaillancourt C, Callaway CW, Morrison LJ, Christenson J, Aufderheide TP, Davis DP, Free C, Hostler D, Stouffer JA, Idris AHResuscitation Outcomes Consortium Investigators. What is the optimal chest compression depth during out-of-hospital cardiac arrest resuscitation of adult patients?Circulation. 2014; 130:1962–1970. doi: 10.1161/CIRCULATIONAHA.114.008671LinkGoogle Scholar
34. Babbs CF, Kemeny AE, Quan W, Freeman G. A new paradigm for human resuscitation research using intelligent devices.Resuscitation. 2008; 77:306–315. doi: 10.1016/j.resuscitation.2007.12.018CrossrefMedlineGoogle Scholar
35. Kilgannon JH, Kirchhoff M, Pierce L, Aunchman N, Trzeciak S, Roberts BW. Association between chest compression rates and clinical outcomes following in-hospital cardiac arrest at an academic tertiary hospital.Resuscitation. 2017; 110:154–161. doi: 10.1016/j.resuscitation.2016.09.015CrossrefMedlineGoogle Scholar
36. Abella BS, Sandbo N, Vassilatos P, Alvarado JP, O’Hearn N, Wigder HN, Hoffman P, Tynus K, Vanden Hoek TL, Becker LB. Chest compression rates during cardiopulmonary resuscitation are suboptimal: a prospective study during in-hospital cardiac arrest.Circulation. 2005; 111:428–434. doi: 10.1161/01.CIR.0000153811.84257.59LinkGoogle Scholar
37. Hwang SO, Cha KC, Kim K, Jo YH, Chung SP, You JS, Shin J, Lee HJ, Park YS, Kim S, et al.. A randomized controlled trial of compression rates during cardiopulmonary resuscitation.J Korean Med Sci. 2016; 31:1491–1498. doi: 10.3346/jkms.2016.31.9.1491CrossrefMedlineGoogle Scholar
38. Cheskes S, Common MR, Byers AP, Zhan C, Silver A, Morrison LJ. The association between chest compression release velocity and outcomes from out-of-hospital cardiac arrest.Resuscitation. 2015; 86:38–43. doi: 10.1016/j.resuscitation.2014.10.020CrossrefMedlineGoogle Scholar
39. Kovacs A, Vadeboncoeur TF, Stolz U, Spaite DW, Irisawa T, Silver A, Bobrow BJ. Chest compression release velocity: Association with survival and favorable neurologic outcome after out-of-hospital cardiac arrest.Resuscitation. 2015; 92:107–114. doi: 10.1016/j.resuscitation.2015.04.026CrossrefMedlineGoogle Scholar
40. Yannopoulos D, McKnite S, Aufderheide TP, Sigurdsson G, Pirrallo RG, Benditt D, Lurie KG. Effects of incomplete chest wall decompression during cardiopulmonary resuscitation on coronary and cerebral perfusion pressures in a porcine model of cardiac arrest.Resuscitation. 2005; 64:363–372. doi: 10.1016/j.resuscitation.2004.10.009CrossrefMedlineGoogle Scholar
41. Zuercher M, Hilwig RW, Ranger-Moore J, Nysaether J, Nadkarni VM, Berg MD, Kern KB, Sutton R, Berg RA. Leaning during chest compressions impairs cardiac output and left ventricular myocardial blood flow in piglet cardiac arrest.Crit Care Med. 2010; 38:1141–1146. doi: 10.1097/CCM.0b013e3181ce1fe2CrossrefMedlineGoogle Scholar
42. Johnson BV, Johnson B, Coult J, Fahrenbruch C, Blackwood J, Sherman L, Kudenchuk P, Sayre M, Rea T. Cardiopulmonary resuscitation duty cycle in out-of-hospital cardiac arrest.Resuscitation. 2015; 87:86–90. doi: 10.1016/j.resuscitation.2014.11.008CrossrefMedlineGoogle Scholar
43. Wolfe H, Morgan RW, Donoghue A, Niles DE, Kudenchuk P, Berg RA, Nadkarni VM, Sutton RM. Quantitative analysis of duty cycle in pediatric and adolescent in-hospital cardiac arrest.Resuscitation. 2016; 106:65–69. doi: 10.1016/j.resuscitation.2016.06.003CrossrefMedlineGoogle Scholar
44. Berg RA, Hemphill R, Abella BS, Aufderheide TP, Cave DM, Hazinski MF, Lerner EB, Rea TD, Sayre MR, Swor RA. Part 5: adult basic life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S685–S705. doi: 10.1161/CIRCULATIONAHA.110.970939LinkGoogle Scholar
45. Goharani R, Vahedian-Azimi A, Farzanegan B, Bashar FR, Hajiesmaeili M, Shojaei S, Madani SJ, Gohari-Moghaddam K, Hatamian S, Mosavinasab SMM, Khoshfetrat M, Khabiri Khatir MA, Miller ACMORZAK Collaborative. Real-time compression feedback for patients with in-hospital cardiac arrest: a multi-center randomized controlled clinical trial.J Intensive Care. 2019; 7:5. doi: 10.1186/s40560-019-0357-5CrossrefMedlineGoogle Scholar
46. Sutton RM, French B, Meaney PA, Topjian AA, Parshuram CS, Edelson DP, Schexnayder S, Abella BS, Merchant RM, Bembea M, Berg RA, Nadkarni VMAmerican Heart Association’s Get With The Guidelines–Resuscitation Investigators. Physiologic monitoring of CPR quality during adult cardiac arrest: A propensity-matched cohort study.Resuscitation. 2016; 106:76–82. doi: 10.1016/j.resuscitation.2016.06.018CrossrefMedlineGoogle Scholar
47. Sheak KR, Wiebe DJ, Leary M, Babaeizadeh S, Yuen TC, Zive D, Owens PC, Edelson DP, Daya MR, Idris AH, Abella BS. Quantitative relationship between end-tidal carbon dioxide and CPR quality during both in-hospital and out-of-hospital cardiac arrest.Resuscitation. 2015; 89:149–154. doi: 10.1016/j.resuscitation.2015.01.026CrossrefMedlineGoogle Scholar
48. Paiva EF, Paxton JH, O’Neil BJ. The use of end-tidal carbon dioxide (ETCO2) measurement to guide management of cardiac arrest: A systematic review.Resuscitation. 2018; 123:1–7. doi: 10.1016/j.resuscitation.2017.12.003CrossrefMedlineGoogle Scholar
49. Berg KM, Soar J, Andersen LW, Böttiger BW, Cacciola S, Callaway CW, Couper K, Cronberg T, D’Arrigo S, Deakin CD, et al.; on behalf of the Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S92–S139. doi: 10.1161/CIR.0000000000000893LinkGoogle Scholar

Ventilation and Compression-to-Ventilation Ratio

Introduction

The provision of rescue breaths for apneic patients with a pulse is essential. The relative contribution of assisted ventilation for patients in cardiac arrest is more controversial.

There is concern that delivery of chest compressions without assisted ventilation for prolonged periods could be less effective than conventional CPR (compressions plus breaths) because the arterial oxygen content will decrease as CPR duration increases. This concern is especially pertinent in the setting of asphyxial cardiac arrest. Much of the published research involves patients whose arrests were presumed to be of cardiac origin and in settings with short EMS response times. It is likely that a time threshold exists beyond which the absence of ventilation may be harmful, and the generalizability of the findings to all settings must be considered with caution.1

Once an advanced airway has been placed, delivering continuous chest compressions increases the compression fraction but makes it more difficult to deliver adequate ventilation. Simultaneous compressions and ventilation should be avoided,2 but delivery of chest compressions without pausing for ventilation seems a reasonable option.3 The use of SGAs adds to this complexity because efficiency of ventilation during cardiac arrest may be worse than when using an endotracheal tube, though this has not been borne out in recently published RCTs.4,5

Recommendation-Specific Supportive Text

Studies have reported that enough tidal volume to cause visible chest rise, or approximately 500 to 600 mL, provides adequate ventilation while minimizing the risk of overdistension or gastric insufflation.6–9
Both mouth-to-mouth rescue breathing and bag-mask ventilation provide oxygen and ventilation to the victim.10 To provide mouth-to-mouth rescue breaths, open the victim’s airway, pinch the victim’s nose, create an airtight mouth-to-mouth seal, and provide a breath.
Taking a regular rather than a deep breath prevents the rescuer from getting dizzy or light-headed and prevents overinflation of the victim’s lungs. The most common cause of ventilation difficulty is an improperly opened airway,11 so if the victim’s chest does not rise with the first rescue breath, reposition the head by performing the head tilt–chin lift again and then give the second rescue breath. The recommendation for 1 second is to keep the pauses in CPR as brief as possible.
Excessive ventilation is unnecessary and can cause gastric inflation, regurgitation, and aspiration.12,14 Excessive ventilation can also be harmful by increasing intrathoracic pressure, decreasing venous return to the heart, and diminishing cardiac output and survival.14

This topic last received formal evidence review in 2010.15

Recommendation-Specific Supportive Text

Mouth-to-nose ventilation may be necessary if ventilation through the victim’s mouth is impossible because of trauma, positioning, or difficulty obtaining a seal. A case series suggests that mouth-to-nose ventilation in adults is feasible, safe, and effective.16
Effective ventilation of the patient with a tracheal stoma may require ventilation through the stoma, either by using mouth-to-stoma rescue breaths or by use of a bag-mask technique that creates a tight seal over the stoma with a round, pediatric face mask. There is no published evidence on the safety, effectiveness, or feasibility of mouth-to-stoma ventilation. One study of patients with laryngectomies showed that a pediatric face mask created a better peristomal seal than a standard ventilation mask.17

This topic last received formal evidence review in 2010.15

Recommendation-Specific Supportive Text

Since the last review in 2010 of rescue breathing in adult patients, there has been no evidence to support a change in previous recommendations. A study in critically ill patients who required ventilatory support found that bag-mask ventilation at a rate of 10 breaths per minute decreased hypoxic events before intubation.18

This topic last received formal evidence review in 2010.15

Recommendation-Specific Supportive Text

A 2017 ILCOR systematic review found that a ratio of 30 compressions to 2 breaths was associated with better survival than alternate ratios, a recommendation that was reaffirmed by the AHA in 2018.19,20 Most of these studies examined “bundles” of cardiac arrest care, making it impossible to know if the improvement was due to the compression-to-ventilation ratio itself. This ratio is supported by a large OHCA RCT in which the use of 30:2 (with a pause in compressions of less than 5 seconds) was at least as good as continuous chest compressions.21
In a large trial, survival and survival with favorable neurological outcome were similar in a group of patients with OHCA treated with ventilations at a rate of 10/min without pausing compressions, compared with a 30:2 ratio before intubation.21
A 2017 systematic review identified 1 observational human study and 10 animal studies comparing different ventilation rates after advanced airway placement.22 No clear benefit from a rate of 10 was identified, but no other rate was found to be superior. A 2017 ILCOR systematic review did not identify any new evidence to alter this recommendation, which was reiterated in the “2017 AHA Focused Update on Adult BLS and CPR Quality: An Update to the AHA Guidelines for CPR and Emergency Cardiovascular Care.”19,20
A 2017 ILCOR systematic review concluded that although the evidence from observational studies supporting the use of bundles of care including minimally interrupted chest compressions was of very low certainty (primarily unadjusted results), systems already using such an approach may continue to do so.19

These recommendations are supported by the 2017 focused update on adult BLS and CPR quality guidelines. 20

References

1. Kleinman ME, Brennan EE, Goldberger ZD, Swor RA, Terry M, Bobrow BJ, Gazmuri RJ, Travers AH, Rea T. Part 5: adult basic life support and cardiopulmonary resuscitation quality: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S414–S435. doi: 10.1161/CIR.0000000000000259LinkGoogle Scholar
2. Krischer JP, Fine EG, Weisfeldt ML, Guerci AD, Nagel E, Chandra N. Comparison of prehospital conventional and simultaneous compression-ventilation cardiopulmonary resuscitation.Crit Care Med. 1989; 17:1263–1269. doi: 10.1097/00003246-198912000-00005CrossrefMedlineGoogle Scholar
3. Jabre P, Penaloza A, Pinero D, Duchateau FX, Borron SW, Javaudin F, Richard O, de Longueville D, Bouilleau G, Devaud ML, Heidet M, Lejeune C, Fauroux S, Greingor JL, Manara A, Hubert JC, Guihard B, Vermylen O, Lievens P, Auffret Y, Maisondieu C, Huet S, Claessens B, Lapostolle F, Javaud N, Reuter PG, Baker E, Vicaut E, Adnet F. Effect of Bag-Mask Ventilation vs Endotracheal Intubation During Cardiopulmonary Resuscitation on Neurological Outcome After Out-of-Hospital Cardiorespiratory Arrest: A Randomized Clinical Trial.JAMA. 2018; 319:779–787. doi: 10.1001/jama.2018.0156CrossrefMedlineGoogle Scholar
4. Benger JR, Kirby K, Black S, Brett SJ, Clout M, Lazaroo MJ, Nolan JP, Reeves BC, Robinson M, Scott LJ, Smartt H, South A, Stokes EA, Taylor J, Thomas M, Voss S, Wordsworth S, Rogers CA. Effect of a Strategy of a Supraglottic Airway Device vs Tracheal Intubation During Out-of-Hospital Cardiac Arrest on Functional Outcome: The AIRWAYS-2 Randomized Clinical Trial.JAMA. 2018; 320:779–791. doi: 10.1001/jama.2018.11597CrossrefMedlineGoogle Scholar
5. Wang HE, Schmicker RH, Daya MR, Stephens SW, Idris AH, Carlson JN, Colella MR, Herren H, Hansen M, Richmond NJ, Puyana JCJ, Aufderheide TP, Gray RE, Gray PC, Verkest M, Owens PC, Brienza AM, Sternig KJ, May SJ, Sopko GR, Weisfeldt ML, Nichol G. Effect of a Strategy of Initial Laryngeal Tube Insertion vs Endotracheal Intubation on 72-Hour Survival in Adults With Out-of-Hospital Cardiac Arrest: A Randomized Clinical Trial.JAMA. 2018; 320:769–778. doi: 10.1001/jama.2018.7044CrossrefMedlineGoogle Scholar
6. Wenzel V, Keller C, Idris AH, Dörges V, Lindner KH, Brimacombe JR. Effects of smaller tidal volumes during basic life support ventilation in patients with respiratory arrest: good ventilation, less risk?Resuscitation. 1999; 43:25–29. doi: 10.1016/s0300-9572(99)00118-5CrossrefMedlineGoogle Scholar
7. Baskett P, Nolan J, Parr M. Tidal volumes which are perceived to be adequate for resuscitation.Resuscitation. 1996; 31:231–234. doi: 10.1016/0300-9572(96)00994-xCrossrefMedlineGoogle Scholar
8. Dörges V, Ocker H, Hagelberg S, Wenzel V, Idris AH, Schmucker P. Smaller tidal volumes with room-air are not sufficient to ensure adequate oxygenation during bag-valve-mask ventilation.Resuscitation. 2000; 44:37–41. doi: 10.1016/s0300-9572(99)00161-6CrossrefMedlineGoogle Scholar
9. Dörges V, Ocker H, Hagelberg S, Wenzel V, Schmucker P. Optimisation of tidal volumes given with self-inflatable bags without additional oxygen.Resuscitation. 2000; 43:195–199. doi: 10.1016/s0300-9572(99)00148-3CrossrefMedlineGoogle Scholar
10. Wenzel V, Idris AH, Banner MJ, Fuerst RS, Tucker KJ. The composition of gas given by mouth-to-mouth ventilation during CPR.Chest. 1994; 106:1806–1810. doi: 10.1378/chest.106.6.1806CrossrefMedlineGoogle Scholar
11. Safar P, Escarraga LA, Chang F. Upper airway obstruction in the unconscious patient.J Appl Physiol. 1959; 14:760–764. doi: 10.1152/jappl.1959.14.5.760CrossrefMedlineGoogle Scholar
12. Berg MD, Idris AH, Berg RA. Severe ventilatory compromise due to gastric distention during pediatric cardiopulmonary resuscitation.Resuscitation. 1998; 36:71–73. doi: 10.1016/s0300-9572(97)00077-4CrossrefMedlineGoogle Scholar
13. Deleted in proof.Google Scholar
14. Aufderheide TP, Sigurdsson G, Pirrallo RG, Yannopoulos D, McKnite S, von Briesen C, Sparks CW, Conrad CJ, Provo TA, Lurie KG. Hyperventilation-induced hypotension during cardiopulmonary resuscitation.Circulation. 2004; 109:1960–1965. doi: 10.1161/01.CIR.0000126594.79136.61LinkGoogle Scholar
15. Berg RA, Hemphill R, Abella BS, Aufderheide TP, Cave DM, Hazinski MF, Lerner EB, Rea TD, Sayre MR, Swor RA. Part 5: adult basic life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S685–S705. doi: 10.1161/CIRCULATIONAHA.110.970939LinkGoogle Scholar
16. Ruben H. The immediate treatment of respiratory failure.Br J Anaesth. 1964; 36:542–549. doi: 10.1093/bja/36.9.542CrossrefMedlineGoogle Scholar
17. Bhalla RK, Corrigan A, Roland NJ. Comparison of two face masks used to deliver early ventilation to laryngectomized patients.Ear Nose Throat J. 2004; 83:414, 416.CrossrefMedlineGoogle Scholar
18. Casey JD, Janz DR, Russell DW, Vonderhaar DJ, Joffe AM, Dischert KM, Brown RM, Zouk AN, Gulati S, Heideman BE, et al.; and the PreVent Investigators and the Pragmatic Critical Care Research Group. Bag-mask ventilation during tracheal intubation of critically ill adults.N Engl J Med. 2019; 380:811–821. doi: 10.1056/NEJMoa1812405CrossrefMedlineGoogle Scholar
19. Ashoor HM, Lillie E, Zarin W, Pham B, Khan PA, Nincic V, Yazdi F, Ghassemi M, Ivory J, Cardoso R, Perkins GD, de Caen AR, Tricco ACILCOR Basic Life Support Task Force. Effectiveness of different compression-to-ventilation methods for cardiopulmonary resuscitation: A systematic review.Resuscitation. 2017; 118:112–125. doi: 10.1016/j.resuscitation.2017.05.032CrossrefMedlineGoogle Scholar
20. Kleinman ME, Goldberger ZD, Rea T, Swor RA, Bobrow BJ, Brennan EE, Terry M, Hemphill R, Gazmuri RJ, Hazinski MF, Travers AH. 2017 American Heart Association Focused Update on Adult Basic Life Support and Cardiopulmonary Resuscitation Quality: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2018; 137:e7–e13. doi: 10.1161/CIR.0000000000000539LinkGoogle Scholar
21. Nichol G, Leroux B, Wang H, Callaway CW, Sopko G, Weisfeldt M, Stiell I, Morrison LJ, Aufderheide TP, Cheskes S, Christenson J, Kudenchuk P, Vaillancourt C, Rea TD, Idris AH, Colella R, Isaacs M, Straight R, Stephens S, Richardson J, Condle J, Schmicker RH, Egan D, May S, Ornato JPROC Investigators. Trial of Continuous or Interrupted Chest Compressions during CPR.N Engl J Med. 2015; 373:2203–2214. doi: 10.1056/NEJMoa1509139CrossrefMedlineGoogle Scholar
22. Vissers G, Soar J, Monsieurs KG. Ventilation rate in adults with a tracheal tube during cardiopulmonary resuscitation: A systematic review.Resuscitation. 2017; 119:5–12. doi: 10.1016/j.resuscitation.2017.07.018CrossrefMedlineGoogle Scholar

Defibrillation

Introduction

Along with CPR, early defibrillation is critical to survival when sudden cardiac arrest is caused by VF or pulseless VT (pVT).1,2 Defibrillation is most successful when administered as soon as possible after onset of VF/VT and a reasonable immediate treatment when the interval from onset to shock is very brief. Conversely, when VF/VT is more protracted, depletion of the heart’s energy reserves can compromise the efficacy of defibrillation unless replenished by a prescribed period of CPR before the rhythm analysis. Minimizing disruptions in CPR surrounding shock administration is also a high priority.

Currently marketed defibrillators use proprietary shock waveforms that differ in their electric characteristics. These deliver different peak currents even at the same programmed energy setting, making comparisons of shock efficacy between devices challenging. Energy setting specifications for cardioversion also differ between defibrillators. Refer to the device manufacturer’s recommended energy for a particular waveform.

Technologies are now in development to diagnose the underlying cardiac rhythm during ongoing CPR and to derive prognostic information from the ventricular waveform that can help guide patient management. These still require further testing and validation before routine use.

Recommendation-Specific Supportive Text

Emergent electric cardioversion and defibrillation are highly effective at terminating VF/VT and other tachyarrhythmias. No shock waveform has distinguished itself as achieving a consistently higher rate of ROSC or survival. Biphasic and monophasic shock waveforms are likely equivalent in their clinical outcome efficacy.3
No shock waveform has proved to be superior in improving the rate of ROSC or survival. However, biphasic waveform defibrillators (which deliver pulses of opposite polarity) expose patients to a much lower peak electric current with equivalent or greater efficacy for terminating atrial4 and ventricular tachyarrhythmias than monophasic (single polarity) defibrillators do.5–10,13 These potential differences in safety and efficacy favor preferential use of a biphasic defibrillator, when available. Biphasic defibrillators have largely replaced monophasic shock defibrillators, which are no longer manufactured.
The rationale for a single shock strategy, in which CPR is immediately resumed after the first shock rather than after serial “stacked” shocks (if required) is based on a number of considerations. These include the high success rate of the first shock with biphasic waveforms (lessening the need for successive shocks), the declining success of immediate second and third serial shocks when the first shock has failed,14 and the protracted interruption in CPR required for a series of stacked shocks. A single shock strategy results in shorter interruptions in CPR and a significantly improved survival to hospital admission and discharge (although not 1-year survival) compared with serial “stacked” shocks.15–17 It is unknown whether stacked shocks or single shocks are more effective in settings of a monitored witnessed arrest (for example, see the section on Cardiac Arrest After Cardiac Surgery).
Regardless of waveform, successful defibrillation requires that a shock be of sufficient energy to terminate VF/VT. In cases where the initial shock fails to terminate VF/VT, subsequent shocks may be effective when repeated at the same or an escalating energy setting.18,19 An optimal energy setting for first or subsequent biphasic defibrillation, whether fixed or escalating, has not been identified, and its selection can be based on the defibrillator’s manufacturer specification.
There is no conclusive evidence of superiority of one biphasic shock waveform over another for defibrillation.20 Given the variability in electric characteristics between proprietary biphasic waveforms, it is reasonable to use the energy settings specified by the manufacturer for that specific device. If a manufacturer’s specified energy setting for defibrillation is not known at the time of intended use, the maximum dose setting for that device may be considered.
Commercially available defibrillators either provide fixed energy settings or allow for escalating energy settings; both approaches are highly effective in terminating VF/VT.18 An optimal energy setting for first or subsequent biphasic defibrillation, whether fixed or escalating, has not been identified and is best deferred to the defibrillator’s manufacturer. A randomized trial comparing fixed 150 J biphasic defibrillation with escalating higher shock energies (200–300–360 J) observed similar rates of successful defibrillation and conversion to an organized rhythm after the first shock. However, among patients who required multiple shocks, escalating shock energy resulted in a significantly higher rate of conversion to an organized rhythm, although overall survival did not differ between the 2 treatment groups.19 When VF/VT is refractory to the first shock, an equivalent or higher energy setting than the first shock may be considered. As yet, there is no conclusive evidence of superiority of one biphasic shock waveform over another for defibrillation.20 It is reasonable to use the energy settings specified by the manufacturer for that specific device. If a manufacturer’s specified energy setting for defibrillation is not known at the time of intended use, the maximum dose setting for that device may be considered.

Recommendations 1, 2, and 6 last received formal evidence review in 2015.21 Recommendations 3, 4, and 5 are supported by the 2020 CoSTR for BLS.22

Recommendation-Specific Supportive Text

Anterolateral, anteroposterior, anterior-left infrascapular, and anterior-right infrascapular electrode placements are comparably effective for treating supraventricular and ventricular arrhythmias.24–28 A larger pad/paddle size (within the limits of 8–12 cm in diameter) lowers transthoracic impedance.29,30 Self-adhesive pads have largely replaced defibrillation paddles in clinical practice. Before pad placement, remove all clothing and jewelry from the chest.

This recommendation is supported by a 2020 ILCOR scoping review, which found no new information to update the 2010 recommendations.22,31

Recommendation-Specific Supportive Text

AEDs are highly accurate in their detection of shockable arrhythmias but require a pause in CPR for automated rhythm analysis.32,33 Manual defibrillation can result in a shorter hands-off period for rhythm confirmation in operators with a sufficient skill for rapid and reliable rhythm interpretation.34,35

This recommendation is supported by a 2020 ILCOR scoping review,22 which found no new information to update the 2010 recommendations.31

Recommendation-Specific Supportive Text

CPR is the single-most important intervention for a patient in cardiac arrest and should be provided until a defibrillator is applied to minimize interruptions in compressions.
When VF/VT has been present for more than a few minutes, myocardial reserves of oxygen and other energy substrates are rapidly depleted. If replenished by a period of CPR before shock, defibrillation success improves significantly.1,2,36,37 Because no differences in outcome were seen in studies comparing short (typically approximately about 30 seconds) with prolonged (up to 3 minutes) periods of CPR preceding the initial rhythm analysis, a brief period of CPR while the defibrillator is readied for use may be sufficient in unmonitored cardiac arrest.38–40 Even in monitored arrests, it can take time to attach pads, power on a defibrillator, and charge the capacitor before shock delivery, during which there is good reason to administer CPR.
Early defibrillation improves outcome from cardiac arrest.41–43 When VF is of short duration, myocardial reserves of oxygen and other energy substrates are likely to remain intact. During this early electric phase, the rhythm is most responsive to defibrillation.44,45 Thus, if the onset of VF is monitored or witnessed with a defibrillator that is already applied, or to which there is immediate access, it is reasonable to administer a shock as soon as possible. Interim CPR should be provided if there is any delay in obtaining or readying the defibrillator for use.

Recommendations 1 and 2 are supported by the 2020 CoSTR for BLS.22 Recommendation 3 last received formal evidence review in 2010.46

Recommendation-Specific Supportive Text

There are differing approaches to charging a manual defibrillator during resuscitation. It is not uncommon for chest compressions to be paused for rhythm detection and continue to be withheld while the defibrillator is charged and prepared for shock delivery. This approach results in a protracted hands-off period before shock. Precharging the defibrillator during ongoing chest compressions shortens the hands-off chest time surrounding defibrillation, without evidence of harm.47 Although no study has directly evaluated the effect of precharging itself on cardiac arrest outcome, shorter perishock pauses (which could result from such a strategy) are associated with improved survival from VF arrest.48 Two approaches are reasonable: either charging the defibrillator before a rhythm check or resuming compressions briefly after a rhythm check while the defibrillator charges. Either approach may reduce no-flow time.49,50

This recommendation is supported by the 2020 CoSTR for ALS.51

Recommendation-Specific Supportive Text

Immediate resumption of chest compressions after shock results in a shorter perishock pause and improves the overall hands-on time (chest compression fraction) during resuscitation, which is associated with improved survival from VF arrest.16,48 Even when successful, defibrillation is often followed by a variable (and sometimes protracted) period of asystole or pulseless electrical activity, during which providing CPR while awaiting a return of rhythm and pulse is advisable. Whether resumption of CPR immediately after shock might reinduce VF/VT is controversial.52–54 This potential concern has not been borne out by any evidence of worsened survival from such a strategy. Should there be physiological evidence of return of circulation such as an arterial waveform or abrupt rise in ETCO2 after shock, a pause of chest compressions briefly for confirmatory rhythm analysis may be warranted.

This recommendation is supported by the 2020 CoSTR for BLS.22

Recommendation-Specific Supportive Text

CPR obscures interpretation of the underlying rhythm because of the artifact created by chest compressions on the ECG. This makes it difficult to plan the next step of care and can potentially delay or even misdirect drug therapies if given empirically (blindly) based on the patient’s presumed, but not actual, underlying rhythm. Time taken for rhythm analysis also disrupts CPR. Artifact-filtering and other innovative techniques to disclose the underlying rhythm beneath ongoing CPR can surmount these challenges and minimize interruptions in chest compressions while offering a diagnostic advantage to better direct therapies.55–60 Despite the theoretical advantages, no study has evaluated these technologies in a real-time clinical setting or validated their clinical effectiveness compared to current resuscitation strategies. At present, filtering algorithms are strictly used for visual (manual) rhythm interpretation and not for automated VF/VT rhythm detection in AEDs during ongoing CPR. This added potential application remains untested. Recognizing the need for further clinical research, a 2020 ILCOR systematic review recommended against adopting artifact-filtering algorithms for rhythm analysis during CPR at the present time.51 The writing group also endorses the need for further investigation and clinical validation before these technologies are adopted into clinical practice.
The electric characteristics of the VF waveform are known to change over time.61 VF waveform analysis may be of value in predicting the success of defibrillation or other therapies during the course of resuscitation.62–64 The prospect of basing therapies on a prognostic analysis of the VF waveform in real-time is an exciting and developing avenue of new research. However, the validity, reliability, and clinical effectiveness of an approach that prompts or withholds shock or other therapies on the basis of predictive analyses is currently uncertain. The only prospective clinical trial comparing a standard shock-first protocol with a waveform analysis-guided shock algorithm observed no differences in outcome.65 The consensus of the writing group is that there is currently insufficient evidence to support the routine use of waveform analysis to guide resuscitation care, but it is an area in which further research with clinical validation is needed and encouraged.

Recommendation 1 is supported by the 2020 CoSTR for ALS.51 Recommendation 2 is supported by a 2020 ILCOR evidence update,51 which found no new information to update the 2010 recommendations.66

Recommendation-Specific Supportive Text

There is limited evidence examining double sequential defibrillation in clinical practice. A number of case reports have shown good outcomes in patients who received double sequential defibrillation. However, these case reports are subject to publication bias and should not be used to support its effectiveness.67 A handful of observational studies demonstrated no difference in outcomes (ROSC, survival, neurological outcome) with the use of double sequential defibrillation compared with standard defibrillation.68–71 These studies should also be interpreted with caution, because the use of double sequential defibrillation was not protocolized and was often used late in the resuscitation after standard resuscitation was unsuccessful. Published reports also do not distinguish the application of double sequential defibrillation for truly shock-refractory (incessant) VF versus VF that recurs during the period of CPR after a successful shock, which is the more common clinical scenario.3,7 A 2020 ILCOR systematic review found no evidence to support double sequential defibrillation and recommended against its routine use compared with standard defibrillation.51 A recent pilot RCT (not included in the systematic review) of 152 patients who remained in VF after at least 3 shocks found higher rates of VF termination and ROSC with double sequential defibrillation or alternative defibrillator pad placement compared with standard defibrillation but was not powered for these outcomes and did not report patient survival.72 A number of unanswered questions remain about double sequential defibrillation, including intershock timing, pad positioning, technique, and the possibility of harm with increased energy and defibrillator damage.73,74 It is premature for double sequential defibrillation to be incorporated into routine clinical practice given the lack of evidence. Its usefulness should be explored in the context of clinical trials. An ongoing RCT (NCT04080986) may provide answers to some of these questions.

This recommendation is supported by the 2020 CoSTR for ALS.51

References

1. Larsen MP, Eisenberg MS, Cummins RO, Hallstrom AP. Predicting survival from out-of-hospital cardiac arrest: a graphic model.Ann Emerg Med. 1993; 22:1652–1658. doi: 10.1016/s0196-0644(05)81302-2CrossrefMedlineGoogle Scholar
2. Swor RA, Jackson RE, Cynar M, Sadler E, Basse E, Boji B, Rivera-Rivera EJ, Maher A, Grubb W, Jacobson R. Bystander CPR, ventricular fibrillation, and survival in witnessed, unmonitored out-of-hospital cardiac arrest.Ann Emerg Med. 1995; 25:780–784. doi: 10.1016/s0196-0644(95)70207-5CrossrefMedlineGoogle Scholar
3. Kudenchuk PJ, Cobb LA, Copass MK, Olsufka M, Maynard C, Nichol G. Transthoracic incremental monophasic versus biphasic defibrillation by emergency responders (TIMBER): a randomized comparison of monophasic with biphasic waveform ascending energy defibrillation for the resuscitation of out-of-hospital cardiac arrest due to ventricular fibrillation.Circulation. 2006; 114:2010–2018. doi: 10.1161/CIRCULATIONAHA.106.636506LinkGoogle Scholar
4. Inácio JF, da Rosa Mdos S, Shah J, Rosário J, Vissoci JR, Manica AL, Rodrigues CG. Monophasic and biphasic shock for transthoracic conversion of atrial fibrillation: systematic review and network meta-analysis.Resuscitation. 2016; 100:66–75. doi: 10.1016/j.resuscitation.2015.12.009CrossrefMedlineGoogle Scholar
5. Higgins SL, O’Grady SG, Banville I, Chapman FW, Schmitt PW, Lank P, Walker RG, Ilina M. Efficacy of lower-energy biphasic shocks for transthoracic defibrillation: a follow-up clinical study.Prehosp Emerg Care. 2004; 8:262–267. doi: 10.1016/j.prehos.2004.02.002MedlineGoogle Scholar
6. Didon JP, Fontaine G, White RD, Jekova I, Schmid JJ, Cansell A. Clinical experience with a low-energy pulsed biphasic waveform in out-of-hospital cardiac arrest.Resuscitation. 2008; 76:350–353. doi: 10.1016/j.resuscitation.2007.08.010CrossrefMedlineGoogle Scholar
7. van Alem AP, Chapman FW, Lank P, Hart AA, Koster RW. A prospective, randomised and blinded comparison of first shock success of monophasic and biphasic waveforms in out-of-hospital cardiac arrest.Resuscitation. 2003; 58:17–24. doi: 10.1016/s0300-9572(03)00106-0CrossrefMedlineGoogle Scholar
8. Morrison LJ, Dorian P, Long J, Vermeulen M, Schwartz B, Sawadsky B, Frank J, Cameron B, Burgess R, Shield J, Bagley P, Mausz V, Brewer JE, Lerman BBSteering Committee, Central Validation Committee, Safety and Efficacy Committee. Out-of-hospital cardiac arrest rectilinear biphasic to monophasic damped sine defibrillation waveforms with advanced life support intervention trial (ORBIT).Resuscitation. 2005; 66:149–157. doi: 10.1016/j.resuscitation.2004.11.031CrossrefMedlineGoogle Scholar
9. Schneider T, Martens PR, Paschen H, Kuisma M, Wolcke B, Gliner BE, Russell JK, Weaver WD, Bossaert L, Chamberlain D. Multicenter, randomized, controlled trial of 150-J biphasic shocks compared with 200- to 360-J monophasic shocks in the resuscitation of out-of-hospital cardiac arrest victims. Optimized Response to Cardiac Arrest (ORCA) Investigators.Circulation. 2000; 102:1780–1787. doi: 10.1161/01.cir.102.15.1780LinkGoogle Scholar
10. White RD, Hankins DG, Bugliosi TF. Seven years’ experience with early defibrillation by police and paramedics in an emergency medical services system.Resuscitation. 1998; 39:145–151. doi: 10.1016/s0300-9572(98)00135-xCrossrefMedlineGoogle Scholar
11. Deleted in proof.Google Scholar
12. Deleted in proof.Google Scholar
13. Leng CT, Paradis NA, Calkins H, Berger RD, Lardo AC, Rent KC, Halperin HR. Resuscitation after prolonged ventricular fibrillation with use of monophasic and biphasic waveform pulses for external defibrillation.Circulation. 2000; 101:2968–2974. doi: 10.1161/01.cir.101.25.2968LinkGoogle Scholar
14. Koster RW, Walker RG, Chapman FW. Recurrent ventricular fibrillation during advanced life support care of patients with prehospital cardiac arrest.Resuscitation. 2008; 78:252–257. doi: 10.1016/j.resuscitation.2008.03.231CrossrefMedlineGoogle Scholar
15. Bobrow BJ, Clark LL, Ewy GA, Chikani V, Sanders AB, Berg RA, Richman PB, Kern KB. Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest.JAMA. 2008; 299:1158–1165. doi: 10.1001/jama.299.10.1158CrossrefMedlineGoogle Scholar
16. Rea TD, Helbock M, Perry S, Garcia M, Cloyd D, Becker L, Eisenberg M. Increasing use of cardiopulmonary resuscitation during out-of-hospital ventricular fibrillation arrest: survival implications of guideline changes.Circulation. 2006; 114:2760–2765. doi: 10.1161/CIRCULATIONAHA.106.654715LinkGoogle Scholar
17. Jost D, Degrange H, Verret C, Hersan O, Banville IL, Chapman FW, Lank P, Petit JL, Fuilla C, Migliani R, et al.; and the DEFI 2005 Work Group. DEFI 2005: a randomized controlled trial of the effect of automated external defibrillator cardiopulmonary resuscitation protocol on outcome from out-of-hospital cardiac arrest.Circulation. 2010; 121:1614–1622. doi: 10.1161/CIRCULATIONAHA.109.878389LinkGoogle Scholar
18. Hess EP, Russell JK, Liu PY, White RD. A high peak current 150-J fixed-energy defibrillation protocol treats recurrent ventricular fibrillation (VF) as effectively as initial VF.Resuscitation. 2008; 79:28–33. doi: 10.1016/j.resuscitation.2008.04.028CrossrefMedlineGoogle Scholar
19. Stiell IG, Walker RG, Nesbitt LP, Chapman FW, Cousineau D, Christenson J, Bradford P, Sookram S, Berringer R, Lank P, Wells GA. BIPHASIC Trial: a randomized comparison of fixed lower versus escalating higher energy levels for defibrillation in out-of-hospital cardiac arrest.Circulation. 2007; 115:1511–1517. doi: 10.1161/CIRCULATIONAHA.106.648204LinkGoogle Scholar
20. Morrison LJ, Henry RM, Ku V, Nolan JP, Morley P, Deakin CD. Single-shock defibrillation success in adult cardiac arrest: a systematic review.Resuscitation. 2013; 84:1480–1486. doi: 10.1016/j.resuscitation.2013.07.008CrossrefMedlineGoogle Scholar
21. Link MS, Berkow LC, Kudenchuk PJ, Halperin HR, Hess EP, Moitra VK, Neumar RW, O’Neil BJ, Paxton JH, Silvers SM, et al.. Part 7: adult advanced cardiovascular life support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S444–S464. doi: 10.1161/CIR.0000000000000261LinkGoogle Scholar
22. Olasveengen TM, Mancini ME, Perkins GD, Avis S, Brooks S, Castrén M, Chung SP, Considine J, Couper K, Escalante R, et al.; on behalf of the Adult Basic Life Support Collaborators. Adult basic life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S41–S91. doi: 10.1161/CIR.0000000000000892LinkGoogle Scholar
23. Deleted in proof.Google Scholar
24. Boodhoo L, Mitchell AR, Bordoli G, Lloyd G, Patel N, Sulke N. DC cardioversion of persistent atrial fibrillation: a comparison of two protocols.Int J Cardiol. 2007; 114:16–21. doi: 10.1016/j.ijcard.2005.11.108CrossrefMedlineGoogle Scholar
25. Brazdzionyte J, Babarskiene RM, Stanaitiene G. Anterior-posterior versus anterior-lateral electrode position for biphasic cardioversion of atrial fibrillation.Medicina (Kaunas). 2006; 42:994–998.MedlineGoogle Scholar
26. Chen CJ, Guo GB. External cardioversion in patients with persistent atrial fibrillation: a reappraisal of the effects of electrode pad position and transthoracic impedance on cardioversion success.Jpn Heart J. 2003; 44:921–932. doi: 10.1536/jhj.44.921CrossrefMedlineGoogle Scholar
27. Stanaitiene G, Babarskiene RM. [Impact of electrical shock waveform and paddle positions on efficacy of direct current cardioversion for atrial fibrillation].Medicina (Kaunas). 2008; 44:665–672.CrossrefMedlineGoogle Scholar
28. Krasteva V, Matveev M, Mudrov N, Prokopova R. Transthoracic impedance study with large self-adhesive electrodes in two conventional positions for defibrillation.Physiol Meas. 2006; 27:1009–1022. doi: 10.1088/0967-3334/27/10/007CrossrefMedlineGoogle Scholar
29. Kerber RE, Grayzel J, Hoyt R, Marcus M, Kennedy J. Transthoracic resistance in human defibrillation. Influence of body weight, chest size, serial shocks, paddle size and paddle contact pressure.Circulation. 1981; 63:676–682. doi: 10.1161/01.cir.63.3.676LinkGoogle Scholar
30. Connell PN, Ewy GA, Dahl CF, Ewy MD. Transthoracic impedance to defibrillator discharge. Effect of electrode size and electrode-chest wall interface.J Electrocardiol. 1973; 6:313–31M. doi: 10.1016/s0022-0736(73)80053-6CrossrefMedlineGoogle Scholar
31. Jacobs I, Sunde K, Deakin CD, Hazinski MF, Kerber RE, Koster RW, Morrison LJ, Nolan JP, Sayre MRDefibrillation Chapter C. Part 6: Defibrillation: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2010; 122(Suppl 2):S325–337. doi: 10.1161/CIRCULATIONAHA.110.971010LinkGoogle Scholar
32. Loma-Osorio P, Nunez M, Aboal J, Bosch D, Batlle P, Ruiz de Morales E, Ramos R, Brugada J, Onaga H, Morales A, et al.. The Girona Territori Cardioprotegit Project: performance evaluation of public defibrillators.Rev Esp Cardiol (Engl Ed). 2018; 71:79–85. doi: 10.1016/j.rec.2017.04.011CrossrefMedlineGoogle Scholar
33. Zijlstra JA, Bekkers LE, Hulleman M, Beesems SG, Koster RW. Automated external defibrillator and operator performance in out-of-hospital cardiac arrest.Resuscitation. 2017; 118:140–146. doi: 10.1016/j.resuscitation.2017.05.017CrossrefMedlineGoogle Scholar
34. Kramer-Johansen J, Edelson DP, Abella BS, Becker LB, Wik L, Steen PA. Pauses in chest compression and inappropriate shocks: a comparison of manual and semi-automatic defibrillation attempts.Resuscitation. 2007; 73:212–220. doi: 10.1016/j.resuscitation.2006.09.006CrossrefMedlineGoogle Scholar
35. Cheskes S, Hillier M, Byers A, Verbeek PR, Drennan IR, Zhan C, Morrison LJ. The association between manual mode defibrillation, pre-shock pause duration and appropriate shock delivery when employed by basic life support paramedics during out-of-hospital cardiac arrest.Resuscitation. 2015; 90:61–66. doi: 10.1016/j.resuscitation.2015.02.022CrossrefMedlineGoogle Scholar
36. Eftestøl T, Wik L, Sunde K, Steen PA. Effects of cardiopulmonary resuscitation on predictors of ventricular fibrillation defibrillation success during out-of-hospital cardiac arrest.Circulation. 2004; 110:10–15. doi: 10.1161/01.CIR.0000133323.15565.75LinkGoogle Scholar
37. Holmberg M, Holmberg S, Herlitz J. Incidence, duration and survival of ventricular fibrillation in out-of-hospital cardiac arrest patients in sweden.Resuscitation. 2000; 44:7–17. doi: 10.1016/s0300-9572(99)00155-0CrossrefMedlineGoogle Scholar
38. Baker PW, Conway J, Cotton C, Ashby DT, Smyth J, Woodman RJ, Grantham HClinical Investigators. Defibrillation or cardiopulmonary resuscitation first for patients with out-of-hospital cardiac arrests found by paramedics to be in ventricular fibrillation? A randomised control trial.Resuscitation. 2008; 79:424–431. doi: 10.1016/j.resuscitation.2008.07.017CrossrefMedlineGoogle Scholar
39. Jacobs IG, Finn JC, Oxer HF, Jelinek GA. CPR before defibrillation in out-of-hospital cardiac arrest: a randomized trial.Emerg Med Australas. 2005; 17:39–45. doi: 10.1111/j.1742-6723.2005.00694.xCrossrefMedlineGoogle Scholar
40. Stiell IG, Nichol G, Leroux BG, Rea TD, Ornato JP, Powell J, Christenson J, Callaway CW, Kudenchuk PJ, Aufderheide TP, Idris AH, Daya MR, Wang HE, Morrison LJ, Davis D, Andrusiek D, Stephens S, Cheskes S, Schmicker RH, Fowler R, Vaillancourt C, Hostler D, Zive D, Pirrallo RG, Vilke GM, Sopko G, Weisfeldt MROC Investigators. Early versus later rhythm analysis in patients with out-of-hospital cardiac arrest.N Engl J Med. 2011; 365:787–797. doi: 10.1056/NEJMoa1010076CrossrefMedlineGoogle Scholar
41. Bircher NG, Chan PS, Xu YAmerican Heart Association’s Get With The Guidelines–Resuscitation Investigators. Delays in Cardiopulmonary Resuscitation, Defibrillation, and Epinephrine Administration All Decrease Survival in In-hospital Cardiac Arrest.Anesthesiology. 2019; 130:414–422. doi: 10.1097/ALN.0000000000002563CrossrefMedlineGoogle Scholar
42. Valenzuela TD, Roe DJ, Nichol G, Clark LL, Spaite DW, Hardman RG. Outcomes of rapid defibrillation by security officers after cardiac arrest in casinos.N Engl J Med. 2000; 343:1206–1209. doi: 10.1056/NEJM200010263431701CrossrefMedlineGoogle Scholar
43. White RD, Asplin BR, Bugliosi TF, Hankins DG. High discharge survival rate after out-of-hospital ventricular fibrillation with rapid defibrillation by police and paramedics.Ann Emerg Med. 1996; 28:480–485. doi: 10.1016/s0196-0644(96)70109-9CrossrefMedlineGoogle Scholar
44. Weisfeldt ML, Becker LB. Resuscitation after cardiac arrest: a 3-phase time-sensitive model.JAMA. 2002; 288:3035–3038. doi: 10.1001/jama.288.23.3035CrossrefMedlineGoogle Scholar
45. Kern KB, Garewal HS, Sanders AB, Janas W, Nelson J, Sloan D, Tacker WA, Ewy GA. Depletion of myocardial adenosine triphosphate during prolonged untreated ventricular fibrillation: effect on defibrillation success.Resuscitation. 1990; 20:221–229. doi: 10.1016/0300-9572(90)90005-yCrossrefMedlineGoogle Scholar
46. Link MS, Atkins DL, Passman RS, Halperin HR, Samson RA, White RD, Cudnik MT, Berg MD, Kudenchuk PJ, Kerber RE. Part 6: electrical therapies: automated external defibrillators, defibrillation, cardioversion, and pacing: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S706–S719. doi: 10.1161/CIRCULATIONAHA.110.970954LinkGoogle Scholar
47. Edelson DP, Robertson-Dick BJ, Yuen TC, Eilevstjønn J, Walsh D, Bareis CJ, Vanden Hoek TL, Abella BS. Safety and efficacy of defibrillator charging during ongoing chest compressions: a multi-center study.Resuscitation. 2010; 81:1521–1526. doi: 10.1016/j.resuscitation.2010.07.014CrossrefMedlineGoogle Scholar
48. Cheskes S, Schmicker RH, Christenson J, Salcido DD, Rea T, Powell J, Edelson DP, Sell R, May S, Menegazzi JJ, Van Ottingham L, Olsufka M, Pennington S, Simonini J, Berg RA, Stiell I, Idris A, Bigham B, Morrison LResuscitation Outcomes Consortium (ROC) Investigators. Perishock pause: an independent predictor of survival from out-of-hospital shockable cardiac arrest.Circulation. 2011; 124:58–66. doi: 10.1161/CIRCULATIONAHA.110.010736LinkGoogle Scholar
49. Hansen LK, Folkestad L, Brabrand M. Defibrillator charging before rhythm analysis significantly reduces hands-off time during resuscitation: a simulation study.Am J Emerg Med. 2013; 31:395–400. doi: 10.1016/j.ajem.2012.08.029CrossrefMedlineGoogle Scholar
50. Kemper M, Zech A, Lazarovici M, Zwissler B, Prückner S, Meyer O. Defibrillator charging before rhythm analysis causes peri-shock pauses exceeding guideline recommended maximum 5 s: A randomized simulation trial.Anaesthesist. 2019; 68:546–554. doi: 10.1007/s00101-019-0623-xCrossrefMedlineGoogle Scholar
51. Berg KM, Soar J, Andersen LW, Böttiger BW, Cacciola S, Callaway CW, Couper K, Cronberg T, D’Arrigo S, Deakin CD, et al.; on behalf of the Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S92–S139. doi: 10.1161/CIR.0000000000000893LinkGoogle Scholar
52. Berdowski J, ten Haaf M, Tijssen JG, Chapman FW, Koster RW. Time in recurrent ventricular fibrillation and survival after out-of-hospital cardiac arrest.Circulation. 2010; 122:1101–1108. doi: 10.1161/CIRCULATIONAHA.110.958173LinkGoogle Scholar
53. Hess EP, White RD. Ventricular fibrillation is not provoked by chest compression during post-shock organized rhythms in out-of-hospital cardiac arrest.Resuscitation. 2005; 66:7–11. doi: 10.1016/j.resuscitation.2005.01.011CrossrefMedlineGoogle Scholar
54. Berdowski J, Tijssen JG, Koster RW. Chest compressions cause recurrence of ventricular fibrillation after the first successful conversion by defibrillation in out-of-hospital cardiac arrest.Circ Arrhythm Electrophysiol. 2010; 3:72–78. doi: 10.1161/CIRCEP.109.902114LinkGoogle Scholar
55. Li Y, Bisera J, Tang W, Weil MH. Automated detection of ventricular fibrillation to guide cardiopulmonary resuscitation.Crit Pathw Cardiol. 2007; 6:131–134. doi: 10.1097/HPC.0b013e31813429b0CrossrefMedlineGoogle Scholar
56. Tan Q, Freeman GA, Geheb F, Bisera J. Electrocardiographic analysis during uninterrupted cardiopulmonary resuscitation.Crit Care Med. 2008; 3611 SupplS409–S412. doi: 10.1097/ccm.0b013e31818a7fbfCrossrefMedlineGoogle Scholar
57. Li Y, Bisera J, Weil MH, Tang W. An algorithm used for ventricular fibrillation detection without interrupting chest compression.IEEE Trans Biomed Eng. 2012; 59:78–86. doi: 10.1109/TBME.2011.2118755CrossrefMedlineGoogle Scholar
58. Babaeizadeh S, Firoozabadi R, Han C, Helfenbein ED. Analyzing cardiac rhythm in the presence of chest compression artifact for automated shock advisory.J Electrocardiol. 2014; 47:798–803. doi: 10.1016/j.jelectrocard.2014.07.021CrossrefMedlineGoogle Scholar
59. Fumagalli F, Silver AE, Tan Q, Zaidi N, Ristagno G. Cardiac rhythm analysis during ongoing cardiopulmonary resuscitation using the Analysis During Compressions with Fast Reconfirmation technology.Heart Rhythm. 2018; 15:248–255. doi: 10.1016/j.hrthm.2017.09.003CrossrefMedlineGoogle Scholar
60. Hu Y, Tang H, Liu C, Jing D, Zhu H, Zhang Y, Yu X, Zhang G, Xu J. The performance of a new shock advisory algorithm to reduce interruptions during CPR.Resuscitation. 2019; 143:1–9. doi: 10.1016/j.resuscitation.2019.07.026CrossrefMedlineGoogle Scholar
61. Asano Y, Davidenko JM, Baxter WT, Gray RA, Jalife J. Optical mapping of drug-induced polymorphic arrhythmias and torsade de pointes in the isolated rabbit heart.J Am Coll Cardiol. 1997; 29:831–842. doi: 10.1016/s0735-1097(96)00588-8CrossrefMedlineGoogle Scholar
62. Callaway CW, Sherman LD, Mosesso VN, Dietrich TJ, Holt E, Clarkson MC. Scaling exponent predicts defibrillation success for out-of-hospital ventricular fibrillation cardiac arrest.Circulation. 2001; 103:1656–1661. doi: 10.1161/01.cir.103.12.1656LinkGoogle Scholar
63. Coult J, Blackwood J, Sherman L, Rea TD, Kudenchuk PJ, Kwok H. Ventricular Fibrillation Waveform Analysis During Chest Compressions to Predict Survival From Cardiac Arrest.Circ Arrhythm Electrophysiol. 2019; 12:e006924. doi: 10.1161/CIRCEP.118.006924LinkGoogle Scholar
64. Coult J, Kwok H, Sherman L, Blackwood J, Kudenchuk PJ, Rea TD. Ventricular fibrillation waveform measures combined with prior shock outcome predict defibrillation success during cardiopulmonary resuscitation.J Electrocardiol. 2018; 51:99–106. doi: 10.1016/j.jelectrocard.2017.07.016CrossrefMedlineGoogle Scholar
65. Freese JP, Jorgenson DB, Liu PY, Innes J, Matallana L, Nammi K, Donohoe RT, Whitbread M, Silverman RA, Prezant DJ. Waveform analysis-guided treatment versus a standard shock-first protocol for the treatment of out-of-hospital cardiac arrest presenting in ventricular fibrillation: results of an international randomized, controlled trial.Circulation. 2013; 128:995–1002. doi: 10.1161/CIRCULATIONAHA.113.003273LinkGoogle Scholar
66. Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, et al.. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122:S729–S767. doi: 10.1161/CIRCULATIONAHA.110.970988LinkGoogle Scholar
67. Clemency BM, Pastwik B, Gillen D. Double sequential defibrillation and the tyranny of the case study.Am J Emerg Med. 2019; 37:792–793. doi: 10.1016/j.ajem.2018.09.002CrossrefMedlineGoogle Scholar
68. Beck LR, Ostermayer DG, Ponce JN, Srinivasan S, Wang HE. Effectiveness of Prehospital Dual Sequential Defibrillation for Refractory Ventricular Fibrillation and Ventricular Tachycardia Cardiac Arrest.Prehosp Emerg Care. 2019; 23:597–602. doi: 10.1080/10903127.2019.1584256CrossrefMedlineGoogle Scholar
69. Mapp JG, Hans AJ, Darrington AM, Ross EM, Ho CC, Miramontes DA, Harper SA, Wampler DAPrehospital Research and Innovation in Military and Expeditionary Environments (PRIME) Research Group. Prehospital Double Sequential Defibrillation: A Matched Case-Control Study.Acad Emerg Med. 2019; 26:994–1001. doi: 10.1111/acem.13672CrossrefMedlineGoogle Scholar
70. Ross EM, Redman TT, Harper SA, Mapp JG, Wampler DA, Miramontes DA. Dual defibrillation in out-of-hospital cardiac arrest: A retrospective cohort analysis.Resuscitation. 2016; 106:14–17. doi: 10.1016/j.resuscitation.2016.06.011CrossrefMedlineGoogle Scholar
71. Emmerson AC, Whitbread M, Fothergill RT. Double sequential defibrillation therapy for out-of-hospital cardiac arrests: The London experience.Resuscitation. 2017; 117:97–101. doi: 10.1016/j.resuscitation.2017.06.011CrossrefMedlineGoogle Scholar
72. Cheskes S, Dorian P, Feldman M, McLeod S, Scales DC, Pinto R, Turner L, Morrison LJ, Drennan IR, Verbeek PR. Double sequential external defibrillation for refractory ventricular fibrillation: the DOSE VF pilot randomized controlled trial.Resuscitation. 2020; 150:178–184. doi: 10.1016/j.resuscitation.2020.02.010CrossrefMedlineGoogle Scholar
73. Gerstein NS, McLean AR, Stecker EC, Schulman PM. External Defibrillator Damage Associated With Attempted Synchronized Dual-Dose Cardioversion.Ann Emerg Med. 2018; 71:109–112. doi: 10.1016/j.annemergmed.2017.04.005CrossrefMedlineGoogle Scholar
74. Kudenchuk PJ. Shocking insights on double defibrillation: How, when and why not?Resuscitation. 2019; 140:209–210. doi: 10.1016/j.resuscitation.2019.05.022CrossrefMedlineGoogle Scholar

Other Electric or Pseudo-Electric Therapies for Cardiac Arrest

Introduction

In addition to defibrillation, several alternative electric and pseudoelectrical therapies have been explored as possible treatment options during cardiac arrest. Transcutaneous pacing has been studied during cardiac arrest with bradyasystolic cardiac rhythm. The theory is that the heart will respond to electric stimuli by producing myocardial contraction and generating forward movement of blood, but clinical trials have not shown pacing to improve patient outcomes.

Other pseudoelectrical therapies, such as cough CPR, fist or percussion pacing, and precordial thump have all been described as temporizing measures in select patients who are either periarrest or in the initial seconds of witnessed cardiac arrest (before losing consciousness in the case of cough CPR) when definitive therapy is not readily available. Precordial thump is a single, sharp, high-velocity impact (or “punch”) to the middle sternum by the ulnar aspect of a tightly clenched fist. The force from a precordial thump is intended to transmit electric energy to the heart, similar to a low-energy shock, in hope of terminating the underlying tachyarrhythmia.

Fist (or percussion) pacing is the delivery of a serial, rhythmic, relatively low-velocity impact to the sternum by a closed fist.1 Fist pacing is administered in an attempt to stimulate an electric impulse sufficient to cause myocardial depolarization. Cough CPR is described as repeated deep breaths followed immediately by a cough every few seconds in an attempt to increase aortic and intracardiac pressures, providing transient hemodynamic support before a loss of consciousness.

Recommendation-Specific Supportive Text

Existing evidence, including observational and quasi-RCT data, suggests that pacing by a transcutaneous, transvenous, or transmyocardial approach in cardiac arrest does not improve the likelihood of ROSC or survival, regardless of the timing of pacing administration in established asystole, location of arrest (in-hospital or out-of-hospital), or primary cardiac rhythm (asystole, pulseless electrical activity).2–6 Protracted interruptions in chest compressions while the success of pacing is assessed can also be detrimental to survival. It is not known whether the timing of pacing initiation may influence pacing success such that pacing may be useful in the initial seconds of select cases of witnessed, monitored cardiac arrest (see the section on Cardiac Arrest After Cardiac Surgery). If pacing is attempted during cardiac arrest related to the special circumstances described above, providers are cautioned against its performance at the expense of high-quality CPR, particularly when assessing electric and mechanical capture.

This topic last underwent formal evidence review in 2010.7

Recommendation-Specific Supportive Text

1 and 2. The intent of precordial thump is to transmit the mechanical force of the “thump” to the heart as electric energy analogous to a pacing stimulus or very low-energy shock (depending on its force) and is referred to as electromechanical transduction.1 There is no evidence that the use of precordial thump during routine cardiac arrest care in the out-of-hospital or in-hospital settings improves rates of ROSC or survival to hospital discharge.8–12 It may be beneficial only at the very early onset of VT when the arrhythmia is most vulnerable to lower-energy termination such as in responder-witnessed, monitored events, or in a controlled laboratory environment, but even then it is rarely effective.13 Although there are case reports of success without evidence of harm from a precordial thump,9,14,15 if fortuitously administered on the electrically vulnerable portion of an organized rhythm (T wave), the thump (like an unsynchronized shock) risks acceleration or conversion of the rhythm to VF,16–19 analogous to commotio cordis.20 Thus, although the thump may be useful as a single brief intervention under specific circumstances (ie, when a cardiac arrest is witnessed by the responder and monitor-confirmed to be due to VF/VT and a defibrillator is not readily available for use), it should not delay CPR or deployment of a defibrillator.

These recommendations are supported by the 2020 CoSTR for BLS.21

Recommendation-Specific Supportive Text

Fist, or percussion, pacing is administered with the goal of stimulating an electric impulse sufficient to cause depolarization and contraction of the myocardium, resulting in a pulse. There are a number of case reports and case series that examined the use of fist pacing during asystolic or “life-threatening bradycardic” events1,22–25 showing favorable outcomes of survival22 and ROSC.23 None of these studies, however, were controlled or comparative, and it is not known if the use of fist pacing itself improves rates of ROSC or survival compared with standard therapy. There is no role for fist pacing in patients in cardiac arrest.

This recommendation is supported by the 2020 CoSTR for BLS.21

Recommendation-Specific Supportive Text

It is important to underscore that while cough CPR by definition cannot be used for an unconscious patient, it can be harmful in any setting if diverting time, effort, and attention from performing high-quality CPR. Cough CPR is described as a repetitive deep inspiration followed by a cough every few seconds before the loss of consciousness. It is feasible only at the onset of a hemodynamically significant arrhythmia in a cooperative, conscious patient who has ideally been previously instructed on its performance, and as a bridge to definitive care. There are no studies comparing cough CPR to standard resuscitation care. Limited evidence from case reports and case series demonstrates transient increases in aortic and intracardiac pressure with the use of cough CPR at the onset of tachyarrhythmias or bradyarrhythmias in conscious patients.10,26–28 These studies suffer from considerable selection bias and lack of comparison groups, and do not control for the confounding effect of other treatments, making them hard to interpret.

This recommendation is supported by the 2020 CoSTR for BLS.21

References

1. Tucker KJ, Shaburihvili TS, Gedevanishvili AT. Manual external (fist) pacing during high-degree atrioventricular block: a lifesaving intervention.Am J Emerg Med. 1995; 13:53–54. doi: 10.1016/0735-6757(95)90243-0CrossrefMedlineGoogle Scholar
2. Sherbino J, Verbeek PR, MacDonald RD, Sawadsky BV, McDonald AC, Morrison LJ. Prehospital transcutaneous cardiac pacing for symptomatic bradycardia or bradyasystolic cardiac arrest: a systematic review.Resuscitation. 2006; 70:193–200. doi: 10.1016/j.resuscitation.2005.11.019CrossrefMedlineGoogle Scholar
3. White JD, Brown CG. Immediate transthoracic pacing for cardiac asystole in an emergency department setting.Am J Emerg Med. 1985; 3:125–128. doi: 10.1016/0735-6757(85)90034–8CrossrefMedlineGoogle Scholar
4. Hedges JR, Syverud SA, Dalsey WC, Feero S, Easter R, Shultz B. Prehospital trial of emergency transcutaneous cardiac pacing.Circulation. 1987; 76:1337–1343. doi: 10.1161/01.cir.76.6.1337LinkGoogle Scholar
5. Barthell E, Troiano P, Olson D, Stueven HA, Hendley G. Prehospital external cardiac pacing: a prospective, controlled clinical trial.Ann Emerg Med. 1988; 17:1221–1226. doi: 10.1016/s0196-0644(88)80074-xCrossrefMedlineGoogle Scholar
6. Cummins RO, Graves JR, Larsen MP, Hallstrom AP, Hearne TR, Ciliberti J, Nicola RM, Horan S. Out-of-hospital transcutaneous pacing by emergency medical technicians in patients with asystolic cardiac arrest.N Engl J Med. 1993; 328:1377–1382. doi: 10.1056/NEJM199305133281903CrossrefMedlineGoogle Scholar
7. Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, et al.. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122:S729–S767. doi: 10.1161/CIRCULATIONAHA.110.970988LinkGoogle Scholar
8. Nehme Z, Andrew E, Bernard SA, Smith K. Treatment of monitored out-of-hospital ventricular fibrillation and pulseless ventricular tachycardia utilising the precordial thump.Resuscitation. 2013; 84:1691–1696. doi: 10.1016/j.resuscitation.2013.08.011CrossrefMedlineGoogle Scholar
9. Pellis T, Kette F, Lovisa D, Franceschino E, Magagnin L, Mercante WP, Kohl P. Utility of pre-cordial thump for treatment of out of hospital cardiac arrest: a prospective study.Resuscitation. 2009; 80:17–23. doi: 10.1016/j.resuscitation.2008.10.018CrossrefMedlineGoogle Scholar
10. Caldwell G, Millar G, Quinn E, Vincent R, Chamberlain DA. Simple mechanical methods for cardioversion: defence of the precordial thump and cough version.BMJ. (Clin Res Ed). 1985; 291:627–630. doi: 10.1136/bmj.291.6496.627CrossrefMedlineGoogle Scholar
11. Gertsch M, Hottinger S, Hess T. Serial chest thumps for the treatment of ventricular tachycardia in patients with coronary artery disease.Clin Cardiol. 1992; 15:181–188. doi: 10.1002/clc.4960150309CrossrefMedlineGoogle Scholar
12. Rajagopalan RS, Appu KS, Sultan SK, Jagannadhan TG, Nityanandan K, Sethuraman S. Precordial thump in ventricular tachycardia.J Assoc Physicians India. 1971; 19:725–729.MedlineGoogle Scholar
13. Haman L, Parizek P, Vojacek J. Precordial thump efficacy in termination of induced ventricular arrhythmias.Resuscitation. 2009; 80:14–16. doi: 10.1016/j.resuscitation.2008.07.022CrossrefMedlineGoogle Scholar
14. Befeler B. Mechanical stimulation of the heart: its therapeutic value in tachyarrhythmias.Chest. 1978; 73:832–838. doi: 10.1378/chest.73.6.832CrossrefMedlineGoogle Scholar
15. Volkmann H, Klumbies A, Kühnert H, Paliege R, Dannberg G, Siegert K. [Terminating ventricular tachycardias by mechanical heart stimulation with precordial thumps].Z Kardiol. 1990; 79:717–724.MedlineGoogle Scholar
16. Morgera T, Baldi N, Chersevani D, Medugno G, Camerini F. Chest thump and ventricular tachycardia.Pacing Clin Electrophysiol. 1979; 2:69–75. doi: 10.1111/j.1540-8159.1979.tb05178.xCrossrefMedlineGoogle Scholar
17. Krijne R. Rate acceleration of ventricular tachycardia after a precordial chest thump.Am J Cardiol. 1984; 53:964–965. doi: 10.1016/0002-9149(84)90539-3CrossrefMedlineGoogle Scholar
18. Sclarovsky S, Kracoff OH, Agmon J. Acceleration of ventricular tachycardia induced by a chest thump.Chest. 1981; 80:596–599. doi: 10.1378/chest.80.5.596CrossrefMedlineGoogle Scholar
19. Yakaitis RW, Redding JS. Precordial thumping during cardiac resuscitation.Crit Care Med. 1973; 1:22–26. doi: 10.1097/00003246-197301000-00004CrossrefMedlineGoogle Scholar
20. Link MS, Maron BJ, Wang PJ, VanderBrink BA, Zhu W, Estes NA. Upper and lower limits of vulnerability to sudden arrhythmic death with chest-wall impact (commotio cordis).J Am Coll Cardiol. 2003; 41:99–104. doi: 10.1016/s0735-1097(02)02669-4CrossrefMedlineGoogle Scholar
21. Olasveengen TM, Mancini ME, Perkins GD, Avis S, Brooks S, Castrén M, Chung SP, Considine J, Couper K, Escalante R, et al.; on behalf of the Adult Basic Life Support Collaborators. Adult basic life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S41–S91. doi: 10.1161/CIR.0000000000000892LinkGoogle Scholar
22. Klumbies A, Paliege R, Volkmann H. [Mechanical emergency stimulation in asystole and extreme bradycardia].Z Gesamte Inn Med. 1988; 43:348–352.MedlineGoogle Scholar
23. Iseri LT, Allen BJ, Baron K, Brodsky MA. Fist pacing, a forgotten procedure in bradyasystolic cardiac arrest.Am Heart J. 1987; 113:1545–1550. doi: 10.1016/0002-8703(87)90697-1CrossrefMedlineGoogle Scholar
24. Paliege R, Volkmann H, Klumbies A. The fist as a pacemaker for the heart—investigations about the mechanical stimulation of the heart in case of emergency.Deutsche Gesundheitswesen Zeitschrift für Klinische Medizin. 1982; 37:1094–1100.Google Scholar
25. Scherf D, Bornemann C. Thumping of the precordium in ventricular standstill.Am J Cardiol. 1960; 5:30–40. doi: 10.1016/0002-9149(60)90006-0CrossrefMedlineGoogle Scholar
26. Petelenz T, Iwiński J, Chlebowczyk J, Czyz Z, Flak Z, Fiutowski L, Zaorski K, Petelenz T, Zeman S. Self–administered cough cardiopulmonary resuscitation (c-CPR) in patients threatened by MAS events of cardiovascular origin.Wiad Lek. 1998; 51:326–336.MedlineGoogle Scholar
27. Niemann JT, Rosborough J, Hausknecht M, Brown D, Criley JM. Cough-CPR: documentation of systemic perfusion in man and in an experimental model: a “window” to the mechanism of blood flow in external CPR.Crit Care Med. 1980; 8:141–146. doi: 10.1097/00003246-198003000-00011CrossrefMedlineGoogle Scholar
28. Marozsán I, Albared JL, Szatmáry LJ. Life-threatening arrhythmias stopped by cough.Cor Vasa. 1990; 32:401–408.MedlineGoogle Scholar

Vascular Access

Synopsis

The traditional approach for giving emergency pharmacotherapy is by the peripheral IV route. However, obtaining IV access under emergent conditions can prove to be challenging based on patient characteristics and operator experience leading to delay in pharmacological treatments.

Alternatives to IV access for acute drug administration include IO, central venous, intracardiac, and endotracheal routes. Intracardiac drug administration was discouraged in the 2000 AHA Guidelines for CPR and Emergency Cardiovascular Care given its highly specialized skill set, potential morbidity, and other available options for access.1,2 Endotracheal drug administration results in low blood concentrations and unpredictable pharmacological effect and has also largely fallen into disuse given other access options. Central venous access is primarily used in the hospital setting because it requires appropriate training to acquire and maintain the needed skill set.

IO access has grown in popularity given the relative ease and speed with which it can be achieved, a higher successful placement rate compared with IV cannulation, and the relatively low procedural risk. However, the efficacy of IV versus IO drug administration in cardiac arrest remains to be elucidated.

Recommendation-Specific Supportive Text

The peripheral IV route has been the traditional approach to vascular access for emergency drug and fluid administration during resuscitation. The pharmacokinetic properties, acute effects, and clinical efficacy of emergency drugs have primarily been described when given intravenously.3–6 The IV route has precedence, is usually accessible, and affords a potentially more predictable drug response, making it a reasonable initial approach for vascular access.
The paucity of information on the efficacy of IO drug administration during CPR was acknowledged in 2010, but since then the IO route has grown in popularity. IO access is increasingly implemented as a first-line approach for emergent vascular access. A 2020 ILCOR systematic review7 comparing IV versus IO (principally pretibial placement) drug administration during cardiac arrest found the IV route was associated with better clinical outcomes compared with IO in 5 retrospective studies.8–12 There were significant concerns for bias, particularly due to the fact that need for IO placement may indicate patient or arrest characteristics that are also risk factors for poor outcome. Subgroup analyses of IV versus IO route from 2 RCTs were also included in this systematic review. In these, no statistically significant effect modification by route of administration was identified. Point estimates favored IV access except for the outcome of ROSC in the PARAMEDIC2 trial, where the effect of epinephrine was similar regardless of route.13,14 Site specificity may also be an issue with IO administration, because IO access was nearly always pretibial in these studies. On the basis of these results, the writing group concluded that establishing a peripheral IV remains a reasonable initial approach, but IO access may be considered when an IV is not successful or feasible. Further research is needed to assess the efficacy of drugs delivered intravenously as compared with intraosseously (tibial and humeral).
Drug administration by central venous access (by internal jugular or subclavian vein) achieves higher peak concentrations and more rapid circulation times than drugs administered by peripheral IV do,15–17 but there are currently no data comparing clinical outcomes between these access routes. Central access is associated with higher morbidity, takes time to perform, and may also require interruption of CPR. Current use of this approach is largely in the hospital and may be considered by skilled providers when IV and IO access are not successful or feasible.
Endotracheal drug administration is regarded as the least-preferred route of drug administration because it is associated with unpredictable (but generally low) drug concentrations18–20 and lower rates of ROSC and survival.21

Recommendations 1 and 2 are supported by the 2020 CoSTR for ALS.22 Recommendations 3 and 4 last received formal evidence review in 2010.20

References

1. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: advanced cardiovascular life support: section 6: pharmacology II: agents to optimize cardiac output and blood pressure.Circulation. 2000; 102(suppl):I129–I135.MedlineGoogle Scholar
2. Aitkenhead AR. Drug administration during CPR: what route?Resuscitation. 1991; 22:191–195. doi: 10.1016/0300-9572(91)90011-mCrossrefMedlineGoogle Scholar
3. Collinsworth KA, Kalman SM, Harrison DC. The clinical pharmacology of lidocaine as an antiarrhythymic drug.Circulation. 1974; 50:1217–1230. doi: 10.1161/01.cir.50.6.1217LinkGoogle Scholar
4. Greenblatt DJ, Bolognini V, Koch-Weser J, Harmatz JS. Pharmacokinetic approach to the clinical use of lidocaine intravenously.JAMA. 1976; 236:273–277.CrossrefMedlineGoogle Scholar
5. Riva E, Gerna M, Latini R, Giani P, Volpi A, Maggioni A. Pharmacokinetics of amiodarone in man.J Cardiovasc Pharmacol. 1982; 4:264–269. doi: 10.1097/00005344-198203000-00015CrossrefMedlineGoogle Scholar
6. Orlowski JP, Porembka DT, Gallagher JM, Lockrem JD, VanLente F. Comparison study of intraosseous, central intravenous, and peripheral intravenous infusions of emergency drugs.Am J Dis Child. 1990; 144:112–117. doi: 10.1001/archpedi.1990.02150250124049MedlineGoogle Scholar
7. Granfeldt A, Avis SR, Lind PC, Holmberg MJ, Kleinman M, Maconochie I, Hsu CH, Fernanda de Almeida M, Wang TL, Neumar RW, Andersen LW. Intravenous vs. intraosseous administration of drugs during cardiac arrest: A systematic review.Resuscitation. 2020; 149:150–157. doi: 10.1016/j.resuscitation.2020.02.025CrossrefMedlineGoogle Scholar
8. Feinstein BA, Stubbs BA, Rea T, Kudenchuk PJ. Intraosseous compared to intravenous drug resuscitation in out-of-hospital cardiac arrest.Resuscitation. 2017; 117:91–96. doi: 10.1016/j.resuscitation.2017.06.014CrossrefMedlineGoogle Scholar
9. Kawano T, Grunau B, Scheuermeyer FX, Gibo K, Fordyce CB, Lin S, Stenstrom R, Schlamp R, Jenneson S, Christenson J. Intraosseous Vascular Access Is Associated With Lower Survival and Neurologic Recovery Among Patients With Out-of-Hospital Cardiac Arrest.Ann Emerg Med. 2018; 71:588–596. doi: 10.1016/j.annemergmed.2017.11.015CrossrefMedlineGoogle Scholar
10. Clemency B, Tanaka K, May P, Innes J, Zagroba S, Blaszak J, Hostler D, Cooney D, McGee K, Lindstrom H. Intravenous vs. intraosseous access and return of spontaneous circulation during out of hospital cardiac arrest.Am J Emerg Med. 2017; 35:222–226. doi: 10.1016/j.ajem.2016.10.052CrossrefMedlineGoogle Scholar
11. Nguyen L, Suarez S, Daniels J, Sanchez C, Landry K, Redfield C. Effect of Intravenous Versus Intraosseous Access in Prehospital Cardiac Arrest.Air Med J. 2019; 38:147–149. doi: 10.1016/j.amj.2019.02.005CrossrefMedlineGoogle Scholar
12. Mody P, Brown SP, Kudenchuk PJ, Chan PS, Khera R, Ayers C, Pandey A, Kern KB, de Lemos JA, Link MS, Idris AH. Intraosseous versus intravenous access in patients with out-of-hospital cardiac arrest: Insights from the resuscitation outcomes consortium continuous chest compression trial.Resuscitation. 2019; 134:69–75. doi: 10.1016/j.resuscitation.2018.10.031CrossrefMedlineGoogle Scholar
13. Daya MR, Leroux BG, Dorian P, Rea TD, Newgard CD, Morrison LJ, Lupton JR, Menegazzi JJ, Ornato JP, Sopko G, Christenson J, Idris A, Mody P, Vilke GM, Herdeman C, Barbic D, Kudenchuk PJResuscitation Outcomes Consortium Investigators. Survival After Intravenous Versus Intraosseous Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Shock-Refractory Cardiac Arrest.Circulation. 2020; 141:188–198. doi: 10.1161/CIRCULATIONAHA.119.042240LinkGoogle Scholar
14. Nolan JP, Deakin CD, Ji C, Gates S, Rosser A, Lall R, Perkins GD. Intraosseous versus intravenous administration of adrenaline in patients with out-of-hospital cardiac arrest: a secondary analysis of the PARAMEDIC2 placebo-controlled trial [published online January 30, 2020].Intensive Care Med. 2020:Epub ahead of print. doi: 10.1007/s00134-019-05920-7CrossrefGoogle Scholar
15. Barsan WG, Levy RC, Weir H. Lidocaine levels during CPR: differences after peripheral venous, central venous, and intracardiac injections.Ann Emerg Med. 1981; 10:73–78. doi: 10.1016/s0196-0644(81)80339-3CrossrefMedlineGoogle Scholar
16. Kuhn GJ, White BC, Swetnam RE, Mumey JF, Rydesky MF, Tintinalli JE, Krome RL, Hoehner PJ. Peripheral vs central circulation times during CPR: a pilot study.Ann Emerg Med. 1981; 10:417–419. doi: 10.1016/s0196-0644(81)80308-3CrossrefMedlineGoogle Scholar
17. Emerman CL, Pinchak AC, Hancock D, Hagen JF. Effect of injection site on circulation times during cardiac arrest.Crit Care Med. 1988; 16:1138–1141. doi: 10.1097/00003246-198811000-00011CrossrefMedlineGoogle Scholar
18. Schüttler J, Bartsch A, Ebeling BJ, Hörnchen U, Kulka P, Sühling B, Stoeckel H. [Endobronchial administration of adrenaline in preclinical cardiopulmonary resuscitation].Anasth Intensivther Notfallmed. 1987; 22:63–68.MedlineGoogle Scholar
19. Hörnchen U, Schüttler J, Stoeckel H, Eichelkraut W, Hahn N. Endobronchial instillation of epinephrine during cardiopulmonary resuscitation.Crit Care Med. 1987; 15:1037–1039. doi: 10.1097/00003246-198711000-00009CrossrefMedlineGoogle Scholar
20. Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, et al.. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122:S729–S767. doi: 10.1161/CIRCULATIONAHA.110.970988LinkGoogle Scholar
21. Niemann JT, Stratton SJ, Cruz B, Lewis RJ. Endotracheal drug administration during out-of-hospital resuscitation: where are the survivors?Resuscitation. 2002; 53:153–157. doi: 10.1016/s0300-9572(02)00004-7CrossrefMedlineGoogle Scholar
22. Berg KM, Soar J, Andersen LW, Böttiger BW, Cacciola S, Callaway CW, Couper K, Cronberg T, D’Arrigo S, Deakin CD, et al.; on behalf of the Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S92–S139. doi: 10.1161/CIR.0000000000000893LinkGoogle Scholar

Vasopressor Medications During Cardiac Arrest

Synopsis

Epinephrine has been hypothesized to have beneficial effects during cardiac arrest primarily because of its α-adrenergic effects, leading to increased coronary and cerebral perfusion pressure during CPR. Conversely, the β-adrenergic effects may increase myocardial oxygen demand, reduce subendocardial perfusion, and may be proarrhythmic. Two randomized, placebo-controlled trials, enrolling over 8500 patients, evaluated the efficacy of epinephrine for OHCA.1,2 A systematic review and meta-analysis of these and other studies3 concluded that epinephrine significantly increased ROSC and survival to hospital discharge. Epinephrine did not lead to increased survival with favorable or unfavorable neurological outcome at 3 months, although both of these outcomes occurred slightly more frequently in the epinephrine group.2 Observational data suggest better outcomes when epinephrine is given sooner, and the low survival with favorable neurological outcome in the available trials may be due in part to the median time of 21 minutes from arrest to receipt of epinephrine. This time delay is a consistent issue in OHCA trials. Time to drug in IHCA is generally much shorter, and the effect of epinephrine on outcomes in the IHCA population may therefore be different. No trials to date have found any benefit of either higher-dose epinephrine or other vasopressors over standard-dose epinephrine during CPR.

Recommendation-Specific Supportive Text

The suggestion to administer epinephrine was strengthened to a recommendation based on a systematic review and meta-analysis,3 which included results of 2 randomized trials of epinephrine for OHCA, 1 of which included over 8000 patients,1,2 showing that epinephrine increased ROSC and survival. At 3 months, the time point felt to be most meaningful for neurological recovery, there was a nonsignificant increase in survivors with both favorable and unfavorable neurological outcome in the epinephrine group.2 Any drug that increases the rate of ROSC and survival, but is given after several minutes of downtime, will likely increase both favorable and unfavorable neurological outcome. Determining the likelihood of favorable or unfavorable neurological outcome at the time of arrest is currently not feasible. Therefore, continuing to use a drug that has been shown to increase survival, while focusing our broader efforts on shortening time to drug for all patients so that more survivors will have a favorable neurological outcome, seems the most beneficial approach.
The existing trials have used a protocol of 1 mg every 3 to 5 minutes. Operationally, administering epinephrine every second cycle of CPR, after the initial dose, may also be reasonable.
Of 16 observational studies on timing in the recent systematic review, all found an association between earlier epinephrine and ROSC for patients with nonshockable rhythms, although improvements in survival were not universally seen.3
For shockable rhythms, trial protocols have directed that epinephrine be given after the third shock. The literature supports prioritizing defibrillation and CPR initially and giving epinephrine if initial attempts with CPR and defibrillation are not successful.3
The recent systematic review3 found no difference in outcomes in trials comparing vasopressin alone or vasopressin combined with epinephrine to epinephrine alone for cardiac arrest, although these studies were underpowered.
Multiple RCTs have compared high-dose with standard-dose epinephrine, and although some have shown higher rates of ROSC with high-dose epinephrine, none have shown improvement in survival to discharge or any longer-term outcomes.4–11

These recommendations are supported by the “2019 AHA Focused Update on Advanced Cardiovascular Life Support: Use of Advanced Airways, Vasopressors, and Extracorporeal CPR During Cardiac Arrest: An Update to the AHA Guidelines for CPR and Emergency Cardiovascular Care.”12

References

1. Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Effect of adrenaline on survival in out-of-hospital cardiac arrest: a randomised double-blind placebo-controlled trial.Resuscitation. 2011; 82:1138–1143. doi: 10.1016/j.resuscitation.2011.06.029CrossrefMedlineGoogle Scholar
2. Perkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, Black JJM, Moore F, Fothergill RT, Rees N, O’Shea L, Docherty M, Gunson I, Han K, Charlton K, Finn J, Petrou S, Stallard N, Gates S, Lall RPARAMEDIC2 Collaborators. A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest.N Engl J Med. 2018; 379:711–721. doi: 10.1056/NEJMoa1806842CrossrefMedlineGoogle Scholar
3. Holmberg MJ, Issa MS, Moskowitz A, Morley P, Welsford M, Neumar RW, Paiva EF, Coker A, Hansen CK, Andersen LW, Donnino MW, Berg KMInternational Liaison Committee on Resuscitation Advanced Life Support Task Force Collaborators. Vasopressors during adult cardiac arrest: A systematic review and meta-analysis.Resuscitation. 2019; 139:106–121. doi: 10.1016/j.resuscitation.2019.04.008CrossrefMedlineGoogle Scholar
4. Brown CG, Martin DR, Pepe PE, Stueven H, Cummins RO, Gonzalez E, Jastremski M. A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital. The Multicenter High-Dose Epinephrine Study Group.N Engl J Med. 1992; 327:1051–1055. doi: 10.1056/NEJM199210083271503CrossrefMedlineGoogle Scholar
5. Choux C, Gueugniaud PY, Barbieux A, Pham E, Lae C, Dubien PY, Petit P. Standard doses versus repeated high doses of epinephrine in cardiac arrest outside the hospital.Resuscitation. 1995; 29:3–9. doi: 10.1016/0300-9572(94)00810-3CrossrefMedlineGoogle Scholar
6. Gueugniaud PY, Mols P, Goldstein P, Pham E, Dubien PY, Deweerdt C, Vergnion M, Petit P, Carli P. A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest outside the hospital. European Epinephrine Study Group.N Engl J Med. 1998; 339:1595–1601. doi: 10.1056/NEJM199811263392204CrossrefMedlineGoogle Scholar
7. Lindner KH, Ahnefeld FW, Prengel AW. Comparison of standard and high-dose adrenaline in the resuscitation of asystole and electromechanical dissociation.Acta Anaesthesiol Scand. 1991; 35:253–256. doi: 10.1111/j.1399-6576.1991.tb03283.xCrossrefMedlineGoogle Scholar
8. Lipman J, Wilson W, Kobilski S, Scribante J, Lee C, Kraus P, Cooper J, Barr J, Moyes D. High-dose adrenaline in adult in-hospital asystolic cardiopulmonary resuscitation: a double-blind randomised trial.Anaesth Intensive Care. 1993; 21:192–196. doi: 10.1177/0310057X9302100210CrossrefMedlineGoogle Scholar
9. Sherman BW, Munger MA, Foulke GE, Rutherford WF, Panacek EA. High-dose versus standard-dose epinephrine treatment of cardiac arrest after failure of standard therapy.Pharmacotherapy. 1997; 17:242–247.MedlineGoogle Scholar
10. Stiell IG, Hebert PC, Weitzman BN, Wells GA, Raman S, Stark RM, Higginson LA, Ahuja J, Dickinson GE. High-dose epinephrine in adult cardiac arrest.N Engl J Med. 1992; 327:1045–1050. doi: 10.1056/NEJM199210083271502CrossrefMedlineGoogle Scholar
11. Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J. A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest.JAMA. 1992; 268:2667–2672.CrossrefMedlineGoogle Scholar
12. Panchal AR, Berg KM, Hirsch KG, Kudenchuk PJ, Del Rios M, Cabañas JG, Link MS, Kurz MC, Chan PS, Morley PT, et al.. 2019 American Heart Association focused update on advanced cardiovascular life support: use of advanced airways, vasopressors, and extracorporeal cardiopulmonary resuscitation during cardiac arrest: an update to the American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care.Circulation. 2019; 140:e881–e894. doi: 10.1161/CIR.0000000000000732LinkGoogle Scholar

Nonvasopressor Medications During Cardiac Arrest

Synopsis

Pharmacological treatment of cardiac arrest is typically deployed when CPR with or without attempted defibrillation fails to achieve ROSC. This may include vasopressor agents such as epinephrine (discussed in Vasopressor Medications During Cardiac Arrest) as well as drugs without direct hemodynamic effects (“nonpressors”) such as antiarrhythmic medications, magnesium, sodium bicarbonate, calcium, or steroids (discussed here). Although theoretically attractive and of some proven benefit in animal studies, none of the latter therapies has been definitively proved to improve overall survival after cardiac arrest, although some may have possible benefit in selected populations and/or special circumstances.

Recommendations for the treatment of cardiac arrest due to hyperkalemia, including the use of calcium and sodium bicarbonate, are presented in Electrolyte Abnormalities. Recommendations for management of torsades de pointes are also presented in Torsades de Pointes.

Recommendation-Specific Supportive Text

Administration of amiodarone or lidocaine to patients with OHCA was last formally reviewed in 20181 and demonstrated improved survival to hospital admission but did not improve overall survival to hospital discharge or survival with good neurological outcome.1,2 However, amiodarone and lidocaine each significantly improved survival to hospital discharge in a prespecified subgroup of patients with bystander-witnessed arrest, potentially arguing for a time-dependent benefit and a group for whom these drugs may be more useful. Other antiarrhythmic agents were not specifically addressed in the most recent evidence review and merit further evaluation. These include bretylium tosylate, which was recently reintroduced in the United States for treatment of immediately life-threatening ventricular arrhythmias but without any new information on its effectiveness or safety.3 Sotalol requires administration as a slow infusion, rendering it impractical to use in cardiac arrest.4 Similar limitations also apply to procainamide, although it has been given by rapid infusion as a second-line agent in cardiac arrest, with uncertain benefit.5 The efficacy of antiarrhythmic drugs when given in combination for cardiac arrest has not been systematically addressed and remains a knowledge gap. The role of prophylactic antiarrhythmic medications on ROSC after successful defibrillation is also uncertain. Though not associated with improved survival to hospital discharge, lidocaine decreased the recurrence of VF/pVT when administered prophylactically after successful defibrillation and ROSC.6 The “2018 AHA Focused Update on Advanced Cardiovascular Life Support Use of Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: An Update to the AHA Guidelines for CPR and Emergency Cardiovascular Care”1 concluded that lidocaine use could be considered in specific circumstances (such as during EMS transport) when treatment of recurrent VF/pVT might be compromised. There is no evidence addressing the use of other antiarrhythmic drugs for this specific indication.
Two randomized trials from the same center reported improved survival and neurological outcome when steroids were bundled in combination with vasopressin and epinephrine during cardiac arrest and also administered after successful resuscitation from cardiac arrest.7,8 However, nonrandomized studies of strictly intra-arrest corticosteroid administration, in addition to standard resuscitation, show mixed outcomes.9,10 Due to the only studies suggesting benefit being from a single center with a bundled intervention, and observational data having conflicting results, whether steroids are beneficial during cardiac arrest remains unclear. At least 1 trial attempting to validate the findings of Mentzelopoulos et al is ongoing (NCT03640949).
Since last addressed by the 2010 Guidelines, a 2013 systematic review found little evidence to support the routine use of calcium in undifferentiated cardiac arrest, though the evidence is very weak due to lack of clinical trials and the tendency to use calcium as a “last resort” medication in refractory cardiac arrest.11 Administration of calcium in special circumstances such as hyperkalemia and calcium blocker overdose is addressed in Electrolyte Abnormalities and in Toxicity: β-Adrenergic Blockers and Calcium Channel Blockers.
Clinical trials and observational studies since the 2010 Guidelines have yielded no new evidence that routine administration of sodium bicarbonate improves outcomes from undifferentiated cardiac arrest and evidence suggests that it may worsen survival and neurological recovery.12–14 Use of sodium bicarbonate in special circumstances such as hyperkalemia and drug overdose is addressed in Electrolyte Abnormalities and in Toxicity: Sodium Channel Blockers, Including Tricyclic Antidepressants.
Magnesium’s role as an antiarrhythmic agent was last addressed by the 2018 focused update on advanced cardiovascular life support (ACLS) guidelines.1 RCTs have not found it to improve ROSC, survival, or neurological outcome regardless of the presenting cardiac arrest rhythm,15–18 nor useful for monomorphic VT.19 There are anecdotal reports and small case series attesting to magnesium’s efficacy in the treatment of torsades de pointes (See Torsades de Pointes).

Recommendations 1 and 5 are supported by the 2018 focused update on ACLS guidelines.1 Recommendation 2 last received formal evidence review in 2015.20 Recommendations 3 and 4 last received formal evidence review in 2010.21

References

1. Panchal AR, Berg KM, Kudenchuk PJ, Del Rios M, Hirsch KG, Link MS, Kurz MC, Chan PS, Cabañas JG, Morley PT, Hazinski MF, Donnino MW. 2018 American Heart Association Focused Update on Advanced Cardiovascular Life Support Use of Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2018; 138:e740–e749. doi: 10.1161/CIR.0000000000000613LinkGoogle Scholar
2. Kudenchuk PJ, Brown SP, Daya M, Rea T, Nichol G, Morrison LJ, Leroux B, Vaillancourt C, Wittwer L, Callaway CW, Christenson J, Egan D, Ornato JP, Weisfeldt ML, Stiell IG, Idris AH, Aufderheide TP, Dunford JV, Colella MR, Vilke GM, Brienza AM, Desvigne-Nickens P, Gray PC, Gray R, Seals N, Straight R, Dorian PResuscitation Outcomes Consortium Investigators. Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest.N Engl J Med. 2016; 374:1711–1722. doi: 10.1056/NEJMoa1514204CrossrefMedlineGoogle Scholar
3. Chowdhury A, Fernandes B, Melhuish TM, White LD. Antiarrhythmics in Cardiac Arrest: A Systematic Review and Meta-Analysis.Heart Lung Circ. 2018; 27:280–290. doi: 10.1016/j.hlc.2017.07.004CrossrefMedlineGoogle Scholar
4. Batul SA, Gopinathannair R. Intravenous Sotalol - Reintroducing a Forgotten Agent to the Electrophysiology Therapeutic Arsenal.J Atr Fibrillation. 2017; 9:1499. doi: 10.4022/jafib.1499CrossrefMedlineGoogle Scholar
5. Markel DT, Gold LS, Allen J, Fahrenbruch CE, Rea TD, Eisenberg MS, Kudenchuk PJ. Procainamide and survival in ventricular fibrillation out-of-hospital cardiac arrest.Acad Emerg Med. 2010; 17:617–623. doi: 10.1111/j.1553-2712.2010.00763.xCrossrefMedlineGoogle Scholar
6. Kudenchuk PJ, Newell C, White L, Fahrenbruch C, Rea T, Eisenberg M. Prophylactic lidocaine for post resuscitation care of patients with out-of-hospital ventricular fibrillation cardiac arrest.Resuscitation. 2013; 84:1512–1518. doi: 10.1016/j.resuscitation.2013.05.022CrossrefMedlineGoogle Scholar
7. Mentzelopoulos SD, Zakynthinos SG, Tzoufi M, Katsios N, Papastylianou A, Gkisioti S, Stathopoulos A, Kollintza A, Stamataki E, Roussos C. Vasopressin, epinephrine, and corticosteroids for in-hospital cardiac arrest.Arch Intern Med. 2009; 169:15–24. doi: 10.1001/archinternmed.2008.509CrossrefMedlineGoogle Scholar
8. Mentzelopoulos SD, Malachias S, Chamos C, Konstantopoulos D, Ntaidou T, Papastylianou A, Kolliantzaki I, Theodoridi M, Ischaki H, Makris D, Zakynthinos E, Zintzaras E, Sourlas S, Aloizos S, Zakynthinos SG. Vasopressin, steroids, and epinephrine and neurologically favorable survival after in-hospital cardiac arrest: a randomized clinical trial.JAMA. 2013; 310:270–279. doi: 10.1001/jama.2013.7832CrossrefMedlineGoogle Scholar
9. Tsai MS, Chuang PY, Yu PH, Huang CH, Tang CH, Chang WT, Chen WJ. Glucocorticoid use during cardiopulmonary resuscitation may be beneficial for cardiac arrest.Int J Cardiol. 2016; 222:629–635. doi: 10.1016/j.ijcard.2016.08.017CrossrefMedlineGoogle Scholar
10. Tsai MS, Huang CH, Chang WT, Chen WJ, Hsu CY, Hsieh CC, Yang CW, Chiang WC, Ma MH, Chen SC. The effect of hydrocortisone on the outcome of out-of-hospital cardiac arrest patients: a pilot study.Am J Emerg Med. 2007; 25:318–325. doi: 10.1016/j.ajem.2006.12.007CrossrefMedlineGoogle Scholar
11. Kette F, Ghuman J, Parr M. Calcium administration during cardiac arrest: a systematic review.Eur J Emerg Med. 2013; 20:72–78. doi: 10.1097/MEJ.0b013e328358e336CrossrefMedlineGoogle Scholar
12. Vukmir RB, Katz LSodium Bicarbonate Study Group. Sodium bicarbonate improves outcome in prolonged prehospital cardiac arrest.Am J Emerg Med. 2006; 24:156–161. doi: 10.1016/j.ajem.2005.08.016CrossrefMedlineGoogle Scholar
13. Ahn S, Kim YJ, Sohn CH, Seo DW, Lim KS, Donnino MW, Kim WY. Sodium bicarbonate on severe metabolic acidosis during prolonged cardiopulmonary resuscitation: a double-blind, randomized, placebo-controlled pilot study.J Thorac Dis. 2018; 10:2295–2302. doi: 10.21037/jtd.2018.03.124CrossrefMedlineGoogle Scholar
14. Kawano T, Grunau B, Scheuermeyer FX, Gibo K, Dick W, Fordyce CB, Dorian P, Stenstrom R, Straight R, Christenson J. Prehospital sodium bicarbonate use could worsen long term survival with favorable neurological recovery among patients with out-of-hospital cardiac arrest.Resuscitation. 2017; 119:63–69. doi: 10.1016/j.resuscitation.2017.08.008CrossrefMedlineGoogle Scholar
15. Fatovich DM, Prentice DA, Dobb GJ. Magnesium in cardiac arrest (the magic trial).Resuscitation. 1997; 35:237–241. doi: 10.1016/s0300-9572(97)00062-2CrossrefMedlineGoogle Scholar
16. Allegra J, Lavery R, Cody R, Birnbaum G, Brennan J, Hartman A, Horowitz M, Nashed A, Yablonski M. Magnesium sulfate in the treatment of refractory ventricular fibrillation in the prehospital setting.Resuscitation. 2001; 49:245–249. doi: 10.1016/s0300-9572(00)00375-0CrossrefMedlineGoogle Scholar
17. Hassan TB, Jagger C, Barnett DB. A randomised trial to investigate the efficacy of magnesium sulphate for refractory ventricular fibrillation.Emerg Med J. 2002; 19:57–62.CrossrefMedlineGoogle Scholar
18. Thel MC, Armstrong AL, McNulty SE, Califf RM, O’Connor CM. Randomised trial of magnesium in in-hospital cardiac arrest. Duke Internal Medicine Housestaff.Lancet. 1997; 350:1272–1276. doi: 10.1016/s0140-6736(97)05048-4CrossrefMedlineGoogle Scholar
19. Manz M, Jung W, Lüderitz B. Effect of magnesium on sustained ventricular tachycardia [in German].Herz. 1997; 22(suppl 1):51–55. doi: 10.1007/bf03042655CrossrefMedlineGoogle Scholar
20. Link MS, Berkow LC, Kudenchuk PJ, Halperin HR, Hess EP, Moitra VK, Neumar RW, O’Neil BJ, Paxton JH, Silvers SM, et al.. Part 7: adult advanced cardiovascular life support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S444–S464. doi: 10.1161/CIR.0000000000000261LinkGoogle Scholar
21. Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, et al.. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122:S729–S767. doi: 10.1161/CIRCULATIONAHA.110.970988LinkGoogle Scholar

Adjuncts to CPR

Synopsis

Although the vast majority of cardiac arrest trials have been conducted in OHCA, IHCA comprises almost half of the arrests that occur in the United States annually, and many OHCA resuscitations continue into the emergency department. IHCA patients often have invasive monitoring devices in place such as central venous or arterial lines, and personnel to perform advanced procedures such as arterial blood gas analysis or point-of-care ultrasound are often present. Advanced monitoring such as ETCO2 monitoring is being increasingly used. Determining the utility of such physiological monitoring or diagnostic procedures is important. High-quality CPR, defibrillation when appropriate, vasopressors and/or antiarrhythmics, and airway management remain the cornerstones of cardiac arrest resuscitation, but some emerging data suggest that incorporating patient-specific imaging and physiological data into our approach to resuscitation holds some promise. See Metrics for High-Quality CPR for recommendations on physiological monitoring during CPR. More research in this area is clearly needed.

Recommendation-Specific Supportive Text

Point-of-care cardiac ultrasound can identify cardiac tamponade or other potentially reversible causes of cardiac arrest and identify cardiac motion in pulseless electrical activity.1,2 However, cardiac ultrasound is also associated with longer interruptions in chest compressions.3 A single small RCT found no improvement in outcomes with the use of cardiac ultrasound during CPR.4
No adult human studies directly compare levels of inspired oxygen concentration during CPR. A small number of studies has shown that higher Pao2 during CPR is associated with ROSC, but this is likely due to differences in patients or resuscitation quality.5–7
Observational studies have found that increases in ETCO2 of more than 10 mm Hg may indicate ROSC, although no specific cutoff value indicative of ROSC has been identified.8
Arterial Po2 and Pco2 values are dependent on cardiac output and ventilation and therefore will depend on both patient characteristics and CPR quality. One small study found wide discrepancies in blood gases between mixed venous and arterial samples during CPR and concluded that arterial samples are not accurate during resuscitation.9
If an arterial line is in place, an abrupt increase in diastolic pressure or the presence of an arterial waveform during a rhythm check showing an organized rhythm may indicate ROSC.

Recommendations 1, 3, and 5 last received formal evidence review in 2015.10. Recommendation 2 last received formal evidence review in 2015,10 with an evidence update completed in 2020.11 Recommendation 4 last received formal evidence review in 2010.12

References

1. Breitkreutz R, Price S, Steiger HV, Seeger FH, Ilper H, Ackermann H, Rudolph M, Uddin S, Weigand MA, Müller E, Walcher FEmergency Ultrasound Working Group of the Johann Wolfgang Goethe-University Hospital, Frankfurt am Main. Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients: a prospective trial.Resuscitation. 2010; 81:1527–1533. doi: 10.1016/j.resuscitation.2010.07.013CrossrefMedlineGoogle Scholar
2. Gaspari R, Weekes A, Adhikari S, Noble VE, Nomura JT, Theodoro D, Woo M, Atkinson P, Blehar D, Brown SM, Caffery T, Douglass E, Fraser J, Haines C, Lam S, Lanspa M, Lewis M, Liebmann O, Limkakeng A, Lopez F, Platz E, Mendoza M, Minnigan H, Moore C, Novik J, Rang L, Scruggs W, Raio C. Emergency department point-of-care ultrasound in out-of-hospital and in-ED cardiac arrest.Resuscitation. 2016; 109:33–39. doi: 10.1016/j.resuscitation.2016.09.018CrossrefMedlineGoogle Scholar
3. Clattenburg EJ, Wroe P, Brown S, Gardner K, Losonczy L, Singh A, Nagdev A. Point-of-care ultrasound use in patients with cardiac arrest is associated prolonged cardiopulmonary resuscitation pauses: A prospective cohort study.Resuscitation. 2018; 122:65–68. doi: 10.1016/j.resuscitation.2017.11.056CrossrefMedlineGoogle Scholar
4. Chardoli M, Heidari F, Rabiee H, Sharif-Alhoseini M, Shokoohi H, Rahimi-Movaghar V. Echocardiography integrated ACLS protocol versus conventional cardiopulmonary resuscitation in patients with pulseless electrical activity cardiac arrest.Chin J Traumatol. 2012; 15:284–287.MedlineGoogle Scholar
5. Spindelboeck W, Schindler O, Moser A, Hausler F, Wallner S, Strasser C, Haas J, Gemes G, Prause G. Increasing arterial oxygen partial pressure during cardiopulmonary resuscitation is associated with improved rates of hospital admission.Resuscitation. 2013; 84:770–775. doi: 10.1016/j.resuscitation.2013.01.012CrossrefMedlineGoogle Scholar
6. Spindelboeck W, Gemes G, Strasser C, Toescher K, Kores B, Metnitz P, Haas J, Prause G. Arterial blood gases during and their dynamic changes after cardiopulmonary resuscitation: A prospective clinical study.Resuscitation. 2016; 106:24–29. doi: 10.1016/j.resuscitation.2016.06.013CrossrefMedlineGoogle Scholar
7. Patel JK, Schoenfeld E, Parikh PB, Parnia S. Association of Arterial Oxygen Tension During In-Hospital Cardiac Arrest With Return of Spontaneous Circulation and Survival.J Intensive Care Med. 2018; 33:407–414. doi: 10.1177/0885066616658420CrossrefMedlineGoogle Scholar
8. Sandroni C, De Santis P, D’Arrigo S. Capnography during cardiac arrest.Resuscitation. 2018; 132:73–77. doi: 10.1016/j.resuscitation.2018.08.018CrossrefMedlineGoogle Scholar
9. Weil MH, Rackow EC, Trevino R, Grundler W, Falk JL, Griffel MI. Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation.N Engl J Med. 1986; 315:153–156. doi: 10.1056/NEJM198607173150303CrossrefMedlineGoogle Scholar
10. Link MS, Berkow LC, Kudenchuk PJ, Halperin HR, Hess EP, Moitra VK, Neumar RW, O’Neil BJ, Paxton JH, Silvers SM, et al.. Part 7: adult advanced cardiovascular life support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S444–S464. doi: 10.1161/CIR.0000000000000261LinkGoogle Scholar
11. Berg KM, Soar J, Andersen LW, Böttiger BW, Cacciola S, Callaway CW, Couper K, Cronberg T, D’Arrigo S, Deakin CD, et al.; on behalf of the Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S92–S139. doi: 10.1161/CIR.0000000000000893LinkGoogle Scholar
12. Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, et al.. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122:S729–S767. doi: 10.1161/CIRCULATIONAHA.110.970988LinkGoogle Scholar

Termination of Resuscitation

Synopsis

OHCA is a resource-intensive condition most often associated with low rates of survival. It is important for EMS providers to be able to differentiate patients in whom continued resuscitation is futile from patients with a chance of survival who should receive continued resuscitation and transportation to hospital. This will aid in both resource utilization and optimizing a patient’s chance for survival. Using a validated TOR rule will help ensure accuracy in determining futile patients (Figures 5 and 6). Futility is often defined as less than 1% chance of survival,1 suggesting that for a TOR rule to be valid it should demonstrate high accuracy for predicting futility with the lower confidence limit greater than 99% on external validation.

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Figure 5. Adult basic life support termination of resuscitation rule.2 AED indicates automated external defibrillator; and BLS, basic life support.

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Figure 6. Adult advanced life support termination of resuscitation rule.2 ACLS indicates advanced cardiovascular life support; and CPR, cardiopulmonary resuscitation.

Recommendation-Specific Supportive Text

The BLS TOR rule recommends TOR when all of the following criteria apply before moving to the ambulance for transport: (1) arrest was not witnessed by EMS providers or first responder; (2) no ROSC obtained; and (3) no shocks were delivered. In a recent meta-analysis of 7 published studies (33 795 patients), only 0.13% (95% CI, 0.03%–0.58%) of patients who fulfilled the BLS termination criteria survived to hospital discharge.3
The ALS TOR rule recommends TOR when all of the following criteria apply before moving to the ambulance for transport: (1) arrest was not witnessed; (2) no bystander CPR was provided; (3) no ROSC after full ALS care in the field; and (4) no AED shocks were delivered. In a recent meta-analysis of 2 published studies (10 178 patients), only 0.01% (95% CI, 0.00%–0.07%) of patients who fulfilled the ALS termination criteria survived to hospital discharge.3
The BLS TOR rule, otherwise known as the universal TOR rule (arrest not witnessed by EMS providers; no shock delivered; no ROSC), has been prospectively validated in combined BLS and ALS systems.4 Although the rule did not have adequate specificity after 6 minutes of resuscitation (false-positive rate: 2.1%) it did achieve better than 99% specificity after approximately 15 minutes of attempted resuscitation, while still reducing transportation by half. A retrospective analysis found that application of the universal TOR at 20 minutes of resuscitation was able to predict futility, identifying over 99% of survivors and patients with good neurological outcome.5
In intubated patients, an ETCO2 measurement less than 10 mm Hg indicates low to no blood flow. Several small studies provide evidence showing that an ETCO2 less than 10 mm Hg after 20 minutes of ALS resuscitation is strongly but not perfectly predictive of futility.6–9 These small observational studies suffer from high risk of bias. Alternative ETCO2 thresholds and timepoints have been proposed. The use of ETCO2 alone to predict patient outcome needs to be validated in a large prospective study.
A recent systematic review found that no sonographic finding had consistently high sensitivity for clinical outcomes to be used as the sole criterion to terminate cardiac arrest resuscitation.10 Although some findings demonstrated higher ranges of sensitivity and/or specificity, studies examining the use of point-of-care ultrasound during cardiac arrest demonstrate varying results and are hindered by significant bias. There is considerable heterogeneity between studies in terms of timing and application of point-of-care ultrasound as well as inconsistent definitions and terminology in terms of cardiac motion. Further there is little research examining the interrater reliability of ultrasound findings during cardiac arrest.11,12 In addition, see Adjuncts to CPR for ultrasound as an adjunct to CPR.
No studies were found that specifically examined the use of ETCO2 in cardiac arrest patients without an advanced airway. It is not known whether ETCO2 values during bag-mask ventilation are as reliable as those with an advanced airway in place. Because of the lack of evidence, there is nothing to support using any cutoff value of ETCO2 for decisions about TOR in a nonintubated patient.

Recommendations 1, 2, 3, and 5 are supported by the 2020 CoSTRs for BLS and ALS.13,14 Recommendations 4 and 6 last received formal evidence review in 2015.15

References

1. Schneiderman LJ. Defining Medical Futility and Improving Medical Care.J Bioeth Inq. 2011; 8:123–131. doi: 10.1007/s11673-011-9293-3CrossrefMedlineGoogle Scholar
2. Morrison LJ, Kierzek G, Diekema DS, Sayre MR, Silvers SM, Idris AH, Mancini ME. Part 3: ethics: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S665–S675. doi: 10.1161/CIRCULATIONAHA.110.970905LinkGoogle Scholar
3. Ebell MH, Vellinga A, Masterson S, Yun P. Meta-analysis of the accuracy of termination of resuscitation rules for out-of-hospital cardiac arrest.Emerg Med J. 2019; 36:479–484. doi: 10.1136/emermed-2018-207833CrossrefMedlineGoogle Scholar
4. Grunau B, Taylor J, Scheuermeyer FX, Stenstrom R, Dick W, Kawano T, Barbic D, Drennan I, Christenson J. External Validation of the Universal Termination of Resuscitation Rule for Out-of-Hospital Cardiac Arrest in British Columbia.Ann Emerg Med. 2017; 70:374–381.e1. doi: 10.1016/j.annemergmed.2017.01.030CrossrefMedlineGoogle Scholar
5. Drennan IR, Case E, Verbeek PR, Reynolds JC, Goldberger ZD, Jasti J, Charleston M, Herren H, Idris AH, Leslie PR, Austin MA, Xiong Y, Schmicker RH, Morrison LJResuscitation Outcomes Consortium Investigators. A comparison of the universal TOR Guideline to the absence of prehospital ROSC and duration of resuscitation in predicting futility from out-of-hospital cardiac arrest.Resuscitation. 2017; 111:96–102. doi: 10.1016/j.resuscitation.2016.11.021CrossrefMedlineGoogle Scholar
6. Ahrens T, Schallom L, Bettorf K, Ellner S, Hurt G, O’Mara V, Ludwig J, George W, Marino T, Shannon W. End-tidal carbon dioxide measurements as a prognostic indicator of outcome in cardiac arrest.Am J Crit Care. 2001; 10:391–398.CrossrefMedlineGoogle Scholar
7. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest.N Engl J Med. 1997; 337:301–306. doi: 10.1056/NEJM199707313370503CrossrefMedlineGoogle Scholar
8. Wayne MA, Levine RL, Miller CC. Use of end-tidal carbon dioxide to predict outcome in prehospital cardiac arrest.Ann Emerg Med. 1995; 25:762–767. doi: 10.1016/s0196-0644(95)70204-0CrossrefMedlineGoogle Scholar
9. Akinci E, Ramadan H, Yuzbasioglu Y, Coskun F. Comparison of end-tidal carbon dioxide levels with cardiopulmonary resuscitation success presented to emergency department with cardiopulmonary arrest.Pak J Med Sci. 2014; 30:16–21. doi: 10.12669/pjms.301.4024MedlineGoogle Scholar
10. Reynolds JC, Mahmoud SI, Nicholson T, Drennan IR, Berg K, O’Neil BJ, Welsford Mon behalf of the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation. Prognostication with point-of-care echocardiography during cardiac arrest: a systematic review.Resuscitation. 2020:In pressCrossrefGoogle Scholar
11. Flato UA, Paiva EF, Carballo MT, Buehler AM, Marco R, Timerman A. Echocardiography for prognostication during the resuscitation of intensive care unit patients with non-shockable rhythm cardiac arrest.Resuscitation. 2015; 92:1–6. doi: 10.1016/j.resuscitation.2015.03.024CrossrefMedlineGoogle Scholar
12. Gaspari R, Weekes A, Adhikari S, Noble VE, Nomura JT, Theodoro D, Woo M, Atkinson P, Blehar D, Brown SM, Caffery T, Douglass E, Fraser J, Haines C, Lam S, Lanspa M, Lewis M, Liebmann O, Limkakeng A, Lopez F, Platz E, Mendoza M, Minnigan H, Moore C, Novik J, Rang L, Scruggs W, Raio C. Emergency department point-of-care ultrasound in out-of-hospital and in-ED cardiac arrest.Resuscitation. 2016; 109:33–39. doi: 10.1016/j.resuscitation.2016.09.018CrossrefMedlineGoogle Scholar
13. Olasveengen TM, Mancini ME, Perkins GD, Avis S, Brooks S, Castrén M, Chung SP, Considine J, Couper K, Escalante R, et al.; on behalf of the Adult Basic Life Support Collaborators. Adult basic life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S41–S91. doi: 10.1161/CIR.0000000000000892LinkGoogle Scholar
14. Berg KM, Soar J, Andersen LW, Böttiger BW, Cacciola S, Callaway CW, Couper K, Cronberg T, D’Arrigo S, Deakin CD, et al.; on behalf of the Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S92–S139. doi: 10.1161/CIR.0000000000000893LinkGoogle Scholar
15. Link MS, Berkow LC, Kudenchuk PJ, Halperin HR, Hess EP, Moitra VK, Neumar RW, O’Neil BJ, Paxton JH, Silvers SM, et al.. Part 7: adult advanced cardiovascular life support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S444–S464. doi: 10.1161/CIR.0000000000000261LinkGoogle Scholar

Advanced Techniques and Devices for Resuscitation

Advanced Airway Placement

Introduction

Airway management during cardiac arrest usually commences with a basic strategy such as bag-mask ventilation. In addition, it may be helpful for providers to master an advanced airway strategy as well as a second (backup) strategy for use if they are unable to establish the first-choice airway adjunct. Because placement of an advanced airway may result in interruption of chest compressions, a malpositioned device, or undesirable hyperventilation, providers should carefully weigh these risks against the potential benefits of an advanced airway. The 2019 focused update on ACLS guidelines addressed the use of advanced airways in cardiac arrest and noted that either bag-mask ventilation or an advanced airway strategy may be considered during CPR for adult cardiac arrest in any setting.1 Outcomes from advanced airway and bag-mask ventilation interventions are highly dependent on the skill set and experience of the provider (Figure 7). Thus, the ultimate decision of the use, type, and timing of an advanced airway will require consideration of a host of patient and provider characteristics that are not easily defined in a global recommendation. Important considerations for determining airway management strategies is provider airway management skill and experience, frequent retraining for providers, and ongoing quality improvement to minimize airway management complications.

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Figure 7. Schematic representation of ALS recommendations for use of advanced airways during CPR. ALS indicates advanced life support; CPR, cardiopulmonary resuscitation; and EMS, emergency medical services.

Recommendation-Specific Supportive Text

One large RCT in OHCA comparing bag-mask ventilation with endotracheal intubation (ETI) in a physician-based EMS system showed no significant benefit for either technique for 28-day survival or survival with favorable neurological outcome.2 The success rate of ETI in this study was 98%, suggesting a relatively optimal setting for the potential success of ETI as an intervention. Further research is required to determine equivalence or superiority between the 2 approaches for acute airway management.

These recommendations are supported by the 2019 focused update on ACLS guidelines.1

Recommendation-Specific Supportive Text

1, 2, and 3. One RCT in OHCA comparing SGA (with iGel) to ETI in a non–physician-based EMS system (ETI success, 69%) found no difference in survival or survival with favorable neurological outcome at hospital discharge.3 A second RCT in OHCA comparing SGA (with laryngeal tube) with ETI in a non–physician-based EMS system (ETI success, 52%) found both better survival to hospital discharge and better survival to hospital discharge with good neurological outcome in the patients managed with SGA.4 These results are challenging to contextualize because they both allowed for provider deviation from protocol based on clinical judgment. Additionally, precise thresholds for high or low tracheal intubation success rates have not been identified, though guidance can be taken from the existing clinical trials. Thus, it is difficult to understand the potential benefit (or harm), per individual, that drove the decision to place the specific advanced airway device. The decision on placement of an advanced airway requires an understanding of patient and provider characteristics that are not easily defined in a global recommendation. Because of a paucity of studies on advanced airway management for IHCA, the IHCA recommendations are extrapolated from OHCA data. Based on these issues, there is a need for further research specifically on the interface between patient factors and the experience, training, tools, and skills of the provider. Given these reasons, a recommendation for SGA in preference to ETI would be premature.

These recommendations are supported by the 2019 focused update on ACLS guidelines.1

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To maintain provider skills from initial training, frequent retraining is important.5,6 However, future research will need to address the specific type, amount, and duration between training experiences.
Although an advanced airway can be placed without interrupting chest compressions,7 unfortunately, such interruptions still occur. Therefore, providers should weigh the potential benefits of an advanced airway with the benefits of maintaining a high chest compression fraction.8–10
In a small clinical trial and several observational studies, waveform capnography was 100% specific for confirming endotracheal tube position during cardiac arrest.11–13 The sensitivity of waveform capnography decreases after a prolonged cardiac arrest.11–13 The use of waveform capnography to assess the placement of other advanced airways (eg, Combitube, laryngeal mask airway) has not been studied.
The rationale for tracking the overall success rate for systems performing ETI is to make informed decisions as to whether practice should allow for ETI, move toward SGA, or simply use bag-mask ventilation for patients in cardiac arrest; recommendations will vary depending on the overall success rate in a given system.

These recommendations are supported by the 2019 focused update on ACLS guidelines.1

References

1. Panchal AR, Berg KM, Hirsch KG, Kudenchuk PJ, Del Rios M, Cabañas JG, Link MS, Kurz MC, Chan PS, Morley PT, et al.. 2019 American Heart Association focused update on advanced cardiovascular life support: use of advanced airways, vasopressors, and extracorporeal cardiopulmonary resuscitation during cardiac arrest: an update to the American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care.Circulation. 2019; 140:e881–e894. doi: 10.1161/CIR.0000000000000732LinkGoogle Scholar
2. Jabre P, Penaloza A, Pinero D, Duchateau FX, Borron SW, Javaudin F, Richard O, de Longueville D, Bouilleau G, Devaud ML, Heidet M, Lejeune C, Fauroux S, Greingor JL, Manara A, Hubert JC, Guihard B, Vermylen O, Lievens P, Auffret Y, Maisondieu C, Huet S, Claessens B, Lapostolle F, Javaud N, Reuter PG, Baker E, Vicaut E, Adnet F. Effect of Bag-Mask Ventilation vs Endotracheal Intubation During Cardiopulmonary Resuscitation on Neurological Outcome After Out-of-Hospital Cardiorespiratory Arrest: A Randomized Clinical Trial.JAMA. 2018; 319:779–787. doi: 10.1001/jama.2018.0156CrossrefMedlineGoogle Scholar
3. Benger JR, Kirby K, Black S, Brett SJ, Clout M, Lazaroo MJ, Nolan JP, Reeves BC, Robinson M, Scott LJ, Smartt H, South A, Stokes EA, Taylor J, Thomas M, Voss S, Wordsworth S, Rogers CA. Effect of a Strategy of a Supraglottic Airway Device vs Tracheal Intubation During Out-of-Hospital Cardiac Arrest on Functional Outcome: The AIRWAYS-2 Randomized Clinical Trial.JAMA. 2018; 320:779–791. doi: 10.1001/jama.2018.11597CrossrefMedlineGoogle Scholar
4. Wang HE, Schmicker RH, Daya MR, Stephens SW, Idris AH, Carlson JN, Colella MR, Herren H, Hansen M, Richmond NJ, Puyana JCJ, Aufderheide TP, Gray RE, Gray PC, Verkest M, Owens PC, Brienza AM, Sternig KJ, May SJ, Sopko GR, Weisfeldt ML, Nichol G. Effect of a Strategy of Initial Laryngeal Tube Insertion vs Endotracheal Intubation on 72-Hour Survival in Adults With Out-of-Hospital Cardiac Arrest: A Randomized Clinical Trial.JAMA. 2018; 320:769–778. doi: 10.1001/jama.2018.7044CrossrefMedlineGoogle Scholar
5. Wong ML, Carey S, Mader TJ, Wang HEAmerican Heart Association National Registry of Cardiopulmonary Resuscitation Investigators. Time to invasive airway placement and resuscitation outcomes after inhospital cardiopulmonary arrest.Resuscitation. 2010; 81:182–186. doi: 10.1016/j.resuscitation.2009.10.027CrossrefMedlineGoogle Scholar
6. Warner KJ, Carlbom D, Cooke CR, Bulger EM, Copass MK, Sharar SR. Paramedic training for proficient prehospital endotracheal intubation.Prehosp Emerg Care. 2010; 14:103–108. doi: 10.3109/10903120903144858CrossrefMedlineGoogle Scholar
7. Gatward JJ, Thomas MJ, Nolan JP, Cook TM. Effect of chest compressions on the time taken to insert airway devices in a manikin.Br J Anaesth. 2008; 100:351–356. doi: 10.1093/bja/aem364CrossrefMedlineGoogle Scholar
8. Talikowska M, Tohira H, Finn J. Cardiopulmonary resuscitation quality and patient survival outcome in cardiac arrest: A systematic review and meta-analysis.Resuscitation. 2015; 96:66–77. doi: 10.1016/j.resuscitation.2015.07.036CrossrefMedlineGoogle Scholar
9. Vaillancourt C, Everson-Stewart S, Christenson J, Andrusiek D, Powell J, Nichol G, Cheskes S, Aufderheide TP, Berg R, Stiell IGResuscitation Outcomes Consortium Investigators. The impact of increased chest compression fraction on return of spontaneous circulation for out-of-hospital cardiac arrest patients not in ventricular fibrillation.Resuscitation. 2011; 82:1501–1507. doi: 10.1016/j.resuscitation.2011.07.011CrossrefMedlineGoogle Scholar
10. Christenson J, Andrusiek D, Everson-Stewart S, Kudenchuk P, Hostler D, Powell J, Callaway CW, Bishop D, Vaillancourt C, Davis D, Aufderheide TP, Idris A, Stouffer JA, Stiell I, Berg RResuscitation Outcomes Consortium Investigators. Chest compression fraction determines survival in patients with out-of-hospital ventricular fibrillation.Circulation. 2009; 120:1241–1247. doi: 10.1161/CIRCULATIONAHA.109.852202LinkGoogle Scholar
11. Grmec S. Comparison of three different methods to confirm tracheal tube placement in emergency intubation.Intensive Care Med. 2002; 28:701–704. doi: 10.1007/s00134-002-1290-xCrossrefMedlineGoogle Scholar
12. Takeda T, Tanigawa K, Tanaka H, Hayashi Y, Goto E, Tanaka K. The assessment of three methods to verify tracheal tube placement in the emergency setting.Resuscitation. 2003; 56:153–157. doi: 10.1016/s0300-9572(02)00345-3CrossrefMedlineGoogle Scholar
13. Tanigawa K, Takeda T, Goto E, Tanaka K. Accuracy and reliability of the self-inflating bulb to verify tracheal intubation in out-of-hospital cardiac arrest patients.Anesthesiology. 2000; 93:1432–1436. doi: 10.1097/00000542-200012000-00015CrossrefMedlineGoogle Scholar

Alternative CPR Techniques and Devices

Introduction

Many alternatives and adjuncts to conventional CPR have been developed. These include mechanical CPR, impedance threshold devices (ITD), active compression-decompression (ACD) CPR, and interposed abdominal compression CPR. Many of these techniques and devices require specialized equipment and training.

Mechanical CPR devices deliver automated chest compressions, thereby eliminating the need for manual chest compressions. There are 2 different types of mechanical CPR devices: a load-distributing compression band that compresses the entire thorax circumferentially and a pneumatic piston device that compresses the chest in an anteroposterior direction. A recent systematic review of 11 RCTs (overall moderate to low certainty of evidence) found no evidence of improved survival with good neurological outcome with mechanical CPR compared with manual CPR in either OHCA or IHCA.1 Given the perceived logistic advantages related to limited personnel and safety during patient transport, mechanical CPR remains popular among some providers and systems.

ACD-CPR is performed by using a handheld device with a suction cup applied to the midsternum, actively lifting up the chest during decompressions, thereby enhancing the negative intrathoracic pressure generated by chest recoil and increasing venous return and cardiac output during the next chest compression. The ITD is a pressure-sensitive valve attached to an advanced airway or face mask that limits air entry into the lungs during the decompression phase of CPR, enhancing the negative intrathoracic pressure generated during chest wall recoil and improving venous return and cardiac output during CPR.

There are many alternative CPR techniques being used, and many are unproven. As an example, there is insufficient evidence concerning the cardiac arrest bundle of care with the inclusion of “heads-up” CPR to provide a recommendation concerning its use.2 Further investigation in this and other alternative CPR techniques is best explored in the context of formal controlled clinical research.

Recommendation-Specific Supportive Text

1 and 2. Studies of mechanical CPR devices have not demonstrated a benefit when compared with manual CPR, with a suggestion of worse neurological outcome in some studies. In the ASPIRE trial (1071 patients), use of the load-distributing band device was associated with similar odds of survival to hospital discharge (adjusted odds ratio [aOR], 0.56; CI, 0.31–1.00; P=0.06), and worse survival with good neurological outcome (3.1% versus 7.5%; P=0.006), compared with manual CPR.3 In the CIRC trial (n=4231), use of load-distributing band–CPR resulted in statistically equivalent rates of survival to hospital discharge (aOR, 1.06; CI, 0.83–1.37) and survival with good neurological outcome (aOR, 0.80; CI, 0.47–1.37).4 In the PARAMEDIC trial (n=4470), use of a mechanical piston device produced similar rates of 30-day survival (aOR, 0.86; CI, 0.64–1.15), and worse survival with good neurological outcome (aOR, 0.72; CI, 0.52–0.99), compared with manual CPR.5 In the LINC trial (n=2589), survival with good neurological outcome was similar in both groups (8.3% versus 7.8%; risk difference, 0.55%; 95% CI, –1.5% to 2.6%).6

Acknowledging these data, the use of mechanical CPR devices by trained personnel may be beneficial in settings where reliable, high-quality manual compressions are not possible or may cause risk to personnel (ie, limited personnel, moving ambulance, angiography suite, prolonged resuscitation, or with concerns for infectious disease exposure).

This topic last received formal evidence review in 2015.7

Recommendation-Specific Supportive Text

A 2013 Cochrane review of 10 trials comparing ACD-CPR with standard CPR found no differences in mortality and neurological function in adults with OHCA or IHCA.8 An important added consideration with this modality is that of increased rescuer fatigue, which could impair the overall quality of CPR.
ACD-CPR and ITD may act synergistically to enhance venous return during chest decompression and improve blood flow to vital organs during CPR. The ResQTrial demonstrated that ACD plus ITD was associated with improved survival to hospital discharge with favorable neurological function for OHCA compared with standard CPR, though this study was limited by a lack of blinding, different CPR feedback elements between the study arms (ie, cointervention), lack of CPR quality assessment, and early TOR.9,10 The 2015 AHA Guidelines Update for CPR and Emergency Cardiovascular Care7 evaluated this topic and noted that though a large RCT of low-quality demonstrated benefit of its use, additional trials were needed to confirm the results because of study limitations noted. Thus, ACD-CPR plus ITD was not recommended in previous versions of the AHA Guidelines. However, in settings where the equipment and trained personnel are available, ACD-CPR plus ITD could be an alternative to standard CPR.
In the PRIMED study (n=8178), the use of the ITD (compared with a sham device) did not significantly improve survival to hospital discharge or survival with good neurological function in patients with OHCA.11 Despite the addition of a post hoc analysis of the PRIMED trial for ITD,12 the routine use of the ITD as an adjunct during conventional CPR is not recommended.

This topic last received formal evidence review in 2015.7

Recommendation-Specific Supportive Text

Interposed abdominal compression CPR is a 3-rescuer technique that includes conventional chest compressions combined with alternating abdominal compressions. The dedicated rescuer who provides manual abdominal compressions will compress the abdomen midway between the xiphoid and the umbilicus during the relaxation phase of chest compression. This topic was last reviewed in 2010 and identified 2 randomized trials, interposed abdominal compression CPR performed by trained rescuers improved short-term survival13 and survival to hospital discharge,14 compared with conventional CPR for adult IHCA. One RCT of adult OHCA15 did not show any survival advantage to interposed abdominal compression CPR. More evaluation is needed to further define the routine use of this technique.

This topic last received formal evidence review in 2010.16

References

1. Wang PL, Brooks SC. Mechanical versus manual chest compressions for cardiac arrest.Cochrane Database Syst Rev. 2018; 8:CD007260. doi: 10.1002/14651858.CD007260.pub4MedlineGoogle Scholar
2. Pepe PE, Scheppke KA, Antevy PM, Crowe RP, Millstone D, Coyle C, Prusansky C, Garay S, Ellis R, Fowler RL, Moore JC. Confirming the Clinical Safety and Feasibility of a Bundled Methodology to Improve Cardiopulmonary Resuscitation Involving a Head-Up/Torso-Up Chest Compression Technique.Crit Care Med. 2019; 47:449–455. doi: 10.1097/CCM.0000000000003608CrossrefMedlineGoogle Scholar
3. Hallstrom A, Rea TD, Sayre MR, Christenson J, Anton AR, Mosesso VN, Van Ottingham L, Olsufka M, Pennington S, White LJ, Yahn S, Husar J, Morris MF, Cobb LA. Manual chest compression vs use of an automated chest compression device during resuscitation following out-of-hospital cardiac arrest: a randomized trial.JAMA. 2006; 295:2620–2628. doi: 10.1001/jama.295.22.2620CrossrefMedlineGoogle Scholar
4. Wik L, Olsen JA, Persse D, Sterz F, Lozano M, Brouwer MA, Westfall M, Souders CM, Malzer R, van Grunsven PM, Travis DT, Whitehead A, Herken UR, Lerner EB. Manual vs. integrated automatic load-distributing band CPR with equal survival after out of hospital cardiac arrest. The randomized CIRC trial.Resuscitation. 2014; 85:741–748. doi: 10.1016/j.resuscitation.2014.03.005CrossrefMedlineGoogle Scholar
5. Perkins GD, Lall R, Quinn T, Deakin CD, Cooke MW, Horton J, Lamb SE, Slowther AM, Woollard M, Carson A, Smyth M, Whitfield R, Williams A, Pocock H, Black JJ, Wright J, Han K, Gates SPARAMEDIC trial collaborators. Mechanical versus manual chest compression for out-of-hospital cardiac arrest (PARAMEDIC): a pragmatic, cluster randomised controlled trial.Lancet. 2015; 385:947–955. doi: 10.1016/S0140-6736(14)61886-9CrossrefMedlineGoogle Scholar
6. Rubertsson S, Lindgren E, Smekal D, Östlund O, Silfverstolpe J, Lichtveld RA, Boomars R, Ahlstedt B, Skoog G, Kastberg R, et al.. Mechanical chest compressions and simultaneous defibrillation vs conventional cardiopulmonary resuscitation in out-of-hospital cardiac arrest: the LINC randomized trial.JAMA. 2014; 311:53–61. doi: 10.1001/jama.2013.282538CrossrefMedlineGoogle Scholar
7. Brooks SC, Anderson ML, Bruder E, Daya MR, Gaffney A, Otto CW, Singer AJ, Thiagarajan RR, Travers AH. Part 6: alternative techniques and ancillary devices for cardiopulmonary resuscitation: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S436–S443. doi: 10.1161/CIR.0000000000000260LinkGoogle Scholar
8. Lafuente-Lafuente C, Melero-Bascones M. Active chest compression-decompression for cardiopulmonary resuscitation.Cochrane Database Syst Rev. 2013CD002751. doi: 10.1002/14651858.CD002751.pub3MedlineGoogle Scholar
9. Aufderheide TP, Frascone RJ, Wayne MA, Mahoney BD, Swor RA, Domeier RM, Olinger ML, Holcomb RG, Tupper DE, Yannopoulos D, Lurie KG. Standard cardiopulmonary resuscitation versus active compression-decompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: a randomised trial.Lancet. 2011; 377:301–311. doi: 10.1016/S0140-6736(10)62103-4CrossrefMedlineGoogle Scholar
10. Frascone RJ, Wayne MA, Swor RA, Mahoney BD, Domeier RM, Olinger ML, Tupper DE, Setum CM, Burkhart N, Klann L, Salzman JG, Wewerka SS, Yannopoulos D, Lurie KG, O’Neil BJ, Holcomb RG, Aufderheide TP. Treatment of non-traumatic out-of-hospital cardiac arrest with active compression decompression cardiopulmonary resuscitation plus an impedance threshold device.Resuscitation. 2013; 84:1214–1222. doi: 10.1016/j.resuscitation.2013.05.002CrossrefMedlineGoogle Scholar
11. Aufderheide TP, Nichol G, Rea TD, Brown SP, Leroux BG, Pepe PE, Kudenchuk PJ, Christenson J, Daya MR, Dorian P, Callaway CW, Idris AH, Andrusiek D, Stephens SW, Hostler D, Davis DP, Dunford JV, Pirrallo RG, Stiell IG, Clement CM, Craig A, Van Ottingham L, Schmidt TA, Wang HE, Weisfeldt ML, Ornato JP, Sopko GResuscitation Outcomes Consortium (ROC) Investigators. A trial of an impedance threshold device in out-of-hospital cardiac arrest.N Engl J Med. 2011; 365:798–806. doi: 10.1056/NEJMoa1010821CrossrefMedlineGoogle Scholar
12. Sugiyama A, Duval S, Nakamura Y, Yoshihara K, Yannopoulos D. Impedance Threshold Device Combined With High-Quality Cardiopulmonary Resuscitation Improves Survival With Favorable Neurological Function After Witnessed Out-of-Hospital Cardiac Arrest.Circ J. 2016; 80:2124–2132. doi: 10.1253/circj.CJ-16-0449CrossrefMedlineGoogle Scholar
13. Sack JB, Kesselbrenner MB, Jarrad A. Interposed abdominal compression-cardiopulmonary resuscitation and resuscitation outcome during asystole and electromechanical dissociation.Circulation. 1992; 86:1692–1700. doi: 10.1161/01.cir.86.6.1692LinkGoogle Scholar
14. Sack JB, Kesselbrenner MB, Bregman D. Survival from in-hospital cardiac arrest with interposed abdominal counterpulsation during cardiopulmonary resuscitation.JAMA. 1992; 267:379–385.CrossrefMedlineGoogle Scholar
15. Mateer JR, Stueven HA, Thompson BM, Aprahamian C, Darin JC. Pre-hospital IAC-CPR versus standard CPR: paramedic resuscitation of cardiac arrests.Am J Emerg Med. 1985; 3:143–146. doi: 10.1016/0735-6757(85)90038-5CrossrefMedlineGoogle Scholar
16. Cave DM, Gazmuri RJ, Otto CW, Nadkarni VM, Cheng A, Brooks SC, Daya M, Sutton RM, Branson R, Hazinski MF. Part 7: CPR techniques and devices: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122:S720–728. doi: 10.1161/CIRCULATIONAHA.110.970970LinkGoogle Scholar

Extracorporeal CPR

Synopsis

ECPR refers to the initiation of cardiopulmonary bypass during the resuscitation of a patient in cardiac arrest. This involves the cannulation of a large vein and artery and initiation of venoarterial extracorporeal circulation and membrane oxygenation (ECMO) (Figure 8). The goal of ECPR is to support end organ perfusion while potentially reversible conditions are addressed. ECPR is a complex intervention that requires a highly trained team, specialized equipment, and multidisciplinary support within a healthcare system. The 2019 focused update on ACLS guidelines1 addressed the use of ECPR for cardiac arrest and noted that there is insufficient evidence to recommend the routine use of ECPR in cardiac arrest. However, ECPR may be considered if there is a potentially reversible cause of an arrest that would benefit from temporary cardiorespiratory support. One important consideration is the selection of patients for ECPR and further research is needed to define patients who would most benefit from the intervention. Furthermore, the resource intensity required to begin and maintain an ECPR program should be considered in the context of strengthening other links in the Chain of Survival. Additional investigations are necessary to evaluate cost-effectiveness, resource allocation, and ethics surrounding the routine use of ECPR in resuscitation.

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Figure 8. Schematic depiction of components of extracorporeal membrane oxygenator circuit as used for ECPR. Components include venous cannula, a pump, an oxygenator, and an arterial cannula. ECPR indicates extracorporeal cardiopulmonary resuscitation.

Recommendation-Specific Supportive Text

There are no RCTs on the use of ECPR for OHCA or IHCA. Fifteen observational studies were identified for OHCA that varied in inclusion criteria, ECPR settings, and study design, with the majority of studies reporting improved neurological outcome associated with ECPR.2 For ECPR use in the in-hospital setting, all studies were assessed as having very serious risk of bias (primarily due to confounding) and the overall certainty of evidence was rated as very low for all outcomes.2 In 3 studies, ECPR was not associated with beneficial effects for short- or long-term neurological outcomes,3–5 while 1 study6 did report associated short- and long-term neurological outcome benefit. Despite many studies reporting favorable outcomes with the use of ECPR, the vast majority of the studies are from single centers with varying inclusion criteria and settings, with decisions to perform ECPR made on a case-by-case basis. While there is currently no evidence to clearly define what should constitute “selected patients,” most of the studies analyzed included younger patients with fewer comorbidities. More data are clearly needed from studies of higher methodologic quality, including randomized trials.

These recommendations are supported by the 2019 focused update on ACLS guidelines.1

References

1. Panchal AR, Berg KM, Hirsch KG, Kudenchuk PJ, Del Rios M, Cabañas JG, Link MS, Kurz MC, Chan PS, Morley PT, et al.. 2019 American Heart Association focused update on advanced cardiovascular life support: use of advanced airways, vasopressors, and extracorporeal cardiopulmonary resuscitation during cardiac arrest: an update to the American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care.Circulation. 2019; 140:e881–e894. doi: 10.1161/CIR.0000000000000732LinkGoogle Scholar
2. Holmberg MJ, Geri G, Wiberg S, Guerguerian AM, Donnino MW, Nolan JP, Deakin CD, Andersen LWInternational Liaison Committee on Resuscitation’s (ILCOR) Advanced Life Support and Pediatric Task Forces. Extracorporeal cardiopulmonary resuscitation for cardiac arrest: A systematic review.Resuscitation. 2018; 131:91–100. doi: 10.1016/j.resuscitation.2018.07.029CrossrefMedlineGoogle Scholar
3. Blumenstein J, Leick J, Liebetrau C, Kempfert J, Gaede L, Groß S, Krug M, Berkowitsch A, Nef H, Rolf A, Arlt M, Walther T, Hamm CW, Möllmann H. Extracorporeal life support in cardiovascular patients with observed refractory in-hospital cardiac arrest is associated with favourable short and long-term outcomes: A propensity-matched analysis.Eur Heart J Acute Cardiovasc Care. 2016; 5:13–22. doi: 10.1177/2048872615612454CrossrefMedlineGoogle Scholar
4. Chen YS, Lin JW, Yu HY, Ko WJ, Jerng JS, Chang WT, Chen WJ, Huang SC, Chi NH, Wang CH, Chen LC, Tsai PR, Wang SS, Hwang JJ, Lin FY. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and propensity analysis.Lancet. 2008; 372:554–561. doi: 10.1016/S0140-6736(08)60958-7CrossrefMedlineGoogle Scholar
5. Lin JW, Wang MJ, Yu HY, Wang CH, Chang WT, Jerng JS, Huang SC, Chou NK, Chi NH, Ko WJ, Wang YC, Wang SS, Hwang JJ, Lin FY, Chen YS. Comparing the survival between extracorporeal rescue and conventional resuscitation in adult in-hospital cardiac arrests: propensity analysis of three-year data.Resuscitation. 2010; 81:796–803. doi: 10.1016/j.resuscitation.2010.03.002CrossrefMedlineGoogle Scholar
6. Shin TG, Choi JH, Jo IJ, Sim MS, Song HG, Jeong YK, Song YB, Hahn JY, Choi SH, Gwon HC, Jeon ES, Sung K, Kim WS, Lee YT. Extracorporeal cardiopulmonary resuscitation in patients with inhospital cardiac arrest: A comparison with conventional cardiopulmonary resuscitation.Crit Care Med. 2011; 39:1–7. doi: 10.1097/CCM.0b013e3181feb339CrossrefMedlineGoogle Scholar

Specific Arrhythmia Management

Wide-Complex Tachycardia

Synopsis

A wide-complex tachycardia is defined as a rapid rhythm (generally 150 beats/min or more when attributable to an arrhythmia) with a QRS duration of 0.12 seconds or more. It can represent any aberrantly conducted supraventricular tachycardia (SVT), including paroxysmal SVT caused by atrioventricular (AV) reentry, aberrantly conducted atrial fibrillation, atrial flutter, or ectopic atrial tachycardia. A wide-complex tachycardia can also be caused by any of these supraventricular arrhythmias when conducted by an accessory pathway (called pre-excited arrhythmias). Conversely, a wide-complex tachycardia can also be due to VT or a rapid ventricular paced rhythm in patients with a pacemaker.

Initial management of wide-complex tachycardia requires a rapid assessment of the patient’s hemodynamic stability. Unstable patients require immediate electric cardioversion. If hemodynamically stable, a presumptive rhythm diagnosis should be attempted by obtaining a 12-lead ECG to evaluate the tachycardia’s features. This includes identifying P waves and their relationship to QRS complexes and (in the case of patients with a pacemaker) pacing spikes preceding QRS complexes.

A wide-complex tachycardia can be regular or irregularly irregular and have uniform (monomorphic) or differing (polymorphic) QRS complexes from beat to beat. Each of these features can also be useful in making a presumptive rhythm diagnosis. An irregularly irregular wide-complex tachycardia with monomorphic QRS complexes suggests atrial fibrillation with aberrancy, whereas pre-excited atrial fibrillation or polymorphic VT are likely when QRS complexes change in their configuration from beat to beat. Conversely, a regular wide-complex tachycardia could represent monomorphic VT or an aberrantly conducted reentrant paroxysmal SVT, ectopic atrial tachycardia, or atrial flutter. Distinguishing between these rhythm etiologies is the key to proper drug selection for treatment. While hemodynamically stable rhythms afford an opportunity for evaluation and pharmacological treatment, the need for prompt electric cardioversion should be anticipated in the event the arrhythmia proves unresponsive to these measures or rapid decompensation occurs. A more detailed approach to rhythm management is found elsewhere.1–3

Recommendation-Specific Supportive Text

Before embarking on empirical drug therapy, obtaining a 12-lead ECG and/or seeking expert consultation for diagnosis is encouraged, if available. If a regular wide-complex tachycardia is suspected to be paroxysmal SVT, vagal maneuvers can be considered before initiating pharmacological therapies (see Regular Narrow-Complex Tachycardia). Adenosine is an ultra–short-acting drug that is effective in terminating regular tachycardias when caused by AV reentry. Adenosine will not typically terminate atrial arrhythmias (such as atrial flutter or atrial tachycardia) but will transiently slow the ventricular rate by blocking conduction of P waves through the AV node, afford their recognition, and help establish the rhythm diagnosis. While ineffective in terminating ventricular arrhythmias, adenosine’s relatively short-lived effect on blood pressure makes it less likely to destabilize monomorphic VT in an otherwise hemodynamically stable patient. These features make adenosine relatively safe for treating a hemodynamically stable, regular, monomorphic wide-complex tachycardia of unknown type4 and as an aid in rhythm diagnosis, although its use is not completely without risk.5,6
IV antiarrhythmic medications may be considered in stable patients with wide-complex tachycardia, particularly if suspected to be VT or having failed adenosine. Because of their longer duration of action, antiarrhythmic agents may also be useful to prevent recurrences of wide-complex tachycardia. Lidocaine is not included as a treatment option for undifferentiated wide-complex tachycardia because it is a relatively “narrow-spectrum” drug that is ineffective for SVT, probably because its kinetic properties are less effective for VT at hemodynamically tolerated rates than amiodarone, procainamide, or sotalol are.7–10 In contrast, amiodarone, procainamide, and sotalol are “broader-spectrum” antiarrhythmics than lidocaine and can treat both SVT and VT, but they can cause hypotension. Since the 2010 Guidelines, a new branded bioequivalent formulation of amiodarone has become available for IV infusion with less hypotensive effects than the older generic formulation.11 There are few direct comparisons of efficacy between amiodarone, procainamide, and sotalol themselves,12 which the writing group felt were insufficient to favor one of these drugs over another, apart from cautioning about their use in patients with long QT, amiodarone in suspected pre-excited arrhythmias, or giving these drugs in combination without prior expert consultation. Any of these drugs can also worsen wide-complex tachycardia, converting it to an arrhythmia that is more rapid, less hemodynamically stable, or more malignant, such that availability of a defibrillator is encouraged when these drugs are administered.13
Verapamil is a calcium channel blocking agent that slows AV node conduction, shortens the refractory period of accessory pathways, and acts as a negative inotrope and vasodilator. Its effects are mediated by a different mechanism and are longer lasting than adenosine. Though effective for treating a wide-complex tachycardia known to be of supraventricular origin and not involving accessory pathway conduction, verapamil’s negative inotropic and hypotensive effects can destabilize VT14 and accelerate pre-excited atrial fibrillation and flutter.15 Similar concerns may also apply to other drugs commonly used to treat SVTs, such as diltiazem and β-adrenergic blockers, which are not addressed in this recommendation and require evidence review.
The combination of adenosine’s short-lived slowing of AV node conduction, shortening of refractoriness in the myocardium and accessory pathways, and hypotensive effects make it unsuitable in hemodynamically unstable patients and for treating irregularly irregular and polymorphic wide-complex tachycardias. Adenosine only transiently slows irregularly irregular rhythms, such as atrial fibrillation, rendering it unsuitable for their management. The drug’s hypotensive and tissue refractoriness–shortening effects can accelerate ventricular rates in polymorphic VT and, when atrial fibrillation or flutter are conducted by an accessory pathway, risk degeneration to VF.16 Thus, the drug is not recommended in hemodynamically unstable patients or for treating irregularly irregular or polymorphic wide-complex tachycardias.

This topic last received formal evidence review in 2010.17

Recommendation-Specific Supportive Text

When available, expert consultation can be helpful to assist in the diagnosis and management of treatment-refractory wide-complex tachycardia. Electric cardioversion can be useful either as first-line treatment or for drug-refractory wide-complex tachycardia due to reentry rhythms (such as atrial fibrillation, atrial flutter, AV reentry, and VT). However, electric cardioversion may not be effective for automatic tachycardias (such as ectopic atrial tachycardias), entails risks associated with sedation, and does not prevent recurrences of the wide-complex tachycardia. Notably, when the QRS complex is of uniform morphology, shock synchronized to the QRS is encouraged because this minimizes the risk of provoking VF by a mistimed shock during the vulnerable period of the cardiac cycle (T wave).18 In contrast, polymorphic wide-complex tachycardias cannot be synchronized reliably because of the differing characteristics of each QRS complex, and require high-energy defibrillation.19

This topic last received formal evidence review in 2010.17

References

1. Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, et al.. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.Circulation. 2018; 138:e272–e391. doi: 10.1161/CIR.0000000000000549LinkGoogle Scholar
2. Page RL, Joglar JA, Caldwell MA, Calkins H, Conti JB, Deal BJ, Estes NA, Field ME, Goldberger ZD, Hammill SC, Indik JH, Lindsay BD, Olshansky B, Russo AM, Shen WK, Tracy CM, Al-Khatib SMEvidence Review Committee Chair‡. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.Circulation. 2016; 133:e506–e574. doi: 10.1161/CIR.0000000000000311LinkGoogle Scholar
3. January CT, Wann LS, Calkins H, Chen LY, Cigarroa JE, Cleveland JC, Ellinor PT, Ezekowitz MD, Field ME, Furie KL, Heidenreich PA, Murray KT, Shea JB, Tracy CM, Yancy CW. 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society in Collaboration With the Society of Thoracic Surgeons.Circulation. 2019; 140:e125–e151. doi: 10.1161/CIR.0000000000000665LinkGoogle Scholar
4. Marill KA, Wolfram S, Desouza IS, Nishijima DK, Kay D, Setnik GS, Stair TO, Ellinor PT. Adenosine for wide-complex tachycardia: efficacy and safety.Crit Care Med. 2009; 37:2512–2518. doi: 10.1097/CCM.0b013e3181a93661CrossrefMedlineGoogle Scholar
5. Shah CP, Gupta AK, Thakur RK, Hayes OW, Mehrotra A, Lokhandwala YY. Adenosine-induced ventricular fibrillation.Indian Heart J. 2001; 53:208–210.MedlineGoogle Scholar
6. Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Case report: adenosine induced ventricular fibrillation in a patient with stable ventricular tachycardia.J Interv Card Electrophysiol. 2001; 5:71–74. doi: 10.1023/a:1009810025584CrossrefMedlineGoogle Scholar
7. Josephson ME. Lidocaine and sustained monomorphic ventricular tachycardia: fact or fiction.Am J Cardiol. 1996; 78:82–83. doi: 10.1016/s0002-9149(96)00271-8CrossrefMedlineGoogle Scholar
8. Somberg JC, Bailin SJ, Haffajee CI, Paladino WP, Kerin NZ, Bridges D, Timar S, Molnar JAmio-Aqueous Investigators. Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia.Am J Cardiol. 2002; 90:853–859. doi: 10.1016/s0002-9149(02)02707-8CrossrefMedlineGoogle Scholar
9. Gorgels AP, van den Dool A, Hofs A, Mulleneers R, Smeets JL, Vos MA, Wellens HJ. Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia.Am J Cardiol. 1996; 78:43–46. doi: 10.1016/s0002-9149(96)00224-xCrossrefMedlineGoogle Scholar
10. Ho DS, Zecchin RP, Richards DA, Uther JB, Ross DL. Double-blind trial of lignocaine versus sotalol for acute termination of spontaneous sustained ventricular tachycardia.Lancet. 1994; 344:18–23. doi: 10.1016/s0140-6736(94)91048-0CrossrefMedlineGoogle Scholar
11. Cushing DJ, Cooper WD, Gralinski MR, Lipicky RJ. The hypotensive effect of intravenous amiodarone is sustained throughout the maintenance infusion period.Clin Exp Pharmacol Physiol. 2010; 37:358–361. doi: 10.1111/j.1440-1681.2009.05303.xCrossrefMedlineGoogle Scholar
12. Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral JPROCAMIO Study Investigators. Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study.Eur Heart J. 2017; 38:1329–1335. doi: 10.1093/eurheartj/ehw230MedlineGoogle Scholar
13. Friedman PL, Stevenson WG. Proarrhythmia.Am J Cardiol. 1998; 82:50N–58N. doi: 10.1016/s0002-9149(98)00586-4CrossrefMedlineGoogle Scholar
14. Buxton AE, Marchlinski FE, Doherty JU, Flores B, Josephson ME. Hazards of intravenous verapamil for sustained ventricular tachycardia.Am J Cardiol. 1987; 59:1107–1110. doi: 10.1016/0002-9149(87)90857-5CrossrefMedlineGoogle Scholar
15. Gulamhusein S, Ko P, Carruthers SG, Klein GJ. Acceleration of the ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome after verapamil.Circulation. 1982; 65:348–354. doi: 10.1161/01.cir.65.2.348LinkGoogle Scholar
16. Gupta AK, Shah CP, Maheshwari A, Thakur RK, Hayes OW, Lokhandwala YY. Adenosine induced ventricular fibrillation in Wolff-Parkinson-White syndrome.Pacing Clin Electrophysiol. 2002; 254 Pt 1477–480. doi: 10.1046/j.1460-9592.2002.00477.xCrossrefMedlineGoogle Scholar
17. Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, et al.. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122:S729–S767. doi: 10.1161/CIRCULATIONAHA.110.970988LinkGoogle Scholar
18. Trohman RG, Parrillo JE. Direct current cardioversion: indications, techniques, and recent advances.Crit Care Med. 2000; 28(suppl):N170–N173. doi: 10.1097/00003246-200010001-00010CrossrefMedlineGoogle Scholar
19. Dell’Orfano JT, Naccarelli GV. Update on external cardioversion and defibrillation.Curr Opin Cardiol. 2001; 16:54–57. doi: 10.1097/00001573-200101000-00008CrossrefMedlineGoogle Scholar

Torsades de Pointes

Synopsis

Polymorphic VT refers to a wide-complex tachycardia of ventricular origin with differing configurations of the QRS complex from beat to beat. However, the most critical feature in the diagnosis and treatment of polymorphic VT is not the morphology of rhythm but rather what is known (or suspected) about the patient’s underlying QT interval. Torsades de pointes is a form of polymorphic VT that is associated with a prolonged heart rate–corrected QT interval when the rhythm is normal and VT is not present. The risk for developing torsades increases when the corrected QT interval is greater than 500 milliseconds and accompanied by bradycardia.1 Torsades can be due to an inherited genetic abnormality2 and can also be caused by drugs and electrolyte imbalances that cause lengthening of the QT interval.3

Conversely, polymorphic VT not associated with a long QT is most often due to acute myocardial ischemia.4,5 Other potential causes include catecholaminergic polymorphic VT, a genetic abnormality in which polymorphic VT is provoked by exercise or emotion in the absence of QT prolongation6; “short QT” syndrome, a form of polymorphic VT associated with an unusually short QT interval (corrected QT interval less than 330–370 milliseconds)7,8; and bidirectional VT seen in digitalis toxicity in which the axis of alternate QRS complexes shifts by 180 degrees.9 Supportive data for the acute pharmacological treatment of polymorphic VT, with and without long corrected QT interval, is largely based on case reports and case series, because no RCTs exist.

Recommendation-Specific Supportive Text

Regardless of the underlying QT interval, all forms of polymorphic VT tend to be hemodynamically and electrically unstable. They may repeatedly recur and remit spontaneously, become sustained, or degenerate to VF, for which electric shock may be required. When the QRS complex of a VT is of uniform morphology, electric cardioversion with the shock synchronized to the QRS minimizes the risk of provoking VF by a mistimed shock during the vulnerable period of the cardiac cycle (T wave).10 In contrast, polymorphic VT cannot be synchronized reliably because of the differing characteristics of each QRS complex and requires high-energy unsynchronized defibrillation.11 While effective in terminating polymorphic VT, electric shock may not prevent its recurrence, for which pharmacological therapies are often required and the primary focus of the ensuing recommendations

This topic last received formal evidence review in 2010.12

Recommendation-Specific Supportive Text

Torsades de pointes typically presents in a recurring pattern of self-terminating, hemodynamically unstable polymorphic VT in context of a known or suspected long QT abnormality, often with an associated bradycardia. Immediate defibrillation is the treatment of choice when torsades is sustained or degenerates to VF. However, termination of torsades by shock does not prevent its recurrence, which requires additional measures. In small case series, IV magnesium has been effective in suppressing and preventing recurrences of torsades.13–16 Magnesium is believed to suppress early afterdepolarizations, which are fluctuations in the myocardial action potential that can trigger the salvos of VT seen in torsades.17 Correcting any electrolyte abnormalities, particularly hypokalemia, is also advisable. Torsades is not treatable with antiarrhythmic medications, which can themselves prolong the QT interval and promote the arrhythmia. When given acutely, β-adrenergic blockers can also precipitate torsades by causing or worsening bradycardia. In patients with bradycardia or pause-precipitated torsades, expert consultation is best sought for additional measures such as overdrive pacing or isoproterenol,18–20 if needed. The use of magnesium in torsades de pointes was addressed by the 2010 Guidelines and updated in a 2018 focused update on ACLS guidelines,21 with an interim evidence review that identified no new information that would modify previous recommendations.

This topic last received formal evidence review in 2010.12

Recommendation-Specific Supportive Text

Polymorphic VT that is not associated with QT prolongation is often triggered by acute myocardial ischemia and infarction,4,5 often rapidly degenerates into VF, and is treated similarly to other ventricular arrhythmias (VT and VF). However, termination of polymorphic VT with defibrillation may not prevent its recurrence, which often requires additional measures. No RCTs have been performed to determine the best practice for pharmacological management of polymorphic VT. However measures to treat myocardial ischemia (eg, β-adrenergic blockers or emergent coronary intervention) as well as lidocaine and amiodarone may be effective22–29 in concert with defibrillation when the arrhythmia is sustained. β-Adrenergic blockers have also been shown to reduce the incidence of ventricular arrhythmias in acute coronary syndromes.30,31 Expert consultation is advisable when other causes of polymorphic VT are suspected, for which β-adrenergic blockers and antiarrhythmics may also have efficacy.6,32 This topic was last addressed by the 2010 Guidelines, with an interim evidence update that identified no new information that would modify previous recommendations. Newer defined diagnostic entities causing polymorphic VT merit future evidence evaluation.
In the absence of long QT, magnesium has not been shown to be effective in the treatment of polymorphic VT 13 or to afford benefit in the acute management of other ventricular tachyarrhythmias.16

These recommendations are supported by the 2018 focused update on ACLS guidelines.21

References

1. Chan A, Isbister GK, Kirkpatrick CM, Dufful SB. Drug-induced QT prolongation and torsades de pointes: evaluation of a QT nomogram.QJM. 2007; 100:609–615. doi: 10.1093/qjmed/hcm072CrossrefMedlineGoogle Scholar
2. Saprungruang A, Khongphatthanayothin A, Mauleekoonphairoj J, Wandee P, Kanjanauthai S, Bhuiyan ZA, Wilde AAM, Poovorawan Y. Genotype and clinical characteristics of congenital long QT syndrome in Thailand.Indian Pacing Electrophysiol J. 2018; 18:165–171. doi: 10.1016/j.ipej.2018.07.007CrossrefMedlineGoogle Scholar
3. Drew BJ, Ackerman MJ, Funk M, Gibler WB, Kligfield P, Menon V, Philippides GJ, Roden DM, Zareba WAmerican Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology; Council on Cardiovascular Nursing; American College of Cardiology Foundation. Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation.J Am Coll Cardiol. 2010; 55:934–947. doi: 10.1016/j.jacc.2010.01.001CrossrefMedlineGoogle Scholar
4. Pogwizd SM, Corr PB. Electrophysiologic mechanisms underlying arrhythmias due to reperfusion of ischemic myocardium.Circulation. 1987; 76:404–426. doi: 10.1161/01.cir.76.2.404LinkGoogle Scholar
5. Wolfe CL, Nibley C, Bhandari A, Chatterjee K, Scheinman M. Polymorphous ventricular tachycardia associated with acute myocardial infarction.Circulation. 1991; 84:1543–1551. doi: 10.1161/01.cir.84.4.1543LinkGoogle Scholar
6. Liu N, Ruan Y, Priori SG. Catecholaminergic polymorphic ventricular tachycardia.Prog Cardiovasc Dis. 2008; 51:23–30. doi: 10.1016/j.pcad.2007.10.005CrossrefMedlineGoogle Scholar
7. Cross B, Homoud M, Link M, Foote C, Garlitski AC, Weinstock J, Estes NA. The short QT syndrome.J Interv Card Electrophysiol. 2011; 31:25–31. doi: 10.1007/s10840-011-9566-0CrossrefMedlineGoogle Scholar
8. Gollob MH, Redpath CJ, Roberts JD. The short QT syndrome: proposed diagnostic criteria.J Am Coll Cardiol. 2011; 57:802–812. doi: 10.1016/j.jacc.2010.09.048CrossrefMedlineGoogle Scholar
9. Chapman M, Hargreaves M, Schneider H, Royle M. Bidirectional ventricular tachycardia associated with digoxin toxicity and with normal digoxin levels.Heart Rhythm. 2014; 11:1222–1225. doi: 10.1016/j.hrthm.2014.03.050CrossrefMedlineGoogle Scholar
10. Trohman RG, Parrillo JE. Direct current cardioversion: indications, techniques, and recent advances.Crit Care Med. 2000; 28(suppl):N170–N173. doi: 10.1097/00003246-200010001-00010CrossrefMedlineGoogle Scholar
11. Dell’Orfano JT, Naccarelli GV. Update on external cardioversion and defibrillation.Curr Opin Cardiol. 2001; 16:54–57. doi: 10.1097/00001573-200101000-00008CrossrefMedlineGoogle Scholar
12. Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, et al.. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122:S729–S767. doi: 10.1161/CIRCULATIONAHA.110.970988LinkGoogle Scholar
13. Tzivoni D, Banai S, Schuger C, Benhorin J, Keren A, Gottlieb S, Stern S. Treatment of torsade de pointes with magnesium sulfate.Circulation. 1988; 77:392–397. doi: 10.1161/01.cir.77.2.392LinkGoogle Scholar
14. Tzivoni D, Keren A, Cohen AM, Loebel H, Zahavi I, Chenzbraun A, Stern S. Magnesium therapy for torsades de pointes.Am J Cardiol. 1984; 53:528–530. doi: 10.1016/0002-9149(84)90025-0CrossrefMedlineGoogle Scholar
15. Hoshino K, Ogawa K, Hishitani T, Isobe T, Etoh Y. Successful uses of magnesium sulfate for torsades de pointes in children with long QT syndrome.Pediatr Int. 2006; 48:112–117. doi: 10.1111/j.1442-200X.2006.02177.xCrossrefMedlineGoogle Scholar
16. Manz M, Jung W, Lüderitz B. Effect of magnesium on sustained ventricular tachycardia [in German].Herz. 1997; 22(suppl 1):51–55. doi: 10.1007/bf03042655CrossrefMedlineGoogle Scholar
17. Baker WL. Treating arrhythmias with adjunctive magnesium: identifying future research directions.Eur Heart J Cardiovasc Pharmacother. 2017; 3:108–117. doi: 10.1093/ehjcvp/pvw028MedlineGoogle Scholar
18. DiSegni E, Klein HO, David D, Libhaber C, Kaplinsky E. Overdrive pacing in quinidine syncope and other long QT-interval syndromes.Arch Intern Med. 1980; 140:1036–1040.CrossrefMedlineGoogle Scholar
19. Damiano BP, Rosen MR. Effects of pacing on triggered activity induced by early afterdepolarizations.Circulation. 1984; 69:1013–1025. doi: 10.1161/01.cir.69.5.1013LinkGoogle Scholar
20. Suarez K, Mack R, Hardegree EL, Chiles C, Banchs JE, Gonzalez MD. Isoproterenol suppresses recurrent torsades de pointes in a patient with long QT syndrome type 2.HeartRhythm Case Rep. 2018; 4:576–579. doi: 10.1016/j.hrcr.2018.08.013CrossrefMedlineGoogle Scholar
21. Panchal AR, Berg KM, Kudenchuk PJ, Del Rios M, Hirsch KG, Link MS, Kurz MC, Chan PS, Cabañas JG, Morley PT, Hazinski MF, Donnino MW. 2018 American Heart Association Focused Update on Advanced Cardiovascular Life Support Use of Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2018; 138:e740–e749. doi: 10.1161/CIR.0000000000000613LinkGoogle Scholar
22. Vrana M, Pokorny J, Marcian P, Fejfar Z. Class I and III antiarrhythmic drugs for prevention of sudden cardiac death and management of postmyocardial infarction arrhythmias. A review.Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2013; 157:114–124. doi: 10.5507/bp.2013.030CrossrefMedlineGoogle Scholar
23. Nalliah CJ, Zaman S, Narayan A, Sullivan J, Kovoor P. Coronary artery reperfusion for ST elevation myocardial infarction is associated with shorter cycle length ventricular tachycardia and fewer spontaneous arrhythmias.Europace. 2014; 16:1053–1060. doi: 10.1093/europace/eut307CrossrefMedlineGoogle Scholar
24. Brady W, Meldon S, DeBehnke D. Comparison of prehospital monomorphic and polymorphic ventricular tachycardia: prevalence, response to therapy, and outcome.Ann Emerg Med. 1995; 25:64–70. doi: 10.1016/s0196-0644(95)70357-8CrossrefMedlineGoogle Scholar
25. Brady WJ, DeBehnke DJ, Laundrie D. Prevalence, therapeutic response, and outcome of ventricular tachycardia in the out-of-hospital setting: a comparison of monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, and torsades de pointes.Acad Emerg Med. 1999; 6:609–617. doi: 10.1111/j.1553-2712.1999.tb00414.xCrossrefMedlineGoogle Scholar
26. Luqman N, Sung RJ, Wang CL, Kuo CT. Myocardial ischemia and ventricular fibrillation: pathophysiology and clinical implications.Int J Cardiol. 2007; 119:283–290. doi: 10.1016/j.ijcard.2006.09.016CrossrefMedlineGoogle Scholar
27. Gorenek B, Lundqvist CB, Terradellas JB, Camm AJ, Hindricks G, Huber K, Kirchhof P, Kuck KH, Kudaiberdieva G, Lin T, Raviele A, Santini M, Tilz RR, Valgimigli M, Vos MA, Vrints C, Zeymer U. Cardiac arrhythmias in acute coronary syndromes: position paper from the joint EHRA, ACCA, and EAPCI task force.Eur Heart J Acute Cardiovasc Care. 2015; 4:386. doi: 10.1177/2048872614550583CrossrefMedlineGoogle Scholar
28. Carmeliet E. Cardiac ionic currents and acute ischemia: from channels to arrhythmias.Physiol Rev. 1999; 79:917–1017. doi: 10.1152/physrev.1999.79.3.917CrossrefMedlineGoogle Scholar
29. Steg PG, James SK, Atar D, Badano LP, Blömstrom-Lundqvist C, Borger MA, Di Mario C, Dickstein K, Ducrocq G, Fernandez-Aviles F, et al.; and the Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation.Eur Heart J. 2012; 33:2569–2619. doi: 10.1093/eurheartj/ehs215CrossrefMedlineGoogle Scholar
30. Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, et al.. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.Circulation. 2018; 138:e272–e391. doi: 10.1161/CIR.0000000000000549LinkGoogle Scholar
31. Chatterjee S, Chaudhuri D, Vedanthan R, Fuster V, Ibanez B, Bangalore S, Mukherjee D. Early intravenous beta-blockers in patients with acute coronary syndrome—a meta-analysis of randomized trials.Int J Cardiol. 2013; 168:915–921. doi: 10.1016/j.ijcard.2012.10.050CrossrefMedlineGoogle Scholar
32. Van Houzen NE, Alsheikh-Ali AA, Garlitski AC, Homoud MK, Weinstock J, Link MS, Estes NA. Short QT syndrome review.J Interv Card Electrophysiol. 2008; 23:1–5. doi: 10.1007/s10840-008-9201-xCrossrefMedlineGoogle Scholar

Regular Narrow-Complex Tachycardia

Introduction

Management of SVTs is the subject of a recent joint treatment guideline from the AHA, the American College of Cardiology, and the Heart Rhythm Society.1

Narrow-complex tachycardia represents a range of tachyarrhythmias originating from a circuit or focus involving the atria or the AV node. Clinicians must determine if the tachycardia is narrow-complex or wide-complex tachycardia and if it has a regular or irregular rhythm. For patients with a sinus tachycardia (heart rate greater than 100/min, P waves), no specific drug treatment is needed, and clinicians should focus on identification and treatment of the underlying cause of the tachycardia (fever, dehydration, pain). If the patient presents with SVT, the primary goal of treatment is to quickly identify and treat patients who are hemodynamically unstable (ischemic chest pain, altered mental status, shock, hypotension, acute heart failure) or symptomatic due to the arrhythmia. Synchronized cardioversion or drugs or both may be used to control unstable or symptomatic regular narrow-complex tachycardia. The available evidence suggests no appreciable differences in success or major adverse event rates between calcium channel blockers and adenosine.2

In patients with narrow-complex tachycardia who are refractory to the measures described, this may indicate a more complicated rhythm abnormality for which expert consultation may be advisable.

Recommendation-Specific Supportive Text

1 and 2. Management of hemodynamically unstable patients with SVT must start with prompt restoration of sinus rhythm through the use of cardioversion. Cardioversion has been shown to be both safe and effective in the prehospital setting for hemodynamically unstable patients with SVT who had failed to respond to vagal maneuvers and IV pharmacological therapies.3 Cardioversion is advised in patients who present with hypotension, acutely altered mental status, signs of shock, chest pain, or acute heart failure. Though rare, cardioversion may also be necessary in stable patients with SVT. Most stable patients with SVT have high conversion success rates of 80% to 98% with pharmacological management (eg, adenosine, diltiazem).4,5 However, if drugs fail to restore sinus rhythm, cardioversion is safe and effective for stable patients after adequate sedation and anesthesia.

These recommendations are supported by the “2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With SVT: A Report of the American College of Cardiology/AHA Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.”6

Recommendation-Specific Supportive Text

Success rates for the Valsalva maneuver in terminating SVT range from 19% to 54%.7 Augmenting the Valsalva maneuver with passive leg raise is more effective.8 Caution is advised when deploying carotid massage in older patients given the potential thromboembolic risk.
The 2015 American College of Cardiology, AHA, and Heart Rhythm Society Guidelines evaluated and recommended adenosine as a first-line treatment for regular SVT because of its effectiveness, extremely short half-life, and favorable side-effect profile.6 A Cochrane systematic review of 7 RCTs (622 patients) found similar rates of conversion to sinus rhythm with adenosine or calcium channel blockers (90% versus 93%) and no significant difference in hypotension.2 Adenosine may have profound effects in post–heart transplant patients and can cause severe bronchospasm in asthma patients.
Treatment of hemodynamically stable patients with IV diltiazem or verapamil have been shown to convert SVT to normal sinus rhythm in 64% to 98% of patients.4,9–11 These agents are particularly useful in patients who cannot tolerate β-adrenergic blockers or who have recurrent SVT after treatment with adenosine. Caution should be taken to administer these medications slowly to decrease the potential for hypotension.11 Diltiazem and verapamil are not appropriate in the setting of suspected systolic heart failure.6
Evidence for the effectiveness of β-adrenergic blockers in terminating SVT is limited. In a trial that compared esmolol with diltiazem, diltiazem was more effective in terminating SVT.5 Nonetheless, β-adrenergic blockers are generally safe, and it is reasonable to use them to terminate SVT in hemodynamically stable patients.6

These recommendations are supported by the 2015 American College of Cardiology, AHA, and Heart Rhythm Society Guidelines for the Management of Adult Patients With SVT.6

References

1. Page RL, Joglar JA, Caldwell MA, Calkins H, Conti JB, Deal BJ, Estes NAM, Field ME, Goldberger ZD, Hammill SC, Indik JH, Lindsay BD, Olshansky B, Russo AM, Shen WK, Tracy CM, Al-Khatib SM. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.J Am Coll Cardiol. 2016; 67:e27–e115. doi: 10.1016/j.jacc.2015.08.856CrossrefMedlineGoogle Scholar
2. Alabed S, Sabouni A, Providencia R, Atallah E, Qintar M, Chico TJ. Adenosine versus intravenous calcium channel antagonists for supraventricular tachycardia.Cochrane Database Syst Rev. 2017; 10:CD005154. doi: 10.1002/14651858.CD005154.pub4MedlineGoogle Scholar
3. Roth A, Elkayam I, Shapira I, Sander J, Malov N, Kehati M, Golovner M. Effectiveness of prehospital synchronous direct-current cardioversion for supraventricular tachyarrhythmias causing unstable hemodynamic states.Am J Cardiol. 2003; 91:489–491. doi: 10.1016/s0002-9149(02)03257-5CrossrefMedlineGoogle Scholar
4. Brady WJ, DeBehnke DJ, Wickman LL, Lindbeck G. Treatment of out-of-hospital supraventricular tachycardia: adenosine vs verapamil.Acad Emerg Med. 1996; 3:574–585. doi: 10.1111/j.1553-2712.1996.tb03467.xCrossrefMedlineGoogle Scholar
5. Gupta A, Naik A, Vora A, Lokhandwala Y. Comparison of efficacy of intravenous diltiazem and esmolol in terminating supraventricular tachycardia.J Assoc Physicians India. 1999; 47:969–972.MedlineGoogle Scholar
6. Page RL, Joglar JA, Caldwell MA, Calkins H, Conti JB, Deal BJ, Estes NA, Field ME, Goldberger ZD, Hammill SC, Indik JH, Lindsay BD, Olshansky B, Russo AM, Shen WK, Tracy CM, Al-Khatib SMEvidence Review Committee Chair‡. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.Circulation. 2016; 133:e506–e574. doi: 10.1161/CIR.0000000000000311LinkGoogle Scholar
7. Smith GD, Fry MM, Taylor D, Morgans A, Cantwell K. Effectiveness of the Valsalva Manoeuvre for reversion of supraventricular tachycardia.Cochrane Database Syst Rev. 2015Cd009502. doi: 10.1002/14651858.CD009502.pub3MedlineGoogle Scholar
8. Appelboam A, Reuben A, Mann C, Gagg J, Ewings P, Barton A, Lobban T, Dayer M, Vickery J, Benger JREVERT trial collaborators. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial.Lancet. 2015; 386:1747–1753. doi: 10.1016/S0140-6736(15)61485-4CrossrefMedlineGoogle Scholar
9. Lim SH, Anantharaman V, Teo WS, Chan YH. Slow infusion of calcium channel blockers compared with intravenous adenosine in the emergency treatment of supraventricular tachycardia.Resuscitation. 2009; 80:523–528. doi: 10.1016/j.resuscitation.2009.01.017CrossrefMedlineGoogle Scholar
10. Madsen CD, Pointer JE, Lynch TG. A comparison of adenosine and verapamil for the treatment of supraventricular tachycardia in the prehospital setting.Ann Emerg Med. 1995; 25:649–655. doi: 10.1016/s0196-0644(95)70179-6CrossrefMedlineGoogle Scholar
11. Lim SH, Anantharaman V, Teo WS. Slow-infusion of calcium channel blockers in the emergency management of supraventricular tachycardia.Resuscitation. 2002; 52:167–174. doi: 10.1016/s0300-9572(01)00459-2CrossrefMedlineGoogle Scholar

Atrial Fibrillation or Flutter With Rapid Ventricular Response

Introduction

Atrial fibrillation is an SVT consisting of disorganized atrial electric activation and uncoordinated atrial contraction. Atrial flutter is an SVT with a macroreentrant circuit resulting in rapid atrial activation but intermittent ventricular response. These arrhythmias are common and often coexist, and their treatment recommendations are similar.

Treatment of atrial fibrillation/flutter depends on the hemodynamic stability of the patient as well as prior history of arrhythmia, comorbidities, and responsiveness to medication. Hemodynamically unstable patients and those with rate-related ischemia should receive urgent electric cardioversion. Hemodynamically stable patients can be treated with a rate-control or rhythm-control strategy. Rate control is more common in the emergency setting, using IV administration of a nondihydropyridine calcium channel antagonist (eg, diltiazem, verapamil) or a β-adrenergic blocker (eg, metoprolol, esmolol). While amiodarone is typically considered a rhythm-control agent, it can effectively reduce ventricular rate with potential use in patients with congestive heart failure where β-adrenergic blockers may not be tolerated and nondihydropyridine calcium channel antagonists are contraindicated. Long-term anticoagulation may be necessary for patients at risk for thromboembolic events based on their CHA2DS2-VASc score. The choice of anticoagulation is beyond the scope of these guidelines.

The rhythm-control strategy (sometimes called chemical cardioversion) includes antiarrhythmic medications given to convert the rhythm to sinus and/or prevent recurrent atrial fibrillation/flutter (Table 3). Patient selection, evaluation, timing, drug selection, and anticoagulation for patients undergoing rhythm control are beyond the scope of these guidelines and are presented elsewhere.1,2

Table 3. IV Medications Commonly Used for Acute Rate Control in Atrial Fibrillation and Atrial Flutter18

MedicationBolus DoseInfusion RateNotes

Nondihydropyridine Calcium Channel Blockers
Diltiazem	0.25 mg/kg IV bolus over 2 min	5–10 mg/h	Avoid in hypotension, heart failure, cardiomyopathy, and acute coronary syndromes
Verapamil	0.075–0.15 mg/kg IV bolus over 2 min; may give an additional dose after 30 min if no response	0.005 mg/kg per min	Avoid in hypotension, heart failure, cardiomyopathy, acute and coronary syndromes
β-Adrenergic Blockers
Metoprolol	2.5–5 mg over 2 min, up to 3 doses		Avoid in decompensated heart failure
Esmolol	500 μg/kg IV over 1 min	50–300 μg/kg per min	Short duration of action; avoid in decompensated heart failure
Propranolol	1 mg IV over 1 min, up to 3 doses		Avoid in decompensated heart failure
Other Medications
Amiodarone	300 mg IV over 1 h	10–50 mg/h over 24 h	Multiple dosing schemes exist for amiodarone
Digoxin	0.25 mg IV, repeated to maximum dose 1.5 mg over 24 h		Typically used as adjunctive therapy with another option from above; caution in patients with renal impairment

The management of patients with preexcitation syndromes (aka Wolff-Parkinson-White) is covered in the Wide-Complex Tachycardia section.

Recommendation-Specific Supportive Text

1 and 2. Uncontrolled tachycardia may impair ventricular filling, cardiac output, and coronary perfusion while increasing myocardial oxygen demand. While an expeditious trial of medications and/or fluids may be appropriate in some cases, unstable patients or patients with ongoing cardiac ischemia with atrial fibrillation or atrial flutter need to be cardioverted promptly.1–3 When making the decision for cardioversion, one should also consider whether the arrhythmia is the cause of the tachycardia. Potential exacerbation of rapid ventricular response by secondary causes (eg, sepsis) should be considered and may inform initial attempts at hemodynamic stabilization with pharmacotherapy. There are few data addressing these strategies in hemodynamically unstable patients. However, studies demonstrating hemodynamic benefits of successful cardioversion have been published.4,5 In addition, risks of hypotension and hypoperfusion with use of negative inotropes have been demonstrated even in normotensive patients.6–8 Hemodynamically unstable patients and those with ongoing cardiac ischemia are likely to benefit from the improved hemodynamic status associated with restoration of sinus rhythm and avoidance of hypotension caused by the alternative pharmacological therapies. Depending on the clinical scenario, patients cardioverted from atrial fibrillation or atrial flutter of 48 hours’ duration or longer are candidates for anticoagulation. Details about anticoagulation selection can be found elsewhere.2
3 and 4. The electric energy required to successfully cardiovert a patient from atrial fibrillation or atrial flutter to sinus rhythm varies and is generally less in patients with new-onset arrhythmia, thin body habitus, and when biphasic waveform shocks are delivered.9–15 Obese patients may require greater energy.16 If initial cardioversion is unsuccessful, energy is increased in subsequent attempts. Less energy is generally required for atrial flutter than for atrial fibrillation.11 Higher energies of 200 J or more are associated with improved first shock success and decreased total energy delivery. In addition, a retrospective analysis found that lower energy shocks were associated with higher risk of cardioversion-induced VF.17 Previous guidelines included a comparison of monophasic and biphasic waveforms. This recommendation now focuses primarily on biphasic waveforms. Recommended energy levels vary with different devices, reducing the validity of generalized recommendations. This topic requires further study with a comprehensive systematic review to better understand the optimal electric doses with current devices. The writing group assessment of the LOE as C-LD is consistent with the limited evidence using modern devices and energy waveforms.

These recommendations are supported by the “2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/AHA Task Force on Practice Guidelines and the Heart Rhythm Society”18 as well as the focused update of those guidelines published in 2019.2

Recommendation-Specific Supportive Text

1 and 2. Clinical trial evidence shows that nondihydropyridine calcium channel antagonists (eg, diltiazem, verapamil), β-adrenergic blockers (eg, esmolol, propranolol), amiodarone, and digoxin are all effective for rate control in patients with atrial fibrillation/flutter.6–8,19–23 Calcium channel blockers may be more effective than amiodarone, and cause more hypotension.6 Digoxin is rarely used in the acute setting because of slow onset of effect.1,2
3. Based on limited case reports and small case series, there is concern that patients with concomitant preexcitation and atrial fibrillation or atrial flutter may develop VF in response to accelerated ventricular response after the administration of AV nodal blocking agents such as digoxin, nondihydropyridine calcium channel antagonists, β-adrenergic blockers, or IV amiodarone.24–27 In this setting, cardioversion is recommended as the most appropriate management.
4. Because of their negative inotropic effect, nondihydropyridine calcium channel antagonists (eg, diltiazem, verapamil) may further decompensate patients with left ventricular systolic dysfunction and symptomatic heart failure. They may be used in patients with heart failure with preserved ejection fraction. β-Adrenergic blockers may be used in compensated patients with cardiomyopathy; however, they should be used with caution or avoided altogether in patients with decompensated heart failure. This recommendation is based on expert consensus and pathophysiologic rationale.2,18,28 β-Adrenergic blockers may be used in patients with chronic obstructive pulmonary disease because multiple studies have shown no negative effects.29

These recommendations are supported by 2014 AHA, American College of Cardiology, and Heart Rhythm Society Guideline for the Management of Patients With Atrial Fibrillation18 as well as the focused update of those guidelines published in 2019.2

References

1. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC, Conti JB, Ellinor PT, Ezekowitz MD, Field ME, Murray KT, Sacco RL, Stevenson WG, Tchou PJ, Tracy CM, Yancy CWACC/AHA Task Force Members. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society.Circulation. 2014; 130:2071–2104. doi: 10.1161/CIR.0000000000000040LinkGoogle Scholar
2. January CT, Wann LS, Calkins H, Chen LY, Cigarroa JE, Cleveland JC, Ellinor PT, Ezekowitz MD, Field ME, Furie KL, Heidenreich PA, Murray KT, Shea JB, Tracy CM, Yancy CW. 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society in Collaboration With the Society of Thoracic Surgeons.Circulation. 2019; 140:e125–e151. doi: 10.1161/CIR.0000000000000665LinkGoogle Scholar
3. McMurray J, Køber L, Robertson M, Dargie H, Colucci W, Lopez-Sendon J, Remme W, Sharpe DN, Ford I. Antiarrhythmic effect of carvedilol after acute myocardial infarction: results of the Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction (CAPRICORN) trial.J Am Coll Cardiol. 2005; 45:525–530. doi: 10.1016/j.jacc.2004.09.076CrossrefMedlineGoogle Scholar
4. DeMaria AN, Lies JE, King JF, Miller RR, Amsterdam EA, Mason DT. Echographic assessment of atrial transport, mitral movement, and ventricular performance following electroversion of supraventricular arrhythmias.Circulation. 1975; 51:273–282. doi: 10.1161/01.cir.51.2.273LinkGoogle Scholar
5. Raymond RJ, Lee AJ, Messineo FC, Manning WJ, Silverman DI. Cardiac performance early after cardioversion from atrial fibrillation.Am Heart J. 1998; 136:435–442. doi: 10.1016/s0002-8703(98)70217-0CrossrefMedlineGoogle Scholar
6. Delle Karth G, Geppert A, Neunteufl T, Priglinger U, Haumer M, Gschwandtner M, Siostrzonek P, Heinz G. Amiodarone versus diltiazem for rate control in critically ill patients with atrial tachyarrhythmias.Crit Care Med. 2001; 29:1149–1153. doi: 10.1097/00003246-200106000-00011CrossrefMedlineGoogle Scholar
7. Platia EV, Michelson EL, Porterfield JK, Das G. Esmolol versus verapamil in the acute treatment of atrial fibrillation or atrial flutter.Am J Cardiol. 1989; 63:925–929. doi: 10.1016/0002-9149(89)90141-0CrossrefMedlineGoogle Scholar
8. Ellenbogen KA, Dias VC, Plumb VJ, Heywood JT, Mirvis DM. A placebo-controlled trial of continuous intravenous diltiazem infusion for 24-hour heart rate control during atrial fibrillation and atrial flutter: a multicenter study.J Am Coll Cardiol. 1991; 18:891–897. doi: 10.1016/0735-1097(91)90743-sCrossrefMedlineGoogle Scholar
9. Glover BM, Walsh SJ, McCann CJ, Moore MJ, Manoharan G, Dalzell GW, McAllister A, McClements B, McEneaney DJ, Trouton TG, Mathew TP, Adgey AA. Biphasic energy selection for transthoracic cardioversion of atrial fibrillation. The BEST AF Trial.Heart. 2008; 94:884–887. doi: 10.1136/hrt.2007.120782CrossrefMedlineGoogle Scholar
10. Inácio JF, da Rosa Mdos S, Shah J, Rosário J, Vissoci JR, Manica AL, Rodrigues CG. Monophasic and biphasic shock for transthoracic conversion of atrial fibrillation: systematic review and network meta-analysis.Resuscitation. 2016; 100:66–75. doi: 10.1016/j.resuscitation.2015.12.009CrossrefMedlineGoogle Scholar
11. Gallagher MM, Guo XH, Poloniecki JD, Guan Yap Y, Ward D, Camm AJ. Initial energy setting, outcome and efficiency in direct current cardioversion of atrial fibrillation and flutter.J Am Coll Cardiol. 2001; 38:1498–1504. doi: 10.1016/s0735-1097(01)01540-6CrossrefMedlineGoogle Scholar
12. Scholten M, Szili-Torok T, Klootwijk P, Jordaens L. Comparison of monophasic and biphasic shocks for transthoracic cardioversion of atrial fibrillation.Heart. 2003; 89:1032–1034. doi: 10.1136/heart.89.9.1032CrossrefMedlineGoogle Scholar
13. Page RL, Kerber RE, Russell JK, Trouton T, Waktare J, Gallik D, Olgin JE, Ricard P, Dalzell GW, Reddy R, Lazzara R, Lee K, Carlson M, Halperin B, Bardy GHBiCard Investigators. Biphasic versus monophasic shock waveform for conversion of atrial fibrillation: the results of an international randomized, double-blind multicenter trial.J Am Coll Cardiol. 2002; 39:1956–1963. doi: 10.1016/s0735-1097(02)01898-3CrossrefMedlineGoogle Scholar
14. Reisinger J, Gstrein C, Winter T, Zeindlhofer E, Höllinger K, Mori M, Schiller A, Winter A, Geiger H, Siostrzonek P. Optimization of initial energy for cardioversion of atrial tachyarrhythmias with biphasic shocks.Am J Emerg Med. 2010; 28:159–165. doi: 10.1016/j.ajem.2008.10.028CrossrefMedlineGoogle Scholar
15. Alatawi F, Gurevitz O, White RD, Ammash NM, Malouf JF, Bruce CJ, Moon BS, Rosales AG, Hodge D, Hammill SC, Gersh BJ, Friedman PA. Prospective, randomized comparison of two biphasic waveforms for the efficacy and safety of transthoracic biphasic cardioversion of atrial fibrillation.Heart Rhythm. 2005; 2:382–387. doi: 10.1016/j.hrthm.2004.12.024CrossrefMedlineGoogle Scholar
16. Voskoboinik A, Moskovitch J, Plunkett G, Bloom J, Wong G, Nalliah C, Prabhu S, Sugumar H, Paramasweran R, McLellan A, et al.. Cardioversion of atrial fibrillation in obese patients: Results from the Cardioversion-BMI randomized controlled trial.J Cardiovasc Electrophysiol. 2019; 30:155–161. doi: 10.1111/jce.13786CrossrefMedlineGoogle Scholar
17. Gallagher MM, Yap YG, Padula M, Ward DE, Rowland E, Camm AJ. Arrhythmic complications of electrical cardioversion: relationship to shock energy.Int J Cardiol. 2008; 123:307–312. doi: 10.1016/j.ijcard.2006.12.014CrossrefMedlineGoogle Scholar
18. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC, Conti JB, Ellinor PT, Ezekowitz MD, Field ME, et al.. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society.Circulation. 2014; 130:e199–e267. doi: 10.1161/CIR.0000000000000041LinkGoogle Scholar
19. Abrams J, Allen J, Allin D, Anderson J, Anderson S, Blanski L, Chadda K, DiBianco R, Favrot L, Gonzalez J. Efficacy and safety of esmolol vs propranolol in the treatment of supraventricular tachyarrhythmias: a multicenter double-blind clinical trial.Am Heart J. 1985; 110:913–922. doi: 10.1016/0002-8703(85)90185-1CrossrefMedlineGoogle Scholar
20. Siu CW, Lau CP, Lee WL, Lam KF, Tse HF. Intravenous diltiazem is superior to intravenous amiodarone or digoxin for achieving ventricular rate control in patients with acute uncomplicated atrial fibrillation.Crit Care Med. 2009; 37:2174–9; quiz 2180. doi: 10.1097/CCM.0b013e3181a02f56CrossrefMedlineGoogle Scholar
21. Clemo HF, Wood MA, Gilligan DM, Ellenbogen KA. Intravenous amiodarone for acute heart rate control in the critically ill patient with atrial tachyarrhythmias.Am J Cardiol. 1998; 81:594–598. doi: 10.1016/s0002-9149(97)00962-4CrossrefMedlineGoogle Scholar
22. Hou ZY, Chang MS, Chen CY, Tu MS, Lin SL, Chiang HT, Woosley RL. Acute treatment of recent-onset atrial fibrillation and flutter with a tailored dosing regimen of intravenous amiodarone. A randomized, digoxin-controlled study.Eur Heart J. 1995; 16:521–528. doi: 10.1093/oxfordjournals.eurheartj.a060945CrossrefMedlineGoogle Scholar
23. Salerno DM, Dias VC, Kleiger RE, Tschida VH, Sung RJ, Sami M, Giorgi LV. Efficacy and safety of intravenous diltiazem for treatment of atrial fibrillation and atrial flutter. The Diltiazem-Atrial Fibrillation/Flutter Study Group.Am J Cardiol. 1989; 63:1046–1051. doi: 10.1016/0002-9149(89)90076-3CrossrefMedlineGoogle Scholar
24. Gulamhusein S, Ko P, Carruthers SG, Klein GJ. Acceleration of the ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome after verapamil.Circulation. 1982; 65:348–354. doi: 10.1161/01.cir.65.2.348LinkGoogle Scholar
25. Jacob AS, Nielsen DH, Gianelly RE. Fatal ventricular fibrillation following verapamil in Wolff-Parkinson-White syndrome with atrial fibrillation.Ann Emerg Med. 1985; 14:159–160. doi: 10.1016/s0196-0644(85)81080-5CrossrefMedlineGoogle Scholar
26. Boriani G, Biffi M, Frabetti L, Azzolini U, Sabbatani P, Bronzetti G, Capucci A, Magnani B. Ventricular fibrillation after intravenous amiodarone in Wolff-Parkinson-White syndrome with atrial fibrillation.Am Heart J. 1996; 131:1214–1216. doi: 10.1016/s0002-8703(96)90098-8CrossrefMedlineGoogle Scholar
27. Kim RJ, Gerling BR, Kono AT, Greenberg ML. Precipitation of ventricular fibrillation by intravenous diltiazem and metoprolol in a young patient with occult Wolff-Parkinson-White syndrome.Pacing Clin Electrophysiol. 2008; 31:776–779. doi: 10.1111/j.1540-8159.2008.01086.xCrossrefMedlineGoogle Scholar
28. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE, Drazner MH, Fonarow GC, Geraci SA, Horwich T, Januzzi JL, et al.; on behalf of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines.Circulation. 2013; 128:e240–e327. doi: 10.1161/CIR.0b013e31829e8776LinkGoogle Scholar
29. Salpeter S, Ormiston T, Salpeter E. Cardioselective beta-blockers for chronic obstructive pulmonary disease.Cochrane Database Syst Rev. 2005CD003566. doi: 10.1002/14651858.CD003566.pub2MedlineGoogle Scholar

Bradycardia

Introduction

Bradycardia is generally defined as a heart rate less than 60/min. Bradycardia can be a normal finding, especially for athletes or during sleep. When bradycardia occurs secondary to a pathological cause, it can lead to decreased cardiac output with resultant hypotension and tissue hypoperfusion. The clinical manifestations of bradycardia can range from an absence of symptoms to symptomatic bradycardia (bradycardia associated with acutely altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock that persist despite adequate airway and breathing). The cause of the bradycardia may dictate the severity of the presentation. For example, patients with severe hypoxia and impending respiratory failure may suddenly develop a profound bradycardia that leads to cardiac arrest if not addressed immediately. In contrast, a patient who develops third-degree heart block but is otherwise well compensated might experience relatively low blood pressure but otherwise be stable. Therefore, the management of bradycardia will depend on both the underlying cause and severity of the clinical presentation. In 2018, the AHA, American College of Cardiology, and Heart Rhythm Society published an extensive guideline on the evaluation and management of stable and unstable bradycardia.2 This guideline focuses exclusively on symptomatic bradycardia in the ACLS setting and maintains consistency with the 2018 guideline.

Recommendation-Specific Supportive Text

Symptomatic bradycardia may be caused by a number of potentially reversible or treatable causes, including structural heart disease, increased vagal tone, hypoxemia, myocardial ischemia, or medications.2 Bradycardia may be difficult to resolve until the underlying cause is treated, making evaluation of underlying cause imperative, simultaneous with emergent treatments for stabilization.
Atropine has been shown to be effective for the treatment of symptomatic bradycardia in both observational studies and in 1 limited RCT.3–7
If atropine is ineffective, either alternative agents to increase heart rate and blood pressure or transcutaneous pacing are reasonable next steps. For medical management of a periarrest patient, epinephrine has gained popularity, including IV infusion and utilization of “push-dose” administration for acute bradycardia and hypotension. Studies on push-dose epinephrine for bradycardia specifically are lacking, although limited data support its use for hypotension.8 Use of push-dose vasopressor requires careful attention to correct dosing. Medication errors leading to adverse effects have been reported.9 Dopamine infusion can also increase heart rate.10 There are limited studies comparing medications to transcutaneous pacing for the treatment of bradycardia. A randomized feasibility study in patients failing atropine compared dopamine to transcutaneous pacing and found no difference in survival to discharge.10 Whether to trial transcutaneous pacing, epinephrine, dopamine, or other vasoactive agent will likely therefore depend on clinician experience and resources available.
For severe symptomatic bradycardia causing shock, if no IV or IO access is available, immediate transcutaneous pacing while access is being pursued may be undertaken. A 2006 systematic review involving 7 studies of transcutaneous pacing for symptomatic bradycardia and bradyasystolic cardiac arrest in the prehospital setting did not find a benefit from pacing compared with standard ACLS, although a subgroup analysis from 1 trial suggested a possible benefit in patients with symptomatic bradycardia.11

These recommendations are supported by the “2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/AHA Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.”2

Recommendation-Specific Supportive Text

When bradycardia is refractory to medical management and results in severe symptoms, the reasonable next step is placement of a temporary pacing catheter for transvenous pacing. Limited evidence for this intervention consists largely of observational studies, many of which have focused on indications and the relatively high complication rate (including bloodstream infections and pneumothorax, among others).12–14 However, when the heart rate does not improve with medications and shock persists, transvenous pacing can improve the heart rate and symptoms until more definitive treatment (correction of underlying cause or permanent pacemaker placement) can be implemented.

These recommendations are supported by the 2018 American College of Cardiology, AHA, and Heart Rhythm Society guideline on the evaluation and management of patients with bradycardia and cardiac conduction delay.2

References

1. Deleted in proof.Google Scholar
2. Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA, Thompson A, Varosy PD. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.Circulation. 2019; 140:e382–e482. doi: 10.1161/CIR.0000000000000628LinkGoogle Scholar
3. Smith I, Monk TG, White PF. Comparison of transesophageal atrial pacing with anticholinergic drugs for the treatment of intraoperative bradycardia.Anesth Analg. 1994; 78:245–252. doi: 10.1213/00000539-199402000-00009CrossrefMedlineGoogle Scholar
4. Brady WJ, Swart G, DeBehnke DJ, Ma OJ, Aufderheide TP. The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: prehospital and emergency department considerations.Resuscitation. 1999; 41:47–55. doi: 10.1016/s0300-9572(99)00032-5CrossrefMedlineGoogle Scholar
5. Chadda KD, Lichstein E, Gupta PK, Kourtesis P. Effects of atropine in patients with bradyarrhythmia complicating myocardial infarction. Usefulness of an optimum dose for overdrive.Am J Med. 1977; 63:503–510. doi: 10.1016/0002-9343(77)90194-2CrossrefMedlineGoogle Scholar
6. Swart G, Brady WJ, DeBehnke DJ, MA OJ, Aufderheide TP. Acute myocardial infarction complicated by hemodynamically unstable bradyarrhythmia: prehospital and ED treatment with atropine.Am J Emerg Med. 1999; 17:647–652. doi: 10.1016/s0735-6757(99)90151-1CrossrefMedlineGoogle Scholar
7. Chadda KD, Lichstein E, Gupta PK, Choy R. Bradycardia-hypotension syndrome in acute myocardial infarction. Reappraisal of the overdrive effects of atropine.Am J Med. 1975; 59:158–164. doi: 10.1016/0002-9343(75)90349-6CrossrefMedlineGoogle Scholar
8. Nawrocki PS, Poremba M, Lawner BJ. Push Dose Epinephrine Use in the Management of Hypotension During Critical Care Transport.Prehosp Emerg Care. 2020; 24:188–195. doi: 10.1080/10903127.2019.1588443CrossrefMedlineGoogle Scholar
9. Cole JB, Knack SK, Karl ER, Horton GB, Satpathy R, Driver BE. Human Errors and Adverse Hemodynamic Events Related to “Push Dose Pressors” in the Emergency Department.J Med Toxicol. 2019; 15:276–286. doi: 10.1007/s13181-019-00716-zCrossrefMedlineGoogle Scholar
10. Morrison LJ, Long J, Vermeulen M, Schwartz B, Sawadsky B, Frank J, Cameron B, Burgess R, Shield J, Bagley P, Mausz V, Brewer JE, Dorian P. A randomized controlled feasibility trial comparing safety and effectiveness of prehospital pacing versus conventional treatment: ‘PrePACE’.Resuscitation. 2008; 76:341–349. doi: 10.1016/j.resuscitation.2007.08.008CrossrefMedlineGoogle Scholar
11. Sherbino J, Verbeek PR, MacDonald RD, Sawadsky BV, McDonald AC, Morrison LJ. Prehospital transcutaneous cardiac pacing for symptomatic bradycardia or bradyasystolic cardiac arrest: a systematic review.Resuscitation. 2006; 70:193–200. doi: 10.1016/j.resuscitation.2005.11.019CrossrefMedlineGoogle Scholar
12. Ferguson JD, Banning AP, Bashir Y. Randomised trial of temporary cardiac pacing with semirigid and balloon-flotation electrode catheters.Lancet. 1997; 349:1883. doi: 10.1016/S0140-6736(97)24026-2CrossrefMedlineGoogle Scholar
13. McCann P. A review of temporary cardiac pacing wires.Indian Pacing Electrophysiol J. 2007; 7:40–49.MedlineGoogle Scholar
14. Jou YL, Hsu HP, Tuan TC, Wang KL, Lin YJ, Lo LW, Hu YF, Kong CW, Chang SL, Chen SA. Trends of temporary pacemaker implant and underlying disease substrate.Pacing Clin Electrophysiol. 2010; 33:1475–1484. doi: 10.1111/j.1540-8159.2010.02893.xCrossrefMedlineGoogle Scholar

Care After ROSC

Postresuscitation Care

Introduction

Post–cardiac arrest care is a critical component of the Chain of Survival. What defines optimal hospital care for patients with ROSC after cardiac arrest is not completely known, but there is increasing interest in identifying and optimizing practices that are likely to improve outcomes. The systemic impact of the ischemia-reperfusion injury caused by cardiac arrest and subsequent resuscitation requires post–cardiac arrest care to simultaneously support the multiple organ systems that are affected. After initial stabilization, care of critically ill postarrest patients hinges on hemodynamic support, mechanical ventilation, temperature management, diagnosis and treatment of underlying causes, diagnosis and treatment of seizures, vigilance for and treatment of infection, and management of the critically ill state of the patient. Many cardiac arrest patients who survive the initial event will eventually die because of withdrawal of life-sustaining treatment in the setting of neurological injury. This cause of death is especially prominent in those with OHCA but is also frequent after IHCA.1,2 Thus, much of postarrest care focuses on mitigating injury to the brain. Possible contributors to this goal include optimization of cerebral perfusion pressure, management of oxygen and carbon dioxide levels, control of core body temperature, and detection and treatment of seizures (Figure 9). Cardiac arrest results in heterogeneous injury; thus, death can also result from multiorgan dysfunction or shock. In light of the complexity of postarrest patients, a multidisciplinary team with expertise in cardiac arrest care is preferred, and the development of multidisciplinary protocols is critical to optimize survival and neurological outcome.

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Figure 9. Adult Post–Cardiac Arrest Care Algorithm. CT indicates computed tomography; ROSC, return of spontaneous circulation; and STEMI, ST-segment elevation myocardial infarction.

Key topics in postresuscitation care that are not covered in this section, but are discussed later, are targeted temperature management (TTM) (Targeted Temperature Management), percutaneous coronary intervention (PCI) in cardiac arrest (PCI After Cardiac Arrest), neuroprognostication (Neuroprognostication), and recovery (Recovery).

Recommendation-Specific Supportive Text

Observational studies evaluating the utility of cardiac receiving centers suggest that a strong system of care may represent a logical clinical link between successful resuscitation and ultimate survival.3 Although data are limited, taken together with experience from regionalized approaches to other emergencies such as trauma, stroke, and ST-segment elevation acute myocardial infarction, consistent implementation of a system of care to manage cardiac arrest patients may improve outcomes.
Patients with 12-lead identification of ST-segment elevation myocardial infarction (STEMI) should have coronary angiography for possible PCI, highlighting the importance of obtaining an ECG for diagnostic purposes.4 However, multiple studies have reported that absence of ST-segment elevations does not rule out an intervenable coronary lesion.5–7
Several RCTs have compared a titrated approach to oxygen administration with an approach of administering 100% oxygen in the first 1 to 2 hours after ROSC.8–10 All of these were conducted in the prehospital setting. However, these trials only titrated oxygen once an oxygen saturation could be measured with a pulse oximeter. No studies have investigated titration of oxygen in patients for whom oxygen saturation (by pulse oximeter) or partial pressure of oxygen in the blood (by arterial blood gas) cannot be measured. The recommendation to administer 100% oxygen until measurement of this vital sign is possible is therefore based on physiology and the expert opinion that hypoxia could worsen end-organ damage and should be avoided.

Recommendation 1 is supported by the 2019 focused update on ACLS guidelines.3 Recommendation 2 last received formal evidence review in 2015.4 Recommendation 3 is supported by the 2020 CoSTR for ALS.11

Recommendation-Specific Supportive Text

Hypotension may worsen brain and other organ injury after cardiac arrest by decreasing oxygen delivery to tissues. The optimal MAP target after ROSC, however, is not clear. This topic was previously reviewed by ILCOR in 2015,12 and a detailed evidence update was conducted by the Australia and New Zealand Council of Resuscitation on behalf of ILCOR for 2020.11 Several observational studies have found that postresuscitation hypotension is associated with worse survival and neurological outcome.13–19 One study found no association between higher MAP during TTM treatment and outcome, although shock at admission was associated with poor outcome.20 Definitions of hypotension vary between studies, with systolic blood pressure of 90 mm Hg and MAP of 65 mm Hg being common cutoffs used. Two RCTs conducted since 2015 compared a lower blood pressure target (standard care or MAP greater than 65 mm Hg in one study and MAP 65–75 mm Hg in the other) with a higher target (MAP 85–100 in one study and MAP 80–100 mm Hg in the other).21,22 Both studies failed to detect any difference in survival or survival with favorable neurological outcome, although neither study was appropriately powered for these outcomes. One trial did find improvement in cerebral oxygenation with higher MAP,21 which is a proposed mechanism for the benefit effect of higher MAP in hypoxic ischemic encephalopathy. A recent observational study comparing outcomes in patients with MAP 70 to 90 mm Hg to those with MAP greater than 90 mm Hg also found that higher MAP was associated with better neurological outcome.23 Although some of these data suggest targeting a MAP of 80 mm Hg or higher in those at risk for neurological injury after cardiac arrest might be beneficial, this remains unproven.

These recommendations are supported by the 2015 Guidelines Update24 and a 2020 evidence update.11

Recommendation-Specific Supportive Text

In a 2020 ILCOR systematic review,11 1 observational study reported that hypoxemia after return of circulation was associated with worse outcome.25 This was not seen in other studies,26–28 and all studies were at high risk of bias. This recommendation is therefore based primarily on the physiological rationale that hypoxia increases the risk of end-organ damage, and the fact that hypoxemia is the best available surrogate for hypoxia.
There are some physiological basis and preclinical data for hyperoxemia leading to increased inflammation and exacerbating brain injury in postarrest patients.29 A 2020 ILCOR systematic review11 identified 5 RCTs comparing a titrated or lower oxygen administration strategy with usual care or a higher oxygen administration strategy in postarrest patients: 3 in the prehospital setting and 2 in the ICU setting.8–10,30,31 Overall, these trials found no difference in clinical outcomes, but all were underpowered for these outcomes. A recent large RCT compared usual care with aggressive avoidance of hyperoxemia in mechanically ventilated critically ill patients and found no difference between groups in the overall cohort but increased survival in the intervention arm in the subgroup of 164 postarrest patients.32 Observational data are inconsistent and very limited by confounding.11 Three RCTs on this topic are ongoing (NCT03138005, NCT03653325, NCT03141099). The suggested range of 92% to 98% is intended as a practical approximation of the normal range.
Two RCTs compared a strategy of targeting high-normal Paco2 (44–46 mm Hg) with one targeting low-normal Paco2 (33–35 mm Hg)31 and a strategy targeting moderate hypercapnia (Paco2 50–55 mm Hg) compared with normocapnia (Paco2 35–45 mm Hg).33 Neither trial found a difference in any clinical outcomes. Results across 6 observational studies were inconsistent, and all studies were limited by significant risk of bias.25,34–38 There is a large ongoing RCT addressing this question (NCT03114033).

These recommendations are supported by the 2020 CoSTR for ALS.11

Recommendation-Specific Supportive Text

A 2020 ILCOR systematic review11 identified no controlled studies comparing treatment of seizures with no treatment of seizures in this population. In spite of the lack of evidence, untreated clinically apparent seizure activity is thought to be potentially harmful to the brain, and treatment of seizures is recommended in other settings39 and likely also warranted after cardiac arrest.
The writing group acknowledged that there is no direct evidence that EEG to detect nonconvulsive seizures improves outcomes. This recommendation is based on the fact that nonconvulsive seizures are common in postarrest patients and that the presence of seizures may be important prognostically, although whether treatment of nonconvulsive seizures affects outcome in this setting remains uncertain. An ILCOR systematic review done for 2020 did not specifically address the timing and method of obtaining EEGs in postarrest patients who remain unresponsive. Data on the relative benefit of continuous versus intermittent EEG are limited. One study found no difference in survival with good neurological outcome at 3 months in patients monitored with routine (one to two 20-minute EEGs over 24 hours) versus continuous (for 18–24 hours) EEG.40
Nonconvulsive seizures are common after cardiac arrest. Whether treatment of seizure activity on EEG that is not associated with clinically evident seizures affects outcome is currently unknown. A randomized trial investigating this question is ongoing (NCT02056236).
The 2020 CoSTR recommends that seizures be treated when diagnosed in postarrest patients.11 No specific agent was recommended. However, the CoSTR described 2 retrospective studies suggesting valproate, levetiracetam, and fosphenytoin may all be effective, with fosphenytoin found to be associated with more hypotension in 1 study.41,42 Common sedatives such as propofol and midazolam have also been found to be effective in suppressing seizure activity after cardiac arrest.43–45
A 2020 ILCOR systematic review11 identified 2 RCTs comparing seizure prophylaxis with no seizure prophylaxis in comatose postarrest patients.46,47 Neither study found any difference in occurrence of seizures or survival with favorable neurological outcome between groups.

These recommendations are supported by the 2020 CoSTR for ALS.11

Recommendation-Specific Supportive Text

One small RCT from 2007,48 found no difference in survival between strict and moderate glucose control. In the absence of other evidence specific to cardiac arrest, it seems reasonable to manage blood glucose levels in postarrest patients with the same approach used for the general critically ill population, namely using insulin therapy when needed to maintain a blood glucose of 150 to 180 mg/dL.49
A 2020 ILCOR systematic review found 2 RCTs and a small number of observational studies evaluating the effect of prophylactic antibiotics on outcomes in postarrest patients.11,50 The RCTs found no difference in survival or neurological outcome.51,52 One RCT51 did find lower incidence of early pneumonia in those who received prophylactic antibiotics, but this did not translate to a difference in other outcomes. When data from the 2 RCTs were pooled, there was no overall difference in infections.51,52
The topic of neuroprotective agents was last reviewed in detail in 2010. Multiple agents, including magnesium, coenzyme Q10 (ubiquinol), exanatide, xenon gas, methylphenidate, and amantadine, have been considered as possible agents to either mitigate neurological injury or facilitate patient awakening. This work has been largely observational,53–57 although randomized trials have been conducted on coenzyme Q10, xenon gas, and exanatide.58–60 A small trial on the effect of coenzyme Q10 reported better survival in those receiving coenzyme Q10, but there was no significant difference in favorable neurological outcome and these findings have yet to be validated.58 One additional coenzyme Q10 trial was recently completed but results are not yet available (NCT02934555). None of the other studies identified have been able to show a difference in any clinical outcomes with use of any of the agents studied.
Since this topic was last updated in detail in 2015, at least 2 randomized trials have been completed on the effect of steroids on shock and other outcomes after ROSC, only 1 of which has been published to date.61 In this study, shock reversal and other outcomes did not differ between groups. A large retrospective observational study did find that steroid use after cardiac arrest was associated with survival.62 Steroid use for septic shock has been evaluated extensively, with a recent trial of over 1200 patients finding improved survival in those treated with steroids.63 A trial enrolling 3800 patients did not find a mortality benefit, although time to discharge from ICU and time to shock reversal were both shorter in the steroid group.64 Taken together, there is no definitive evidence of benefit from steroids after ROSC. However, the data in sepsis suggest that some patients with severe shock may benefit from steroids and that the co-occurrence of sepsis and cardiac arrest is important to consider.

Recommendation 1 last received formal evidence review in 2010 and is supported by the “Guidelines for the Use of an Insulin Infusion for the Management of Hyperglycemia in Critically Ill Patients” from the Society for Critical Care Medicine.49 Recommendation 2 is supported by the 2020 CoSTR for ALS.11 Recommendations 3 and 4 last received formal evidence review in 2015.24

References

1. Witten L, Gardner R, Holmberg MJ, Wiberg S, Moskowitz A, Mehta S, Grossestreuer AV, Yankama T, Donnino MW, Berg KM . Reasons for death in patients successfully resuscitated from out-of-hospital and in-hospital cardiac arrest.Resuscitation. 2019; 136:93–99. doi: 10.1016/j.resuscitation.2019.01.031CrossrefMedlineGoogle Scholar
2. Laver S, Farrow C, Turner D, Nolan J. Mode of death after admission to an intensive care unit following cardiac arrest.Intensive Care Med. 2004; 30:2126–2128. doi: 10.1007/s00134-004-2425-zCrossrefMedlineGoogle Scholar
3. Panchal AR, Berg KM, Cabanas JG, Kurz MC, Link MS, Del Rios M, Hirsch KG, Chan PS, Hazinski MF, Morley PT, et al.. 2019 American Heart Association focused update on systems of care: dispatcher-assisted cardiopulmonary resuscitation and cardiac arrest centers: an update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2019; 140:e895–e903. doi: 10.1161/CIR.0000000000000733LinkGoogle Scholar
4. Levine GN, Bates ER, Blankenship JC, Bailey SR, Bittl JA, Cercek B, Chambers CE, Ellis SG, Guyton RA, Hollenberg SM, Khot UN, Lange RA, Mauri L, Mehran R, Moussa ID, Mukherjee D, Ting HH, O’Gara PT, Kushner FG, Ascheim DD, Brindis RG, Casey DE, Chung MK, de Lemos JA, Diercks DB, Fang JC, Franklin BA, Granger CB, Krumholz HM, Linderbaum JA, Morrow DA, Newby LK, Ornato JP, Ou N, Radford MJ, Tamis-Holland JE, Tommaso CL, Tracy CM, Woo YJ, Zhao DX. 2015 ACC/AHA/SCAI Focused Update on Primary Percutaneous Coronary Intervention for Patients With ST-Elevation Myocardial Infarction: An Update of the 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention and the 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction.Circulation. 2016; 133:1135–1147. doi: 10.1161/CIR.0000000000000336AbstractGoogle Scholar
5. Stær-Jensen H, Nakstad ER, Fossum E, Mangschau A, Eritsland J, Draegni T, Jacobsen D, Sunde K, Andersen GO. Post-resuscitation ECG for selection of patients for immediate coronary angiography in out-of-hospital cardiac arrest.Circ Cardiovasc Interv. 2015; 8doi: 10.1161/CIRCINTERVENTIONS.115.002784LinkGoogle Scholar
6. Zanuttini D, Armellini I, Nucifora G, Grillo MT, Morocutti G, Carchietti E, Trillò G, Spedicato L, Bernardi G, Proclemer A. Predictive value of electrocardiogram in diagnosing acute coronary artery lesions among patients with out-of-hospital-cardiac-arrest.Resuscitation. 2013; 84:1250–1254. doi: 10.1016/j.resuscitation.2013.04.023CrossrefMedlineGoogle Scholar
7. Sideris G, Voicu S, Dillinger JG, Stratiev V, Logeart D, Broche C, Vivien B, Brun PY, Deye N, Capan D, Aout M, Megarbane B, Baud FJ, Henry P. Value of post-resuscitation electrocardiogram in the diagnosis of acute myocardial infarction in out-of-hospital cardiac arrest patients.Resuscitation. 2011; 82:1148–1153. doi: 10.1016/j.resuscitation.2011.04.023CrossrefMedlineGoogle Scholar
8. Kuisma M, Boyd J, Voipio V, Alaspää A, Roine RO, Rosenberg P. Comparison of 30 and the 100% inspired oxygen concentrations during early post-resuscitation period: a randomised controlled pilot study.Resuscitation. 2006; 69:199–206. doi: 10.1016/j.resuscitation.2005.08.010CrossrefMedlineGoogle Scholar
9. Bray JE, Hein C, Smith K, Stephenson M, Grantham H, Finn J, Stub D, Cameron P, Bernard SEXACT Investigators. Oxygen titration after resuscitation from out-of-hospital cardiac arrest: A multi-centre, randomised controlled pilot study (the EXACT pilot trial).Resuscitation. 2018; 128:211–215. doi: 10.1016/j.resuscitation.2018.04.019CrossrefMedlineGoogle Scholar
10. Thomas M, Voss S, Benger J, Kirby K, Nolan JP. Cluster randomised comparison of the effectiveness of 100% oxygen versus titrated oxygen in patients with a sustained return of spontaneous circulation following out of hospital cardiac arrest: a feasibility study. PROXY: post ROSC OXYgenation study.BMC Emerg Med. 2019; 19:16. doi: 10.1186/s12873-018-0214-1CrossrefMedlineGoogle Scholar
11. Berg KM, Soar J, Andersen LW, Böttiger BW, Cacciola S, Callaway CW, Couper K, Cronberg T, D’Arrigo S, Deakin CD, et al.; on behalf of the Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S92–S139. doi: 10.1161/CIR.0000000000000893LinkGoogle Scholar
12. Soar J, Nolan JP, Böttiger BW, Perkins GD, Lott C, Carli P, Pellis T, Sandroni C, Skrifvars MB, Smith GB, Sunde K, Deakin CDAdult advanced life support section Collaborators. European Resuscitation Council Guidelines for Resuscitation 2015: Section 3. Adult advanced life support.Resuscitation. 2015; 95:100–147. doi: 10.1016/j.resuscitation.2015.07.016CrossrefMedlineGoogle Scholar
13. Trzeciak S, Jones AE, Kilgannon JH, Milcarek B, Hunter K, Shapiro NI, Hollenberg SM, Dellinger P, Parrillo JE. Significance of arterial hypotension after resuscitation from cardiac arrest.Crit Care Med. 2009; 37:2895–903; quiz 2904. doi: 10.1097/ccm.0b013e3181b01d8cCrossrefMedlineGoogle Scholar
14. Chiu YK, Lui CT, Tsui KL. Impact of hypotension after return of spontaneous circulation on survival in patients of out-of-hospital cardiac arrest.Am J Emerg Med. 2018; 36:79–83. doi: 10.1016/j.ajem.2017.07.019CrossrefMedlineGoogle Scholar
15. Bray JE, Bernard S, Cantwell K, Stephenson M, Smith Kand the VACAR Steering Committee. The association between systolic blood pressure on arrival at hospital and outcome in adults surviving from out-of-hospital cardiac arrests of presumed cardiac aetiology.Resuscitation. 2014; 85:509–515. doi: 10.1016/j.resuscitation.2013.12.005CrossrefMedlineGoogle Scholar
16. Russo JJ, Di Santo P, Simard T, James TE, Hibbert B, Couture E, Marbach J, Osborne C, Ramirez FD, Wells GA, Labinaz M, Le May MRfrom the CAPITAL study group. Optimal mean arterial pressure in comatose survivors of out-of-hospital cardiac arrest: An analysis of area below blood pressure thresholds.Resuscitation. 2018; 128:175–180. doi: 10.1016/j.resuscitation.2018.04.028CrossrefMedlineGoogle Scholar
17. Laurikkala J, Wilkman E, Pettilä V, Kurola J, Reinikainen M, Hoppu S, Ala-Kokko T, Tallgren M, Tiainen M, Vaahersalo J, Varpula T, Skrifvars MBFINNRESUSCI Study Group. Mean arterial pressure and vasopressor load after out-of-hospital cardiac arrest: Associations with one-year neurologic outcome.Resuscitation. 2016; 105:116–122. doi: 10.1016/j.resuscitation.2016.05.026CrossrefMedlineGoogle Scholar
18. Annoni F, Dell’Anna AM, Franchi F, Creteur J, Scolletta S, Vincent JL, Taccone FS. The impact of diastolic blood pressure values on the neurological outcome of cardiac arrest patients.Resuscitation. 2018; 130:167–173. doi: 10.1016/j.resuscitation.2018.07.017CrossrefMedlineGoogle Scholar
19. Janiczek JA, Winger DG, Coppler P, Sabedra AR, Murray H, Pinsky MR, Rittenberger JC, Reynolds JC, Dezfulian C. Hemodynamic Resuscitation Characteristics Associated with Improved Survival and Shock Resolution After Cardiac Arrest.Shock. 2016; 45:613–619. doi: 10.1097/SHK.0000000000000554CrossrefMedlineGoogle Scholar
20. Young MN, Hollenbeck RD, Pollock JS, Giuseffi JL, Wang L, Harrell FE, McPherson JA. Higher achieved mean arterial pressure during therapeutic hypothermia is not associated with neurologically intact survival following cardiac arrest.Resuscitation. 2015; 88:158–164. doi: 10.1016/j.resuscitation.2014.12.008CrossrefMedlineGoogle Scholar
21. Ameloot K, De Deyne C, Eertmans W, Ferdinande B, Dupont M, Palmers PJ, Petit T, Nuyens P, Maeremans J, Vundelinckx J, Vanhaverbeke M, Belmans A, Peeters R, Demaerel P, Lemmens R, Dens J, Janssens S. Early goal-directed haemodynamic optimization of cerebral oxygenation in comatose survivors after cardiac arrest: the Neuroprotect post-cardiac arrest trial.Eur Heart J. 2019; 40:1804–1814. doi: 10.1093/eurheartj/ehz120CrossrefMedlineGoogle Scholar
22. Jakkula P, Pettilä V, Skrifvars MB, Hästbacka J, Loisa P, Tiainen M, Wilkman E, Toppila J, Koskue T, Bendel S, Birkelund T, Laru-Sompa R, Valkonen M, Reinikainen MCOMACARE study group. Targeting low-normal or high-normal mean arterial pressure after cardiac arrest and resuscitation: a randomised pilot trial.Intensive Care Med. 2018; 44:2091–2101. doi: 10.1007/s00134-018-5446-8CrossrefMedlineGoogle Scholar
23. Roberts BW, Kilgannon JH, Hunter BR, Puskarich MA, Shea L, Donnino M, Jones C, Fuller BM, Kline JA, Jones AE, Shapiro NI, Abella BS, Trzeciak S. Association Between Elevated Mean Arterial Blood Pressure and Neurologic Outcome After Resuscitation From Cardiac Arrest: Results From a Multicenter Prospective Cohort Study.Crit Care Med. 2019; 47:93–100. doi: 10.1097/CCM.0000000000003474CrossrefMedlineGoogle Scholar
24. Callaway CW, Donnino MW, Fink EL, Geocadin RG, Golan E, Kern KB, Leary M, Meurer WJ, Peberdy MA, Thompson TM, et al.. Part 8: post–cardiac arrest care: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S465–482. doi: 10.1161/cir.0000000000000262LinkGoogle Scholar
25. Wang HE, Prince DK, Drennan IR, Grunau B, Carlbom DJ, Johnson N, Hansen M, Elmer J, Christenson J, Kudenchuk P, Aufderheide T, Weisfeldt M, Idris A, Trzeciak S, Kurz M, Rittenberger JC, Griffiths D, Jasti J, May SResuscitation Outcomes Consortium (ROC) Investigators. Post-resuscitation arterial oxygen and carbon dioxide and outcomes after out-of-hospital cardiac arrest.Resuscitation. 2017; 120:113–118. doi: 10.1016/j.resuscitation.2017.08.244CrossrefMedlineGoogle Scholar
26. Ebner F, Ullén S, Åneman A, Cronberg T, Mattsson N, Friberg H, Hassager C, Kjærgaard J, Kuiper M, Pelosi P, Undén J, Wise MP, Wetterslev J, Nielsen N. Associations between partial pressure of oxygen and neurological outcome in out-of-hospital cardiac arrest patients: an explorative analysis of a randomized trial.Crit Care. 2019; 23:30. doi: 10.1186/s13054-019-2322-zCrossrefMedlineGoogle Scholar
27. Humaloja J, Litonius E, Efendijev I, Folger D, Raj R, Pekkarinen PT, Skrifvars MB. Early hyperoxemia is not associated with cardiac arrest outcome.Resuscitation. 2019; 140:185–193. doi: 10.1016/j.resuscitation.2019.04.035CrossrefMedlineGoogle Scholar
28. Johnson NJ, Dodampahala K, Rosselot B, Perman SM, Mikkelsen ME, Goyal M, Gaieski DF, Grossestreuer AV. The Association Between Arterial Oxygen Tension and Neurological Outcome After Cardiac Arrest.Ther Hypothermia Temp Manag. 2017; 7:36–41. doi: 10.1089/ther.2016.0015CrossrefMedlineGoogle Scholar
29. Pilcher J, Weatherall M, Shirtcliffe P, Bellomo R, Young P, Beasley R. The effect of hyperoxia following cardiac arrest - A systematic review and meta-analysis of animal trials.Resuscitation. 2012; 83:417–422. doi: 10.1016/j.resuscitation.2011.12.021CrossrefMedlineGoogle Scholar
30. Young P, Bailey M, Bellomo R, Bernard S, Dicker B, Freebairn R, Henderson S, Mackle D, McArthur C, McGuinness S, Smith T, Swain A, Weatherall M, Beasley R. HyperOxic Therapy OR NormOxic Therapy after out-of-hospital cardiac arrest (HOT OR NOT): a randomised controlled feasibility trial.Resuscitation. 2014; 85:1686–1691. doi: 10.1016/j.resuscitation.2014.09.011CrossrefMedlineGoogle Scholar
31. Jakkula P, Reinikainen M, Hästbacka J, Loisa P, Tiainen M, Pettilä V, Toppila J, Lähde M, Bäcklund M, Okkonen M, et al.; and the COMACARE study group. Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial.Intensive Care Med. 2018; 44:2112–2121. doi: 10.1007/s00134-018-5453-9CrossrefMedlineGoogle Scholar
32. Mackle D, Bellomo R, Bailey M, Beasley R, Deane A, Eastwood G, Finfer S, Freebairn R, King V, Linke N, et al.; and the ICU-ROX Investigators the Australian New Zealand Intensive Care Society Clinical Trials Group. Conservative oxygen therapy during mechanical ventilation in the ICU.N Engl J Med. 2020; 382:989–998. doi: 10.1056/NEJMoa1903297CrossrefMedlineGoogle Scholar
33. Eastwood GM, Schneider AG, Suzuki S, Peck L, Young H, Tanaka A, Mårtensson J, Warrillow S, McGuinness S, Parke R, Gilder E, Mccarthy L, Galt P, Taori G, Eliott S, Lamac T, Bailey M, Harley N, Barge D, Hodgson CL, Morganti-Kossmann MC, Pébay A, Conquest A, Archer JS, Bernard S, Stub D, Hart GK, Bellomo R. Targeted therapeutic mild hypercapnia after cardiac arrest: A phase II multi-centre randomised controlled trial (the CCC trial).Resuscitation. 2016; 104:83–90. doi: 10.1016/j.resuscitation.2016.03.023CrossrefMedlineGoogle Scholar
34. Vaahersalo J, Bendel S, Reinikainen M, Kurola J, Tiainen M, Raj R, Pettilä V, Varpula T, Skrifvars MBFINNRESUSCI Study Group. Arterial blood gas tensions after resuscitation from out-of-hospital cardiac arrest: associations with long-term neurologic outcome.Crit Care Med. 2014; 42:1463–1470. doi: 10.1097/CCM.0000000000000228CrossrefMedlineGoogle Scholar
35. Hope Kilgannon J, Hunter BR, Puskarich MA, Shea L, Fuller BM, Jones C, Donnino M, Kline JA, Jones AE, Shapiro NI, Abella BS, Trzeciak S, Roberts BW. Partial pressure of arterial carbon dioxide after resuscitation from cardiac arrest and neurological outcome: A prospective multi-center protocol-directed cohort study.Resuscitation. 2019; 135:212–220. doi: 10.1016/j.resuscitation.2018.11.015CrossrefMedlineGoogle Scholar
36. Roberts BW, Kilgannon JH, Chansky ME, Mittal N, Wooden J, Trzeciak S. Association between postresuscitation partial pressure of arterial carbon dioxide and neurological outcome in patients with post-cardiac arrest syndrome.Circulation. 2013; 127:2107–2113. doi: 10.1161/CIRCULATIONAHA.112.000168LinkGoogle Scholar
37. von Auenmueller KI, Christ M, Sasko BM, Trappe HJ. The Value of Arterial Blood Gas Parameters for Prediction of Mortality in Survivors of Out-of-hospital Cardiac Arrest.J Emerg Trauma Shock. 2017; 10:134–139. doi: 10.4103/JETS.JETS_146_16CrossrefMedlineGoogle Scholar
38. Ebner F, Harmon MBA, Aneman A, Cronberg T, Friberg H, Hassager C, Juffermans N, Kjærgaard J, Kuiper M, Mattsson N, Pelosi P, Ullén S, Undén J, Wise MP, Nielsen N. Carbon dioxide dynamics in relation to neurological outcome in resuscitated out-of-hospital cardiac arrest patients: an exploratory Target Temperature Management Trial substudy.Crit Care. 2018; 22:196. doi: 10.1186/s13054-018-2119-5CrossrefMedlineGoogle Scholar
39. Glauser T, Shinnar S, Gloss D, Alldredge B, Arya R, Bainbridge J, Bare M, Bleck T, Dodson WE, Garrity L, Jagoda A, Lowenstein D, Pellock J, Riviello J, Sloan E, Treiman DM. Evidence-Based Guideline: Treatment of Convulsive Status Epilepticus in Children and Adults: Report of the Guideline Committee of the American Epilepsy Society.Epilepsy Curr. 2016; 16:48–61. doi: 10.5698/1535-7597-16.1.48CrossrefMedlineGoogle Scholar
40. Fatuzzo D, Beuchat I, Alvarez V, Novy J, Oddo M, Rossetti AO. Does continuous EEG influence prognosis in patients after cardiac arrest?Resuscitation. 2018; 132:29–32. doi: 10.1016/j.resuscitation.2018.08.023CrossrefMedlineGoogle Scholar
41. Solanki P, Coppler PJ, Kvaløy JT, Baldwin MA, Callaway CW, Elmer JPittsburgh Post-Cardiac Arrest Service. Association of antiepileptic drugs with resolution of epileptiform activity after cardiac arrest.Resuscitation. 2019; 142:82–90. doi: 10.1016/j.resuscitation.2019.07.007CrossrefMedlineGoogle Scholar
42. Kapur J, Elm J, Chamberlain JM, Barsan W, Cloyd J, Lowenstein D, Shinnar S, Conwit R, Meinzer C, Cock H, Fountain N, Connor JT, Silbergleit RNETT and PECARN Investigators. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus.N Engl J Med. 2019; 381:2103–2113. doi: 10.1056/NEJMoa1905795CrossrefMedlineGoogle Scholar
43. Thömke F, Weilemann SL. Poor prognosis despite successful treatment of postanoxic generalized myoclonus.Neurology. 2010; 74:1392–1394. doi: 10.1212/WNL.0b013e3181dad5b9CrossrefMedlineGoogle Scholar
44. Aicua RI, Rapun I, Novy J, Solari D, Oddo M, Rossetti AO. Early Lance-Adams syndrome after cardiac arrest: prevalence, time to return to awareness, and outcome in a large cohort.Resuscitation. 2017; 115:169–172. doi: 10.1016/j.resuscitation.2017.03.020CrossrefMedlineGoogle Scholar
45. Koutroumanidis M, Sakellariou D. Low frequency nonevolving generalized periodic epileptiform discharges and the borderland of hypoxic nonconvulsive status epilepticus in comatose patients after cardiac arrest.Epilepsy Behav. 2015; 49:255–262. doi: 10.1016/j.yebeh.2015.04.060CrossrefMedlineGoogle Scholar
46. Brain Resuscitation Clinical Trial I Study Group. Randomized clinical study of thiopental loading in comatose survivors of cardiac arrest.N Engl J Med. 1986; 314:397–403. doi: 10.1056/nejm198602133140701CrossrefMedlineGoogle Scholar
47. Longstreth WT, Fahrenbruch CE, Olsufka M, Walsh TR, Copass MK, Cobb LA. Randomized clinical trial of magnesium, diazepam, or both after out-of-hospital cardiac arrest.Neurology. 2002; 59:506–514. doi: 10.1212/wnl.59.4.506CrossrefMedlineGoogle Scholar
48. Oksanen T, Skrifvars MB, Varpula T, Kuitunen A, Pettilä V, Nurmi J, Castrén M. Strict versus moderate glucose control after resuscitation from ventricular fibrillation.Intensive Care Med. 2007; 33:2093–2100. doi: 10.1007/s00134-007-0876-8CrossrefMedlineGoogle Scholar
49. Jacobi J, Bircher N, Krinsley J, Agus M, Braithwaite SS, Deutschman C, Freire AX, Geehan D, Kohl B, Nasraway SA, Rigby M, Sands K, Schallom L, Taylor B, Umpierrez G, Mazuski J, Schunemann H. Guidelines for the use of an insulin infusion for the management of hyperglycemia in critically ill patients.Crit Care Med. 2012; 40:3251–3276. doi: 10.1097/CCM.0b013e3182653269CrossrefMedlineGoogle Scholar
50. Couper K, Laloo R, Field R, Perkins GD, Thomas M, Yeung J. Prophylactic antibiotic use following cardiac arrest: A systematic review and meta-analysis.Resuscitation. 2019; 141:166–173. doi: 10.1016/j.resuscitation.2019.04.047CrossrefMedlineGoogle Scholar
51. François B, Cariou A, Clere-Jehl R, Dequin PF, Renon-Carron F, Daix T, Guitton C, Deye N, Legriel S, Plantefève G, Quenot JP, Desachy A, Kamel T, Bedon-Carte S, Diehl JL, Chudeau N, Karam E, Durand-Zaleski I, Giraudeau B, Vignon P, Le Gouge ACRICS-TRIGGERSEP Network and the ANTHARTIC Study Group. Prevention of Early Ventilator-Associated Pneumonia after Cardiac Arrest.N Engl J Med. 2019; 381:1831–1842. doi: 10.1056/NEJMoa1812379CrossrefMedlineGoogle Scholar
52. Ribaric SF, Turel M, Knafelj R, Gorjup V, Stanic R, Gradisek P, Cerovic O, Mirkovic T, Noc M. Prophylactic versus clinically-driven antibiotics in comatose survivors of out-of-hospital cardiac arrest-A randomized pilot study.Resuscitation. 2017; 111:103–109. doi: 10.1016/j.resuscitation.2016.11.025CrossrefMedlineGoogle Scholar
53. Pearce A, Lockwood C, van den Heuvel C, Pearce J. The use of therapeutic magnesium for neuroprotection during global cerebral ischemia associated with cardiac arrest and cardiac surgery in adults: a systematic review.JBI Database System Rev Implement Rep. 2017; 15:86–118. doi: 10.11124/JBISRIR-2016-003236CrossrefMedlineGoogle Scholar
54. Perucki WH, Hiendlmayr B, O’Sullivan DM, Gunaseelan AC, Fayas F, Fernandez AB. Magnesium Levels and Neurologic Outcomes in Patients Undergoing Therapeutic Hypothermia After Cardiac Arrest.Ther Hypothermia Temp Manag. 2018; 8:14–17. doi: 10.1089/ther.2017.0016CrossrefMedlineGoogle Scholar
55. Suzuki M, Hatakeyama T, Nakamura R, Saiki T, Kamisasanuki T, Sugiki D, Matsushima H. Serum Magnesium Levels and Neurological Outcomes in Patients Undergoing Targeted Temperature Management After Cardiac Arrest.J Emerg Nurs. 2020; 46:59–65. doi: 10.1016/j.jen.2019.10.006CrossrefMedlineGoogle Scholar
56. Cocchi MN, Giberson B, Berg K, Salciccioli JD, Naini A, Buettner C, Akuthota P, Gautam S, Donnino MW. Coenzyme Q10 levels are low and associated with increased mortality in post-cardiac arrest patients.Resuscitation. 2012; 83:991–995. doi: 10.1016/j.resuscitation.2012.03.023CrossrefMedlineGoogle Scholar
57. Reynolds JC, Rittenberger JC, Callaway CW. Methylphenidate and amantadine to stimulate reawakening in comatose patients resuscitated from cardiac arrest.Resuscitation. 2013; 84:818–824. doi: 10.1016/j.resuscitation.2012.11.014CrossrefMedlineGoogle Scholar
58. Damian MS, Ellenberg D, Gildemeister R, Lauermann J, Simonis G, Sauter W, Georgi C. Coenzyme Q10 combined with mild hypothermia after cardiac arrest: a preliminary study.Circulation. 2004; 110:3011–3016. doi: 10.1161/01.CIR.0000146894.45533.C2LinkGoogle Scholar
59. Laitio R, Hynninen M, Arola O, Virtanen S, Parkkola R, Saunavaara J, Roine RO, Grönlund J, Ylikoski E, Wennervirta J, Bäcklund M, Silvasti P, Nukarinen E, Tiainen M, Saraste A, Pietilä M, Airaksinen J, Valanne L, Martola J, Silvennoinen H, Scheinin H, Harjola VP, Niiranen J, Korpi K, Varpula M, Inkinen O, Olkkola KT, Maze M, Vahlberg T, Laitio T. Effect of Inhaled Xenon on Cerebral White Matter Damage in Comatose Survivors of Out-of-Hospital Cardiac Arrest: A Randomized Clinical Trial.JAMA. 2016; 315:1120–1128. doi: 10.1001/jama.2016.1933CrossrefMedlineGoogle Scholar
60. Wiberg S, Hassager C, Schmidt H, Thomsen JH, Frydland M, Lindholm MG, Høfsten DE, Engstrøm T, Køber L, Møller JE, Kjaergaard J. Neuroprotective Effects of the Glucagon-Like Peptide-1 Analog Exenatide After Out-of-Hospital Cardiac Arrest: A Randomized Controlled Trial.Circulation. 2016; 134:2115–2124. doi: 10.1161/CIRCULATIONAHA.116.024088LinkGoogle Scholar
61. Donnino MW, Andersen LW, Berg KM, Chase M, Sherwin R, Smithline H, Carney E, Ngo L, Patel PV, Liu X, Cutlip D, Zimetbaum P, Cocchi MNCollaborating Authors from the Beth Israel Deaconess Medical Center’s Center for Resuscitation Science Research Group. Corticosteroid therapy in refractory shock following cardiac arrest: a randomized, double-blind, placebo-controlled, trial.Crit Care. 2016; 20:82. doi: 10.1186/s13054-016-1257-xCrossrefMedlineGoogle Scholar
62. Tsai MS, Chuang PY, Huang CH, Tang CH, Yu PH, Chang WT, Chen WJ. Postarrest Steroid Use May Improve Outcomes of Cardiac Arrest Survivors.Crit Care Med. 2019; 47:167–175. doi: 10.1097/CCM.0000000000003468CrossrefMedlineGoogle Scholar
63. Annane D, Renault A, Brun-Buisson C, Megarbane B, Quenot JP, Siami S, Cariou A, Forceville X, Schwebel C, Martin C, Timsit JF, Misset B, Ali Benali M, Colin G, Souweine B, Asehnoune K, Mercier E, Chimot L, Charpentier C, François B, Boulain T, Petitpas F, Constantin JM, Dhonneur G, Baudin F, Combes A, Bohé J, Loriferne JF, Amathieu R, Cook F, Slama M, Leroy O, Capellier G, Dargent A, Hissem T, Maxime V, Bellissant ECRICS-TRIGGERSEP Network. Hydrocortisone plus Fludrocortisone for Adults with Septic Shock.N Engl J Med. 2018; 378:809–818. doi: 10.1056/NEJMoa1705716CrossrefMedlineGoogle Scholar
64. Venkatesh B, Finfer S, Cohen J, Rajbhandari D, Arabi Y, Bellomo R, Billot L, Correa M, Glass P, Harward M, et al.; on behalf of the ADRENAL Trial Investigators and the Australian–New Zealand Intensive Care Society Clinical Trials Group. Adjunctive glucocorticoid therapy in patients with septic shock.N Engl J Med. 2018; 378:797–808. doi: 10.1056/NEJMoa1705835CrossrefMedlineGoogle Scholar

Targeted Temperature Management

Introduction

TTM between 32°C and 36°C for at least 24 hours is currently recommended for all cardiac rhythms in both OHCA and IHCA. Multiple randomized trials have been performed in various domains of TTM and were summarized in a systematic review published in 2015.1 Subsequent to the 2015 recommendations, additional randomized trials have evaluated TTM for nonshockable rhythms as well as TTM duration. Many of these were reviewed in an evidence update provided in the 2020 COSTR for ALS.2 Many uncertainties within the topic of TTM remain, including whether temperature should vary on the basis of patient characteristics, how long TTM should be maintained, and how quickly it should be started. An updated systematic review on several aspects of this important topic is needed once currently ongoing clinical trials have been completed.

Recommendation-Specific Supportive Text

Two RCTs of patients with OHCA with an initially shockable rhythm published in 2002 reported benefit from mild hypothermia when compared with no temperature management.1,3,4 A more recent trial comparing a target temperature of 33°C to 37°C in patients (IHCA and OHCA) with initial nonshockable rhythm also found better outcomes in those treated with a temperature of 33°C.5 A large trial is currently underway testing TTM compared with normothermia (NCT03114033).
An RCT published in 2019 compared TTM at 33°C to 37°C for patients who were not following commands after ROSC from cardiac arrest with initial nonshockable rhythm. Survival with a favorable neurological outcome (Cerebral Performance Category 1–2) was higher in the group treated with 33°C.5 This trial included both OHCA and IHCA and is the first randomized trial on TTM after cardiac arrest to include IHCA patients. In a subgroup analysis, the benefit of TTM did not appear to differ significantly by IHCA/OHCA subgroups.
No RCTs of TTM have included IHCA patients with an initial shockable rhythm, and this recommendation is therefore based largely on extrapolation from OHCA studies and the study of patients with initially nonshockable rhythms that included IHCA patients. Observational studies on TTM for IHCA with any initial rhythm have reported mixed results. Two studies that included patients enrolled in the AHA Get With The Guidelines-Resuscitation registry reported either no benefit or worse outcome from TTM.6,7 Both were limited by very low overall usage of TTM in the registry and lack of data on presence of coma, making it difficult to determine if TTM was indicated for a given IHCA patient.

This topic last received formal evidence review in 2015,8 with an evidence update conducted for the 2020 CoSTR for ALS.2

Recommendation-Specific Supportive Text

In 2013, a trial of over 900 patients compared TTM at 33°C to 36°C for patients with OHCA and any initial rhythm, excluding unwitnessed asystole, and found that 33°C was not superior to 36°C.9 A more recent trial compared 33°C to 37°C for patients with ROSC after initial nonshockable rhythm and found improved survival with favorable neurological outcome in the group treated with 33°C.5 There have been reports of decreasing utilization of TTM in recent years, with one hypothesis being that some clinicians interpret the inclusion of 36°C as a target temperature as being equivalent to normothermia, or no strict temperature control.10 An updated systematic review is needed on the question of which target temperature is most beneficial. Based on the available evidence, however, TTM at a temp between 32°C and 36°C remains a Class 1 recommendation.
One RCT including 355 patients found no difference in outcome between TTM for 24 and 48 hours.11 This study may have been underpowered to detect differences in clinical outcomes. The initial 2002 trials cooled patients for 123 and 24 hours4 while the 2013 trial used 28 hours.9 A larger, adaptive clinical trial is currently underway investigating multiple different durations of hypothermia ranging from 6 to 72 hours, using a target temperature of 33°C for all patients enrolled (NCT04217551). There is no clear best approach to rewarming after TTM, although a protocol of 0.5°C per hour was followed in the 2013 trial.9 The optimal rate of rewarming, and specifically whether slower rates are beneficial, is a knowledge gap, and at least 1 trial is ongoing (NCT02555254).
Fever after ROSC is associated with poor neurological outcome in patients not treated with TTM, although this finding is reported less consistently in patients treated with TTM.12–20 It has not been established whether treatment of fever is associated with an improvement in outcome, but treatment or prevention of fever appears to be a reasonable approach.
A 2015 systematic review found that prehospital cooling with the specific method of the rapid infusion of cold IV fluids was associated with more pulmonary edema and a higher risk of rearrest.1 Since this review, a number of RCTs on prehospital cooling have been conducted. One trial compared the prehospital induction of hypothermia with any method (including ice packs and cold IV fluids) with no prehospital cooling, and found higher receipt of in-hospital TTM in those who had prehospital initiation. That trial found no increased adverse events in those treated with prehospital cooling.21 Other methods of prehospital cooling, such as esophageal or nasal devices, have also been investigated; whether these affect outcomes is a knowledge gap.

This topic last received formal evidence review in 2015,8 with an evidence update conducted for the 2020 CoSTR for ALS.2

References

1. Donnino MW, Andersen LW, Berg KM, Reynolds JC, Nolan JP, Morley PT, Lang E, Cocchi MN, Xanthos T, Callaway CW, Soar JILCOR ALS Task Force. Temperature Management After Cardiac Arrest: An Advisory Statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation and the American Heart Association Emergency Cardiovascular Care Committee and the Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation.Circulation. 2015; 132:2448–2456. doi: 10.1161/CIR.0000000000000313LinkGoogle Scholar
2. Berg KM, Soar J, Andersen LW, Böttiger BW, Cacciola S, Callaway CW, Couper K, Cronberg T, D’Arrigo S, Deakin CD, et al.; on behalf of the Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S92–S139. doi: 10.1161/CIR.0000000000000893LinkGoogle Scholar
3. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, Smith K. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia.N Engl J Med. 2002; 346:557–563. doi: 10.1056/NEJMoa003289CrossrefMedlineGoogle Scholar
4. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest.N Engl J Med. 2002; 346:549–556. doi: 10.1056/NEJMoa012689CrossrefMedlineGoogle Scholar
5. Lascarrou JB, Merdji H, Le Gouge A, Colin G, Grillet G, Girardie P, Coupez E, Dequin PF, Cariou A, Boulain T, Brule N, Frat JP, Asfar P, Pichon N, Landais M, Plantefeve G, Quenot JP, Chakarian JC, Sirodot M, Legriel S, Letheulle J, Thevenin D, Desachy A, Delahaye A, Botoc V, Vimeux S, Martino F, Giraudeau B, Reignier JCRICS-TRIGGERSEP Group. Targeted Temperature Management for Cardiac Arrest with Nonshockable Rhythm.N Engl J Med. 2019; 381:2327–2337. doi: 10.1056/NEJMoa1906661CrossrefMedlineGoogle Scholar
6. Nichol G, Huszti E, Kim F, Fly D, Parnia S, Donnino M, Sorenson T, Callaway CWAmerican Heart Association Get With the Guideline-Resuscitation Investigators. Does induction of hypothermia improve outcomes after in-hospital cardiac arrest?Resuscitation. 2013; 84:620–625. doi: 10.1016/j.resuscitation.2012.12.009CrossrefMedlineGoogle Scholar
7. Chan PS, Berg RA, Tang Y, Curtis LH, Spertus JAAmerican Heart Association’s Get With the Guidelines–Resuscitation Investigators. Association Between Therapeutic Hypothermia and Survival After In-Hospital Cardiac Arrest.JAMA. 2016; 316:1375–1382. doi: 10.1001/jama.2016.14380CrossrefMedlineGoogle Scholar
8. Callaway CW, Donnino MW, Fink EL, Geocadin RG, Golan E, Kern KB, Leary M, Meurer WJ, Peberdy MA, Thompson TM, et al.. Part 8: post–cardiac arrest care: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S465–482. doi: 10.1161/cir.0000000000000262LinkGoogle Scholar
9. Nielsen N, Wetterslev J, Cronberg T, Erlinge D, Gasche Y, Hassager C, Horn J, Hovdenes J, Kjaergaard J, Kuiper M, Pellis T, Stammet P, Wanscher M, Wise MP, Åneman A, Al-Subaie N, Boesgaard S, Bro-Jeppesen J, Brunetti I, Bugge JF, Hingston CD, Juffermans NP, Koopmans M, Køber L, Langørgen J, Lilja G, Møller JE, Rundgren M, Rylander C, Smid O, Werer C, Winkel P, Friberg HTTM Trial Investigators. Targeted temperature management at 33°C versus 36°C after cardiac arrest.N Engl J Med. 2013; 369:2197–2206. doi: 10.1056/NEJMoa1310519CrossrefMedlineGoogle Scholar
10. Khera R, Humbert A, Leroux B, Nichol G, Kudenchuk P, Scales D, Baker A, Austin M, Newgard CD, Radecki R, Vilke GM, Sawyer KN, Sopko G, Idris AH, Wang H, Chan PS, Kurz MC. Hospital Variation in the Utilization and Implementation of Targeted Temperature Management in Out-of-Hospital Cardiac Arrest.Circ Cardiovasc Qual Outcomes. 2018; 11:e004829. doi: 10.1161/CIRCOUTCOMES.118.004829LinkGoogle Scholar
11. Kirkegaard H, Søreide E, de Haas I, Pettilä V, Taccone FS, Arus U, Storm C, Hassager C, Nielsen JF, Sørensen CA, Ilkjær S, Jeppesen AN, Grejs AM, Duez CHV, Hjort J, Larsen AI, Toome V, Tiainen M, Hästbacka J, Laitio T, Skrifvars MB. Targeted Temperature Management for 48 vs 24 Hours and Neurologic Outcome After Out-of-Hospital Cardiac Arrest: A Randomized Clinical Trial.JAMA. 2017; 318:341–350. doi: 10.1001/jama.2017.8978CrossrefMedlineGoogle Scholar
12. Nolan JP, Laver SR, Welch CA, Harrison DA, Gupta V, Rowan K. Outcome following admission to UK intensive care units after cardiac arrest: a secondary analysis of the ICNARC Case Mix Programme Database.Anaesthesia. 2007; 62:1207–1216. doi: 10.1111/j.1365-2044.2007.05232.xCrossrefMedlineGoogle Scholar
13. Langhelle A, Tyvold SS, Lexow K, Hapnes SA, Sunde K, Steen PA. In-hospital factors associated with improved outcome after out-of-hospital cardiac arrest. A comparison between four regions in Norway.Resuscitation. 2003; 56:247–263. doi: 10.1016/s0300-9572(02)00409-4CrossrefMedlineGoogle Scholar
14. Suffoletto B, Peberdy MA, van der Hoek T, Callaway C. Body temperature changes are associated with outcomes following in-hospital cardiac arrest and return of spontaneous circulation.Resuscitation. 2009; 80:1365–1370. doi: 10.1016/j.resuscitation.2009.08.020CrossrefMedlineGoogle Scholar
15. Gebhardt K, Guyette FX, Doshi AA, Callaway CW, Rittenberger JCPost Cardiac Arrest Service. Prevalence and effect of fever on outcome following resuscitation from cardiac arrest.Resuscitation. 2013; 84:1062–1067. doi: 10.1016/j.resuscitation.2013.03.038CrossrefMedlineGoogle Scholar
16. Benz-Woerner J, Delodder F, Benz R, Cueni-Villoz N, Feihl F, Rossetti AO, Liaudet L, Oddo M. Body temperature regulation and outcome after cardiac arrest and therapeutic hypothermia.Resuscitation. 2012; 83:338–342. doi: 10.1016/j.resuscitation.2011.10.026CrossrefMedlineGoogle Scholar
17. Leary M, Grossestreuer AV, Iannacone S, Gonzalez M, Shofer FS, Povey C, Wendell G, Archer SE, Gaieski DF, Abella BS. Pyrexia and neurologic outcomes after therapeutic hypothermia for cardiac arrest.Resuscitation. 2013; 84:1056–1061. doi: 10.1016/j.resuscitation.2012.11.003CrossrefMedlineGoogle Scholar
18. Cocchi MN, Boone MD, Giberson B, Giberson T, Farrell E, Salciccioli JD, Talmor D, Williams D, Donnino MW. Fever after rewarming: incidence of pyrexia in postcardiac arrest patients who have undergone mild therapeutic hypothermia.J Intensive Care Med. 2014; 29:365–369. doi: 10.1177/0885066613491932CrossrefMedlineGoogle Scholar
19. Bro-Jeppesen J, Hassager C, Wanscher M, Søholm H, Thomsen JH, Lippert FK, Møller JE, Køber L, Kjaergaard J. Post-hypothermia fever is associated with increased mortality after out-of-hospital cardiac arrest.Resuscitation. 2013; 84:1734–1740. doi: 10.1016/j.resuscitation.2013.07.023CrossrefMedlineGoogle Scholar
20. Winters SA, Wolf KH, Kettinger SA, Seif EK, Jones JS, Bacon-Baguley T. Assessment of risk factors for post-rewarming “rebound hyperthermia” in cardiac arrest patients undergoing therapeutic hypothermia.Resuscitation. 2013; 84:1245–1249. doi: 10.1016/j.resuscitation.2013.03.027CrossrefMedlineGoogle Scholar
21. Scales DC, Cheskes S, Verbeek PR, Pinto R, Austin D, Brooks SC, Dainty KN, Goncharenko K, Mamdani M, Thorpe KE, Morrison LJStrategies for Post-Arrest Care SPARC Network. Prehospital cooling to improve successful targeted temperature management after cardiac arrest: A randomized controlled trial.Resuscitation. 2017; 121:187–194. doi: 10.1016/j.resuscitation.2017.10.002CrossrefMedlineGoogle Scholar

PCI After Cardiac Arrest

Synopsis

Coronary artery disease (CAD) is prevalent in the setting of cardiac arrest.1–4 Patients with cardiac arrest due to shockable rhythms have demonstrated particularly high rates of severe CAD: up to 96% of patients with STEMI on their postresuscitation ECG,2,5 up to 42% for patients without ST-segment elevation,2,5–7 and 85% of refractory out-of-hospital VF/VT arrest patients have severe CAD.8 The role of CAD in cardiac arrest with nonshockable rhythms is unknown.

When significant CAD is observed during post-ROSC coronary angiography, revascularization can be achieved safely in most cases.5,7,9 Further, successful PCI is associated with improved survival in multiple observational studies.2,6,7,10,11 Additional benefits of evaluation in the cardiac catheterization laboratory include discovery of anomalous coronary anatomy, the opportunity to assess left ventricular function and hemodynamic status, and the potential for insertion of temporary mechanical circulatory support devices.

The 2015 Guidelines Update recommended emergent coronary angiography for patients with ST-segment elevation on the post-ROSC ECG. Emergent coronary angiography and PCI have also been also associated with improved neurological outcomes in patients without STEMI on their post-ROSC resuscitation ECG.4,12 However, a large randomized trial found no improvement in survival in patients resuscitated from OHCA with an initial shockable rhythm in whom no ST-segment elevations or signs of shock were present.13 Multiple RCTs are underway. It remains to be tested whether patients with signs of shock benefit from emergent coronary angiography and PCI.

Recommendation-Specific Supportive Text

Several observational studies have demonstrated improved neurologically favorable survival when early coronary angiography is performed followed by PCI in patients with cardiac arrest who have a STEMI.5,14–17 This led to a Class 1 recommendation in the 2015 Guidelines Update that has not been contradicted by any other recent studies. This recommendation is consistent with global recommendations for all patients with STEMI.
Multiple observational studies have shown an association between emergent coronary angiography and PCI and improved neurological outcomes in patients without ST-segment elevation.5,7,14,15,18 A meta-analysis also supported the use of early coronary angiography in patients without ST-segment elevation.19 However, a large randomized trial found no improvement in survival in patients resuscitated from OHCA with an initial shockable rhythm in whom no ST-segment elevation or signs of shock were present.20 In addition, while coronary artery disease was found in 65% of patients who underwent coronary angiography, only 5% of patients had acute thrombotic coronary occlusions. Multiple RCTs are underway, but the role of emergent coronary angiography and PCI in patients without ST-elevation but with signs of shock remains to be tested. The use of emergent coronary angiography in patients with hemodynamic or electric instability is consistent with guidelines for non-STEMI patients.21–23 The optimal treatment of hemodynamically and electrically stable patients without ST-segment elevation remains unclear. This area was last reviewed systematically in 2015 and requires additional systematic review after the completion of currently active trials (NCT03119571, NCT02309151, NCT02387398, NCT02641626, NCT02750462, NCT02876458).
Evidence suggests that patients who are comatose after ROSC benefit from invasive angiography, when indicated, as do patients who are awake.4,14,18 Therefore, invasive coronary angiography is reasonable independent of neurological status.

This topic last received formal evidence review in 2015.24

References

1. Spaulding CM, Joly LM, Rosenberg A, Monchi M, Weber SN, Dhainaut JF, Carli P. Immediate coronary angiography in survivors of out-of-hospital cardiac arrest.N Engl J Med. 1997; 336:1629–1633. doi: 10.1056/NEJM199706053362302CrossrefMedlineGoogle Scholar
2. Dumas F, Cariou A, Manzo-Silberman S, Grimaldi D, Vivien B, Rosencher J, Empana JP, Carli P, Mira JP, Jouven X, Spaulding C. Immediate percutaneous coronary intervention is associated with better survival after out-of-hospital cardiac arrest: insights from the PROCAT (Parisian Region Out of hospital Cardiac ArresT) registry.Circ Cardiovasc Interv. 2010; 3:200–207. doi: 10.1161/CIRCINTERVENTIONS.109.913665LinkGoogle Scholar
3. Davies MJ. Anatomic features in victims of sudden coronary death. Coronary artery pathology.Circulation. 1992; 851 SupplI19–I24.MedlineGoogle Scholar
4. Yannopoulos D, Bartos JA, Aufderheide TP, Callaway CW, Deo R, Garcia S, Halperin HR, Kern KB, Kudenchuk PJ, Neumar RW, Raveendran GAmerican Heart Association Emergency Cardiovascular Care Committee. The Evolving Role of the Cardiac Catheterization Laboratory in the Management of Patients With Out-of-Hospital Cardiac Arrest: A Scientific Statement From the American Heart Association.Circulation. 2019; 139:e530–e552. doi: 10.1161/CIR.0000000000000630LinkGoogle Scholar
5. Kern KB, Lotun K, Patel N, Mooney MR, Hollenbeck RD, McPherson JA, McMullan PW, Unger B, Hsu CH, Seder DBINTCAR-Cardiology Registry. Outcomes of Comatose Cardiac Arrest Survivors With and Without ST-Segment Elevation Myocardial Infarction: Importance of Coronary Angiography.J AM COLL CARDIOL. Cardiovasc Interv. 2015; 8:1031–1040. doi: 10.1016/j.jcin.2015.02.021CrossrefGoogle Scholar
6. Dumas F, Bougouin W, Geri G, Lamhaut L, Rosencher J, Pène F, Chiche JD, Varenne O, Carli P, Jouven X, Mira JP, Spaulding C, Cariou A. Emergency Percutaneous Coronary Intervention in Post-Cardiac Arrest Patients Without ST-Segment Elevation Pattern: Insights From the PROCAT II Registry.J AM COLL CARDIOL. Cardiovasc Interv. 2016; 9:1011–1018. doi: 10.1016/j.jcin.2016.02.001CrossrefGoogle Scholar
7. Garcia S, Drexel T, Bekwelem W, Raveendran G, Caldwell E, Hodgson L, Wang Q, Adabag S, Mahoney B, Frascone R, et al.. Early access to the cardiac catheterization laboratory for patients resuscitated from cardiac arrest due to a shockable rhythm: the Minnesota Resuscitation Consortium Twin Cities Unified Protocol.J Am Heart Assoc. 2016; 5:e002670. doi: 10.1161/JAHA.115.002670LinkGoogle Scholar
8. Yannopoulos D, Bartos JA, Raveendran G, Conterato M, Frascone RJ, Trembley A, John R, Connett J, Benditt DG, Lurie KG, Wilson RF, Aufderheide TP. Coronary Artery Disease in Patients With Out-of-Hospital Refractory Ventricular Fibrillation Cardiac Arrest.J Am Coll Cardiol. 2017; 70:1109–1117. doi: 10.1016/j.jacc.2017.06.059CrossrefMedlineGoogle Scholar
9. Sideris G, Voicu S, Yannopoulos D, Dillinger JG, Adjedj J, Deye N, Gueye P, Manzo-Silberman S, Malissin I, Logeart D, Magkoutis N, Capan DD, Makhloufi S, Megarbane B, Vivien B, Cohen-Solal A, Payen D, Baud FJ, Henry P. Favourable 5-year postdischarge survival of comatose patients resuscitated from out-of-hospital cardiac arrest, managed with immediate coronary angiogram on admission.Eur Heart J Acute Cardiovasc Care. 2014; 3:183–191. doi: 10.1177/2048872614523348CrossrefMedlineGoogle Scholar
10. Geri G, Dumas F, Bougouin W, Varenne O, Daviaud F, Pene F, Lamhaut L, Chiche JD, Spaulding C, Mira JP, et al.. Immediate percutaneous coronary intervention is associated with improved short- and long-term survival after out-of-hospital cardiac arrest.Circ Cardiovasc Interv. 2015; 8doi: 10.1161/circinterventions.114.002303LinkGoogle Scholar
11. Zanuttini D, Armellini I, Nucifora G, Carchietti E, Trillò G, Spedicato L, Bernardi G, Proclemer A. Impact of emergency coronary angiography on in-hospital outcome of unconscious survivors after out-of-hospital cardiac arrest.Am J Cardiol. 2012; 110:1723–1728. doi: 10.1016/j.amjcard.2012.08.006CrossrefMedlineGoogle Scholar
12. Patel N, Patel NJ, Macon CJ, Thakkar B, Desai M, Rengifo-Moreno P, Alfonso CE, Myerburg RJ, Bhatt DL, Cohen MG. Trends and Outcomes of Coronary Angiography and Percutaneous Coronary Intervention After Out-of-Hospital Cardiac Arrest Associated With Ventricular Fibrillation or Pulseless Ventricular Tachycardia.JAMA Cardiol. 2016; 1:890–899. doi: 10.1001/jamacardio.2016.2860CrossrefMedlineGoogle Scholar
13. Lemkes JS, Janssens GN, van der Hoeven NW, Jewbali LSD, Dubois EA, Meuwissen M, Rijpstra TA, Bosker HA, Blans MJ, Bleeker GB, Baak R, Vlachojannis GJ, Eikemans BJW, van der Harst P, van der Horst ICC, Voskuil M, van der Heijden JJ, Beishuizen A, Stoel M, Camaro C, van der Hoeven H, Henriques JP, Vlaar APJ, Vink MA, van den Bogaard B, Heestermans TACM, de Ruijter W, Delnoij TSR, Crijns HJGM, Jessurun GAJ, Oemrawsingh PV, Gosselink MTM, Plomp K, Magro M, Elbers PWG, van de Ven PM, Oudemans-van Straaten HM, van Royen N. Coronary Angiography after Cardiac Arrest without ST-Segment Elevation.N Engl J Med. 2019; 380:1397–1407. doi: 10.1056/NEJMoa1816897CrossrefMedlineGoogle Scholar
14. Bro-Jeppesen J, Kjaergaard J, Wanscher M, Pedersen F, Holmvang L, Lippert FK, Møller JE, Køber L, Hassager C. Emergency coronary angiography in comatose cardiac arrest patients: do real-life experiences support the guidelines?Eur Heart J Acute Cardiovasc Care. 2012; 1:291–301. doi: 10.1177/2048872612465588CrossrefMedlineGoogle Scholar
15. Vyas A, Chan PS, Cram P, Nallamothu BK, McNally B, Girotra S. Early coronary angiography and survival after out-of-hospital cardiac arrest.Circ Cardiovasc Interv. 2015; 8:e002321. doi: 10.1161/CIRCINTERVENTIONS.114.002321LinkGoogle Scholar
16. Waldo SW, Armstrong EJ, Kulkarni A, Hoffmayer K, Kinlay S, Hsue P, Ganz P, McCabe JM. Comparison of clinical characteristics and outcomes of cardiac arrest survivors having versus not having coronary angiography.Am J Cardiol. 2013; 111:1253–1258. doi: 10.1016/j.amjcard.2013.01.267CrossrefMedlineGoogle Scholar
17. Hosmane VR, Mustafa NG, Reddy VK, Reese CL, DiSabatino A, Kolm P, Hopkins JT, Weintraub WS, Rahman E. Survival and neurologic recovery in patients with ST-segment elevation myocardial infarction resuscitated from cardiac arrest.J Am Coll Cardiol. 2009; 53:409–415. doi: 10.1016/j.jacc.2008.08.076CrossrefMedlineGoogle Scholar
18. Hollenbeck RD, McPherson JA, Mooney MR, Unger BT, Patel NC, McMullan PW, Hsu CH, Seder DB, Kern KB. Early cardiac catheterization is associated with improved survival in comatose survivors of cardiac arrest without STEMI.Resuscitation. 2014; 85:88–95. doi: 10.1016/j.resuscitation.2013.07.027CrossrefMedlineGoogle Scholar
19. Khan MS, Shah SMM, Mubashir A, Khan AR, Fatima K, Schenone AL, Khosa F, Samady H, Menon V. Early coronary angiography in patients resuscitated from out of hospital cardiac arrest without ST-segment elevation: A systematic review and meta-analysis.Resuscitation. 2017; 121:127–134. doi: 10.1016/j.resuscitation.2017.10.019CrossrefMedlineGoogle Scholar
20. Lemkes JS, Janssens GN, van Royen N. Coronary Angiography after Cardiac Arrest without ST-Segment Elevation. Reply.N Engl J Med. 2019; 381:189–190. doi: 10.1056/NEJMc1906523MedlineGoogle Scholar
21. Amsterdam EA, Wenger NK, Brindis RG, Casey DE, Ganiats TG, Holmes DR, Jaffe AS, Jneid H, Kelly RF, Kontos MC, Levine GN, Liebson PR, Mukherjee D, Peterson ED, Sabatine MS, Smalling RW, Zieman SJACC/AHA Task Force Members; Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.Circulation. 2014; 130:2354–2394. doi: 10.1161/CIR.0000000000000133LinkGoogle Scholar
22. Lee L, Bates ER, Pitt B, Walton JA, Laufer N, O’Neill WW. Percutaneous transluminal coronary angioplasty improves survival in acute myocardial infarction complicated by cardiogenic shock.Circulation. 1988; 78:1345–1351. doi: 10.1161/01.cir.78.6.1345LinkGoogle Scholar
23. Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley JD, Buller CE, Jacobs AK, Slater JN, Col J, McKinlay SM, LeJemtel TH. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock.N Engl J Med. 1999; 341:625–634. doi: 10.1056/NEJM199908263410901CrossrefMedlineGoogle Scholar
24. Callaway CW, Donnino MW, Fink EL, Geocadin RG, Golan E, Kern KB, Leary M, Meurer WJ, Peberdy MA, Thompson TM, et al.. Part 8: post–cardiac arrest care: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S465–482. doi: 10.1161/cir.0000000000000262LinkGoogle Scholar

Neuroprognostication

General Considerations for Neuroprognostication

Introduction

Hypoxic-ischemic brain injury is the leading cause of morbidity and mortality in survivors of OHCA and accounts for a smaller but significant portion of poor outcomes after resuscitation from IHCA.1,2 Most deaths attributable to postarrest brain injury are due to active withdrawal of life-sustaining treatment based on a predicted poor neurological outcome. Accurate neurological prognostication is important to avoid inappropriate withdrawal of life-sustaining treatment in patients who may otherwise achieve meaningful neurological recovery and also to avoid ineffective treatment when poor outcome is inevitable (Figure 10).3

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Figure 10. Recommended approach to multimodal neuroprognostication. Neurologic prognostication incorporates multiple diagnostic tests that are synthesized into a comprehensive multimodal assessment at least 72 hours after return to normothermia and with sedation and analgesia limited as possible. Awareness and incorporation of the potential sources of error in the individual diagnostic tests is important. The suggested timing of the multimodal diagnostics is shown here. CT indicates computed tomography; EEG, electroencephalogram; MRI, magnetic resonance imaging; NSE, neuron-specific enolase; ROSC, return of spontaneous circulation; SSEP, somatosensory evoked potential; and TTM, targeted temperature management.

Synopsis

Neuroprognostication relies on interpreting the results of diagnostic tests and correlating those results with outcome. Given that a false-positive test for poor neurological outcome could lead to inappropriate withdrawal of life support from a patient who otherwise would have recovered, the most important test characteristic is specificity. Many of the tests considered are subject to error because of the effects of medications, organ dysfunction, and temperature. Furthermore, many research studies have methodological limitations including small sample sizes, single-center design, lack of blinding, the potential for self-fulfilling prophecies, and the use of outcome at hospital discharge rather than a time point associated with maximal recovery (typically 3–6 months after arrest).3

Because any single method of neuroprognostication has an intrinsic error rate and may be subject to confounding, multiple modalities should be used to improve decision-making accuracy.

Recommendation-Specific Supportive Text

The overall certainty in the evidence of neurological prognostication studies is low because of biases that limit the internal validity of the studies as well as issues of generalizability that limit their external validity. Thus, the confidence in the prognostication of the diagnostic tests studied is also low. Neuroprognostication that uses multimodal testing is felt to be better at predicting outcomes than is relying on the results of a single test to predict poor prognosis.3,4
Sedatives and neuromuscular blockers may be metabolized more slowly in post–cardiac arrest patients, and injured brains may be more sensitive to the depressant effects of various medications. Residual sedation or paralysis can confound the accuracy of clinical examinations.5
Prognostication of neurological recovery is complex and limited by uncertainty in most cases. Discordance in goals of care between clinicians and families/surrogates has been reported in more than 25% of critically ill patients.6 Lack of adequate communication is one important factor, and regular multidisciplinary conversations may help mitigate this.
Operationally, the timing for prognostication is typically at least 5 days after ROSC for patients treated with TTM (which is about 72 hours after normothermia) and should be conducted under conditions that minimize the confounding effects of sedating medications. Individual test modalities may be obtained earlier and the results integrated into the multimodality assessment synthesized at least 72 hours after normothermia. In some instances, prognostication and withdrawal of life support may appropriately occur earlier because of nonneurologic disease, brain herniation, patient’s goals and wishes, or clearly nonsurvivable situations.

These recommendations are supported by the 2020 CoSTR for ALS,4 which supplements the last comprehensive review of this topic conducted in 2015.7

Use of the Clinical Examination in Neuroprognostication

Synopsis

Clinical examination findings correlate with poor outcome but are also subject to confounding by TTM and medications, and prior studies have methodological limitations. In addition to assessing level of consciousness and performing basic neurological examination, clinical examination elements may include the pupillary light reflex, pupillometry, corneal reflex, myoclonus, and status myoclonus when assessed within 1 week after cardiac arrest. The ILCOR systematic review included studies regardless of TTM status, and findings were correlated with neurological outcome at time points ranging from hospital discharge to 12 months after arrest.4 Quantitative pupillometry is the automated assessment of pupillary reactivity, measured by the percent reduction in pupillary size and the degree of reactivity reported as the neurological pupil index. Benefits of this method are a standard and reproducible assessment. Status myoclonus is commonly defined as spontaneous or sound-sensitive, repetitive, irregular brief jerks in both face and limb present most of the day within 24 hours after cardiac arrest.8 Status myoclonus differs from myoclonic status epilepticus; myoclonic status epilepticus is defined as status epilepticus with physical manifestation of persistent myoclonic movements and is considered a subtype of status epilepticus for these guidelines.

Recommendation-Specific Supportive Text

In 17 studies,9–25 absent pupillary light reflex assessed from immediately after ROSC up to 7 days after arrest predicted poor neurological outcome with specificity ranging from 48% to 100%. The specificity varied significantly on the basis of timing, with the highest specificity seen at time points 72 hours or more after arrest.
Three studies evaluated quantitative pupillary light reflex15,26,27 and 3 studies evaluated neurological pupil index15,28,29 at time points ranging from 24 to 72 hours after arrest. Absent pupillary light reflex as assessed by quantitative pupillometry (ie, quantitative pupillary light reflex=0%) is an objective finding and, in 1 study of 271 patients, had high specificity for poor outcome when assessed at 72 hours after arrest.15 Neurological pupil index is nonspecific and may be affected by medications; thus, an absolute neurological pupil index cutoff and a specific threshold that predicts poor prognosis is unknown.15,28,29
Eleven observational studies9–11,14,16,17,19,21,22,30,31 evaluated absence of corneal reflexes at time points ranging from immediately after ROSC to 7 days after arrest. The specificity for poor outcome ranged from 25% to 100% and increased in the studies evaluating corneal reflexes at time points 72 hours or more after arrest (ranging from 89% to 100%). Like other examination findings, corneal reflexes are subject to confounding by medications, and few studies specifically evaluated the potential of residual medication effect.
In 2 studies involving 347 patients,21,32 the presence of status myoclonus within 72 hours predicted poor neurological outcome from hospital discharge to 6 months, with specificity ranging from 97% to 100%.
Obtaining EEG in status myoclonus is important to rule out underlying ictal activity. In addition, status myoclonus may have an EEG correlate that is not clearly ictal but may have prognostic meaning, and additional research is needed to delineate these patterns. Some EEG-correlated patterns of status myoclonus may have poor prognosis, but there may also be more benign subtypes of status myoclonus with EEG correlates.33,34
Six observational studies16,19,30,35–37 evaluated the presence of myoclonus within 96 hours after arrest with specificity for poor outcome ranging from 77.8% to 97.4%. There were methodological limitations in all studies, including a lack of standard definitions, lack of blinding, incomplete data about EEG correlates, and the inability to differentiate subtypes of myoclonus. The literature was so imprecise as to make it potentially harmful if undifferentiated myoclonus is used as a prognostic marker.
Historically, the best motor examination in the upper extremities has been used as a prognostic tool, with extensor or absent movement being correlated with poor outcome. The previous literature was limited by methodological concerns, including around inadequate control for effects of TTM and medications and self-fulfilling prophecies, and there was a lower-than-acceptable false-positive rate (10% to 15%).7 The performance of the motor examination was not evaluated in the 2020 ILCOR systematic review. The updates made to the 2015 recommendations are based on concerns that the motor examination is subject to confounding and has an unacceptably high false-positive rate and, thus, should not be used as a prognostic tool or as a screen for subsequent testing.

These recommendations are supported by the 2020 CoSTR for ALS,4 which supplements the last comprehensive review of this topic conducted in 2015.7

Use of Serum Biomarkers for Neuroprognostication

Synopsis

Serum biomarkers are blood-based tests that measure the concentration of proteins normally found in the central nervous system (CNS). These proteins are absorbed into blood in the setting of neurological injury, and their serum levels reflect the degree of brain injury. Limitations to their prognostic utility include variability in testing methods on the basis of site and laboratory, between-laboratory inconsistency in levels, susceptibility to additional uncertainty due to hemolysis, and potential extracerebral sources of the proteins. NSE and S100B are the 2 most commonly studied markers, but others are included in this review as well. The 2020 ILCOR systematic review evaluated studies that obtained serum biomarkers within the first 7 days after arrest and correlated serum biomarker concentrations with neurological outcome. Other testing of serum biomarkers, including testing levels over serial time points after arrest, was not evaluated. A large observational cohort study investigating these and other novel serum biomarkers and their performance as prognostic biomarkers would be of high clinical significance.

Recommendation-Specific Supportive Text

Twelve observational studies evaluated NSE collected within 72 hours after arrest.10,13,21,23,38–45 The maximal level that correlated with poor outcome ranged from 33 to 120 μg/L with specificity for poor outcome of 75% to 100%. The evidence is limited because of lack of blinding, laboratory inconsistencies, a broad range of thresholds needed to achieve 100% specificity, and imprecision. As such, an absolute value cutoff of NSE that predicts poor prognosis is not known, though very high levels of NSE may be used as part of multimodal prognostication. There is research interest in evaluating serial measures over the first days after arrest as a prognostic tool instead of using a single absolute value.10,46
Three observational studies40,47,48 evaluated S100B levels within the first 72 hours after arrest. The maximal level that correlated with poor outcome ranged broadly depending on the study and the timing when it was measured after arrest. At values reported to achieve 100% specificity, test sensitivity ranged from 2.8% to 77.6%. The evidence is limited by the small number of studies and the broad range of thresholds across the studies required to achieve 100% specificity. The ILCOR review also evaluated 1 study each evaluating glial fibrillary acidic protein44 and Tau49 and 2 studies evaluating neurofilament light chain.50,51 Given the low number of studies, the LOE was low, and these serum biomarkers could not be recommended for clinical practice.

These recommendations are supported by the 2020 CoSTR for ALS,4 which supplements the last comprehensive review of this topic conducted in 2015.7

Use of Electrophysiological Tests for Neuroprognostication

Synopsis

Electroencephalography is widely used in clinical practice to evaluate cortical brain activity and diagnose seizures. Its use as a neuroprognostic tool is promising, but the literature is limited by several factors: lack of standardized terminology and definitions, relatively small sample sizes, single center study design, lack of blinding, subjectivity in the interpretation, and lack of accounting for effects of medications. There is also inconsistency in definitions used to describe specific findings and patterns. EEG patterns that were evaluated in the 2020 ILCOR systematic review include unreactive EEG, epileptiform discharges, seizures, status epilepticus, burst suppression, and “highly malignant” EEG. Unfortunately, different studies define highly malignant EEG differently or imprecisely, making use of this finding unhelpful.

SSEPs are obtained by stimulating the median nerve and evaluating for the presence of a cortical N20 wave. Bilaterally absent N20 SSEP waves have been correlated with poor prognosis, but reliability of this modality is limited by requiring appropriate operator skills and care to avoid electric interference from muscle artifacts or from the ICU environment. One benefit to SSEPs is that they are subject to less interference from medications than are other modalities.

Recommendation-Specific Supportive Text

Five observational studies35,52–55 evaluated the role of electrographic and/or convulsive seizures in neuroprognostication. The studies focused on electrographic seizures, though some studies also included convulsive seizures. Although the specificity of seizures in the studies included in the ILCOR systematic review was 100%, sensitivity of this finding was poor (0.6% to 26.8%), and other studies that were not included in the review found patients with postarrest seizures who had good outcomes.36,56,57 Additional methodological concerns include selection bias for which patients underwent EEG monitoring and inconsistent definitions of seizure. The term seizure encompasses a broad spectrum of pathologies that likely have different prognoses, ranging from a single brief electrographic seizure to refractory status epilepticus, and this imprecision justified the more limited recommendation.
Six observational studies21,55,58–61 evaluated status epilepticus within 5 days after arrest and evaluated outcomes at time points ranging from hospital discharge to 6 months after arrest. The specificity of status epilepticus for poor outcome ranged from 82.6% to 100%. Interestingly, although status epilepticus is a severe form of seizures, the specificity of status epilepticus for poor outcome was less than that which was reported in the studies examining the seizures overall (as above). Additional concerns include the inconsistent definition of status epilepticus, lack of blinding, and the use of status epilepticus to justify withdrawal of life-sustaining therapies leading to potential self-fulfilling prophecies.
Six studies21,35,54,59,62,63 evaluated burst suppression within 120 hours after arrest. One additional study64 subdivided burst suppression into synchronous versus heterogeneous patterns. Definitions of burst suppression varied or were not specified. Specificity ranged from 90.7% to 100%, and sensitivity was 1.1% to 51%. The lack of standardized definitions, potential for self-fulfilling prophecies, and the lack of controlling for medication effects limited the ability to make a stronger recommendation, despite the overall high specificity. Additional focus on identifying subtypes of burst suppression, such as the synchronous subtype (which appeared to be highly specific in a single study), should be investigated further. Burst suppression can be caused by medications, so it is particularly important that providers have knowledge about the potential effects of medication on this prognostic tool.
Fourteen observational studies9,13,15–17,23,59,64–70 evaluated bilaterally absent N20 SSEP waves within 96 hours after arrest and correlated the finding with outcome at time points ranging from hospital discharge to 6 months after arrest. Specificity ranged from 50% to 100%. Three studies had specificity below 100%, and additional methodological limitations included lack of blinding and potential for self-fulfilling prophecies. While the studies evaluated SSEPs obtained at any time starting immediately after arrest, there is a high likelihood of potential confounding factors early after arrest, leading to the recommendation that SSEPs should only be obtained more than 24 hours after arrest.
Discharges on EEG were divided into 2 types: rhythmic/periodic and nonrhythmic/periodic. Nine observational studies evaluated rhythmic/periodic discharges.16,45,52–54,61,63,66,69 The specificity of rhythmic/periodic discharges ranged from 66.7% to 100%, with poor sensitivity (2.4%–50.8%). The studies evaluating rhythmic/periodic discharges were inconsistent in the definitions of discharges. Most did not account for effects of medications, and some studies found unacceptably low specificity. Nonetheless, as the time from the cardiac arrest increased, the specificity of rhythmic/periodic discharges for poor outcome improved. There is opportunity to develop this EEG finding as a prognostic tool. Five observational studies52,53,64,66,69 evaluated nonrhythmic/periodic discharges. Specificity for poor outcome was low over the entire post–cardiac arrest period evaluated in the studies.
Ten observational studies16,30,53–55,62,65,71–73 reported on the prognostic value of unreactive EEG. Specificity ranged from 41.7% to 100% and was below 90% in most studies. There was inconsistency in the definitions of and stimuli used for EEG reactivity. Studies also did not account for effects of temperature and medications. Thus, the overall certainty of the evidence was rated as very low.

These recommendations are supported by the 2020 CoSTR for ALS,4 which supplements the last comprehensive review of this topic conducted in 2015.7

Use of Neuroimaging for Neuroprognostication

Synopsis

Neuroimaging may be helpful after arrest to detect and quantify structural brain injury. CT and MRI are the 2 most common modalities. On CT, brain edema can be quantified as the GWR, defined as the ratio between the density (measured as Hounsfield units) of the gray matter and the white matter. Normal brain has a GWR of approximately 1.3, and this number decreases with edema. On MRI, cytotoxic injury can be measured as restricted diffusion on diffusion-weighted imaging (DWI) and can be quantified by the ADC. DWI/ADC is a sensitive measure of injury, with normal values ranging between 700 and 800×10−6 mm2/s and values decreasing with injury. CT and MRI findings of brain injury evolve over the first several days after arrest, so the timing of the imaging study of interest is of particular importance as it relates to prognosis.

Recommendation-Specific Supportive Text

Twelve studies23,24,31,38,66,74–79 evaluated GWR on head CT. Whole-brain GWR (GWR average) and GWR in specific regions were evaluated. The specificity was 85% to 100%, and only 1 study reported a specificity that was not 100%. Many of the studies evaluated head CTs that were obtained within the first 24 hours after arrest, though some studies included head CTs obtained up to 72 hours after arrest. There were methodological limitations, including selection bias, risk of multiple comparisons, and heterogeneity of measurement techniques, such as anatomic sites and calculation methods. Thus, a specific GWR threshold that predicts poor prognosis with 100% specificity is unknown. Additionally, the optimal timing for obtaining head CT after arrest to optimize the GWR as a prognostic tool is unknown.
Five observational studies11,23,74,80,81 investigated DWI changes on MRI within 5 days after arrest. The studies evaluated MRI qualitatively for “high signal intensity” and “positive findings,” but the definitions of positive findings differed between studies and, in some studies, examined only specific brain regions. Specificity was 55.7% to 100%. The imprecise definition and short-term outcome in some studies led to significant uncertainty about how to use DWI MRI to predict poor prognosis. In the correct setting, a significant burden of DWI MRI findings or DWI MRI findings in specific regions of interest may be correlated with poor prognosis, but a broader recommendation could not be supported.
Three observational studies82–84 investigated ADC on MRI within 7 days after arrest. The studies were designed to determine thresholds that achieved 100% specificity, though the ADC and brain volume thresholds needed to achieve that specificity varied broadly. While quantitative ADC measurements are a promising tool, their broad use is limited by feasibility concerns. Additionally, there are relatively few studies, and per other imaging features, there was heterogeneity of measurement techniques, including in sites and calculation methods. A specific ADC threshold that predicts poor prognosis is not known.

These recommendations are supported by the 2020 CoSTR for ALS,4 which supplements the last comprehensive review of this topic conducted in 2015.7

References

1. Laver S, Farrow C, Turner D, Nolan J. Mode of death after admission to an intensive care unit following cardiac arrest.Intensive Care Med. 2004; 30:2126–2128. doi: 10.1007/s00134-004-2425-zCrossrefMedlineGoogle Scholar
2. Witten L, Gardner R, Holmberg MJ, Wiberg S, Moskowitz A, Mehta S, Grossestreuer AV, Yankama T, Donnino MW, Berg KM. Reasons for death in patients successfully resuscitated from out-of-hospital and in-hospital cardiac arrest.Resuscitation. 2019; 136:93–99. doi: 10.1016/j.resuscitation.2019.01.031CrossrefMedlineGoogle Scholar
3. Geocadin RG, Callaway CW, Fink EL, Golan E, Greer DM, Ko NU, Lang E, Licht DJ, Marino BS, McNair ND, Peberdy MA, Perman SM, Sims DB, Soar J, Sandroni CAmerican Heart Association Emergency Cardiovascular Care Committee. Standards for Studies of Neurological Prognostication in Comatose Survivors of Cardiac Arrest: A Scientific Statement From the American Heart Association.Circulation. 2019; 140:e517–e542. doi: 10.1161/CIR.0000000000000702LinkGoogle Scholar
4. Berg KM, Soar J, Andersen LW, Böttiger BW, Cacciola S, Callaway CW, Couper K, Cronberg T, D’Arrigo S, Deakin CD, et al.; on behalf of the Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S92–S139. doi: 10.1161/CIR.0000000000000893LinkGoogle Scholar
5. Samaniego EA, Mlynash M, Caulfield AF, Eyngorn I, Wijman CA. Sedation confounds outcome prediction in cardiac arrest survivors treated with hypothermia.Neurocrit Care. 2011; 15:113–119. doi: 10.1007/s12028-010-9412-8CrossrefMedlineGoogle Scholar
6. Wilson ME, Dobler CC, Zubek L, Gajic O, Talmor D, Curtis JR, Hinds RF, Banner-Goodspeed VM, Mueller A, Rickett DM, Elo G, Filipe M, Szucs O, Novotny PJ, Piers RD, Benoit DD. Prevalence of Disagreement About Appropriateness of Treatment Between ICU Patients/Surrogates and Clinicians.Chest. 2019; 155:1140–1147. doi: 10.1016/j.chest.2019.02.404CrossrefMedlineGoogle Scholar
7. Callaway CW, Donnino MW, Fink EL, Geocadin RG, Golan E, Kern KB, Leary M, Meurer WJ, Peberdy MA, Thompson TM, et al.. Part 8: post–cardiac arrest care: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S465–482. doi: 10.1161/cir.0000000000000262LinkGoogle Scholar
8. Wijdicks EF, Parisi JE, Sharbrough FW. Prognostic value of myoclonus status in comatose survivors of cardiac arrest.Ann Neurol. 1994; 35:239–243. doi: 10.1002/ana.410350219CrossrefMedlineGoogle Scholar
9. Choi SP, Park KN, Wee JH, Park JH, Youn CS, Kim HJ, Oh SH, Oh YS, Kim SH, Oh JS. Can somatosensory and visual evoked potentials predict neurological outcome during targeted temperature management in post cardiac arrest patients?Resuscitation. 2017; 119:70–75. doi: 10.1016/j.resuscitation.2017.06.022CrossrefMedlineGoogle Scholar
10. Chung-Esaki HM, Mui G, Mlynash M, Eyngorn I, Catabay K, Hirsch KG. The neuron specific enolase (NSE) ratio offers benefits over absolute value thresholds in post-cardiac arrest coma prognosis.J Clin Neurosci. 2018; 57:99–104. doi: 10.1016/j.jocn.2018.08.020CrossrefMedlineGoogle Scholar
11. Ryoo SM, Jeon SB, Sohn CH, Ahn S, Han C, Lee BK, Lee DH, Kim SH, Donnino MW, Kim WYKorean Hypothermia Network Investigators. Predicting Outcome With Diffusion-Weighted Imaging in Cardiac Arrest Patients Receiving Hypothermia Therapy: Multicenter Retrospective Cohort Study.Crit Care Med. 2015; 43:2370–2377. doi: 10.1097/CCM.0000000000001263CrossrefMedlineGoogle Scholar
12. Javaudin F, Leclere B, Segard J, Le Bastard Q, Pes P, Penverne Y, Le Conte P, Jenvrin J, Hubert H, Escutnaire J, Batard E, Montassier E, Gr-RéAC Prognostic performance of early absence of pupillary light reaction after recovery of out of hospital cardiac arrest.Resuscitation. 2018; 127:8–13. doi: 10.1016/j.resuscitation.2018.03.020CrossrefMedlineGoogle Scholar
13. Dhakal LP, Sen A, Stanko CM, Rawal B, Heckman MG, Hoyne JB, Dimberg EL, Freeman ML, Ng LK, Rabinstein AA, Freeman WD. Early Absent Pupillary Light Reflexes After Cardiac Arrest in Patients Treated with Therapeutic Hypothermia.Ther Hypothermia Temp Manag. 2016; 6:116–121. doi: 10.1089/ther.2015.0035CrossrefMedlineGoogle Scholar
14. Matthews EA, Magid-Bernstein J, Sobczak E, Velazquez A, Falo CM, Park S, Claassen J, Agarwal S. Prognostic Value of the Neurological Examination in Cardiac Arrest Patients After Therapeutic Hypothermia.Neurohospitalist. 2018; 8:66–73. doi: 10.1177/1941874417733217CrossrefMedlineGoogle Scholar
15. Oddo M, Sandroni C, Citerio G, Miroz JP, Horn J, Rundgren M, Cariou A, Payen JF, Storm C, Stammet P, Taccone FS. Quantitative versus standard pupillary light reflex for early prognostication in comatose cardiac arrest patients: an international prospective multicenter double-blinded study.Intensive Care Med. 2018; 44:2102–2111. doi: 10.1007/s00134-018-5448-6CrossrefMedlineGoogle Scholar
16. Fatuzzo D, Beuchat I, Alvarez V, Novy J, Oddo M, Rossetti AO. Does continuous EEG influence prognosis in patients after cardiac arrest?Resuscitation. 2018; 132:29–32. doi: 10.1016/j.resuscitation.2018.08.023CrossrefMedlineGoogle Scholar
17. Dragancea I, Horn J, Kuiper M, Friberg H, Ullén S, Wetterslev J, Cranshaw J, Hassager C, Nielsen N, Cronberg TTTM Trial Investigators. Neurological prognostication after cardiac arrest and targeted temperature management 33°C versus 36°C: Results from a randomised controlled clinical trial.Resuscitation. 2015; 93:164–170. doi: 10.1016/j.resuscitation.2015.04.013CrossrefMedlineGoogle Scholar
18. Hofmeijer J, Beernink TM, Bosch FH, Beishuizen A, Tjepkema-Cloostermans MC, van Putten MJ. Early EEG contributes to multimodal outcome prediction of postanoxic coma.Neurology. 2015; 85:137–143. doi: 10.1212/WNL.0000000000001742CrossrefMedlineGoogle Scholar
19. Kongpolprom N, Cholkraisuwat J. Neurological Prognostications for the Therapeutic Hypothermia among Comatose Survivors of Cardiac Arrest.Indian J Crit Care Med. 2018; 22:509–518. doi: 10.4103/ijccm.IJCCM_500_17CrossrefMedlineGoogle Scholar
20. Roger C, Palmier L, Louart B, Molinari N, Claret PG, de la Coussaye JE, Lefrant JY, Muller L. Neuron specific enolase and Glasgow motor score remain useful tools for assessing neurological prognosis after out-of-hospital cardiac arrest treated with therapeutic hypothermia.Anaesth Crit Care Pain Med. 2015; 34:231–237. doi: 10.1016/j.accpm.2015.05.004CrossrefMedlineGoogle Scholar
21. Zhou SE, Maciel CB, Ormseth CH, Beekman R, Gilmore EJ, Greer DM. Distinct predictive values of current neuroprognostic guidelines in post-cardiac arrest patients.Resuscitation. 2019; 139:343–350. doi: 10.1016/j.resuscitation.2019.03.035CrossrefMedlineGoogle Scholar
22. Greer DM, Yang J, Scripko PD, Sims JR, Cash S, Wu O, Hafler JP, Schoenfeld DA, Furie KL. Clinical examination for prognostication in comatose cardiac arrest patients.Resuscitation. 2013; 84:1546–1551. doi: 10.1016/j.resuscitation.2013.07.028CrossrefMedlineGoogle Scholar
23. Kim JH, Kim MJ, You JS, Lee HS, Park YS, Park I, Chung SP. Multimodal approach for neurologic prognostication of out-of-hospital cardiac arrest patients undergoing targeted temperature management.Resuscitation. 2019; 134:33–40. doi: 10.1016/j.resuscitation.2018.11.007CrossrefMedlineGoogle Scholar
24. Lee KS, Lee SE, Choi JY, Gho YR, Chae MK, Park EJ, Choi MH, Hong JM. Useful Computed Tomography Score for Estimation of Early Neurologic Outcome in Post-Cardiac Arrest Patients With Therapeutic Hypothermia.Circ J. 2017; 81:1628–1635. doi: 10.1253/circj.CJ-16-1327CrossrefMedlineGoogle Scholar
25. Scarpino M, Carrai R, Lolli F, Lanzo G, Spalletti M, Valzania F, Lombardi M, Audenino D, Contardi S, Celani MG, et al.; on behalf of the ProNeCA Study Group. Neurophysiology for predicting good and poor neurological outcome at 12 and 72 h after cardiac arrest: the ProNeCA multicentre prospective study.Resuscitation. 2020; 147:95–103. doi: 10.1016/j.resuscitation.2019.11.014CrossrefMedlineGoogle Scholar
26. Heimburger D, Durand M, Gaide-Chevronnay L, Dessertaine G, Moury PH, Bouzat P, Albaladejo P, Payen JF. Quantitative pupillometry and transcranial Doppler measurements in patients treated with hypothermia after cardiac arrest.Resuscitation. 2016; 103:88–93. doi: 10.1016/j.resuscitation.2016.02.026CrossrefMedlineGoogle Scholar
27. Solari D, Rossetti AO, Carteron L, Miroz JP, Novy J, Eckert P, Oddo M. Early prediction of coma recovery after cardiac arrest with blinded pupillometry.Ann Neurol. 2017; 81:804–810. doi: 10.1002/ana.24943CrossrefMedlineGoogle Scholar
28. Riker RR, Sawyer ME, Fischman VG, May T, Lord C, Eldridge A, Seder DB. Neurological Pupil Index and Pupillary Light Reflex by Pupillometry Predict Outcome Early After Cardiac Arrest.Neurocrit Care. 2020; 32:152–161. doi: 10.1007/s12028-019-00717-4CrossrefMedlineGoogle Scholar
29. Obling L, Hassager C, Illum C, Grand J, Wiberg S, Lindholm MG, Winther-Jensen M, Kondziella D, Kjaergaard J. Prognostic value of automated pupillometry: an unselected cohort from a cardiac intensive care unit.Eur Heart J Acute Cardiovasc Care. 2019; 2048872619842004. doi: 10.1177/2048872619842004Google Scholar
30. Sivaraju A, Gilmore EJ, Wira CR, Stevens A, Rampal N, Moeller JJ, Greer DM, Hirsch LJ, Gaspard N. Prognostication of post-cardiac arrest coma: early clinical and electroencephalographic predictors of outcome.Intensive Care Med. 2015; 41:1264–1272. doi: 10.1007/s00134-015-3834-xCrossrefMedlineGoogle Scholar
31. Kim SH, Choi SP, Park KN, Youn CS, Oh SH, Choi SM. Early brain computed tomography findings are associated with outcome in patients treated with therapeutic hypothermia after out-of-hospital cardiac arrest.Scand J Trauma. 2013; 21:57. doi: 10.1186/1757-7241-21-57CrossrefMedlineGoogle Scholar
32. Ruknuddeen MI, Ramadoss R, Rajajee V, Grzeskowiak LE, Rajagopalan RE. Early clinical prediction of neurological outcome following out of hospital cardiac arrest managed with therapeutic hypothermia.Indian J Crit Care Med. 2015; 19:304–310. doi: 10.4103/0972-5229.158256CrossrefMedlineGoogle Scholar
33. Elmer J, Rittenberger JC, Faro J, Molyneaux BJ, Popescu A, Callaway CW, Baldwin MPittsburgh Post-Cardiac Arrest Service. Clinically distinct electroencephalographic phenotypes of early myoclonus after cardiac arrest.Ann Neurol. 2016; 80:175–184. doi: 10.1002/ana.24697CrossrefMedlineGoogle Scholar
34. Aicua RI, Rapun I, Novy J, Solari D, Oddo M, Rossetti AO. Early Lance-Adams syndrome after cardiac arrest: prevalence, time to return to awareness, and outcome in a large cohort.Resuscitation. 2017; 115:169–172. doi: 10.1016/j.resuscitation.2017.03.020CrossrefMedlineGoogle Scholar
35. Sadaka F, Doerr D, Hindia J, Lee KP, Logan W. Continuous Electroencephalogram in Comatose Postcardiac Arrest Syndrome Patients Treated With Therapeutic Hypothermia: Outcome Prediction Study.J Intensive Care Med. 2015; 30:292–296. doi: 10.1177/0885066613517214CrossrefMedlineGoogle Scholar
36. Lybeck A, Friberg H, Aneman A, Hassager C, Horn J, Kjærgaard J, Kuiper M, Nielsen N, Ullén S, Wise MP, Westhall E, Cronberg TTTM-trial Investigators. Prognostic significance of clinical seizures after cardiac arrest and target temperature management.Resuscitation. 2017; 114:146–151. doi: 10.1016/j.resuscitation.2017.01.017CrossrefMedlineGoogle Scholar
37. Reynolds AS, Rohaut B, Holmes MG, Robinson D, Roth W, Velazquez A, Couch CK, Presciutti A, Brodie D, Moitra VK, Rabbani LE, Agarwal S, Park S, Roh DJ, Claassen J. Early myoclonus following anoxic brain injury.Neurol Clin Pract. 2018; 8:249–256. doi: 10.1212/CPJ.0000000000000466CrossrefMedlineGoogle Scholar
38. Lee BK, Jeung KW, Lee HY, Jung YH, Lee DH. Combining brain computed tomography and serum neuron specific enolase improves the prognostic performance compared to either alone in comatose cardiac arrest survivors treated with therapeutic hypothermia.Resuscitation. 2013; 84:1387–1392. doi: 10.1016/j.resuscitation.2013.05.026CrossrefMedlineGoogle Scholar
39. Vondrakova D, Kruger A, Janotka M, Malek F, Dudkova V, Neuzil P, Ostadal P. Association of neuron-specific enolase values with outcomes in cardiac arrest survivors is dependent on the time of sample collection.Crit Care. 2017; 21:172. doi: 10.1186/s13054-017-1766-2CrossrefMedlineGoogle Scholar
40. Duez CHV, Grejs AM, Jeppesen AN, Schrøder AD, Søreide E, Nielsen JF, Kirkegaard H. Neuron-specific enolase and S-100b in prolonged targeted temperature management after cardiac arrest: A randomised study.Resuscitation. 2018; 122:79–86. doi: 10.1016/j.resuscitation.2017.11.052CrossrefMedlineGoogle Scholar
41. Stammet P, Collignon O, Hassager C, Wise MP, Hovdenes J, Åneman A, Horn J, Devaux Y, Erlinge D, Kjaergaard J, Gasche Y, Wanscher M, Cronberg T, Friberg H, Wetterslev J, Pellis T, Kuiper M, Gilson G, Nielsen NTTM-Trial Investigators. Neuron-Specific Enolase as a Predictor of Death or Poor Neurological Outcome After Out-of-Hospital Cardiac Arrest and Targeted Temperature Management at 33°C and 36°C.J Am Coll Cardiol. 2015; 65:2104–2114. doi: 10.1016/j.jacc.2015.03.538CrossrefMedlineGoogle Scholar
42. Zellner T, Gärtner R, Schopohl J, Angstwurm M. NSE and S-100B are not sufficiently predictive of neurologic outcome after therapeutic hypothermia for cardiac arrest.Resuscitation. 2013; 84:1382–1386. doi: 10.1016/j.resuscitation.2013.03.021CrossrefMedlineGoogle Scholar
43. Tsetsou S, Novy J, Pfeiffer C, Oddo M, Rossetti AO. Multimodal Outcome Prognostication After Cardiac Arrest and Targeted Temperature Management: Analysis at 36 °C.Neurocrit Care. 2018; 28:104–109. doi: 10.1007/s12028-017-0393-8CrossrefMedlineGoogle Scholar
44. Helwig K, Seeger F, Hölschermann H, Lischke V, Gerriets T, Niessner M, Foerch C. Elevated Serum Glial Fibrillary Acidic Protein (GFAP) is Associated with Poor Functional Outcome After Cardiopulmonary Resuscitation.Neurocrit Care. 2017; 27:68–74. doi: 10.1007/s12028-016-0371-6CrossrefMedlineGoogle Scholar
45. Rossetti AO, Tovar Quiroga DF, Juan E, Novy J, White RD, Ben-Hamouda N, Britton JW, Oddo M, Rabinstein AA. Electroencephalography predicts poor and good outcomes after cardiac arrest: a two-center study.Crit Care Med. 2017; 45:e674–e682. doi: 10.1097/CCM.0000000000002337CrossrefMedlineGoogle Scholar
46. Wiberg S, Hassager C, Stammet P, Winther-Jensen M, Thomsen JH, Erlinge D, Wanscher M, Nielsen N, Pellis T, Åneman A, Friberg H, Hovdenes J, Horn J, Wetterslev J, Bro-Jeppesen J, Wise MP, Kuiper M, Cronberg T, Gasche Y, Devaux Y, Kjaergaard J. Single versus Serial Measurements of Neuron-Specific Enolase and Prediction of Poor Neurological Outcome in Persistently Unconscious Patients after Out-Of-Hospital Cardiac Arrest - A TTM-Trial Substudy.PLoS One. 2017; 12:e0168894. doi: 10.1371/journal.pone.0168894CrossrefMedlineGoogle Scholar
47. Jang JH, Park WB, Lim YS, Choi JY, Cho JS, Woo JH, Choi WS, Yang HJ, Hyun SY. Combination of S100B and procalcitonin improves prognostic performance compared to either alone in patients with cardiac arrest: a prospective observational study.Medicine (Baltimore). 2019; 98:e14496. doi: 10.1097/MD.0000000000014496CrossrefMedlineGoogle Scholar
48. Stammet P, Dankiewicz J, Nielsen N, Fays F, Collignon O, Hassager C, Wanscher M, Undèn J, Wetterslev J, Pellis T, Aneman A, Hovdenes J, Wise MP, Gilson G, Erlinge D, Horn J, Cronberg T, Kuiper M, Kjaergaard J, Gasche Y, Devaux Y, Friberg HTarget Temperature Management after Out-of-Hospital Cardiac Arrest (TTM) trial investigators. Protein S100 as outcome predictor after out-of-hospital cardiac arrest and targeted temperature management at 33 °C and 36 °C.Crit Care. 2017; 21:153. doi: 10.1186/s13054-017-1729-7CrossrefMedlineGoogle Scholar
49. Mattsson N, Zetterberg H, Nielsen N, Blennow K, Dankiewicz J, Friberg H, Lilja G, Insel PS, Rylander C, Stammet P, Aneman A, Hassager C, Kjaergaard J, Kuiper M, Pellis T, Wetterslev J, Wise M, Cronberg T. Serum tau and neurological outcome in cardiac arrest.Ann Neurol. 2017; 82:665–675. doi: 10.1002/ana.25067CrossrefMedlineGoogle Scholar
50. Moseby-Knappe M, Mattsson N, Nielsen N, Zetterberg H, Blennow K, Dankiewicz J, Dragancea I, Friberg H, Lilja G, Insel PS, Rylander C, Westhall E, Kjaergaard J, Wise MP, Hassager C, Kuiper MA, Stammet P, Wanscher MCJ, Wetterslev J, Erlinge D, Horn J, Pellis T, Cronberg T . Serum Neurofilament Light Chain for Prognosis of Outcome After Cardiac Arrest.JAMA Neurol. 2019; 76:64–71. doi: 10.1001/jamaneurol.2018.3223CrossrefMedlineGoogle Scholar
51. Rana OR, Schröder JW, Baukloh JK, Saygili E, Mischke K, Schiefer J, Weis J, Marx N, Rassaf T, Kelm M, Shin DI, Meyer C, Saygili E. Neurofilament light chain as an early and sensitive predictor of long-term neurological outcome in patients after cardiac arrest.Int J Cardiol. 2013; 168:1322–1327. doi: 10.1016/j.ijcard.2012.12.016CrossrefMedlineGoogle Scholar
52. Lamartine Monteiro M, Taccone FS, Depondt C, Lamanna I, Gaspard N, Ligot N, Mavroudakis N, Naeije G, Vincent JL, Legros B. The Prognostic Value of 48-h Continuous EEG During Therapeutic Hypothermia After Cardiac Arrest.Neurocrit Care. 2016; 24:153–162. doi: 10.1007/s12028-015-0215-9CrossrefMedlineGoogle Scholar
53. Benarous L, Gavaret M, Soda Diop M, Tobarias J, de Ghaisne de Bourmont S, Allez C, Bouzana F, Gainnier M, Trebuchon A. Sources of interrater variability and prognostic value of standardized EEG features in post-anoxic coma after resuscitated cardiac arrest.Clin Neurophysiol Pract. 2019; 4:20–26. doi: 10.1016/j.cnp.2018.12.001CrossrefMedlineGoogle Scholar
54. Westhall E, Rossetti AO, van Rootselaar AF, Wesenberg Kjaer T, Horn J, Ullén S, Friberg H, Nielsen N, Rosén I, Åneman A, Erlinge D, Gasche Y, Hassager C, Hovdenes J, Kjaergaard J, Kuiper M, Pellis T, Stammet P, Wanscher M, Wetterslev J, Wise MP, Cronberg TTTM-trial investigators. Standardized EEG interpretation accurately predicts prognosis after cardiac arrest.Neurology. 2016; 86:1482–1490. doi: 10.1212/WNL.0000000000002462CrossrefMedlineGoogle Scholar
55. Amorim E, Rittenberger JC, Zheng JJ, Westover MB, Baldwin ME, Callaway CW, Popescu APost Cardiac Arrest Service. Continuous EEG monitoring enhances multimodal outcome prediction in hypoxic-ischemic brain injury.Resuscitation. 2016; 109:121–126. doi: 10.1016/j.resuscitation.2016.08.012CrossrefMedlineGoogle Scholar
56. Rundgren M, Westhall E, Cronberg T, Rosén I, Friberg H. Continuous amplitude-integrated electroencephalogram predicts outcome in hypothermia-treated cardiac arrest patients.Crit Care Med. 2010; 38:1838–1844. doi: 10.1097/CCM.0b013e3181eaa1e7CrossrefMedlineGoogle Scholar
57. Legriel S, Hilly-Ginoux J, Resche-Rigon M, Merceron S, Pinoteau J, Henry-Lagarrigue M, Bruneel F, Nguyen A, Guezennec P, Troché G, Richard O, Pico F, Bédos JP. Prognostic value of electrographic postanoxic status epilepticus in comatose cardiac-arrest survivors in the therapeutic hypothermia era.Resuscitation. 2013; 84:343–350. doi: 10.1016/j.resuscitation.2012.11.001CrossrefMedlineGoogle Scholar
58. Oh SH, Park KN, Shon YM, Kim YM, Kim HJ, Youn CS, Kim SH, Choi SP, Kim SC. Continuous Amplitude-Integrated Electroencephalographic Monitoring Is a Useful Prognostic Tool for Hypothermia-Treated Cardiac Arrest Patients.Circulation. 2015; 132:1094–1103. doi: 10.1161/CIRCULATIONAHA.115.015754LinkGoogle Scholar
59. Leão RN, Ávila P, Cavaco R, Germano N, Bento L. Therapeutic hypothermia after cardiac arrest: outcome predictors.Rev Bras Ter Intensiva. 2015; 27:322–332. doi: 10.5935/0103-507X.20150056CrossrefMedlineGoogle Scholar
60. Dragancea I, Backman S, Westhall E, Rundgren M, Friberg H, Cronberg T. Outcome following postanoxic status epilepticus in patients with targeted temperature management after cardiac arrest.Epilepsy Behav. 2015; 49:173–177. doi: 10.1016/j.yebeh.2015.04.043CrossrefMedlineGoogle Scholar
61. Beretta S, Coppo A, Bianchi E, Zanchi C, Carone D, Stabile A, Padovano G, Sulmina E, Grassi A, Bogliun G, Foti G, Ferrarese C, Pesenti A, Beghi E, Avalli L. Neurological outcome of postanoxic refractory status epilepticus after aggressive treatment.Epilepsy Behav. 2019; 101Pt B106374. doi: 10.1016/j.yebeh.2019.06.018CrossrefMedlineGoogle Scholar
62. Alvarez V, Reinsberger C, Scirica B, O’Brien MH, Avery KR, Henderson G, Lee JW. Continuous electrodermal activity as a potential novel neurophysiological biomarker of prognosis after cardiac arrest–A pilot study.Resuscitation. 2015; 93:128–135. doi: 10.1016/j.resuscitation.2015.06.006CrossrefMedlineGoogle Scholar
63. Backman S, Cronberg T, Friberg H, Ullén S, Horn J, Kjaergaard J, Hassager C, Wanscher M, Nielsen N, Westhall E. Highly malignant routine EEG predicts poor prognosis after cardiac arrest in the Target Temperature Management trial.Resuscitation. 2018; 131:24–28. doi: 10.1016/j.resuscitation.2018.07.024CrossrefMedlineGoogle Scholar
64. Ruijter BJ, Tjepkema-Cloostermans MC, Tromp SC, van den Bergh WM, Foudraine NA, Kornips FHM, Drost G, Scholten E, Bosch FH, Beishuizen A, van Putten MJAM, Hofmeijer J. Early electroencephalography for outcome prediction of postanoxic coma: A prospective cohort study.Ann Neurol. 2019; 86:203–214. doi: 10.1002/ana.25518CrossrefMedlineGoogle Scholar
65. Grippo A, Carrai R, Scarpino M, Spalletti M, Lanzo G, Cossu C, Peris A, Valente S, Amantini A. Neurophysiological prediction of neurological good and poor outcome in post-anoxic coma.Acta Neurol Scand. 2017; 135:641–648. doi: 10.1111/ane.12659CrossrefMedlineGoogle Scholar
66. Scarpino M, Lolli F, Lanzo G, Carrai R, Spalletti M, Valzania F, Lombardi M, Audenino D, Celani MG, Marrelli A, Contardi S, Peris A, Amantini A, Sandroni C, Grippo AProNeCAStudy Group. Neurophysiological and neuroradiological test for early poor outcome (Cerebral Performance Categories 3-5) prediction after cardiac arrest: Prospective multicentre prognostication data.Data Brief. 2019; 27:104755. doi: 10.1016/j.dib.2019.104755CrossrefMedlineGoogle Scholar
67. De Santis P, Lamanna I, Mavroudakis N, Legros B, Vincent JL, Creteur J, Taccone FS. The potential role of auditory evoked potentials to assess prognosis in comatose survivors from cardiac arrest.Resuscitation. 2017; 120:119–124. doi: 10.1016/j.resuscitation.2017.09.013CrossrefMedlineGoogle Scholar
68. Kim SW, Oh JS, Park J, Jeong HH, Kim JH, Wee JH, Oh SH, Choi SP, Park KNCerebral Resuscitation and Outcome evaluation Within catholic Network (CROWN) Investigators. Short-Latency Positive Peak Following N20 Somatosensory Evoked Potential Is Superior to N20 in Predicting Neurologic Outcome After Out-of-Hospital Cardiac Arrest.Crit Care Med. 2018; 46:e545–e551. doi: 10.1097/CCM.0000000000003083CrossrefMedlineGoogle Scholar
69. Scarpino M, Carrai R, Lolli F, Lanzo G, Spalletti M, Valzania F, Lombardi M, Audenino D, Contardi S, Celani MG, Marrelli A, Mecarelli O, Minardi C, Minicucci F, Politini L, Vitelli E, Peris A, Amantini A, Sandroni C, Grippo AProNeCA study group. Neurophysiology for predicting good and poor neurological outcome at 12 and 72 h after cardiac arrest: The ProNeCA multicentre prospective study.Resuscitation. 2020; 147:95–103. doi: 10.1016/j.resuscitation.2019.11.014CrossrefMedlineGoogle Scholar
70. Maciel CB, Morawo AO, Tsao CY, Youn TS, Labar DR, Rubens EO, Greer DM. SSEP in Therapeutic Hypothermia Era.J Clin Neurophysiol. 2017; 34:469–475. doi: 10.1097/WNP.0000000000000392CrossrefMedlineGoogle Scholar
71. Admiraal MM, van Rootselaar AF, Hofmeijer J, Hoedemaekers CWE, van Kaam CR, Keijzer HM, van Putten MJAM, Schultz MJ, Horn J. Electroencephalographic reactivity as predictor of neurological outcome in postanoxic coma: A multicenter prospective cohort study.Ann Neurol. 2019; 86:17–27. doi: 10.1002/ana.25507CrossrefMedlineGoogle Scholar
72. Duez CHV, Johnsen B, Ebbesen MQ, Kvaløy MB, Grejs AM, Jeppesen AN, Søreide E, Nielsen JF, Kirkegaard H. Post resuscitation prognostication by EEG in 24 vs 48 h of targeted temperature management.Resuscitation. 2019; 135:145–152. doi: 10.1016/j.resuscitation.2018.10.035CrossrefMedlineGoogle Scholar
73. Liu G, Su Y, Liu Y, Jiang M, Zhang Y, Zhang Y, Gao D. Predicting Outcome in Comatose Patients: The Role of EEG Reactivity to Quantifiable Electrical Stimuli.Evid Based Complement Alternat Med. 2016; 2016:8273716. doi: 10.1155/2016/8273716MedlineGoogle Scholar
74. Jeon CH, Park JS, Lee JH, Kim H, Kim SC, Park KH, Yi KS, Kim SM, Youn CS, Kim YM, Lee BK. Comparison of brain computed tomography and diffusion-weighted magnetic resonance imaging to predict early neurologic outcome before target temperature management comatose cardiac arrest survivors.Resuscitation. 2017; 118:21–26. doi: 10.1016/j.resuscitation.2017.06.021CrossrefMedlineGoogle Scholar
75. Kim Y, Ho LJ, Kun HC, Won CK, Hoon YJ, Ju KM, Weon KY, Yul LK, Joo KJ, Youn HS. Feasibility of optic nerve sheath diameter measured on initial brain computed tomography as an early neurologic outcome predictor after cardiac arrest.Academic Emergency Medicine. 2014; 21:1121–1128.CrossrefMedlineGoogle Scholar
76. Lee DH, Lee BK, Jeung KW, Jung YH, Cho YS, Cho IS, Youn CS, Kim JW, Park JS, Min YI. Relationship between ventricular characteristics on brain computed tomography and 6-month neurologic outcome in cardiac arrest survivors who underwent targeted temperature management.Resuscitation. 2018; 129:37–42. doi: 10.1016/j.resuscitation.2018.06.008CrossrefMedlineGoogle Scholar
77. Scarpino M, Lanzo G, Lolli F, Carrai R, Moretti M, Spalletti M, Cozzolino M, Peris A, Amantini A, Grippo A. Neurophysiological and neuroradiological multimodal approach for early poor outcome prediction after cardiac arrest.Resuscitation. 2018; 129:114–120. doi: 10.1016/j.resuscitation.2018.04.016CrossrefMedlineGoogle Scholar
78. Wang GN, Chen XF, Lv JR, Sun NN, Xu XQ, Zhang JS. The prognostic value of gray-white matter ratio on brain computed tomography in adult comatose cardiac arrest survivors.J Chin Med Assoc. 2018; 81:599–604. doi: 10.1016/j.jcma.2018.03.003CrossrefMedlineGoogle Scholar
79. Youn CS, Callaway CW, Rittenberger JCPost Cardiac Arrest Service. Combination of initial neurologic examination, quantitative brain imaging and electroencephalography to predict outcome after cardiac arrest.Resuscitation. 2017; 110:120–125. doi: 10.1016/j.resuscitation.2016.10.024CrossrefMedlineGoogle Scholar
80. Greer DM, Scripko PD, Wu O, Edlow BL, Bartscher J, Sims JR, Camargo EE, Singhal AB, Furie KL. Hippocampal magnetic resonance imaging abnormalities in cardiac arrest are associated with poor outcome.J Stroke.Cerebrovasc Dis. 2013; 22:899–905. doi: 10.1016/j.jstrokecerebrovasdis.2012.08.006CrossrefMedlineGoogle Scholar
81. Jang J, Oh SH, Nam Y, Lee K, Choi HS, Jung SL, Ahn KJ, Park KN, Kim BS. Prognostic value of phase information of 2D T2*-weighted gradient echo brain imaging in cardiac arrest survivors: A preliminary study.Resuscitation. 2019; 140:142–149. doi: 10.1016/j.resuscitation.2019.05.026CrossrefMedlineGoogle Scholar
82. Moon HK, Jang J, Park KN, Kim SH, Lee BK, Oh SH, Jeung KW, Choi SP, Cho IS, Youn CS. Quantitative analysis of relative volume of low apparent diffusion coefficient value can predict neurologic outcome after cardiac arrest.Resuscitation. 2018; 126:36–42. doi: 10.1016/j.resuscitation.2018.02.020CrossrefMedlineGoogle Scholar
83. Kim J, Kim K, Hong S, Kwon B, Yun ID, Choi BS, Jung C, Lee JH, Jo YH, Kim T, et al.. Low apparent diffusion coefficient cluster-based analysis of diffusion-weighted MRI for prognostication of out-of-hospital cardiac arrest survivors.Resuscitation. 2013; 84:1393–1399. doi: 10.1016/j.resuscitation.2013.04.011CrossrefMedlineGoogle Scholar
84. Hirsch KG, Fischbein N, Mlynash M, Kemp S, Bammer R, Eyngorn I, Tong J, Moseley M, Venkatasubramanian C, Caulfield AF, Albers G. Prognostic value of diffusion-weighted MRI for post-cardiac arrest coma.Neurology. 2020; 94:e1684–e1692. doi: 10.1212/WNL.0000000000009289CrossrefMedlineGoogle Scholar

Recovery

Recovery and Survivorship After Cardiac Arrest

Synopsis

Cardiac arrest survivors, like many survivors of critical illness, often experience a spectrum of physical, neurological, cognitive, emotional, or social issues, some of which may not become apparent until after hospital discharge. Survivorship after cardiac arrest is the journey through rehabilitation and recovery and highlights the far-reaching impact on patients, families, healthcare partners, and communities (Figure 11).1–3

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Figure 11. Centralized systems of care in cardiac arrest survivorship.3 CPR indicates cardiopulmonary resuscitation.

The systems-of-care approach to cardiac arrest includes the community and healthcare response to cardiac arrest. However, with more people surviving cardiac arrest, there is a need to organize discharge planning and long-term rehabilitation care resources. Survivorship plans that address treatment, surveillance, and rehabilitation need to be provided at hospital discharge to optimize transitions of care to the outpatient setting. For many patients and families, these plans and resources may be paramount to improved quality of life after cardiac arrest. Survivorship plans help guide the patient, caregivers, and primary care providers and include a summary of the inpatient course, recommended follow-up appointments, and postdischarge recovery expectations (Figure 12).

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Figure 12. Roadmap to recovery in cardiac arrest survivorship.3 OT indicates occupational therapy; PT, physical therapy; PTSD, posttraumatic stress disorder; and SLP, speech-language pathologist.

Cardiac arrest survivors, their families, and families of nonsurvivors may be powerful advocates for community response to cardiac arrest and patient-centered outcomes. Enhancing survivorship and recovery after cardiac arrest needs to be a systematic priority, aligned with treatment recommendations for patients surviving stroke, cancer, and other critical illnesses.3–5

Recommendation-Specific Supportive Text

Approximately one third of cardiac arrest survivors experience anxiety, depression, or posttraumatic stress.6–9 Fatigue is also common and may be due to physical, cognitive, or affective impairments. Family or caregivers may also experience significant stress and benefit from therapy.10–17
Cognitive impairments after cardiac arrest include difficulty with memory, attention, and executive function.18–22 Physical, neurological, and cardiopulmonary impairments are also common.3 Early evaluation for cardiac rehabilitation and physical, occupational, and speech language therapy may be helpful to develop strategies to recover from, overcome, or adapt to impairments.3,23–25
Community reintegration and return to work or other activities may be slow and depend on social support and relationships.26–29 Patients need direction about when to begin driving and when to return to intimacy.30,31
Rescuers may experience anxiety or posttraumatic stress about providing or not providing BLS.23,32 Hospital-based care providers may also experience emotional or psychological effects of caring for a patient with cardiac arrest.34 Team debriefings may allow a review of team performance (education, quality improvement) as well as recognition of the natural stressors associated with caring for a patient near death.35

These recommendations are supported by “Sudden Cardiac Arrest Survivorship: a Scientific Statement From the AHA.”3

References

1. Iwashyna TJ. Survivorship will be the defining challenge of critical care in the 21st century.Ann Intern Med. 2010; 153:204–205. doi: 10.7326/0003-4819-153-3-201008030-00013CrossrefMedlineGoogle Scholar
2. Hope AA, Munro CL. Understanding and Improving Critical Care Survivorship.Am J Crit Care. 2019; 28:410–412. doi: 10.4037/ajcc2019442CrossrefMedlineGoogle Scholar
3. Sawyer KN, Camp-Rogers TR, Kotini-Shah P, Del Rios M, Gossip MR, Moitra VK, Haywood KL, Dougherty CM, Lubitz SA, Rabinstein AA, Rittenberger JC, Callaway CW, Abella BS, Geocadin RG, Kurz MCAmerican Heart Association Emergency Cardiovascular Care Committee; Council on Cardiovascular and Stroke Nursing; Council on Genomic and Precision Medicine; Council on Quality of Care and Outcomes Research; and Stroke Council. Sudden Cardiac Arrest Survivorship: A Scientific Statement From the American Heart Association.Circulation. 2020; 141:e654–e685. doi: 10.1161/CIR.0000000000000747LinkGoogle Scholar
4. Nekhlyudov L, O’Malley D M, Hudson SV. Integrating primary care providers in the care of cancer survivors: gaps in evidence and future opportunities.Lancet Oncol. 2017; 18:e30–e38. doi: 10.1016/S1470-2045(16)30570-8CrossrefMedlineGoogle Scholar
5. Committee on Cancer Survivorship: Improving Care and Quality of life. From Cancer Patient to Cancer Survivor—Lost in Transition. Washington, DC: Institute of Medicine and National Research Council of the National Academies of Sciences; 2006.Google Scholar
6. Wilder Schaaf KP, Artman LK, Peberdy MA, Walker WC, Ornato JP, Gossip MR, Kreutzer JSVirginia Commonwealth University ARCTIC Investigators. Anxiety, depression, and PTSD following cardiac arrest: a systematic review of the literature.Resuscitation. 2013; 84:873–877. doi: 10.1016/j.resuscitation.2012.11.021CrossrefMedlineGoogle Scholar
7. Presciutti A, Verma J, Pavol M, Anbarasan D, Falo C, Brodie D, Rabbani LE, Roh DJ, Park S, Claassen J, Agarwal S. Posttraumatic stress and depressive symptoms characterize cardiac arrest survivors’ perceived recovery at hospital discharge.Gen Hosp Psychiatry. 2018; 53:108–113. doi: 10.1016/j.genhosppsych.2018.02.006CrossrefMedlineGoogle Scholar
8. Presciutti A, Sobczak E, Sumner JA, Roh DJ, Park S, Claassen J, Kronish I, Agarwal S. The impact of psychological distress on long-term recovery perceptions in survivors of cardiac arrest.J Crit Care. 2019; 50:227–233. doi: 10.1016/j.jcrc.2018.12.011CrossrefMedlineGoogle Scholar
9. Lilja G, Nilsson G, Nielsen N, Friberg H, Hassager C, Koopmans M, Kuiper M, Martini A, Mellinghoff J, Pelosi P, Wanscher M, Wise MP, Östman I, Cronberg T. Anxiety and depression among out-of-hospital cardiac arrest survivors.Resuscitation. 2015; 97:68–75. doi: 10.1016/j.resuscitation.2015.09.389CrossrefMedlineGoogle Scholar
10. Doolittle ND, Sauvé MJ. Impact of aborted sudden cardiac death on survivors and their spouses: the phenomenon of different reference points.Am J Crit Care. 1995; 4:389–396.CrossrefMedlineGoogle Scholar
11. Pusswald G, Fertl E, Faltl M, Auff E. Neurological rehabilitation of severely disabled cardiac arrest survivors. Part II. Life situation of patients and families after treatment.Resuscitation. 2000; 47:241–248. doi: 10.1016/s0300-9572(00)00240-9CrossrefMedlineGoogle Scholar
12. Löf S, Sandström A, Engström A. Patients treated with therapeutic hypothermia after cardiac arrest: relatives’ experiences.J Adv Nurs. 2010; 66:1760–1768. doi: 10.1111/j.1365-2648.2010.05352.xCrossrefMedlineGoogle Scholar
13. Weslien M, Nilstun T, Lundqvist A, Fridlund B. When the unreal becomes real: family members’ experiences of cardiac arrest.Nurs Crit Care. 2005; 10:15–22. doi: 10.1111/j.1362-1017.2005.00094.xCrossrefMedlineGoogle Scholar
14. Wallin E, Larsson IM, Rubertsson S, Kristoferzon ML. Relatives’ experiences of everyday life six months after hypothermia treatment of a significant other’s cardiac arrest.J Clin Nurs. 2013; 22:1639–1646. doi: 10.1111/jocn.12112CrossrefMedlineGoogle Scholar
15. Larsson IM, Wallin E, Rubertsson S, Kristoferzon ML. Relatives’ experiences during the next of kin’s hospital stay after surviving cardiac arrest and therapeutic hypothermia.Eur J Cardiovasc Nurs. 2013; 12:353–359. doi: 10.1177/1474515112459618CrossrefMedlineGoogle Scholar
16. Dougherty CM. Longitudinal recovery following sudden cardiac arrest and internal cardioverter defibrillator implantation: survivors and their families.Am J Crit Care. 1994; 3:145–154.CrossrefMedlineGoogle Scholar
17. Dougherty CM. Family-focused interventions for survivors of sudden cardiac arrest.J Cardiovasc Nurs. 1997; 12:45–58. doi: 10.1097/00005082-199710000-00006CrossrefMedlineGoogle Scholar
18. Lilja G, Nielsen N, Friberg H, Horn J, Kjaergaard J, Nilsson F, Pellis T, Wetterslev J, Wise MP, Bosch F, Bro-Jeppesen J, Brunetti I, Buratti AF, Hassager C, Hofgren C, Insorsi A, Kuiper M, Martini A, Palmer N, Rundgren M, Rylander C, van der Veen A, Wanscher M, Watkins H, Cronberg T. Cognitive function in survivors of out-of-hospital cardiac arrest after target temperature management at 33°C versus 36°C.Circulation. 2015; 131:1340–1349. doi: 10.1161/CIRCULATIONAHA.114.014414LinkGoogle Scholar
19. Tiainen M, Poutiainen E, Oksanen T, Kaukonen KM, Pettilä V, Skrifvars M, Varpula T, Castrén M. Functional outcome, cognition and quality of life after out-of-hospital cardiac arrest and therapeutic hypothermia: data from a randomized controlled trial.Scand J Trauma Resusc Emerg Med. 2015; 23:12. doi: 10.1186/s13049-014-0084-9CrossrefMedlineGoogle Scholar
20. Buanes EA, Gramstad A, Søvig KK, Hufthammer KO, Flaatten H, Husby T, Langørgen J, Heltne JK. Cognitive function and health-related quality of life four years after cardiac arrest.Resuscitation. 2015; 89:13–18. doi: 10.1016/j.resuscitation.2014.12.021CrossrefMedlineGoogle Scholar
21. Mateen FJ, Josephs KA, Trenerry MR, Felmlee-Devine MD, Weaver AL, Carone M, White RD. Long-term cognitive outcomes following out-of-hospital cardiac arrest: a population-based study.Neurology. 2011; 77:1438–1445. doi: 10.1212/WNL.0b013e318232ab33CrossrefMedlineGoogle Scholar
22. Steinbusch CVM, van Heugten CM, Rasquin SMC, Verbunt JA, Moulaert VRM. Cognitive impairments and subjective cognitive complaints after survival of cardiac arrest: A prospective longitudinal cohort study.Resuscitation. 2017; 120:132–137. doi: 10.1016/j.resuscitation.2017.08.007CrossrefMedlineGoogle Scholar
23. Nolan JP, Soar J, Cariou A, Cronberg T, Moulaert VR, Deakin CD, Bottiger BW, Friberg H, Sunde K, Sandroni C. European Resuscitation Council and European Society of Intensive Care Medicine 2015 guidelines for post-resuscitation care.Intensive Care Med. 2015; 41:2039–2056. doi: 10.1007/s00134-015-4051-3CrossrefMedlineGoogle Scholar
24. Moulaert VR, Verbunt JA, Bakx WG, Gorgels AP, de Krom MC, Heuts PH, Wade DT, van Heugten CM. ‘Stand still., and move on’, a new early intervention service for cardiac arrest survivors and their caregivers: rationale and description of the intervention.Clin Rehabil. 2011; 25:867–879. doi: 10.1177/0269215511399937CrossrefMedlineGoogle Scholar
25. Cowan MJ, Pike KC, Budzynski HK. Psychosocial nursing therapy following sudden cardiac arrest: impact on two-year survival.Nurs Res. 2001; 50:68–76. doi: 10.1097/00006199-200103000-00002CrossrefMedlineGoogle Scholar
26. Lundgren-Nilsson A, Rosén H, Hofgren C, Sunnerhagen KS. The first year after successful cardiac resuscitation: function, activity, participation and quality of life.Resuscitation. 2005; 66:285–289. doi: 10.1016/j.resuscitation.2005.04.001CrossrefMedlineGoogle Scholar
27. Middelkamp W, Moulaert VR, Verbunt JA, van Heugten CM, Bakx WG, Wade DT. Life after survival: long-term daily life functioning and quality of life of patients with hypoxic brain injury as a result of a cardiac arrest.Clin Rehabil. 2007; 21:425–431. doi: 10.1177/0269215507075307CrossrefMedlineGoogle Scholar
28. Kragholm K, Wissenberg M, Mortensen RN, Fonager K, Jensen SE, Rajan S, Lippert FK, Christensen EF, Hansen PA, Lang-Jensen T, Hendriksen OM, Kober L, Gislason G, Torp-Pedersen C, Rasmussen BS. Return to Work in Out-of-Hospital Cardiac Arrest Survivors: A Nationwide Register-Based Follow-Up Study.Circulation. 2015; 131:1682–1690. doi: 10.1161/CIRCULATIONAHA.114.011366LinkGoogle Scholar
29. Lilja G, Nielsen N, Bro-Jeppesen J, Dunford H, Friberg H, Hofgren C, Horn J, Insorsi A, Kjaergaard J, Nilsson F, Pelosi P, Winters T, Wise MP, Cronberg T. Return to Work and Participation in Society After Out-of-Hospital Cardiac Arrest.Circ Cardiovasc Qual Outcomes. 2018; 11:e003566. doi: 10.1161/CIRCOUTCOMES.117.003566LinkGoogle Scholar
30. Dougherty CM, Benoliel JQ, Bellin C. Domains of nursing intervention after sudden cardiac arrest and automatic internal cardioverter defibrillator implantation.Heart Lung. 2000; 29:79–86.CrossrefMedlineGoogle Scholar
31. Forslund AS, Lundblad D, Jansson JH, Zingmark K, Söderberg S. Risk factors among people surviving out-of-hospital cardiac arrest and their thoughts about what lifestyle means to them: a mixed methods study.BMC Cardiovasc Disord. 2013; 13:62. doi: 10.1186/1471-2261-13-62CrossrefMedlineGoogle Scholar
32. Møller TP, Hansen CM, Fjordholt M, Pedersen BD, Østergaard D, Lippert FK. Debriefing bystanders of out-of-hospital cardiac arrest is valuable.Resuscitation. 2014; 85:1504–1511. doi: 10.1016/j.resuscitation.2014.08.006CrossrefMedlineGoogle Scholar
33. Deleted in proof.Google Scholar
34. Clark R, McLean C. The professional and personal debriefing needs of ward based nurses after involvement in a cardiac arrest: An explorative qualitative pilot study.Intensive Crit Care Nurs. 2018; 47:78–84. doi: 10.1016/j.iccn.2018.03.009CrossrefMedlineGoogle Scholar
35. Ireland S, Gilchrist J, Maconochie I. Debriefing after failed paediatric resuscitation: a survey of current UK practice.Emerg Med J. 2008; 25:328–330. doi: 10.1136/emj.2007.048942CrossrefMedlineGoogle Scholar

Special Circumstances of Resuscitation

Accidental Hypothermia

Synopsis

Severe accidental environmental hypothermia (body temperature less than 30°C [86°F]) causes marked decrease in both heart rate and respiratory rate and may make it difficult to determine if a patient is truly in cardiac arrest. A victim may also appear clinically dead because of the effects of very low body temperature. Lifesaving procedures, including standard BLS and ACLS, are therefore important to continue until a patient is rewarmed unless the victim is obviously dead (eg, rigor mortis or nonsurvivable traumatic injury). Aggressive rewarming, possibly including invasive techniques, may be required and may necessitate transport to the hospital sooner than would be done in other OHCA circumstances.1 The specific care of patients who are victims of an avalanche are not included in these guidelines but can be found elsewhere.2

Recommendation-Specific Supportive Text

Patients with accidental hypothermia often present with marked CNS and cardiovascular depression and the appearance of death or near death, necessitating the need for prompt full resuscitative measures unless there are signs of obvious death. Along with providing standard BLS and ALS treatment, next steps include preventing additional evaporative heat loss by removing wet garments and insulating the victim from further environmental exposures. For patients with severe hypothermia (less than 30°C [86°F]) with a perfusing rhythm, core rewarming is often used. Techniques include administration of warm humidified oxygen, warm IV fluids, and intrathoracic or intraperitoneal warm-water lavage.3–5 For patients with severe hypothermia and cardiac arrest, extracorporeal rewarming allows for most rapid rewarming when available.6–11 Severe hyperkalemia and very low core temperatures may also predict resuscitation futility.12,13
When the victim is hypothermic, pulse and respiratory rates may be slow or difficult to detect,13,14 and the ECG may even show asystole, making it important to perform lifesaving interventions until the victim is warmed and/or obviously dead. Because severe hypothermia is frequently preceded by other disorders (eg, drug overdose, alcohol use, trauma), it is advisable to look for and treat these underlying conditions while simultaneously treating hypothermia.
The hypothermic heart may be unresponsive to cardiovascular drugs, pacemaker stimulation, and defibrillation; however, the data to support this are essentially theoretical.15 If VT or VF persists after a single shock, the value of deferring subsequent defibrillations until a target temperature is achieved is uncertain. There is no evidence to suggest a benefit from deviating from standard BLS protocol for defibrillation.
Evidence in humans of the effect of vasopressors or other medications during cardiac arrest in the setting of hypothermia consists of case reports only.11,16,17 A systematic review of several animal studies concluded that use of vasopressors during hypothermic cardiac arrest did increase ROSC.18 No evidence was identified at the time of prior review for harm from following standard ACLS, including vasopressor medications, during hypothermic cardiac arrest.

This topic last received formal evidence review in 2010.1

References

1. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S829–S861. doi: 10.1161/CIRCULATIONAHA.110.971069LinkGoogle Scholar
2. Brugger H, Durrer B, Elsensohn F, Paal P, Strapazzon G, Winterberger E, Zafren K, Boyd J. Resuscitation of avalanche victims: Evidence-based guidelines of the international commission for mountain emergency medicine (ICAR MEDCOM): intended for physicians and other advanced life support personnel.Resuscitation. 2013; 84:539–546. doi: 10.1016/j.resuscitation.2012.10.020CrossrefMedlineGoogle Scholar
3. Kangas E, Niemelä H, Kojo N. Treatment of hypothermic circulatory arrest with thoracotomy and pleural lavage.Ann Chir Gynaecol. 1994; 83:258–260.MedlineGoogle Scholar
4. Walters DT. Closed thoracic cavity lavage for hypothermia with cardiac arrest.Ann Emerg Med. 1991; 20:439–440. doi: 10.1016/s0196-0644(05)81687-7CrossrefMedlineGoogle Scholar
5. Plaisier BR. Thoracic lavage in accidental hypothermia with cardiac arrest–report of a case and review of the literature.Resuscitation. 2005; 66:99–104. doi: 10.1016/j.resuscitation.2004.12.024CrossrefMedlineGoogle Scholar
6. Farstad M, Andersen KS, Koller ME, Grong K, Segadal L, Husby P. Rewarming from accidental hypothermia by extracorporeal circulation. A retrospective study.Eur J Cardiothorac Surg. 2001; 20:58–64. doi: 10.1016/s1010-7940(01)00713-8CrossrefMedlineGoogle Scholar
7. Sheridan RL, Goldstein MA, Stoddard FJ, Walker TG. Case records of the Massachusetts General Hospital. Case 41-2009. A 16-year-old boy with hypothermia and frostbite.N Engl J Med. 2009; 361:2654–2662. doi: 10.1056/NEJMcpc0910088CrossrefMedlineGoogle Scholar
8. Gilbert M, Busund R, Skagseth A, Nilsen PA, Solbø JP. Resuscitation from accidental hypothermia of 13.7 degrees C with circulatory arrest.Lancet. 2000; 355:375–376. doi: 10.1016/S0140-6736(00)01021-7CrossrefMedlineGoogle Scholar
9. Coleman E, Doddakula K, Meeke R, Marshall C, Jahangir S, Hinchion J. An atypical case of successful resuscitation of an accidental profound hypothermia patient, occurring in a temperate climate.Perfusion. 2010; 25:103–106. doi: 10.1177/0267659110366066CrossrefMedlineGoogle Scholar
10. Althaus U, Aeberhard P, Schüpbach P, Nachbur BH, Mühlemann W. Management of profound accidental hypothermia with cardiorespiratory arrest.Ann Surg. 1982; 195:492–495. doi: 10.1097/00000658-198204000-00018CrossrefMedlineGoogle Scholar
11. Dobson JA, Burgess JJ. Resuscitation of severe hypothermia by extracorporeal rewarming in a child.J Trauma. 1996; 40:483–485. doi: 10.1097/00005373-199603000-00032CrossrefMedlineGoogle Scholar
12. Brugger H, Bouzat P, Pasquier M, Mair P, Fieler J, Darocha T, Blancher M, de Riedmatten M, Falk M, Paal P, Strapazzon G, Zafren K, Brodmann Maeder M. Cut-off values of serum potassium and core temperature at hospital admission for extracorporeal rewarming of avalanche victims in cardiac arrest: A retrospective multi-centre study.Resuscitation. 2019; 139:222–229. doi: 10.1016/j.resuscitation.2019.04.025CrossrefMedlineGoogle Scholar
13. Paal P, Gordon L, Strapazzon G, Brodmann Maeder M, Putzer G, Walpoth B, Wanscher M, Brown D, Holzer M, Broessner G, Brugger H. Accidental hypothermia-an update: The content of this review is endorsed by the International Commission for Mountain Emergency Medicine (ICAR MEDCOM).Scand J Trauma Resusc Emerg Med. 2016; 24:111. doi: 10.1186/s13049-016-0303-7CrossrefMedlineGoogle Scholar
14. Danzl DF, Pozos RS. Accidental hypothermia.N Engl J Med. 1994; 331:1756–1760. doi: 10.1056/NEJM199412293312607CrossrefMedlineGoogle Scholar
15. Clift J, Munro-Davies L. Best evidence topic report. Is defibrillation effective in accidental severe hypothermia in adults?Emerg Med J. 2007; 24:50–51. doi: 10.1136/emj.2006.044404CrossrefMedlineGoogle Scholar
16. Winegard C. Successful treatment of severe hypothermia and prolonged cardiac arrest with closed thoracic cavity lavage.J Emerg Med. 1997; 15:629–632. doi: 10.1016/s0736-4679(97)00139-xCrossrefMedlineGoogle Scholar
17. Lienhart HG, John W, Wenzel V. Cardiopulmonary resuscitation of a near-drowned child with a combination of epinephrine and vasopressin.Pediatr Crit Care Med. 2005; 6:486–488. doi: 10.1097/01.PCC.0000163673.40424.E7CrossrefMedlineGoogle Scholar
18. Wira CR, Becker JU, Martin G, Donnino MW. Anti-arrhythmic and vasopressor medications for the treatment of ventricular fibrillation in severe hypothermia: a systematic review of the literature.Resuscitation. 2008; 78:21–29. doi: 10.1016/j.resuscitation.2008.01.025CrossrefMedlineGoogle Scholar

Anaphylaxis

Introduction

Between 1.6% and 5.1% of US adults have suffered anaphylaxis.1 Approximately 200 Americans die from anaphylaxis annually, mostly from adverse reactions to medication.2 Although anaphylaxis is a multisystem disease, life-threatening manifestations most often involve the respiratory tract (edema, bronchospasm) and/or the circulatory system (vasodilatory shock). Epinephrine is the cornerstone of treatment for anaphylaxis.3–5

Recommendation-Specific Supportive Text

There are no RCTs evaluating alternative treatment algorithms for cardiac arrest due to anaphylaxis. Evidence is limited to case reports and extrapolations from nonfatal cases, interpretation of pathophysiology, and consensus opinion. Urgent support of airway, breathing, and circulation is essential in suspected anaphylactic reactions. Because of limited evidence, the cornerstone of management of cardiac arrest secondary to anaphylaxis is standard BLS and ACLS, including airway management and early epinephrine. There is no proven benefit from the use of antihistamines, inhaled beta agonists, and IV corticosteroids during anaphylaxis-induced cardiac arrest.

Recommendation-Specific Supportive Text

All patients with evidence of anaphylaxis require early treatment with epinephrine. Severe anaphylaxis may cause complete obstruction of the airway and/or cardiovascular collapse from vasogenic shock. Administration of epinephrine may be lifesaving.6 Intramuscular is the preferred initial route because of ease of administration, effectiveness, and safety.7
Injection of epinephrine into the lateral aspect of the thigh produces rapid peak plasma epinephrine concentrations.7 The adult epinephrine intramuscular autoinjector will deliver 0.3 mg of epinephrine, and the pediatric epinephrine intramuscular autoinjector will deliver 0.15 mg of epinephrine. Many patients will require additional doses, with recurrence of symptoms after 5 to 15 minutes reported.8
Patients in anaphylactic shock are critically ill, and cardiovascular and respiratory status can change quickly, making close monitoring imperative.9
When anaphylaxis produces obstructive airway edema, rapid advanced airway management is critical. In some cases, emergency cricothyroidotomy or tracheostomy may be required.10,11
IV epinephrine is an appropriate alternative to intramuscular administration in anaphylactic shock when an IV is in place. An IV dose of 0.05 to 0.1 mg (5% to 10% of the epinephrine dose used routinely in cardiac arrest) has been used successfully for anaphylactic shock.9 Although not specifically studied by this route in anaphylaxis, IO epinephrine is also likely to be effective at comparable doses.
In a canine model of anaphylactic shock, a continuous infusion of epinephrine was more effective at treating hypotension than no treatment or bolus epinephrine treatment were.12 If shock recurs after initial treatment, IV infusion (5–15 μg/min) may also better allow for careful titration and avoidance of overdosing epinephrine.
Although data specific to patients with ROSC after cardiac arrest from anaphylaxis was not identified, an observational study of anaphylactic shock suggests that IV infusion of epinephrine (5–15 μg/min), along with other resuscitative measures such as volume resuscitation, can be successful in the treatment of anaphylactic shock.13 Because of its role in the treatment of anaphylaxis, epinephrine is a logical choice for the treatment of postarrest shock in this setting.

This topic last received formal evidence review in 2010.14

References

1. Wood RA, Camargo CA, Lieberman P, Sampson HA, Schwartz LB, Zitt M, Collins C, Tringale M, Wilkinson M, Boyle J, et al.. Anaphylaxis in America: the prevalence and characteristics of anaphylaxis in the United States.J Allergy Clin Immunol. 2014; 133:461–467. doi: 10.1016/j.jaci.2013.08.016CrossrefMedlineGoogle Scholar
2. Jerschow E, Lin RY, Scaperotti MM, McGinn AP. Fatal anaphylaxis in the United States, 1999-2010: temporal patterns and demographic associations.J Allergy Clin Immunol. 2014; 134:1318.e7–1328.e7. doi: 10.1016/j.jaci.2014.08.018CrossrefGoogle Scholar
3. Dhami S, Panesar SS, Roberts G, Muraro A, Worm M, Bilò MB, Cardona V, Dubois AE, DunnGalvin A, Eigenmann P, Fernandez-Rivas M, Halken S, Lack G, Niggemann B, Rueff F, Santos AF, Vlieg-Boerstra B, Zolkipli ZQ, Sheikh AEAACI Food Allergy and Anaphylaxis Guidelines Group. Management of anaphylaxis: a systematic review.Allergy. 2014; 69:168–175. doi: 10.1111/all.12318CrossrefMedlineGoogle Scholar
4. Sheikh A, Simons FE, Barbour V, Worth A. Adrenaline auto-injectors for the treatment of anaphylaxis with and without cardiovascular collapse in the community.Cochrane Database Syst Rev. 2012CD008935. doi: 10.1002/14651858.CD008935.pub2MedlineGoogle Scholar
5. Shaker MS, Wallace DV, Golden DBK, Oppenheimer J, Bernstein JA, Campbell RL, Dinakar C, Ellis A, Greenhawt M, Khan DA, Lang DM, Lang ES, Lieberman JA, Portnoy J, Rank MA, Stukus DR, Wang J, Riblet N, Bobrownicki AMP, Bontrager T, Dusin J, Foley J, Frederick B, Fregene E, Hellerstedt S, Hassan F, Hess K, Horner C, Huntington K, Kasireddy P, Keeler D, Kim B, Lieberman P, Lindhorst E, McEnany F, Milbank J, Murphy H, Pando O, Patel AK, Ratliff N, Rhodes R, Robertson K, Scott H, Snell A, Sullivan R, Trivedi V, Wickham A, Shaker MS, Wallace DV, Shaker MS, Wallace DV, Bernstein JA, Campbell RL, Dinakar C, Ellis A, Golden DBK, Greenhawt M, Lieberman JA, Rank MA, Stukus DR, Wang J, Shaker MS, Wallace DV, Golden DBK, Bernstein JA, Dinakar C, Ellis A, Greenhawt M, Horner C, Khan DA, Lieberman JA, Oppenheimer J, Rank MA, Shaker MS, Stukus DR, Wang JCollaborators; Chief Editors; Workgroup Contributors; Joint Task Force on Practice Parameters Reviewers. Anaphylaxis-a 2020 practice parameter update, systematic review, and Grading of Recommendations, Assessment, Development and Evaluation (GRADE) analysis.J Allergy Clin Immunol. 2020; 145:1082–1123. doi: 10.1016/j.jaci.2020.01.017CrossrefMedlineGoogle Scholar
6. Sheikh A, Shehata YA, Brown SG, Simons FE. Adrenaline (epinephrine) for the treatment of anaphylaxis with and without shock.Cochrane Database Syst Rev. 2008CD006312. doi: 10.1002/14651858.CD006312.pub2MedlineGoogle Scholar
7. Simons FE, Gu X, Simons KJ. Epinephrine absorption in adults: intramuscular versus subcutaneous injection.J Allergy Clin Immunol. 2001; 108:871–873. doi: 10.1067/mai.2001.119409CrossrefMedlineGoogle Scholar
8. Korenblat P, Lundie MJ, Dankner RE, Day JH. A retrospective study of epinephrine administration for anaphylaxis: how many doses are needed?Allergy Asthma Proc. 1999; 20:383–386. doi: 10.2500/108854199778251834CrossrefMedlineGoogle Scholar
9. Bochner BS, Lichtenstein LM. Anaphylaxis.N Engl J Med. 1991; 324:1785–1790. doi: 10.1056/NEJM199106203242506CrossrefMedlineGoogle Scholar
10. Yilmaz R, Yuksekbas O, Erkol Z, Bulut ER, Arslan MN. Postmortem findings after anaphylactic reactions to drugs in Turkey.Am J Forensic Med Pathol. 2009; 30:346–349. doi: 10.1097/PAF.0b013e3181c0e7bbCrossrefMedlineGoogle Scholar
11. Yunginger JW, Sweeney KG, Sturner WQ, Giannandrea LA, Teigland JD, Bray M, Benson PA, York JA, Biedrzycki L, Squillace DL. Fatal food-induced anaphylaxis.JAMA. 1988; 260:1450–1452.CrossrefMedlineGoogle Scholar
12. Mink SN, Simons FE, Simons KJ, Becker AB, Duke K. Constant infusion of epinephrine, but not bolus treatment, improves haemodynamic recovery in anaphylactic shock in dogs.Clin Exp Allergy. 2004; 34:1776–1783. doi: 10.1111/j.1365-2222.2004.02106.xCrossrefMedlineGoogle Scholar
13. Brown SG, Blackman KE, Stenlake V, Heddle RJ. Insect sting anaphylaxis; prospective evaluation of treatment with intravenous adrenaline and volume resuscitation.Emerg Med J. 2004; 21:149–154. doi: 10.1136/emj.2003.009449CrossrefMedlineGoogle Scholar
14. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S829–S861. doi: 10.1161/CIRCULATIONAHA.110.971069LinkGoogle Scholar

Cardiac Arrest Due to Asthma

Synopsis

Severe exacerbations of asthma can lead to profound respiratory distress, retention of carbon dioxide, and air trapping, resulting in acute respiratory acidosis and high intrathoracic pressure. Deaths from acute asthma have decreased in the United States, but asthma continues to be the acute cause of death for over 3500 adults per year.1,2 Patients with respiratory arrest from asthma develop life-threatening acute respiratory acidosis.3 Both the profound acidemia and the decreased venous return to the heart from elevated intrathoracic pressure are likely causes of cardiac arrest in asthma.

Care of any patient with cardiac arrest in the setting of acute exacerbation of asthma begins with standard BLS. There are also no specific alterations to ACLS for patients with cardiac arrest from asthma, although airway management and ventilation increase in importance given the likelihood of an underlying respiratory cause of arrest. Acute asthma management was reviewed in detail in the 2010 Guidelines.4 For 2020, the writing group focused attention on additional ACLS considerations specific to asthma patients in the immediate periarrest period.

Recommendation-Specific Supportive Text

Tension pneumothorax is a rare life-threatening complication of asthma and a potentially reversible cause of arrest.5 Although usually occurring in patients receiving mechanical ventilation, cases in spontaneously breathing patients have been reported.5–7 High peak airway pressures resulting from positive-pressure ventilation can lead to pneumothorax. While difficulty ventilating an asthmatic patient in extremis is more likely due to hyperinflation and high intrathoracic pressure, evaluation for tension pneumothorax remains important.
The acute respiratory failure that can precipitate cardiac arrest in asthma patients is characterized by severe obstruction leading to air trapping. Because of the limitation in exhalational air flow, delivery of large tidal volumes at a higher respiratory rate can lead to progressive worsening of air trapping and a decrease in effective ventilation. An approach using lower tidal volumes, lower respiratory rate, and increased expiratory time may minimize the risk of auto-PEEP and barotrauma.8
Breath stacking in an asthma patient with limited ability to exhale can lead to increases in intrathoracic pressure, decreases in venous return and coronary perfusion pressure, and cardiac arrest.9–11 This can manifest as increased difficulty ventilating a patient, high airway pressure alarms on a ventilator, or sudden decreases in blood pressure. Brief disconnection from the ventilator or a pause in bag-mask ventilation and compression of the thorax to aid exhalation may relieve hyperinflation.

This topic last received formal evidence review in 2010.4

References

1. Moorman JE, Akinbami LJ, Bailey CM, Zahran HS, King ME, Johnson CA, Liu X . National surveillance of asthma: United States, 2001-2010.Vital Health Stat 3. 20121–58.MedlineGoogle Scholar
2. Centers for Disease Control and Prevention. AsthmaStats: asthma as the underlying cause of death.2016. //www.cdc.gov/asthma/asthma_stats/documents/AsthmStat_Mortality_2001-2016-H.pdf. Accessed April 20, 2020.Google Scholar
3. Molfino NA, Nannini LJ, Martelli AN, Slutsky AS. Respiratory arrest in near-fatal asthma.N Engl J Med. 1991; 324:285–288. doi: 10.1056/NEJM199101313240502CrossrefMedlineGoogle Scholar
4. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S829–S861. doi: 10.1161/CIRCULATIONAHA.110.971069LinkGoogle Scholar
5. Leigh-Smith S, Christey G. Tension pneumothorax in asthma.Resuscitation. 2006; 69:525–527. doi: 10.1016/j.resuscitation.2005.10.011CrossrefMedlineGoogle Scholar
6. Metry AA. Acute severe asthma complicated with tension pneumothorax and hemopneumothorax.Int J Crit Illn Inj Sci. 2019; 9:91–95. doi: 10.4103/IJCIIS.IJCIIS_83_18CrossrefMedlineGoogle Scholar
7. Karakaya Z, Demir S, Sagay SS, Karakaya O, Ozdinç S. Bilateral spontaneous pneumothorax, pneumomediastinum, and subcutaneous emphysema: rare and fatal complications of asthma.Case Rep Emerg Med. 2012; 2012:242579. doi: 10.1155/2012/242579MedlineGoogle Scholar
8. Leatherman J. Mechanical ventilation for severe asthma.Chest. 2015; 147:1671–1680. doi: 10.1378/chest.14-1733CrossrefMedlineGoogle Scholar
9. Myles PS, Madder H, Morgan EB. Intraoperative cardiac arrest after unrecognized dynamic hyperinflation.Br J Anaesth. 1995; 74:340–342. doi: 10.1093/bja/74.3.340CrossrefMedlineGoogle Scholar
10. Mercer M. Cardiac arrest after unrecognized dynamic inflation.Br J Anaesth. 1995; 75:252. doi: 10.1093/bja/75.2.252CrossrefMedlineGoogle Scholar
11. Berlin D. Hemodynamic consequences of auto-PEEP.J Intensive Care Med. 2014; 29:81–86. doi: 10.1177/0885066612445712CrossrefMedlineGoogle Scholar

Cardiac Arrest After Cardiac Surgery

Synopsis

Cardiac arrest occurs after 1% to 8% of cardiac surgery cases.1–8 Etiologies include tachyarrhythmias such as VT or VF, bradyarrhythmias such as heart block or asystole, obstructive causes such as tamponade or pneumothorax, technical factors such as dysfunction of a new valve, occlusion of a grafted artery, or bleeding. Like all patients with cardiac arrest, the immediate goal is restoration of perfusion with CPR, initiation of ACLS, and rapid identification and correction of the cause of cardiac arrest. Unlike most other cardiac arrests, these patients typically develop cardiac arrest in a highly monitored setting such as an ICU, with highly trained staff available to perform rescue therapies.

These guidelines are not meant to be comprehensive. A recent consensus statement on this topic has been published by the Society of Thoracic Surgeons.9

Recommendation-Specific Supportive Text

Case reports have rarely described damage to the heart due to external chest compressions.10–14 However, other case series have not reported such damage,8 and external chest compressions remain the only means of providing perfusion in some circumstances. In this case, the risk of external chest compressions is far outweighed by the certain death in the absence of perfusion.
VF is the presenting rhythm in 25% to 50% of cases of cardiac arrest after cardiac surgery. Immediate defibrillation by a trained provider presents distinct advantages in these patients, whereas the morbidity associated with external chest compressions or resternotomy may substantially impact recovery. Sparse data have been published addressing this question. Limited data are available from defibrillator threshold testing with backup transthoracic defibrillation, using variable waveforms and energy doses.15–17 First shock success over 90% was observed in most of these studies, though pooled results from 15 studies found a defibrillation success rate of 78% for the first shock, 35% for the second, and 14% for the third shock.18 The Society of Thoracic Surgeons Task Force on Resuscitation After Cardiac Surgery9 and the European Association for Cardio-Thoracic Surgery18 recommend 3 stacked defibrillations within 1 minute, before initiation of CPR. This departure from standard ACLS is likely warranted in the post–cardiac surgery setting because of the highly monitored setting and unique risks of compressions and resternotomy.
In post–cardiac surgery patients with asystole or bradycardic arrest in the ICU with pacing leads in place, pacing can be initiated immediately by trained providers. Available hemodynamic monitoring modalities in conjunction with manual pulse detection provide an opportunity to confirm myocardial capture and adequate cardiac function. When pacing attempts are not immediately successful, standard ACLS including CPR is indicated. This protocol is supported by the surgical societies,9,18 though no data are available to support its use.
No RCTs of resternotomy timing have been performed. However, good outcomes have been observed with rapid resternotomy protocols when performed by experienced providers in an appropriately equipped ICU.1,4,8,19–25 Other studies are neutral or show no benefit of resternotomy compared with standard therapy.3,6,26,27 Resternotomy performed outside of the ICU results in poor outcomes.1,3 The Society of Thoracic Surgeons recommends that resternotomy be a standard part of the resuscitation protocols for at least 10 days after surgery.9
No randomized RCTs have been performed comparing open-chest with external CPR. Two small studies have demonstrated improved hemodynamic effects of open-chest CPR when compared with external chest compressions in cardiac surgery patients.3,4
Multiple case series have demonstrated potential benefit from mechanical circulatory support including ECMO and cardiopulmonary bypass in patients who are refractory to standard resuscitation procedures.24,28–34 No RCT has been performed to date.

This topic last received formal evidence review in 2010.35 These recommendations were supplemented by a 2017 review published by the Society of Thoracic Surgeons.9

References

1. Mackay JH, Powell SJ, Osgathorp J, Rozario CJ. Six-year prospective audit of chest reopening after cardiac arrest.Eur J Cardiothorac Surg. 2002; 22:421–425. doi: 10.1016/s1010-7940(02)00294-4CrossrefMedlineGoogle Scholar
2. Birdi I, Chaudhuri N, Lenthall K, Reddy S, Nashef SA. Emergency reinstitution of cardiopulmonary bypass following cardiac surgery: outcome justifies the cost.Eur J Cardiothorac Surg. 2000; 17:743–746. doi: 10.1016/s1010-7940(00)00453-xCrossrefMedlineGoogle Scholar
3. Pottle A, Bullock I, Thomas J, Scott L. Survival to discharge following open chest cardiac compression (OCCC). A 4-year retrospective audit in a cardiothoracic specialist centre–Royal Brompton and Harefield NHS Trust, United Kingdom.Resuscitation. 2002; 52:269–272. doi: 10.1016/s0300-9572(01)00479-8CrossrefMedlineGoogle Scholar
4. Anthi A, Tzelepis GE, Alivizatos P, Michalis A, Palatianos GM, Geroulanos S. Unexpected cardiac arrest after cardiac surgery: incidence, predisposing causes, and outcome of open chest cardiopulmonary resuscitation.Chest. 1998; 113:15–19. doi: 10.1378/chest.113.1.15CrossrefMedlineGoogle Scholar
5. Charalambous CP, Zipitis CS, Keenan DJ. Chest reexploration in the intensive care unit after cardiac surgery: a safe alternative to returning to the operating theater.Ann Thorac Surg. 2006; 81:191–194. doi: 10.1016/j.athoracsur.2005.06.024CrossrefMedlineGoogle Scholar
6. Wahba A, Götz W, Birnbaum DE. Outcome of cardiopulmonary resuscitation following open heart surgery.Scand Cardiovasc J. 1997; 31:147–149. doi: 10.3109/14017439709058084CrossrefMedlineGoogle Scholar
7. LaPar DJ, Ghanta RK, Kern JA, Crosby IK, Rich JB, Speir AM, Kron IL, Ailawadi Gand the Investigators for the Virginia Cardiac Surgery Quality Initiative. Hospital variation in mortality from cardiac arrest after cardiac surgery: an opportunity for improvement?Ann Thorac Surg. 2014; 98:534–539. doi: 10.1016/j.athoracsur.2014.03.030CrossrefMedlineGoogle Scholar
8. el-Banayosy A, Brehm C, Kizner L, Hartmann D, Körtke H, Körner MM, Minami K, Reichelt W, Körfer R. Cardiopulmonary resuscitation after cardiac surgery: a two-year study.J Cardiothorac Vasc Anesth. 1998; 12:390–392. doi: 10.1016/s1053-0770(98)90189-6CrossrefMedlineGoogle Scholar
9. Society of Thoracic Surgeons Task Force on Resuscitation After Cardiac Surgery. The Society of Thoracic Surgeons expert consensus for the resuscitation of patients who arrest after cardiac surgery.Ann Thorac Surg. 2017; 103:1005–1020. doi: 10.1016/j.athoracsur.2016.10.033CrossrefMedlineGoogle Scholar
10. Böhrer H, Gust R, Böttiger BW. Cardiopulmonary resuscitation after cardiac surgery.J Cardiothorac Vasc Anesth. 1995; 9:352. doi: 10.1016/s1053-0770(05)80355-6CrossrefMedlineGoogle Scholar
11. Ricci M, Karamanoukian HL, D’Ancona G, Jajkowski MR, Bergsland J, Salerno TA. Avulsion of an H graft during closed-chest cardiopulmonary resuscitation after minimally invasive coronary artery bypass graft surgery.J Cardiothorac Vasc Anesth. 2000; 14:586–587. doi: 10.1053/jcan.2000.9440CrossrefMedlineGoogle Scholar
12. Kempen PM, Allgood R. Right ventricular rupture during closed-chest cardiopulmonary resuscitation after pneumonectomy with pericardiotomy: a case report.Crit Care Med. 1999; 27:1378–1379. doi: 10.1097/00003246-199907000-00033CrossrefMedlineGoogle Scholar
13. Sokolove PE, Willis-Shore J, Panacek EA. Exsanguination due to right ventricular rupture during closed-chest cardiopulmonary resuscitation.J Emerg Med. 2002; 23:161–164. doi: 10.1016/s0736-4679(02)00504-8CrossrefMedlineGoogle Scholar
14. Fosse E, Lindberg H. Left ventricular rupture following external chest compression.Acta Anaesthesiol Scand. 1996; 40:502–504. doi: 10.1111/j.1399-6576.1996.tb04476.xCrossrefMedlineGoogle Scholar
15. Szili-Torok T, Theuns D, Verblaauw T, Scholten M, Kimman GJ, Res J, Jordaens L. Transthoracic defibrillation of short-lasting ventricular fibrillation: a randomised trial for comparison of the efficacy of low-energy biphasic rectilinear and monophasic damped sine shocks.Acta Cardiol. 2002; 57:329–334. doi: 10.2143/AC.57.5.2005448CrossrefMedlineGoogle Scholar
16. Higgins SL, O’Grady SG, Banville I, Chapman FW, Schmitt PW, Lank P, Walker RG, Ilina M. Efficacy of lower-energy biphasic shocks for transthoracic defibrillation: a follow-up clinical study.Prehosp Emerg Care. 2004; 8:262–267. doi: 10.1016/j.prehos.2004.02.002MedlineGoogle Scholar
17. Bardy GH, Marchlinski FE, Sharma AD, Worley SJ, Luceri RM, Yee R, Halperin BD, Fellows CL, Ahern TS, Chilson DA, Packer DL, Wilber DJ, Mattioni TA, Reddy R, Kronmal RA, Lazzara R. Multicenter comparison of truncated biphasic shocks and standard damped sine wave monophasic shocks for transthoracic ventricular defibrillation. Transthoracic Investigators.Circulation. 1996; 94:2507–2514. doi: 10.1161/01.cir.94.10.2507LinkGoogle Scholar
18. Dunning J, Fabbri A, Kolh PH, Levine A, Lockowandt U, Mackay J, Pavie AJ, Strang T, Versteegh MI, Nashef SAEACTS Clinical Guidelines Committee. Guideline for resuscitation in cardiac arrest after cardiac surgery.Eur J Cardiothorac Surg. 2009; 36:3–28. doi: 10.1016/j.ejcts.2009.01.033CrossrefMedlineGoogle Scholar
19. Mackay JH, Powell SJ, Charman SC, Rozario C. Resuscitation after cardiac surgery: are we ageist?Eur J Anaesthesiol. 2004; 21:66–71. doi: 10.1017/s0265021504001115CrossrefMedlineGoogle Scholar
20. Raman J, Saldanha RF, Branch JM, Esmore DS, Spratt PM, Farnsworth AE, Harrison GA, Chang VP, Shanahan MX. Open cardiac compression in the postoperative cardiac intensive care unit.Anaesth Intensive Care. 1989; 17:129–135. doi: 10.1177/0310057X8901700202CrossrefMedlineGoogle Scholar
21. Karhunen JP, Sihvo EI, Suojaranta-Ylinen RT, Rämö OJ, Salminen US. Predictive factors of hemodynamic collapse after coronary artery bypass grafting: a case-control study.J Cardiothorac Vasc Anesth. 2006; 20:143–148. doi: 10.1053/j.jvca.2005.11.005CrossrefMedlineGoogle Scholar
22. Fairman RM, Edmunds LH. Emergency thoracotomy in the surgical intensive care unit after open cardiac operation.Ann Thorac Surg. 1981; 32:386–391. doi: 10.1016/s0003-4975(10)61761-4CrossrefMedlineGoogle Scholar
23. Ngaage DL, Cowen ME. Survival of cardiorespiratory arrest after coronary artery bypass grafting or aortic valve surgery.Ann Thorac Surg. 2009; 88:64–68. doi: 10.1016/j.athoracsur.2009.03.042CrossrefMedlineGoogle Scholar
24. Rousou JA, Engelman RM, Flack JE, Deaton DW, Owen SG. Emergency cardiopulmonary bypass in the cardiac surgical unit can be a lifesaving measure in postoperative cardiac arrest.Circulation. 1994; 905 Pt 2II280–II284.MedlineGoogle Scholar
25. Dimopoulou I, Anthi A, Michalis A, Tzelepis GE. Functional status and quality of life in long-term survivors of cardiac arrest after cardiac surgery.Crit Care Med. 2001; 29:1408–1411. doi: 10.1097/00003246-200107000-00018CrossrefMedlineGoogle Scholar
26. Feng WC, Bert AA, Browning RA, Singh AK. Open cardiac massage and periresuscitative cardiopulmonary bypass for cardiac arrest following cardiac surgery.J Cardiovasc Surg (Torino). 1995; 36:319–321.MedlineGoogle Scholar
27. Kaiser GC, Naunheim KS, Fiore AC, Harris HH, McBride LR, Pennington DG, Barner HB, Willman VL. Reoperation in the intensive care unit.Ann Thorac Surg. 1990; 49:903–7; discussion 908. doi: 10.1016/0003-4975(90)90863-2CrossrefMedlineGoogle Scholar
28. Chen YS, Chao A, Yu HY, Ko WJ, Wu IH, Chen RJ, Huang SC, Lin FY, Wang SS. Analysis and results of prolonged resuscitation in cardiac arrest patients rescued by extracorporeal membrane oxygenation.J Am Coll Cardiol. 2003; 41:197–203. doi: 10.1016/s0735-1097(02)02716-xCrossrefMedlineGoogle Scholar
29. Dalton HJ, Siewers RD, Fuhrman BP, Del Nido P, Thompson AE, Shaver MG, Dowhy M. Extracorporeal membrane oxygenation for cardiac rescue in children with severe myocardial dysfunction.Crit Care Med. 1993; 21:1020–1028. doi: 10.1097/00003246-199307000-00016CrossrefMedlineGoogle Scholar
30. Ghez O, Feier H, Ughetto F, Fraisse A, Kreitmann B, Metras D. Postoperative extracorporeal life support in pediatric cardiac surgery: recent results.ASAIO J. 2005; 51:513–516. doi: 10.1097/01.mat.0000178039.53714.57CrossrefMedlineGoogle Scholar
31. Duncan BW, Ibrahim AE, Hraska V, del Nido PJ, Laussen PC, Wessel DL, Mayer JE, Bower LK, Jonas RA. Use of rapid-deployment extracorporeal membrane oxygenation for the resuscitation of pediatric patients with heart disease after cardiac arrest.J Thorac Cardiovasc Surg. 1998; 116:305–311. doi: 10.1016/s0022-5223(98)70131-xCrossrefMedlineGoogle Scholar
32. Newsome LR, Ponganis P, Reichman R, Nakaji N, Jaski B, Hartley M. Portable percutaneous cardiopulmonary bypass: use in supported coronary angioplasty, aortic valvuloplasty, and cardiac arrest.J Cardiothorac Vasc Anesth. 1992; 6:328–331. doi: 10.1016/1053-0770(92)90151-vCrossrefMedlineGoogle Scholar
33. Parra DA, Totapally BR, Zahn E, Jacobs J, Aldousany A, Burke RP, Chang AC. Outcome of cardiopulmonary resuscitation in a pediatric cardiac intensive care unit.Crit Care Med. 2000; 28:3296–3300. doi: 10.1097/00003246-200009000-00030CrossrefMedlineGoogle Scholar
34. Overlie PA. Emergency use of cardiopulmonary bypass.J Interv Cardiol. 1995; 8:239–247. doi: 10.1111/j.1540-8183.1995.tb00541.xCrossrefMedlineGoogle Scholar
35. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S829–S861. doi: 10.1161/CIRCULATIONAHA.110.971069LinkGoogle Scholar

Drowning

Synopsis

Each year, drowning is responsible for approximately 0.7% of deaths worldwide, or more than 500 000 deaths per year.1,2 A recent study using data from the United States reported a survival rate of 13% after cardiac arrest associated with drowning.3 People at increased risk for drowning include children, those with seizure disorders, and those intoxicated with alcohol or other drugs.1 Although survival is uncommon after prolonged submersion, successful resuscitations have been reported.4–9 For this reason, scene resuscitation should be initiated and the victim transported to the hospital unless there are obvious signs of death. Standard BLS and ACLS are the cornerstones of treatment, with airway management and ventilation being of particular importance because of the respiratory cause of arrest. The evidence for these recommendations was last reviewed thoroughly in 2010.

Recommendation-Specific Supportive Text

The duration and severity of hypoxia sustained as a result of drowning is the single most important determinant of outcome.10,11 With outcome in mind, as soon as an unresponsive submersion victim is removed from the water, rescuers should provide CPR, with rescue breathing, if appropriately trained. Prompt initiation of rescue breathing increases the victim’s chance of survival.12
Multiple observational evaluations, primarily in pediatric patients, have demonstrated that decompensation after fresh or salt-water drowning can occur in the first 4 to 6 hours after the event.13,14 This supports transporting all victims to a medical facility for monitoring for at least 4 to 6 hours if feasible.
The immediate cause of death in drowning is hypoxemia. Based on the training of the rescuers, and only if scene safety can be maintained for the rescuer, sometimes ventilation can be provided in the water (“in-water resuscitation”), which may lead to improved patient outcomes compared with delaying ventilation until the victim is out of the water.8
The reported incidence of cervical spine injury in drowning victims is low (0.009%).15,16 Routine stabilization of the cervical spine in the absence of circumstances that suggest a spinal injury is unlikely to benefit the patient and may delay needed resuscitation.16,17

These recommendations incorporate the results of a 2020 ILCOR CoSTR, which focused on prognostic factors in drowning.18 Otherwise, this topic last received formal evidence review in 2010.19 These guidelines were supplemented by “Wilderness Medical Society Clinical Practice Guidelines for the Treatment and Prevention of Drowning: 2019 Update.”20

References

1. Szpilman D, Bierens JJ, Handley AJ, Orlowski JP. Drowning.N Engl J Med. 2012; 366:2102–2110. doi: 10.1056/NEJMra1013317CrossrefMedlineGoogle Scholar
2. Peden MM, McGee K . The epidemiology of drowning worldwide.Inj Control Saf Promot. 2003; 10:195–199. doi: 10.1076/icsp.10.4.195.16772CrossrefMedlineGoogle Scholar
3. Reynolds JC, Hartley T, Michiels EA, Quan L. Long-Term Survival After Drowning-Related Cardiac Arrest.J Emerg Med. 2019; 57:129–139. doi: 10.1016/j.jemermed.2019.05.029CrossrefMedlineGoogle Scholar
4. Southwick FS, Dalglish PH. Recovery after prolonged asystolic cardiac arrest in profound hypothermia. A case report and literature review.JAMA. 1980; 243:1250–1253.CrossrefMedlineGoogle Scholar
5. Siebke H, Rod T, Breivik H, Link B. Survival after 40 minutes; submersion without cerebral sequeae.Lancet. 1975; 1:1275–1277. doi: 10.1016/s0140-6736(75)92554-4CrossrefMedlineGoogle Scholar
6. Bolte RG, Black PG, Bowers RS, Thorne JK, Corneli HM. The use of extracorporeal rewarming in a child submerged for 66 minutes.JAMA. 1988; 260:377–379.CrossrefMedlineGoogle Scholar
7. Gilbert M, Busund R, Skagseth A, Nilsen PA, Solbø JP. Resuscitation from accidental hypothermia of 13.7 degrees C with circulatory arrest.Lancet. 2000; 355:375–376. doi: 10.1016/S0140-6736(00)01021-7CrossrefMedlineGoogle Scholar
8. Szpilman D, Soares M. In-water resuscitation–is it worthwhile?Resuscitation. 2004; 63:25–31. doi: 10.1016/j.resuscitation.2004.03.017CrossrefMedlineGoogle Scholar
9. Allman FD, Nelson WB, Pacentine GA, McComb G. Outcome following cardiopulmonary resuscitation in severe pediatric near-drowning.Am J Dis Child. 1986; 140:571–575. doi: 10.1001/archpedi.1986.02140200081033MedlineGoogle Scholar
10. Youn CS, Choi SP, Yim HW, Park KN. Out-of-hospital cardiac arrest due to drowning: An Utstein Style report of 10 years of experience from St. Mary’s Hospital.Resuscitation. 2009; 80:778–783. doi: 10.1016/j.resuscitation.2009.04.007CrossrefMedlineGoogle Scholar
11. Suominen P, Baillie C, Korpela R, Rautanen S, Ranta S, Olkkola KT. Impact of age, submersion time and water temperature on outcome in near-drowning.Resuscitation. 2002; 52:247–254. doi: 10.1016/s0300-9572(01)00478-6CrossrefMedlineGoogle Scholar
12. Kyriacou DN, Arcinue EL, Peek C, Kraus JF. Effect of immediate resuscitation on children with submersion injury.Pediatrics. 1994; 942 Pt 1137–142.CrossrefMedlineGoogle Scholar
13. Causey AL, Tilelli JA, Swanson ME. Predicting discharge in uncomplicated near-drowning.Am J Emerg Med. 2000; 18:9–11. doi: 10.1016/s0735-6757(00)90039-1CrossrefMedlineGoogle Scholar
14. Noonan L, Howrey R, Ginsburg CM. Freshwater submersion injuries in children: a retrospective review of seventy-five hospitalized patients.Pediatrics. 1996; 983 Pt 1368–371.CrossrefMedlineGoogle Scholar
15. Weinstein MD, Krieger BP. Near-drowning: epidemiology, pathophysiology, and initial treatment.J Emerg Med. 1996; 14:461–467. doi: 10.1016/0736-4679(96)00097-2CrossrefMedlineGoogle Scholar
16. Watson RS, Cummings P, Quan L, Bratton S, Weiss NS. Cervical spine injuries among submersion victims.J Trauma. 2001; 51:658–662. doi: 10.1097/00005373-200110000-00006CrossrefMedlineGoogle Scholar
17. Hwang V, Shofer FS, Durbin DR, Baren JM. Prevalence of traumatic injuries in drowning and near drowning in children and adolescents.Arch Pediatr Adolesc Med. 2003; 157:50–53. doi: 10.1001/archpedi.157.1.50CrossrefMedlineGoogle Scholar
18. Olasveengen TM, Mancini ME, Perkins GD, Avis S, Brooks S, Castrén M, Chung SP, Considine J, Couper K, Escalante R, et al.; on behalf of the Adult Basic Life Support Collaborators. Adult basic life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S41–S91. doi: 10.1161/CIR.0000000000000892LinkGoogle Scholar
19. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S829–S861. doi: 10.1161/CIRCULATIONAHA.110.971069LinkGoogle Scholar
20. Schmidt AC, Sempsrott JR, Hawkins SC, Arastu AS, Cushing TA, Auerbach PS. Wilderness Medical Society Clinical Practice Guidelines for the Treatment and Prevention of Drowning: 2019 Update.Wilderness Environ Med. 2019; 304SS70–S86. doi: 10.1016/j.wem.2019.06.007CrossrefMedlineGoogle Scholar

Electrolyte Abnormalities

Synopsis

Electrolyte abnormalities may cause or contribute to cardiac arrest, hinder resuscitative efforts, and affect hemodynamic recovery after cardiac arrest. In addition to standard ACLS, specific interventions may be lifesaving for cases of hyperkalemia and hypermagnesemia.

Hyperkalemia is commonly caused by renal failure and can precipitate cardiac arrhythmias and cardiac arrest. The clinical signs associated with severe hyperkalemia (more than 6.5 mmol/L) include flaccid paralysis, paresthesia, depressed deep tendon reflexes, or shortness of breath.1–3 The early electrocardiographic signs include peaked T waves on the ECG followed by flattened or absent T waves, prolonged PR interval, widened QRS complex, deepened S waves, and merging of S and T waves.4,5 As hyperkalemia progresses, the ECG can develop idioventricular rhythms, form a sine-wave pattern, and develop into an asystolic cardiac arrest.4,5 Severe hypokalemia is less common but can occur in the setting of gastrointestinal or renal losses and can lead to life-threatening ventricular arrhythmias.6–8 Severe hypermagnesemia is most likely to occur in the obstetric setting in patients being treated with IV magnesium for preeclampsia or eclampsia. At very elevated levels, hypermagnesemia can lead to altered consciousness, bradycardia or ventricular arrhythmias, and cardiac arrest.9,10 Hypomagnesemia can occur in the setting of gastrointestinal illness or malnutrition, among other causes, and, when significant, can lead to both atrial and ventricular arrhythmias.11

Recommendation-Specific Supportive Text

In addition to standard ACLS, several therapies have long been recommended to treat life-threatening hyperkalemia.12 These include IV administration of calcium and/or bicarbonate, insulin with glucose, and/or inhaled albuterol. Parenteral calcium may stabilize the myocardial cell membrane and is therefore the most likely to be useful during cardiac arrest and can be given by the IV or IO route. A typical dose is 5 to 10 mL of 10% calcium chloride solution, or 15 to 30 mL of 10% calcium gluconate solution, administered via IV or IO line over 2 to 5 minutes.12 Standard use of sodium polystyrene (Kayexalate) is now discouraged because of poor efficacy and the risk of bowel complications. Emergent hemodialysis in the hospital setting remains a definitive treatment for life-threatening hyperkalemia.
Although the administration of IV magnesium has not been found to be beneficial for VF/VT in the absence of prolonged QT, consideration of its use for cardiac arrest in patients with prolonged QT is advised.13 Hypomagnesemia can cause or aggravate prolonged QT, is associated with multiple arrhythmias, and may precipitate cardiac arrest.11 This provides physiological rationale for the restoration of normal levels, although standard ACLS remains the cornerstone of treatment. Recommendations for treatment of torsades de pointes are provided in the Wide Complex Tachycardia section.
Administration of IV or IO calcium, in the doses suggested for hyperkalemia, may improve hemodynamics in severe magnesium toxicity, supporting its use in cardiac arrest although direct evidence is lacking.14
The controlled administration of IV potassium for ventricular arrhythmias due to severe hypokalemia may be useful, but case reports have generally included infusion of potassium and not bolus dosing.15 Bolus dosing without adverse cardiac effects was reported in at least 1 small case series of cardiac surgery patients where it was administered in a highly monitored setting by an anesthesiologist, but the efficacy of this for cardiac arrest is not known, and safety concerns remain.16

This topic last received formal evidence review in 2010.12

References

1. Weiner ID, Wingo CS. Hyperkalemia: a potential silent killer.J Am Soc Nephrol. 1998; 9:1535–1543.CrossrefMedlineGoogle Scholar
2. Weiner M, Epstein FH. Signs and symptoms of electrolyte disorders.Yale J Biol Med. 1970; 43:76–109.MedlineGoogle Scholar
3. Rastegar A, Soleimani M, Rastergar A. Hypokalaemia and hyperkalaemia.Postgrad Med J. 2001; 77:759–764. doi: 10.1136/pmj.77.914.759CrossrefMedlineGoogle Scholar
4. Mattu A, Brady WJ, Robinson DA. Electrocardiographic manifestations of hyperkalemia.Am J Emerg Med. 2000; 18:721–729. doi: 10.1053/ajem.2000.7344CrossrefMedlineGoogle Scholar
5. Frohnert PP, Giuliani ER, Friedberg M, Johnson WJ, Tauxe WN. Statistical investigation of correlations between serum potassium levels and electrocardiographic findings in patients on intermittent hemodialysis therapy.Circulation. 1970; 41:667–676. doi: 10.1161/01.cir.41.4.667LinkGoogle Scholar
6. Gennari FJ. Hypokalemia.N Engl J Med. 1998; 339:451–458. doi: 10.1056/NEJM199808133390707CrossrefMedlineGoogle Scholar
7. Clausen TG, Brocks K, Ibsen H. Hypokalemia and ventricular arrhythmias in acute myocardial infarction.Acta Med Scand. 1988; 224:531–537. doi: 10.1111/j.0954-6820.1988.tb19623.xCrossrefMedlineGoogle Scholar
8. Slovis C, Jenkins R. ABC of clinical electrocardiography: Conditions not primarily affecting the heart.BMJ. 2002; 324:1320–1323. doi: 10.1136/bmj.324.7349.1320CrossrefMedlineGoogle Scholar
9. McDonnell NJ, Muchatuta NA, Paech MJ. Acute magnesium toxicity in an obstetric patient undergoing general anaesthesia for caesarean delivery.Int J Obstet Anesth. 2010; 19:226–231. doi: 10.1016/j.ijoa.2009.09.009CrossrefMedlineGoogle Scholar
10. McDonnell NJ. Cardiopulmonary arrest in pregnancy: two case reports of successful outcomes in association with perimortem Caesarean delivery.Br J Anaesth. 2009; 103:406–409. doi: 10.1093/bja/aep176CrossrefMedlineGoogle Scholar
11. Hansen BA, Bruserud Ø. Hypomagnesemia in critically ill patients.J Intensive Care. 2018; 6:21. doi: 10.1186/s40560-018-0291-yCrossrefMedlineGoogle Scholar
12. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S829–S861. doi: 10.1161/CIRCULATIONAHA.110.971069LinkGoogle Scholar
13. Panchal AR, Berg KM, Kudenchuk PJ, Del Rios M, Hirsch KG, Link MS, Kurz MC, Chan PS, Cabañas JG, Morley PT, Hazinski MF, Donnino MW. 2018 American Heart Association Focused Update on Advanced Cardiovascular Life Support Use of Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2018; 138:e740–e749. doi: 10.1161/CIR.0000000000000613LinkGoogle Scholar
14. Van Hook JW. Endocrine crises. Hypermagnesemia.Crit Care Clin. 1991; 7:215–223.CrossrefMedlineGoogle Scholar
15. Curry P, Fitchett D, Stubbs W, Krikler D. Ventricular arrhythmias and hypokalaemia.Lancet. 1976; 2:231–233. doi: 10.1016/s0140-6736(76)91029-1CrossrefMedlineGoogle Scholar
16. McCall BB, Mazzei WJ, Scheller MS, Thomas TC. Effects of central bolus injections of potassium chloride on arterial potassium concentration in patients undergoing cardiopulmonary bypass.J Cardiothorac Anesth. 1990; 4:571–576. doi: 10.1016/0888-6296(90)90406-6CrossrefMedlineGoogle Scholar

Opioid Overdose

Introduction

The ongoing opioid epidemic has resulted in an increase in opioid-associated OHCA, leading to approximately 115 deaths per day in the United States and predominantly impacting patients from 25 to 65 years old.1–3 Initially, isolated opioid toxicity is associated with CNS and respiratory depression that progresses to respiratory arrest followed by cardiac arrest. Most opioid-associated deaths also involve the coingestion of multiple drugs or medical and mental health comorbidities.4–7

In creating these recommendations, the writing group considered the difficulty in accurately differentiating opioid-associated resuscitative emergencies from other causes of cardiac and respiratory arrest. Opioid-associated resuscitative emergencies are defined by the presence of cardiac arrest, respiratory arrest, or severe life-threatening instability (such as severe CNS or respiratory depression, hypotension, or cardiac arrhythmia) that is suspected to be due to opioid toxicity. In these situations, the mainstay of care remains the early recognition of an emergency followed by the activation of the emergency response systems (Figures 13 and 14). Opioid overdoses deteriorate to cardiopulmonary arrest because of loss of airway patency and lack of breathing; therefore, addressing the airway and ventilation in a periarrest patient is of the highest priority. The next steps in care, including the performance of CPR and the administration of naloxone, are discussed in detail below.

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Figure 13. Opioid-Associated Emergency for Lay Responders Algorithm. AED indicates automated external defibrillator; CPR, cardiopulmonary resuscitation; and EMS, emergency medical services.

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Figure 14. Opioid-Associated Emergency for Healthcare Providers Algorithm. AED indicates automated external defibrillator; and BLS, basic life support.

Additional recommendations about opioid overdose response education are provided in “Part 6: Resuscitation Education Science.”

Recommendation-Specific Supportive Text

Initial management should focus on support of the patient’s airway and breathing. This begins with opening the airway followed by delivery of rescue breaths, ideally with the use of a bag-mask or barrier device.8–10 Provision of ACLS should continue if return of spontaneous breathing does not occur.
Because there are no studies demonstrating improvement in patient outcomes from administration of naloxone during cardiac arrest, provision of CPR should be the focus of initial care.3 Naloxone can be administered along with standard ACLS care if it does not delay components of high-quality CPR.
Early activation of the emergency response system is critical for patients with suspected opioid overdose. Rescuers cannot be certain that the person’s clinical condition is due to opioid-induced respiratory depression alone. This is particularly true in first aid and BLS, where determination of the presence of a pulse is unreliable.11,12 Naloxone is ineffective in other medical conditions, including overdose involving nonopioids and cardiac arrest from any cause. Second, patients who respond to naloxone administration may develop recurrent CNS and/or respiratory depression and require longer periods of observation before safe discharge.13–16
Twelve studies examined the use of naloxone in respiratory arrest, of which 5 compared intramuscular, intravenous, and/or intranasal routes of naloxone administration (2 RCT,17,18 3 non-RCT19–21) and 9 assessed the safety of naloxone use or were observational studies of naloxone use.22–30 These studies report that naloxone is safe and effective in treatment of opioid-induced respiratory depression and that complications are rare and dose related.

Recommendation-Specific Supportive Text

Patients who respond to naloxone administration may develop recurrent CNS and/or respiratory depression. Although abbreviated observation periods may be adequate for patients with fentanyl, morphine, or heroin overdose,28,30–34 longer periods of observation may be required to safely discharge a patient with life-threatening overdose of a long-acting or sustained-release opioid.13–15 Prehospital providers who are faced with the challenge of a patient refusing transport after treatment for a life-threatening overdose are advised to follow local protocols and practices for determination of patient capacity to refuse care.
Because the duration of action of naloxone may be shorter than the respiratory depressive effect of the opioid, particularly long-acting formulations, repeat doses of naloxone, or a naloxone infusion may be required.13–15

These recommendations are supported by the 2020 AHA scientific statement on opioid-associated OHCA.3

References

1. Scholl L, Seth P, Kariisa M, Wilson N, Baldwin G . Drug and opioid-involved overdose deaths—United States, 2013-2017.MMWR Morb Mortal Wkly Rep. 2018; 67:1419–1427. doi: 10.15585/mmwr.mm675152e1CrossrefMedlineGoogle Scholar
2. Jones CM, Einstein EB, Compton WM. Changes in synthetic opioid involvement in drug overdose deaths in the United States, 2010-2016.JAMA. 2018; 319:1819–1821. doi: 10.1001/jama.2018.2844CrossrefMedlineGoogle Scholar
3. Dezfulian C, Orkin AM, Maron BA, Elmer J, Girota S, Gladwin MT, Merchant RM, Panchal AR, Perman SM, Starks M, et al.; on behalf of the American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular and Stroke Nursing; and Council on Clinical Cardiology. Opioid-associated out-of-hospital cardiac arrest: distinctive clinical features and implications for healthcare and public responses: a scientific statement from the American Heart Association.Circulation. In press.Google Scholar
4. Jones CM, Paulozzi LJ, Mack KACenters for Disease Control and Prevention (CDC). Alcohol involvement in opioid pain reliever and benzodiazepine drug abuse-related emergency department visits and drug-related deaths - United States, 2010.MMWR Morb Mortal Wkly Rep. 2014; 63:881–885.MedlineGoogle Scholar
5. Madadi P, Hildebrandt D, Lauwers AE, Koren G. Characteristics of opioid-users whose death was related to opioid-toxicity: a population-based study in Ontario, Canada.PLoS One. 2013; 8:e60600. doi: 10.1371/journal.pone.0060600CrossrefMedlineGoogle Scholar
6. Paulozzi LJ, Logan JE, Hall AJ, McKinstry E, Kaplan JA, Crosby AE. A comparison of drug overdose deaths involving methadone and other opioid analgesics in West Virginia.Addiction. 2009; 104:1541–1548. doi: 10.1111/j.1360-0443.2009.02650.xCrossrefMedlineGoogle Scholar
7. Webster LR, Cochella S, Dasgupta N, Fakata KL, Fine PG, Fishman SM, Grey T, Johnson EM, Lee LK, Passik SD, Peppin J, Porucznik CA, Ray A, Schnoll SH, Stieg RL, Wakeland W. An analysis of the root causes for opioid-related overdose deaths in the United States.Pain Med. 2011; 12 Suppl 2:S26–S35. doi: 10.1111/j.1526-4637.2011.01134.xCrossrefMedlineGoogle Scholar
8. Kleinman ME, Brennan EE, Goldberger ZD, Swor RA, Terry M, Bobrow BJ, Gazmuri RJ, Travers AH, Rea T. Part 5: adult basic life support and cardiopulmonary resuscitation quality: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S414–S435. doi: 10.1161/CIR.0000000000000259LinkGoogle Scholar
9. Guildner CW. Resuscitation—opening the airway: a comparative study of techniques for opening an airway obstructed by the tongue.JACEP. 1976; 5:588–590. doi: 10.1016/s0361-1124(76)80217-1MedlineGoogle Scholar
10. Wenzel V, Keller C, Idris AH, Dörges V, Lindner KH, Brimacombe JR. Effects of smaller tidal volumes during basic life support ventilation in patients with respiratory arrest: good ventilation, less risk?Resuscitation. 1999; 43:25–29. doi: 10.1016/s0300-9572(99)00118-5CrossrefMedlineGoogle Scholar
11. Bahr J, Klingler H, Panzer W, Rode H, Kettler D. Skills of lay people in checking the carotid pulse.Resuscitation. 1997; 35:23–26. doi: 10.1016/s0300-9572(96)01092-1CrossrefMedlineGoogle Scholar
12. Eberle B, Dick WF, Schneider T, Wisser G, Doetsch S, Tzanova I. Checking the carotid pulse check: diagnostic accuracy of first responders in patients with and without a pulse.Resuscitation. 1996; 33:107–116. doi: 10.1016/s0300-9572(96)01016-7CrossrefMedlineGoogle Scholar
13. Clarke SF, Dargan PI, Jones AL. Naloxone in opioid poisoning: walking the tightrope.Emerg Med J. 2005; 22:612–616. doi: 10.1136/emj.2003.009613CrossrefMedlineGoogle Scholar
14. Etherington J, Christenson J, Innes G, Grafstein E, Pennington S, Spinelli JJ, Gao M, Lahiffe B, Wanger K, Fernandes C. Is early discharge safe after naloxone reversal of presumed opioid overdose?CJEM. 2000; 2:156–162. doi: 10.1017/s1481803500004863CrossrefMedlineGoogle Scholar
15. Zuckerman M, Weisberg SN, Boyer EW. Pitfalls of intranasal naloxone.Prehosp Emerg Care. 2014; 18:550–554. doi: 10.3109/10903127.2014.896961CrossrefMedlineGoogle Scholar
16. Heaton JD, Bhandari B, Faryar KA, Huecker MR. Retrospective Review of Need for Delayed Naloxone or Oxygen in Emergency Department Patients Receiving Naloxone for Heroin Reversal.J Emerg Med. 2019; 56:642–651. doi: 10.1016/j.jemermed.2019.02.015CrossrefMedlineGoogle Scholar
17. Kelly AM, Kerr D, Dietze P, Patrick I, Walker T, Koutsogiannis Z. Randomised trial of intranasal versus intramuscular naloxone in prehospital treatment for suspected opioid overdose.Med J Aust. 2005; 182:24–27.CrossrefMedlineGoogle Scholar
18. Kerr D, Kelly AM, Dietze P, Jolley D, Barger B. Randomized controlled trial comparing the effectiveness and safety of intranasal and intramuscular naloxone for the treatment of suspected heroin overdose.Addiction. 2009; 104:2067–2074. doi: 10.1111/j.1360-0443.2009.02724.xCrossrefMedlineGoogle Scholar
19. Wanger K, Brough L, Macmillan I, Goulding J, MacPhail I, Christenson JM. Intravenous vs subcutaneous naloxone for out-of-hospital management of presumed opioid overdose.Acad Emerg Med. 1998; 5:293–299. doi: 10.1111/j.1553-2712.1998.tb02707.xCrossrefMedlineGoogle Scholar
20. Barton ED, Colwell CB, Wolfe T, Fosnocht D, Gravitz C, Bryan T, Dunn W, Benson J, Bailey J. Efficacy of intranasal naloxone as a needleless alternative for treatment of opioid overdose in the prehospital setting.J Emerg Med. 2005; 29:265–271. doi: 10.1016/j.jemermed.2005.03.007CrossrefMedlineGoogle Scholar
21. Robertson TM, Hendey GW, Stroh G, Shalit M. Intranasal naloxone is a viable alternative to intravenous naloxone for prehospital narcotic overdose.Prehosp Emerg Care. 2009; 13:512–515. doi: 10.1080/10903120903144866CrossrefMedlineGoogle Scholar
22. Cetrullo C, Di Nino GF, Melloni C, Pieri C, Zanoni A. [Naloxone antagonism toward opiate analgesic drugs. Clinical experimental study].Minerva Anestesiol. 1983; 49:199–204.MedlineGoogle Scholar
23. Osterwalder JJ. Naloxone–for intoxications with intravenous heroin and heroin mixtures–harmless or hazardous? A prospective clinical study.J Toxicol Clin Toxicol. 1996; 34:409–416. doi: 10.3109/15563659609013811CrossrefMedlineGoogle Scholar
24. Sporer KA, Firestone J, Isaacs SM. Out-of-hospital treatment of opioid overdoses in an urban setting.Acad Emerg Med. 1996; 3:660–667. doi: 10.1111/j.1553-2712.1996.tb03487.xCrossrefMedlineGoogle Scholar
25. Stokland O, Hansen TB, Nilsen JE. [Prehospital treatment of heroin intoxication in Oslo in 1996].Tidsskr Nor Laegeforen. 1998; 118:3144–3146.MedlineGoogle Scholar
26. Buajordet I, Naess AC, Jacobsen D, Brørs O. Adverse events after naloxone treatment of episodes of suspected acute opioid overdose.Eur J Emerg Med. 2004; 11:19–23. doi: 10.1097/00063110-200402000-00004CrossrefMedlineGoogle Scholar
27. Cantwell K, Dietze P, Flander L. The relationship between naloxone dose and key patient variables in the treatment of non-fatal heroin overdose in the prehospital setting.Resuscitation. 2005; 65:315–319. doi: 10.1016/j.resuscitation.2004.12.012CrossrefMedlineGoogle Scholar
28. Boyd JJ, Kuisma MJ, Alaspää AO, Vuori E, Repo JV, Randell TT. Recurrent opioid toxicity after pre-hospital care of presumed heroin overdose patients.Acta Anaesthesiol Scand. 2006; 50:1266–1270. doi: 10.1111/j.1399-6576.2006.01172.xCrossrefMedlineGoogle Scholar
29. Nielsen K, Nielsen SL, Siersma V, Rasmussen LS. Treatment of opioid overdose in a physician-based prehospital EMS: frequency and long-term prognosis.Resuscitation. 2011; 82:1410–1413. doi: 10.1016/j.resuscitation.2011.05.027CrossrefMedlineGoogle Scholar
30. Wampler DA, Molina DK, McManus J, Laws P, Manifold CA. No deaths associated with patient refusal of transport after naloxone-reversed opioid overdose.Prehosp Emerg Care. 2011; 15:320–324. doi: 10.3109/10903127.2011.569854CrossrefMedlineGoogle Scholar
31. Vilke GM, Sloane C, Smith AM, Chan TC. Assessment for deaths in out-of-hospital heroin overdose patients treated with naloxone who refuse transport.Acad Emerg Med. 2003; 10:893–896. doi: 10.1111/j.1553-2712.2003.tb00636.xCrossrefMedlineGoogle Scholar
32. Rudolph SS, Jehu G, Nielsen SL, Nielsen K, Siersma V, Rasmussen LS. Prehospital treatment of opioid overdose in Copenhagen–is it safe to discharge on-scene?Resuscitation. 2011; 82:1414–1418. doi: 10.1016/j.resuscitation.2011.06.027CrossrefMedlineGoogle Scholar
33. Moss ST, Chan TC, Buchanan J, Dunford JV, Vilke GM. Outcome study of prehospital patients signed out against medical advice by field paramedics.Ann Emerg Med. 1998; 31:247–250. doi: 10.1016/s0196-0644(98)70315-4CrossrefMedlineGoogle Scholar
34. Christenson J, Etherington J, Grafstein E, Innes G, Pennington S, Wanger K, Fernandes C, Spinelli JJ, Gao M. Early discharge of patients with presumed opioid overdose: development of a clinical prediction rule.Acad Emerg Med. 2000; 7:1110–1118. doi: 10.1111/j.1553-2712.2000.tb01260.xCrossrefMedlineGoogle Scholar

Cardiac Arrest in Pregnancy

Introduction

Approximately 1 in 12 000 admissions for delivery in the United States results in a maternal cardiac arrest.1 Although it remains a rare event, the incidence has been increasing.2 Reported maternal and fetal/neonatal survival rates vary widely.3–8 Invariably, the best outcomes for both mother and fetus are through successful maternal resuscitation. Common causes of maternal cardiac arrest are hemorrhage, heart failure, amniotic fluid embolism, sepsis, aspiration pneumonitis, venous thromboembolism, preeclampsia/eclampsia, and complications of anesthesia.1,4,6

Current literature is largely observational, and some treatment decisions are based primarily on the physiology of pregnancy and extrapolations from nonarrest pregnancy states.9 High-quality resuscitative and therapeutic interventions that target the most likely cause of cardiac arrest are paramount in this population. Perimortem cesarean delivery (PMCD) at or greater than 20 weeks uterine size, sometimes referred to as resuscitative hysterotomy, appears to improve outcomes of maternal cardiac arrest when resuscitation does not rapidly result in ROSC (Figure 15).10–14 Further, shorter time intervals from arrest to delivery appear to lead to improved maternal and neonatal outcomes.15 However, the clinical decision to perform PMCD―and its timing with respect to maternal cardiac arrest―is complex because of the variability in level of practitioner and team training, patient factors (eg, etiology of arrest, gestational age), and system resources. Finally, case reports and case series using ECMO in maternal cardiac arrest patients report good maternal survival.16 The treatment of cardiac arrest in late pregnancy represents a major scientific gap.

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Figure 15. Cardiac Arrest in Pregnancy In-Hospital ACLS Algorithm. ACLS indicates advanced cardiovascular life support; BLS, basic life support; CPR, cardiopulmonary resuscitation; ET, endotracheal; IV, intravenous; and ROSC, return of spontaneous circulation.

Recommendation-Specific Supportive Text

To assure successful maternal resuscitation, all potential stakeholders need to be engaged in the planning and training for cardiac arrest in pregnancy, including the possible need for PMCD. Based on similarly rare but time-critical interventions, planning, simulation training and mock emergencies will assist in facility preparedness.17–21
Since initial efforts for maternal resuscitation may not be successful, preparation for PMCD should begin early in the resuscitation, since decreased time to PMCD is associated with better maternal and fetal outcomes.8
In cases of prehospital maternal arrest, rapid transport directly to a facility capable of PMCD and neonatal resuscitation, with early activation of the receiving facility’s adult resuscitation, obstetric, and neonatal resuscitation teams, provides the best chance for a successful outcome.

Recommendation-Specific Supportive Text

The gravid uterus can compress the inferior vena cava, impeding venous return, thereby reducing stroke volume and cardiac output. In the supine position, aortocaval compression can occur for singleton pregnancies starting at approximately 20 weeks of gestational age or when the fundal height is at or above the level of the umbilicus.22 Manual left lateral uterine displacement effectively relieves aortocaval pressure in patients with hypotension (Figure 16).23,23a,23b
Airway, ventilation, and oxygenation are particularly important in the setting of pregnancy because of increased maternal metabolism and decreased functional reserve capacity due to the gravid uterus, making pregnant patients more prone to hypoxia. Furthermore, fetal hypoxia has known detrimental effects. Both of these considerations support earlier advanced airway management for the pregnant patient.
Resuscitation of the pregnant woman, including PMCD when indicated, is the first priority because it may lead to increased survival of both the woman and the fetus.9 Fetal monitoring does not achieve this goal and may distract from maternal resuscitation efforts, particularly defibrillation and preparation of the abdomen for PMCD.
There are no randomized trials of the use of TTM in pregnancy. However, there are several case reports of good maternal and fetal outcome with the use of TTM after cardiac arrest.24,25
After successful maternal resuscitation, the undelivered fetus remains susceptible to the effects of hypothermia, acidosis, hypoxemia, and hypotension, all of which can occur in the setting of post-ROSC care with TTM. In addition, deterioration of fetal status may be an early warning sign of maternal decompensation.

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Figure 16. A, Manual left lateral uterine displacement, performed with 2-handed technique. B, 1-handed technique during resuscitation.

Recommendation-Specific Supportive Text

Evacuation of the gravid uterus relieves aortocaval compression and may increase the likelihood of ROSC.10–14 In the latter half of pregnancy, PMCD may be considered part of maternal resuscitation, regardless of fetal viability.26
Early delivery is associated with better maternal and neonatal survival.15 In situations incompatible with maternal survival, early delivery of the fetus may also improve neonatal survival. 26
The optimal timing for the performance of PMCD is not well established and must logically vary on the basis of provider skill set and available resources as well as patient and/or cardiac arrest characteristics. A systematic review of the literature evaluated all case reports of cardiac arrest in pregnancy about the timing of PMCD, but the wide range of case heterogeneity and reporting bias does not allow for conclusions.15 Survival of the mother has been reported up to 39 minutes after the onset of maternal cardiac arrest.4,10,27–29 In a systematic review of literature published 1980 to 2010, the median time from maternal cardiac arrest to delivery was 9 minutes in surviving mothers and 20 minutes in nonsurviving mothers.15 In the same study, the median time to PMCD was 10 minutes in surviving and 20 minutes in nonsurviving neonates. The time to delivery was within 4 minutes in only 4/57 (7%) reported cases.15 In a UK cohort study,4 the median time from collapse to PMCD was 3 minutes in women who survived compared with 12 minutes in nonsurvivors. In this study, 24/25 infants survived when PMCD occurred within 5 minutes after maternal cardiac arrest compared with 7/10 infants when PMCD occurred more than 5 minutes after cardiac arrest. Neonatal survival has been documented with PMCD performed up to 30 minutes after the onset of maternal cardiac arrest.10 The expert recommendation for timing for PMCD in cardiac arrest at less than 5 minutes remains an important goal, though rarely achieved.9 There is no evidence for a specific survival threshold at 4 minutes.8

These recommendations are supported by “Cardiac Arrest in Pregnancy: a Scientific Statement From the AHA”9 and a 2020 evidence update.30

References

1. Mhyre JM, Tsen LC, Einav S, Kuklina EV, Leffert LR, Bateman BT. Cardiac arrest during hospitalization for delivery in the United States, 1998-2011.Anesthesiology. 2014; 120:810–818. doi: 10.1097/ALN.0000000000000159CrossrefMedlineGoogle Scholar
2. Centers for Disease Control and Prevention. Pregnancy-related deaths: data from 14 U.S. maternal mortality review committees, 2008-2017. //www.cdc.gov/reproductivehealth/maternal-mortality/erase-mm/mmr-data-brief.html. Accessed April 22, 2020.Google Scholar
3. Kobori S, Toshimitsu M, Nagaoka S, Yaegashi N, Murotsuki J. Utility and limitations of perimortem cesarean section: A nationwide survey in Japan.J Obstet Gynaecol Res. 2019; 45:325–330. doi: 10.1111/jog.13819CrossrefMedlineGoogle Scholar
4. Beckett VA, Knight M, Sharpe P. The CAPS Study: incidence, management and outcomes of cardiac arrest in pregnancy in the UK: a prospective, descriptive study.BJOG. 2017; 124:1374–1381. doi: 10.1111/1471-0528.14521CrossrefMedlineGoogle Scholar
5. Maurin O, Lemoine S, Jost D, Lanoë V, Renard A, Travers S, The Paris Fire Brigade Cardiac Arrest Work Group , Lapostolle F, Tourtier JP. Maternal out-of-hospital cardiac arrest: A retrospective observational study.Resuscitation. 2019; 135:205–211. doi: 10.1016/j.resuscitation.2018.11.001CrossrefMedlineGoogle Scholar
6. Schaap TP, Overtoom E, van den Akker T, Zwart JJ, van Roosmalen J, Bloemenkamp KWM. Maternal cardiac arrest in the Netherlands: A nationwide surveillance study.Eur J Obstet Gynecol Reprod Biol. 2019; 237:145–150. doi: 10.1016/j.ejogrb.2019.04.028CrossrefMedlineGoogle Scholar
7. Lipowicz AA, Cheskes S, Gray SH, Jeejeebhoy F, Lee J, Scales DC, Zhan C, Morrison LJRescu Investigators. Incidence, outcomes and guideline compliance of out-of-hospital maternal cardiac arrest resuscitations: A population-based cohort study.Resuscitation. 2018; 132:127–132. doi: 10.1016/j.resuscitation.2018.09.003CrossrefMedlineGoogle Scholar
8. Benson MD, Padovano A, Bourjeily G, Zhou Y. Maternal collapse: Challenging the four-minute rule.EBioMedicine. 2016; 6:253–257. doi: 10.1016/j.ebiom.2016.02.042CrossrefMedlineGoogle Scholar
9. Jeejeebhoy FM, Zelop CM, Lipman S, Carvalho B, Joglar J, Mhyre JM, Katz VL, Lapinsky SE, Einav S, Warnes CA, Page RL, Griffin RE, Jain A, Dainty KN, Arafeh J, Windrim R, Koren G, Callaway CWAmerican Heart Association Emergency Cardiovascular Care Committee, Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation, Council on Cardiovascular Diseases in the Young, and Council on Clinical Cardiology. Cardiac Arrest in Pregnancy: A Scientific Statement From the American Heart Association.Circulation. 2015; 132:1747–1773. doi: 10.1161/CIR.0000000000000300LinkGoogle Scholar
10. Dijkman A, Huisman CM, Smit M, Schutte JM, Zwart JJ, van Roosmalen JJ, Oepkes D. Cardiac arrest in pregnancy: increasing use of perimortem caesarean section due to emergency skills training?BJOG. 2010; 117:282–287. doi: 10.1111/j.1471-0528.2009.02461.xCrossrefMedlineGoogle Scholar
11. Page-Rodriguez A, Gonzalez-Sanchez JA. Perimortem cesarean section of twin pregnancy: case report and review of the literature.Acad Emerg Med. 1999; 6:1072–1074. doi: 10.1111/j.1553-2712.1999.tb01199.xCrossrefMedlineGoogle Scholar
12. Cardosi RJ, Porter KB. Cesarean delivery of twins during maternal cardiopulmonary arrest.Obstet Gynecol. 1998; 924 Pt 2695–697. doi: 10.1016/s0029-7844(98)00127-6MedlineGoogle Scholar
13. Rose CH, Faksh A, Traynor KD, Cabrera D, Arendt KW, Brost BC. Challenging the 4- to 5-minute rule: from perimortem cesarean to resuscitative hysterotomy.Am J Obstetr Gynecol. 2015; 213:653–656. doi: 10.1016/j.ajog.2015.07.019CrossrefMedlineGoogle Scholar
14. Tambawala ZY, Cherawala M, Maqbool S, Hamza LK. Resuscitative hysterotomy for maternal collapse in a triplet pregnancy.BMJ Case Rep. 2020; 13:e235328. doi: 10.1136/bcr-2020-235328CrossrefMedlineGoogle Scholar
15. Einav S, Kaufman N, Sela HY. Maternal cardiac arrest and perimortem caesarean delivery: evidence or expert-based?Resuscitation. 2012; 83:1191–1200. doi: 10.1016/j.resuscitation.2012.05.005CrossrefMedlineGoogle Scholar
16. Biderman P, Carmi U, Setton E, Fainblut M, Bachar O, Einav S. Maternal Salvage With Extracorporeal Life Support: Lessons Learned in a Single Center.Anesth Analg. 2017; 125:1275–1280. doi: 10.1213/ANE.0000000000002262CrossrefMedlineGoogle Scholar
17. Lipman SS, Daniels KI, Arafeh J, Halamek LP. The case for OBLS: a simulation-based obstetric life support program.Semin Perinatol. 2011; 35:74–79. doi: 10.1053/j.semperi.2011.01.006CrossrefMedlineGoogle Scholar
18. Petrone P, Talving P, Browder T, Teixeira PG, Fisher O, Lozornio A, Chan LS. Abdominal injuries in pregnancy: a 155-month study at two level 1 trauma centers.Injury. 2011; 42:47–49. doi: 10.1016/j.injury.2010.06.026CrossrefMedlineGoogle Scholar
19. Al-Foudri H, Kevelighan E, Catling S. CEMACH 2003–5 Saving Mothers’ Lives: lessons for anaesthetists.Continuing Education in Anaesthesia Critical Care & Pain. 2010; 10:81–87. doi: 10.1093/bjaceaccp/mkq009CrossrefGoogle Scholar
20. The Joint Commission. TJC Sentinel Event Alert 44: preventing maternal death. //www.jointcommission.org/resources/patient-safety-topics/sentinel-event/sentinel-event-alert-newsletters/sentinel-event-alert-issue-44-preventing-maternal-death/. Accessed May 11, 2020.Google Scholar
21. The Joint Commission. Sentinel Event Alert: Preventing infant death and injury during delivery.2004. //www.jointcommission.org/resources/patient-safety-topics/sentinel-event/sentinel-event-alert-newsletters/sentinel-event-alert-issue-30-preventing-infant-death-and-injury-during-delivery/. Accessed February 28, 2020.Google Scholar
22. Goodwin AP, Pearce AJ. The human wedge. A manoeuvre to relieve aortocaval compression during resuscitation in late pregnancy.Anaesthesia. 1992; 47:433–434. doi: 10.1111/j.1365-2044.1992.tb02228.xCrossrefMedlineGoogle Scholar
23. Cyna AM, Andrew M, Emmett RS, Middleton P, Simmons SW. Techniques for preventing hypotension during spinal anaesthesia for caesarean section.Cochrane Database Syst Rev. 2006CD002251. doi: 10.1002/14651858.CD002251.pub2MedlineGoogle Scholar
23a. Rees SG, Thurlow JA, Gardner IC, Scrutton MJ, Kinsella SM. Maternal cardiovascular consequences of positioning after spinal anaesthesia for Caesarean section: left 15 degree table tilt vs. left lateral.Anaesthesia. 2002; 57:15–20. doi: 10.1046/j.1365-2044.2002.02325.xCrossrefMedlineGoogle Scholar
23b. Mendonca C, Griffiths J, Ateleanu B, Collis RE. Hypotension following combined spinal-epidural anaesthesia for Caesarean section. Left lateral position vs. tilted supine position.Anaesthesia. 2003; 58:428–431. doi: 10.1046/j.1365-2044.2003.03090.xCrossrefGoogle Scholar
24. Rittenberger JC, Kelly E, Jang D, Greer K, Heffner A. Successful outcome utilizing hypothermia after cardiac arrest in pregnancy: a case report.Crit Care Med. 2008; 36:1354–1356. doi: 10.1097/CCM.0b013e318169ee99CrossrefMedlineGoogle Scholar
25. Chauhan A, Musunuru H, Donnino M, McCurdy MT, Chauhan V, Walsh M. The use of therapeutic hypothermia after cardiac arrest in a pregnant patient.Ann Emerg Med. 2012; 60:786–789. doi: 10.1016/j.annemergmed.2012.06.004CrossrefMedlineGoogle Scholar
26. Svinos H. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 1. Emergency caesarean section in cardiac arrest before the third trimester.Emerg Med J. 2008; 25:764–765. doi: 10.1136/emj.2008.066860CrossrefMedlineGoogle Scholar
27. Kam CW. Perimortem caesarean sections (PMCS).J Accid Emerg Med. 1994; 11:57–58. doi: 10.1136/emj.11.1.57-bCrossrefMedlineGoogle Scholar
28. Kupas DF, Harter SC, Vosk A. Out-of-hospital perimortem cesarean section.Prehosp Emerg Care. 1998; 2:206–208. doi: 10.1080/10903129808958874CrossrefMedlineGoogle Scholar
29. Oates S, Williams GL, Rees GA. Cardiopulmonary resuscitation in late pregnancy.BMJ. 1988; 297:404–405. doi: 10.1136/bmj.297.6645.404CrossrefMedlineGoogle Scholar
30. Berg KM, Soar J, Andersen LW, Böttiger BW, Cacciola S, Callaway CW, Couper K, Cronberg T, D’Arrigo S, Deakin CD, et al.; on behalf of the Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S92–S139. doi: 10.1161/CIR.0000000000000893LinkGoogle Scholar

Pulmonary Embolism

Synopsis

This topic was reviewed in an ILCOR systematic review for 2020.1 PE is a potentially reversible cause of shock and cardiac arrest. Acute increase in right ventricular pressure due to pulmonary artery obstruction and release of vasoactive mediators produces cardiogenic shock that may rapidly progress to cardiovascular collapse. Management of acute PE is determined by disease severity.2 Fulminant PE, characterized by cardiac arrest or severe hemodynamic instability, defines the subset of massive PE that is the focus of these recommendations. Pulseless electrical activity is the presenting rhythm in 36% to 53% of PE-related cardiac arrests, while primary shockable rhythms are uncommon.3–5

Prompt systemic anticoagulation is generally indicated for patients with massive and submassive PE to prevent clot propagation and support endogenous clot dissolution over weeks. Anticoagulation alone is inadequate for patients with fulminant PE. Pharmacological and mechanical therapies to rapidly reverse pulmonary artery occlusion and restore adequate pulmonary and systemic circulation have emerged as primary therapies for massive PE, including fulminant PE.2,6 Current advanced treatment options include systemic thrombolysis, surgical or percutaneous mechanical embolectomy, and ECPR.

Recommendation-Specific Supportive Text

In the 2020 ILCOR systematic review, no randomized trials were identified addressing the treatment of cardiac arrest caused by confirmed PE. Observational studies of fibrinolytic therapy for suspected PE were found to have substantial bias and showed mixed results in terms of improvement in outcomes.3,7–10 Two case series totaling 21 patients with PE undergoing CPR who underwent surgical embolectomy reported 30-day survival rates of 12.5% and 71.4%, respectively.11,12 A case series of patients with PE-related cardiac arrest reported ROSC in 6 of 7 patients (86%) treated with percutaneous mechanical thrombectomy.13 In terms of potential adverse effects, a clinical trial and several observational studies show that the risk of major bleeding in patients receiving thrombolysis and CPR is relatively low.7–9 In spite of the uncertainty of benefit, the risk of death from cardiac arrest outweighs the risk of bleeding from thrombolysis and/or the risks of mechanical or surgical interventions. Because there is no clear benefit to one approach over the other, choice of thrombolysis or surgical or mechanical thrombectomy will depend on timing and available expertise.
The approach to cardiac arrest when PE is suspected but not confirmed is less clear, given that a misdiagnosis could place the patient at risk for bleeding without benefit. Recent evidence, however, suggests that the risk of major bleeding is not significantly higher in cardiac arrest patients receiving thrombolysis.8 PE is difficult to diagnose in the intra-arrest setting, and when ROSC is not obtained and PE is strongly suspected, the evidence supports consideration of thrombolysis.1

These recommendations are supported by a 2020 ILCOR systematic review.1

References

1. Berg KM, Soar J, Andersen LW, Böttiger BW, Cacciola S, Callaway CW, Couper K, Cronberg T, D’Arrigo S, Deakin CD, et al.; on behalf of the Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation. 2020; 142(suppl 1):S92–S139. doi: 10.1161/CIR.0000000000000893LinkGoogle Scholar
2. Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ, Jenkins JS, Kline JA, Michaels AD, Thistlethwaite P, Vedantham S, White RJ, Zierler BKAmerican Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association.Circulation. 2011; 123:1788–1830. doi: 10.1161/CIR.0b013e318214914fLinkGoogle Scholar
3. Kürkciyan I, Meron G, Sterz F, Janata K, Domanovits H, Holzer M, Berzlanovich A, Bankl HC, Laggner AN. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome.Arch Intern Med. 2000; 160:1529–1535. doi: 10.1001/archinte.160.10.1529CrossrefMedlineGoogle Scholar
4. Courtney DM, Kline JA. Prospective use of a clinical decision rule to identify pulmonary embolism as likely cause of outpatient cardiac arrest.Resuscitation. 2005; 65:57–64. doi: 10.1016/j.resuscitation.2004.07.018CrossrefMedlineGoogle Scholar
5. Comess KA, DeRook FA, Russell ML, Tognazzi-Evans TA, Beach KW. The incidence of pulmonary embolism in unexplained sudden cardiac arrest with pulseless electrical activity.Am J Med. 2000; 109:351–356. doi: 10.1016/s0002-9343(00)00511-8CrossrefMedlineGoogle Scholar
6. Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary embolism.Chest. 2002; 121:877–905. doi: 10.1378/chest.121.3.877CrossrefMedlineGoogle Scholar
7. Böttiger BW, Arntz HR, Chamberlain DA, Bluhmki E, Belmans A, Danays T, Carli PA, Adgey JA, Bode C, Wenzel VTROICA Trial Investigators; European Resuscitation Council Study Group. Thrombolysis during resuscitation for out-of-hospital cardiac arrest.N Engl J Med. 2008; 359:2651–2662. doi: 10.1056/NEJMoa070570CrossrefMedlineGoogle Scholar
8. Javaudin F, Lascarrou JB, Le Bastard Q, Bourry Q, Latour C, De Carvalho H, Le Conte P, Escutnaire J, Hubert H, Montassier E, Leclère BResearch Group of the French National Out-of-Hospital Cardiac Arrest Registry (GR-RéAC). Thrombolysis During Resuscitation for Out-of-Hospital Cardiac Arrest Caused by Pulmonary Embolism Increases 30-Day Survival: Findings From the French National Cardiac Arrest Registry.Chest. 2019; 156:1167–1175. doi: 10.1016/j.chest.2019.07.015CrossrefMedlineGoogle Scholar
9. Yousuf T, Brinton T, Ahmed K, Iskander J, Woznicka D, Kramer J, Kopiec A, Chadaga AR, Ortiz K. Tissue Plasminogen Activator Use in Cardiac Arrest Secondary to Fulminant Pulmonary Embolism.J Clin Med Res. 2016; 8:190–195. doi: 10.14740/jocmr2452wCrossrefMedlineGoogle Scholar
10. Janata K, Holzer M, Kürkciyan I, Losert H, Riedmüller E, Pikula B, Laggner AN, Laczika K. Major bleeding complications in cardiopulmonary resuscitation: the place of thrombolytic therapy in cardiac arrest due to massive pulmonary embolism.Resuscitation. 2003; 57:49–55. doi: 10.1016/s0300-9572(02)00430-6CrossrefMedlineGoogle Scholar
11. Doerge HC, Schoendube FA, Loeser H, Walter M, Messmer BJ. Pulmonary embolectomy: review of a 15-year experience and role in the age of thrombolytic therapy.Eur J Cardiothorac Surg. 1996; 10:952–957. doi: 10.1016/s1010-7940(96)80396-4CrossrefMedlineGoogle Scholar
12. Konstantinov IE, Saxena P, Koniuszko MD, Alvarez J, Newman MA. Acute massive pulmonary embolism with cardiopulmonary resuscitation: management and results.Tex Heart Inst J. 2007; 34:41–5; discussion 45.MedlineGoogle Scholar
13. Fava M, Loyola S, Bertoni H, Dougnac A. Massive pulmonary embolism: percutaneous mechanical thrombectomy during cardiopulmonary resuscitation.J Vasc Interv Radiol. 2005; 16:119–123. doi: 10.1097/01.RVI.0000146173.85401.BACrossrefMedlineGoogle Scholar

Toxicity: Benzodiazepines

Synopsis

Benzodiazepine overdose causes CNS and respiratory depression and, particularly when taken with other sedatives (eg, opioids), can cause respiratory arrest and cardiac arrest. Flumazenil, a specific benzodiazepine antagonist, restores consciousness, protective airway reflexes, and respiratory drive but can have significant side effects including seizures and arrhythmia.1 These risks are increased in patients with benzodiazepine dependence and with coingestion of cyclic antidepressant medications. The half-life of flumazenil is shorter than many benzodiazepines, necessitating close monitoring after flumazenil administration.2 An alternative to flumazenil administration is respiratory support with bag-mask ventilation followed by ETI and mechanical ventilation until the benzodiazepine has been metabolized.

Recommendation-Specific Supportive Text

A recent meta-analysis of 13 RCTs (990 evaluable patients) found that adverse events and serious adverse events were more common in patients who were randomized to receive flumazenil than placebo (number needed to harm: 5.5 for all adverse events and 50 for serious adverse events).1 The most commonly encountered adverse events were psychiatric (anxiety, agitation, aggressive behavior); serious adverse events reported included tachycardia, supraventricular arrhythmia, premature ventricular complexes, seizures, and hypotension. Although no patient died in these clinical trials, rare cases of death associated with flumazenil administration have been reported.3,4 Administration of flumazenil to a patient with undifferentiated overdose may confer an unnecessary risk to the patient, making a focus on providing supportive care the best approach.

This topic last received formal evidence review in 2010.5

References

1. Penninga EI, Graudal N, Ladekarl MB, Jürgens G. Adverse Events Associated with Flumazenil Treatment for the Management of Suspected Benzodiazepine Intoxication–A Systematic Review with Meta-Analyses of Randomised Trials.Basic Clin Pharmacol Toxicol. 2016; 118:37–44. doi: 10.1111/bcpt.12434CrossrefMedlineGoogle Scholar
2. Bowden CA, Krenzelok EP. Clinical applications of commonly used contemporary antidotes. A US perspective.Drug Saf. 1997; 16:9–47. doi: 10.2165/00002018-199716010-00002CrossrefMedlineGoogle Scholar
3. Katz Y, Boulos M, Singer P, Rosenberg B. Cardiac arrest associated with flumazenil.BMJ. 1992; 304:1415. doi: 10.1136/bmj.304.6839.1415-bCrossrefMedlineGoogle Scholar
4. Burr W, Sandham P, Judd A. Death after flumazepil.BMJ. 1989; 298:1713. doi: 10.1136/bmj.298.6689.1713-aCrossrefMedlineGoogle Scholar
5. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S829–S861. doi: 10.1161/CIRCULATIONAHA.110.971069LinkGoogle Scholar

Toxicity: β-Adrenergic Blockers and Calcium Channel Blockers

Introduction

β-Adrenergic receptor antagonists (“β-adrenergic blockers”) and L-type calcium channel antagonists (“calcium channel blockers”) are common antihypertensive and cardiac rate control medications. Because the β-adrenergic receptor regulates the activity of the L-type calcium channel,1 overdose of these medications presents similarly, causing life-threatening hypotension and/or bradycardia that may be refractory to standard treatments such as vasopressor infusions.2,3 For patients with refractory hemodynamic instability, therapeutic options include administration of high-dose insulin, IV calcium, or glucagon, and consultation with a medical toxicologist or regional poison center can help determine the optimal therapy. Resuscitation from cardiac arrest caused by β-adrenergic blocker or calcium channel blocker overdose follows standard resuscitation guidelines.

Recommendation-Specific Supportive Text

Animal studies, case reports, and case series have reported increased heart rate and improved hemodynamics after high-dose insulin administration for β-adrenergic blocker toxicity.4–6 The typical insulin dose used in these studies is a bolus of 1 U/kg, followed by an infusion of 1 U/kg per hour titrated to clinical effect; dextrose and potassium infusions are coadministered.2,7 No controlled studies on this topic have been identified.
Although there are no controlled studies, several case reports and small case series have reported improvement in bradycardia and hypotension after glucagon administration.8–10
Limited animal data and rare case reports suggest possible utility of calcium to improve heart rate and hypotension in β-adrenergic blocker toxicity.11–13
Case reports and at least 1 retrospective observational study have been published on survival after ECMO in patients presenting with refractory shock from β-adrenergic blocker overdose.14,15 The evidence for ECMO for any cardiac arrest is very limited, but refractory shock from a reversible cause such as drug toxicity may be a situation when ECMO could convey a benefit.

Recommendation-Specific Supportive Text

No controlled studies examine the effect of IV calcium for calcium channel blocker toxicity.16 Case series and case reports have reported variable efficacy with low incidence of adverse effects. A systematic review noted consistent benefit in animal studies but inconsistent results in human reports.17–21 A 2017 expert consensus statement recommended calcium as first-line treatment for catecholamine-refractory shock from calcium channel blockers, acknowledging a very low certainty of evidence for this intervention.22
Two systematic reviews have identified animal studies, case reports, and human observational studies that have reported increased heart rate and improved hemodynamics after high-dose insulin administration for calcium channel blocker toxicity.4,16,21,23,24 As with β-adrenergic blocker overdose, the typical insulin dose used in these studies is a bolus of 1 U/kg, followed by an infusion of 1 U/kg per hour titrated to clinical effect; dextrose and potassium infusions are coadministered.2,4,7,21
Findings in both animal studies and human case reports/case series on the effect of glucagon in calcium channel blocker toxicity have been inconsistent, with some reporting increase in heart rate and some reporting no effect.21
At least 1 retrospective study on ECMO use for patients with cardiac arrest or refractory shock in the setting of drug toxicity has reported improved outcomes.14 As with all retrospective studies, the risk of bias is high because of other considerations in deciding which patients will be treated with ECMO. A recent consensus statement supports the use of ECMO for refractory shock from a reversible causes such as drug toxicity.22

References

1. van der Heyden MA, Wijnhoven TJ, Opthof T. Molecular aspects of adrenergic modulation of cardiac L-type Ca2+ channels.Cardiovasc Res. 2005; 65:28–39. doi: 10.1016/j.cardiores.2004.09.028CrossrefMedlineGoogle Scholar
2. Graudins A, Lee HM, Druda D. Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies.Br J Clin Pharmacol. 2016; 81:453–461. doi: 10.1111/bcp.12763CrossrefMedlineGoogle Scholar
3. Levine M, Curry SC, Padilla-Jones A, Ruha AM. Critical care management of verapamil and diltiazem overdose with a focus on vasopressors: a 25-year experience at a single center.Ann Emerg Med. 2013; 62:252–258. doi: 10.1016/j.annemergmed.2013.03.018CrossrefMedlineGoogle Scholar
4. Engebretsen KM, Kaczmarek KM, Morgan J, Holger JS. High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning.Clin Toxicol (Phila). 2011; 49:277–283. doi: 10.3109/15563650.2011.582471CrossrefMedlineGoogle Scholar
5. Seegobin K, Maharaj S, Deosaran A, Reddy P. Severe beta blocker and calcium channel blocker overdose: Role of high dose insulin.Am J Emerg Med. 2018; 36:736.e5–736.e6. doi: 10.1016/j.ajem.2018.01.038CrossrefGoogle Scholar
6. Doepker B, Healy W, Cortez E, Adkins EJ. High-dose insulin and intravenous lipid emulsion therapy for cardiogenic shock induced by intentional calcium-channel blocker and Beta-blocker overdose: a case series.J Emerg Med. 2014; 46:486–490. doi: 10.1016/j.jemermed.2013.08.135CrossrefMedlineGoogle Scholar
7. Holger JS, Stellpflug SJ, Cole JB, Harris CR, Engebretsen KM. High-dose insulin: a consecutive case series in toxin-induced cardiogenic shock.Clin Toxicol (Phila). 2011; 49:653–658. doi: 10.3109/15563650.2011.593522CrossrefMedlineGoogle Scholar
8. Love JN, Sachdeva DK, Bessman ES, Curtis LA, Howell JM. A potential role for glucagon in the treatment of drug-induced symptomatic bradycardia.Chest. 1998; 114:323–326. doi: 10.1378/chest.114.1.323CrossrefMedlineGoogle Scholar
9. Bailey B. Glucagon in beta-blocker and calcium channel blocker overdoses: a systematic review.J Toxicol Clin Toxicol. 2003; 41:595–602. doi: 10.1081/clt-120023761CrossrefMedlineGoogle Scholar
10. Peterson CD, Leeder JS, Sterner S. Glucagon therapy for beta-blocker overdose.Drug Intell Clin Pharm. 1984; 18:394–398. doi: 10.1177/106002808401800507CrossrefMedlineGoogle Scholar
11. Pertoldi F, D’Orlando L, Mercante WP. Electromechanical dissociation 48 hours after atenolol overdose: usefulness of calcium chloride.Ann Emerg Med. 1998; 31:777–781. doi: 10.1016/s0196-0644(98)70241-0CrossrefMedlineGoogle Scholar
12. Love JN, Hanfling D, Howell JM. Hemodynamic effects of calcium chloride in a canine model of acute propranolol intoxication.Ann Emerg Med. 1996; 28:1–6. doi: 10.1016/s0196-0644(96)70129-4CrossrefMedlineGoogle Scholar
13. Teo LK, Tham DJW, Chong CP. A case of massive atenolol overdose successfully managed with intravenous calcium chloride.East J Med. 2018; 21:213–215.CrossrefGoogle Scholar
14. Masson R, Colas V, Parienti JJ, Lehoux P, Massetti M, Charbonneau P, Saulnier F, Daubin C. A comparison of survival with and without extracorporeal life support treatment for severe poisoning due to drug intoxication.Resuscitation. 2012; 83:1413–1417. doi: 10.1016/j.resuscitation.2012.03.028CrossrefMedlineGoogle Scholar
15. Rotella JA, Greene SL, Koutsogiannis Z, Graudins A, Hung Leang Y, Kuan K, Baxter H, Bourke E, Wong A. Treatment for beta-blocker poisoning: a systematic review.Clin Toxicol (Phila). 20201–41. doi: 10.1080/15563650.2020.1752918Google Scholar
16. Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA, Thompson A, Varosy PD. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.Circulation. 2019; 140:e382–e482. doi: 10.1161/CIR.0000000000000628LinkGoogle Scholar
17. Howarth DM, Dawson AH, Smith AJ, Buckley N, Whyte IM. Calcium channel blocking drug overdose: an Australian series.Hum Exp Toxicol. 1994; 13:161–166. doi: 10.1177/096032719401300304CrossrefMedlineGoogle Scholar
18. Crump BJ, Holt DW, Vale JA. Lack of response to intravenous calcium in severe verapamil poisoning.Lancet. 1982; 2:939–940. doi: 10.1016/s0140-6736(82)90912-6CrossrefMedlineGoogle Scholar
19. Ghosh S, Sircar M. Calcium channel blocker overdose: experience with amlodipine.Indian J Crit Care Med. 2008; 12:190–193. doi: 10.4103/0972-5229.45080CrossrefMedlineGoogle Scholar
20. Henry M, Kay MM, Viccellio P. Cardiogenic shock associated with calcium-channel and beta blockers: reversal with intravenous calcium chloride.Am J Emerg Med. 1985; 3:334–336. doi: 10.1016/0735-6757(85)90060-9CrossrefMedlineGoogle Scholar
21. St-Onge M, Dubé PA, Gosselin S, Guimont C, Godwin J, Archambault PM, Chauny JM, Frenette AJ, Darveau M, Le Sage N, Poitras J, Provencher J, Juurlink DN, Blais R. Treatment for calcium channel blocker poisoning: a systematic review.Clin Toxicol (Phila). 2014; 52:926–944. doi: 10.3109/15563650.2014.965827CrossrefMedlineGoogle Scholar
22. St-Onge M, Anseeuw K, Cantrell FL, Gilchrist IC, Hantson P, Bailey B, Lavergne V, Gosselin S, Kerns W, Laliberté M, Lavonas EJ, Juurlink DN, Muscedere J, Yang CC, Sinuff T, Rieder M, Mégarbane B. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults.Crit Care Med. 2017; 45:e306–e315. doi: 10.1097/CCM.0000000000002087CrossrefMedlineGoogle Scholar
23. Greene SL, Gawarammana I, Wood DM, Jones AL, Dargan PI. Relative safety of hyperinsulinaemia/euglycaemia therapy in the management of calcium channel blocker overdose: a prospective observational study.Intensive Care Med. 2007; 33:2019–2024. doi: 10.1007/s00134-007-0768-yCrossrefMedlineGoogle Scholar
24. Espinoza TR, Bryant SM, Aks SE. Hyperinsulin therapy for calcium channel antagonist poisoning: a seven-year retrospective study.Am J Ther. 2013; 20:29–31. doi: 10.1097/MJT.0b013e31824d5fbdCrossrefMedlineGoogle Scholar

Toxicity: Cocaine

Synopsis

Cocaine toxicity can cause adverse effects on the cardiovascular system, including dysrhythmia, hypertension, tachycardia and coronary artery vasospasm, and cardiac conduction delays. These effects can also precipitate acute coronary syndrome and stroke. Human experimental data suggest that benzodiazepines (diazepam, lorazepam), alpha blockers (phentolamine), calcium channel blockers (verapamil), morphine, and nitroglycerine are all safe and potentially beneficial in the cocaine-intoxicated patient; no data are available comparing these approaches.1–5 Contradictory data surround the use of β-adrenergic blockers.6–8 Patients suffering from cocaine toxicity can deteriorate quickly depending on the amount and timing of ingestion. If cardiac arrest develops as the result of cocaine toxicity, there is no evidence to suggest deviation from standard BLS and ALS guidelines, with specific treatment strategies used in the post–cardiac arrest phase as needed if there is evidence of severe cardiotoxicity or neurotoxicity. Once ROSC is achieved, urgent consultation with a medical toxicologist or regional poison center is suggested.

Recommendation-Specific Supportive Text

No large RCT evaluating different treatment strategies for patients suffering from acute cocaine toxicity exists. A systematic review of the literature identified 5 small prospective trials, 3 retrospective studies, and multiple case reports and case series with contradictory results. Some literature reports good favorable outcomes while others report significant adverse events.9
A well-conducted human trial showed that administration of propranolol reduces coronary blood flow in patients with cocaine exposure.8 Although recent systematic reviews suggest that β-adrenergic blocker use may not be harmful,6,7 safe alternatives are available.

This topic last received formal evidence review in 2010.10

References

1. Baumann BM, Perrone J, Hornig SE, Shofer FS, Hollander JE. Randomized, double-blind, placebo-controlled trial of diazepam, nitroglycerin, or both for treatment of patients with potential cocaine-associated acute coronary syndromes.Acad Emerg Med. 2000; 7:878–885. doi: 10.1111/j.1553-2712.2000.tb02065.xCrossrefMedlineGoogle Scholar
2. Negus BH, Willard JE, Hillis LD, Glamann DB, Landau C, Snyder RW, Lange RA. Alleviation of cocaine-induced coronary vasoconstriction with intravenous verapamil.Am J Cardiol. 1994; 73:510–513. doi: 10.1016/0002-9149(94)90684-xCrossrefMedlineGoogle Scholar
3. Saland KE, Hillis LD, Lange RA, Cigarroa JE. Influence of morphine sulfate on cocaine-induced coronary vasoconstriction.Am J Cardiol. 2002; 90:810–811. doi: 10.1016/s0002-9149(02)02622-xCrossrefMedlineGoogle Scholar
4. Hollander JE, Hoffman RS, Gennis P, Fairweather P, DiSano MJ, Schumb DA, Feldman JA, Fish SS, Dyer S, Wax P. Nitroglycerin in the treatment of cocaine associated chest pain–clinical safety and efficacy.J Toxicol Clin Toxicol. 1994; 32:243–256. doi: 10.3109/15563659409017957CrossrefMedlineGoogle Scholar
5. Honderick T, Williams D, Seaberg D, Wears R. A prospective, randomized, controlled trial of benzodiazepines and nitroglycerine or nitroglycerine alone in the treatment of cocaine-associated acute coronary syndromes.Am J Emerg Med. 2003; 21:39–42. doi: 10.1053/ajem.2003.50010CrossrefMedlineGoogle Scholar
6. Pham D, Addison D, Kayani W, Misra A, Jneid H, Resar J, Lakkis N, Alam M. Outcomes of beta blocker use in cocaine-associated chest pain: a meta-analysis.Emerg Med J. 2018; 35:559–563. doi: 10.1136/emermed-2017-207065CrossrefMedlineGoogle Scholar
7. Shin D, Lee ES, Bohra C, Kongpakpaisarn K. In-Hospital and Long-Term Outcomes of Beta-Blocker Treatment in Cocaine Users: A Systematic Review and Meta-analysis.Cardiol Res. 2019; 10:40–47. doi: 10.14740/cr831CrossrefMedlineGoogle Scholar
8. Lange RA, Cigarroa RG, Flores ED, McBride W, Kim AS, Wells PJ, Bedotto JB, Danziger RS, Hillis LD. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade.Ann Intern Med. 1990; 112:897–903. doi: 10.7326/0003-4819-112-12-897CrossrefMedlineGoogle Scholar
9. Richards JR, Garber D, Laurin EG, Albertson TE, Derlet RW, Amsterdam EA, Olson KR, Ramoska EA, Lange RA. Treatment of cocaine cardiovascular toxicity: a systematic review.Clin Toxicol (Phila). 2016; 54:345–364. doi: 10.3109/15563650.2016.1142090CrossrefMedlineGoogle Scholar
10. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S829–S861. doi: 10.1161/CIRCULATIONAHA.110.971069LinkGoogle Scholar

Toxicity: Local Anesthetics

Synopsis

Local anesthetic overdose (also known as local anesthetic systemic toxicity, or LAST) is a life-threatening emergency that can present with neurotoxicity or fulminant cardiovascular collapse.1,2 The most commonly reported agents associated with LAST are bupivacaine, lidocaine, and ropivacaine.2

By definition, LAST is a special circumstance in which alternative approaches should be considered in addition to standard BLS and ALS. Case reports and animal data have suggested that IV lipid emulsion may be of benefit.2–5 LAST results in profound inhibition of voltage-gated channels (especially sodium transduction) in the cell membrane. The potential mechanisms of action of IV lipid emulsion include active shuttling of the local anesthetic drug away from the heart and brain, increased cardiac contractility, vasoconstriction, and cardioprotective effects.1

The reported incidence of LAST ranges from 0 to 2 per 1000 nerve blocks2 but appears to be decreasing as a result of increasing awareness of toxicity and improved techniques.1

Recommendation-Specific Supportive Text

Since the last time these recommendations were formally reviewed,6 several detailed systematic reviews of the literature and a practice advisory from the American Society of Regional Anesthesia and Pain Medicine have been published.1–5 There are still no published RCTs or studies with a comparison with standard resuscitative care. Human data come from approximately 100 case reports published until 2014,6 with an additional 47 separate cases in 35 articles between 2014 and November 2016, although patients in only 10 of these 47 cases received any CPR.2 In the identified cases, the results cannot easily be interpreted or attributed to IV lipid emulsion given the lack of a comparative group. The administration of IV lipid emulsion is thought to be relatively benign, although pancreatitis and acute respiratory distress syndrome have been associated with its use.7

This topic last received formal evidence review in 2015.6

References

1. Neal JM, Barrington MJ, Fettiplace MR, Gitman M, Memtsoudis SG, Morwald EE, Rubin DS, Weinberg G. The Third American Society of Regional Anesthesia and Pain Medicine Practice advisory on local anesthetic systemic toxicity: executive summary 2017.Reg Anesth Pain Med. 2018; 43:113–123. doi: 10.1097/AAP.0000000000000720CrossrefMedlineGoogle Scholar
2. Gitman M, Barrington MJ. Local Anesthetic Systemic Toxicity: A Review of Recent Case Reports and Registries.Reg Anesth Pain Med. 2018; 43:124–130. doi: 10.1097/AAP.0000000000000721MedlineGoogle Scholar
3. Cao D, Heard K, Foran M, Koyfman A. Intravenous lipid emulsion in the emergency department: a systematic review of recent literature.J Emerg Med. 2015; 48:387–397. doi: 10.1016/j.jemermed.2014.10.009CrossrefMedlineGoogle Scholar
4. Gosselin S, Hoegberg LC, Hoffman RS, Graudins A, Stork CM, Thomas SH, Stellpflug SJ, Hayes BD, Levine M, Morris M, Nesbitt-Miller A, Turgeon AF, Bailey B, Calello DP, Chuang R, Bania TC, Mégarbane B, Bhalla A, Lavergne V. Evidence-based recommendations on the use of intravenous lipid emulsion therapy in poisoning.Clin Toxicol (Phila). 2016; 54:899–923. doi: 10.1080/15563650.2016.1214275CrossrefMedlineGoogle Scholar
5. Hoegberg LC, Bania TC, Lavergne V, Bailey B, Turgeon AF, Thomas SH, Morris M, Miller-Nesbitt A, Mégarbane B, Magder S, Gosselin SLipid Emulsion Workgroup. Systematic review of the effect of intravenous lipid emulsion therapy for local anesthetic toxicity.Clin Toxicol (Phila). 2016; 54:167–193. doi: 10.3109/15563650.2015.1121270CrossrefMedlineGoogle Scholar
6. Lavonas EJ, Drennan IR, Gabrielli A, Heffner AC, Hoyte CO, Orkin AM, Sawyer KN, Donnino MW. Part 10: special circumstances of resuscitation: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S501–S518. doi: 10.1161/CIR.0000000000000264LinkGoogle Scholar
7. Levine M, Skolnik AB, Ruha AM, Bosak A, Menke N, Pizon AF. Complications following antidotal use of intravenous lipid emulsion therapy.J Med Toxicol. 2014; 10:10–14. doi: 10.1007/s13181-013-0356-1CrossrefMedlineGoogle Scholar

Toxicity: Sodium Channel Blockers, Including Tricyclic Antidepressants

Synopsis

Overdose of sodium channel–blocking medications, such as TCAs and other drugs (eg, cocaine, flecainide, citalopram), can cause hypotension, dysrhythmia, and death by blockade of cardiac sodium channels, among other mechanisms. Characteristic ECG findings include tachycardia and QRS prolongation with a right bundle branch pattern.1,2 TCA toxicity can mimic a Brugada type 1 ECG pattern.3

The standard therapy for hypotension or cardiotoxicity from sodium channel blocker poisoning consists of sodium boluses and serum alkalization, typically achieved through administration of sodium bicarbonate boluses. This approach is supported by animal studies and human case reports and has recently been systematically reviewed.4

A clinical trial studied administration of magnesium in addition to sodium bicarbonate for patients with TCA-induced hypotension, acidosis, and/or QRS prolongation.5 Although overall outcomes were better in the magnesium group, no statistically significant effect was found in mortality, the magnesium patients were significantly less ill than controls at study entry, and methodologic flaws render this work preliminary.

Although case reports describe good outcomes after the use of ECMO6 and IV lipid emulsion therapy7–10 for severe sodium channel blocker cardiotoxicity, no controlled human studies could be found, and limited animal data do not support lipid emulsion efficacy.11

No human controlled studies were found evaluating treatment of cardiac arrest due to TCA toxicity, although 1 study demonstrated termination of amitriptyline-induced VT in dogs.12

Recommendation-Specific Supportive Text

The administration of hypertonic (8.4%, 1 mEq/mL) sodium bicarbonate solution for treatment of sodium channel blockade due to TCAs and other toxicants is supported by human observational studies13,14 and animal experiments.12,15–22 This literature has recently been systematically reviewed.4 Although dose-finding studies are not available, an initial dose of 1 to 2 mEq/kg (1–2 mL/kg of 1 mEq/mL [8.4%]) sodium bicarbonate, repeated as needed to achieve clinical stability while avoiding extreme hypernatremia or alkalemia) has historically been recommended and appears effective.
Case reports support the use of ECMO for patients with refractory shock due to TCA toxicity.23,24 Although the overall evidence for ECPR to improve outcomes is limited, because TCA toxicity is a reversible cause of cardiogenic shock/cardiac arrest, use of ECPR/ECMO in patients with life-threatening toxicity refractory to other therapy is logical.

This topic last received formal evidence review in 2010.25

References

1. Harrigan RA, Brady WJ. ECG abnormalities in tricyclic antidepressant ingestion.Am J Emerg Med. 1999; 17:387–393. doi: 10.1016/s0735-6757(99)90094-3CrossrefMedlineGoogle Scholar
2. Thanacoody HK, Thomas SH. Tricyclic antidepressant poisoning: cardiovascular toxicity.Toxicol Rev. 2005; 24:205–214. doi: 10.2165/00139709-200524030-00013CrossrefMedlineGoogle Scholar
3. Bebarta VS, Phillips S, Eberhardt A, Calihan KJ, Waksman JC, Heard K. Incidence of Brugada electrocardiographic pattern and outcomes of these patients after intentional tricyclic antidepressant ingestion.Am J Cardiol. 2007; 100:656–660. doi: 10.1016/j.amjcard.2007.03.077CrossrefMedlineGoogle Scholar
4. Bruccoleri RE, Burns MM. A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening.J Med Toxicol. 2016; 12:121–129. doi: 10.1007/s13181-015-0483-yCrossrefMedlineGoogle Scholar
5. Emamhadi M, Mostafazadeh B, Hassanijirdehi M. Tricyclic antidepressant poisoning treated by magnesium sulfate: a randomized, clinical trial.Drug Chem Toxicol. 2012; 35:300–303. doi: 10.3109/01480545.2011.614249CrossrefMedlineGoogle Scholar
6. Koschny R, Lutz M, Seckinger J, Schwenger V, Stremmel W, Eisenbach C. Extracorporeal life support and plasmapheresis in a case of severe polyintoxication.J Emerg Med. 2014; 47:527–531. doi: 10.1016/j.jemermed.2014.04.044CrossrefMedlineGoogle Scholar
7. Kiberd MB, Minor SF. Lipid therapy for the treatment of a refractory amitriptyline overdose.CJEM. 2012; 14:193–197. doi: 10.2310/8000.2011.110486CrossrefMedlineGoogle Scholar
8. Agarwala R, Ahmed SZ, Wiegand TJ. Prolonged use of intravenous lipid emulsion in a severe tricyclic antidepressant overdose.J Med Toxicol. 2014; 10:210–214. doi: 10.1007/s13181-013-0353-4CrossrefMedlineGoogle Scholar
9. Cao D, Heard K, Foran M, Koyfman A. Intravenous lipid emulsion in the emergency department: a systematic review of recent literature.J Emerg Med. 2015; 48:387–397. doi: 10.1016/j.jemermed.2014.10.009CrossrefMedlineGoogle Scholar
10. Odigwe CC, Tariq M, Kotecha T, Mustafa U, Senussi N, Ikwu I, Bhattarcharya A, Ngene JI, Ojiako K, Iroegbu N. Tricyclic antidepressant overdose treated with adjunctive lipid rescue and plasmapheresis.Proc (Bayl Univ Med Cent). 2016; 29:284–287. doi: 10.1080/08998280.2016.11929437CrossrefMedlineGoogle Scholar
11. Varney SM, Bebarta VS, Vargas TE, Boudreau S, Castaneda M. Intravenous lipid emulsion therapy does not improve hypotension compared to sodium bicarbonate for tricyclic antidepressant toxicity: a randomized, controlled pilot study in a swine model.Acad Emerg Med. 2014; 21:1212–1219. doi: 10.1111/acem.12513CrossrefMedlineGoogle Scholar
12. Sasyniuk BI, Jhamandas V, Valois M. Experimental amitriptyline intoxication: treatment of cardiac toxicity with sodium bicarbonate.Ann Emerg Med. 1986; 15:1052–1059. doi: 10.1016/s0196-0644(86)80128-7CrossrefMedlineGoogle Scholar
13. Köppel C, Wiegreffe A, Tenczer J. Clinical course, therapy, outcome and analytical data in amitriptyline and combined amitriptyline/chlordiazepoxide overdose.Hum Exp Toxicol. 1992; 11:458–465. doi: 10.1177/096032719201100604CrossrefMedlineGoogle Scholar
14. Hoffman JR, Votey SR, Bayer M, Silver L. Effect of hypertonic sodium bicarbonate in the treatment of moderate-to-severe cyclic antidepressant overdose.Am J Emerg Med. 1993; 11:336–341. doi: 10.1016/0735-6757(93)90163-6CrossrefMedlineGoogle Scholar
15. Brown TC. Tricyclic antidepressant overdosage: experimental studies on the management of circulatory complications.Clin Toxicol. 1976; 9:255–272. doi: 10.3109/15563657608988129CrossrefMedlineGoogle Scholar
16. Nattel S, Mittleman M. Treatment of ventricular tachyarrhythmias resulting from amitriptyline toxicity in dogs.J Pharmacol Exp Ther. 1984; 231:430–435.MedlineGoogle Scholar
17. Pentel P, Benowitz N. Efficacy and mechanism of action of sodium bicarbonate in the treatment of desipramine toxicity in rats.J Pharmacol Exp Ther. 1984; 230:12–19.MedlineGoogle Scholar
18. Hedges JR, Baker PB, Tasset JJ, Otten EJ, Dalsey WC, Syverud SA. Bicarbonate therapy for the cardiovascular toxicity of amitriptyline in an animal model.J Emerg Med. 1985; 3:253–260. doi: 10.1016/0736-4679(85)90427-5CrossrefMedlineGoogle Scholar
19. Knudsen K, Abrahamsson J. Epinephrine and sodium bicarbonate independently and additively increase survival in experimental amitriptyline poisoning.Crit Care Med. 1997; 25:669–674. doi: 10.1097/00003246-199704000-00019CrossrefMedlineGoogle Scholar
20. Tobis JM, Aronow WS. Effect of amitriptyline antidotes on repetitive extrasystole threshold.Clin Pharmacol Ther. 1980; 27:602–606. doi: 10.1038/clpt.1980.85CrossrefMedlineGoogle Scholar
21. McCabe JL, Cobaugh DJ, Menegazzi JJ, Fata J. Experimental tricyclic antidepressant toxicity: a randomized, controlled comparison of hypertonic saline solution, sodium bicarbonate, and hyperventilation.Ann Emerg Med. 1998; 323 Pt 1329–333. doi: 10.1016/s0196-0644(98)70009-5CrossrefMedlineGoogle Scholar
22. Bou-Abboud E, Nattel S. Relative role of alkalosis and sodium ions in reversal of class I antiarrhythmic drug-induced sodium channel blockade by sodium bicarbonate.Circulation. 1996; 94:1954–1961. doi: 10.1161/01.cir.94.8.1954LinkGoogle Scholar
23. Goodwin DA, Lally KP, Null DM. Extracorporeal membrane oxygenation support for cardiac dysfunction from tricyclic antidepressant overdose.Crit Care Med. 1993; 21:625–627. doi: 10.1097/00003246-199304000-00025CrossrefMedlineGoogle Scholar
24. de Lange DW, Sikma MA, Meulenbelt J. Extracorporeal membrane oxygenation in the treatment of poisoned patients.Clin Toxicol (Phila). 2013; 51:385–393. doi: 10.3109/15563650.2013.800876CrossrefMedlineGoogle Scholar
25. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S829–S861. doi: 10.1161/CIRCULATIONAHA.110.971069LinkGoogle Scholar

Toxicity: Carbon Monoxide, Digoxin, and Cyanide

Synopsis

Digoxin poisoning can cause severe bradycardia, AV nodal blockade, and life-threatening ventricular arrhythmias. Poisoning from other cardiac glycosides, such as oleander, foxglove, and digitoxin, have similar effects. Prompt treatment of cardiac glycoside toxicity is imperative to prevent or treat life-threatening arrhythmias.

Carbon monoxide poisoning reduces the ability of hemoglobin to deliver oxygen and also causes direct cellular damage to the brain and myocardium, leading to death or long-term risk of neurological and myocardial injury. Although cardiac arrest due to carbon monoxide poisoning is almost always fatal, studies about neurological sequelae from less-severe carbon monoxide poisoning may be relevant.

The toxicity of cyanide is predominantly due to the cessation of aerobic cell metabolism. Cyanide reversibly binds to the ferric ion cytochrome oxidase in the mitochondria and stops cellular respiration and adenosine triphosphate production. Cyanide poisoning may result from smoke inhalation, industrial exposures, self-poisoning, terrorism, or the administration of sodium nitroprusside. Symptoms typically occur within minutes, and findings may include arrhythmias, apnea, hypotension with bradycardia, seizures, and cardiovascular collapse.1 Lactic acidosis is a sensitive and specific finding.2,3 Immediate antidotes include hydroxocobalamin and nitrites; however, the former has a much better safety profile. Sodium thiosulfate enhances the effectiveness of nitrites by enhancing the detoxification of cyanide, though its role in patients treated with hydroxocobalamin is less certain.4 Novel antidotes are in development.

Recommendation-Specific Supportive Text

There are no data evaluating the use of antidotes to digoxin overdose specifically in the setting of cardiac arrest. Data from 1 RCT5 and 4 case series6–9 concluded that antidigoxin Fab fragments are safe and effective for the treatment of serious cardiac arrhythmias induced by digitalis and other cardiac glycoside overdose.
Few patients who develop cardiac arrest from carbon monoxide poisoning survive to hospital discharge, regardless of the treatment administered after ROSC, though rare good outcomes have been described.10–12 Clinical trials of hyperbaric oxygen therapy to prevent neurological injury from carbon monoxide poisoning yield conflicting results; patients with cardiac arrest were excluded from all trials.13,14 Hyperbaric oxygen therapy has a low incidence of side effects.
Several studies demonstrate that patients with known or suspected cyanide toxicity presenting with cardiovascular instability or cardiac arrest who undergo prompt treatment with IV hydroxocobalamin, a cyanide scavenger,2,15–19 can have reversal of life-threatening toxicity. Whether the addition of sodium thiosulfate, a cofactor for cyanide metabolism, enhances the antidotal effect of hydroxocobalamin is controversial. Four studies in animals20–23 and 2 studies in humans2,24 demonstrated enhanced effectiveness of hydroxocobalamin when sodium thiosulfate was coadministered, though this is not the case in other models.4

This topic last received formal evidence review in 2010.25

References

1. Parker-Cote JL, Rizer J, Vakkalanka JP, Rege SV, Holstege CP. Challenges in the diagnosis of acute cyanide poisoning.Clin Toxicol (Phila). 2018; 56:609–617. doi: 10.1080/15563650.2018.1435886CrossrefMedlineGoogle Scholar
2. Baud FJ, Barriot P, Toffis V, Riou B, Vicaut E, Lecarpentier Y, Bourdon R, Astier A, Bismuth C. Elevated blood cyanide concentrations in victims of smoke inhalation.N Engl J Med. 1991; 325:1761–1766. doi: 10.1056/NEJM199112193252502CrossrefMedlineGoogle Scholar
3. Baud FJ, Borron SW, Bavoux E, Astier A, Hoffman JR. Relation between plasma lactate and blood cyanide concentrations in acute cyanide poisoning.BMJ. 1996; 312:26–27. doi: 10.1136/bmj.312.7022.26CrossrefMedlineGoogle Scholar
4. Bebarta VS, Pitotti RL, Dixon P, Lairet JR, Bush A, Tanen DA. Hydroxocobalamin versus sodium thiosulfate for the treatment of acute cyanide toxicity in a swine (Sus scrofa) model.Ann Emerg Med. 2012; 59:532–539. doi: 10.1016/j.annemergmed.2012.01.022CrossrefMedlineGoogle Scholar
5. Eddleston M, Rajapakse S, Rajakanthan , Jayalath S, Sjöström L, Santharaj W, Thenabadu PN, Sheriff MH, Warrell DA. Anti-digoxin Fab fragments in cardiotoxicity induced by ingestion of yellow oleander: a randomised controlled trial.Lancet. 2000; 355:967–972. doi: 10.1016/s0140-6736(00)90014-xCrossrefMedlineGoogle Scholar
6. Smith TW, Butler VP, Haber E, Fozzard H, Marcus FI, Bremner WF, Schulman IC, Phillips A. Treatment of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments: experience in 26 cases.N Engl J Med. 1982; 307:1357–1362. doi: 10.1056/NEJM198211253072201CrossrefMedlineGoogle Scholar
7. Antman EM, Wenger TL, Butler VP, Haber E, Smith TW. Treatment of 150 cases of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments. Final report of a multicenter study.Circulation. 1990; 81:1744–1752. doi: 10.1161/01.cir.81.6.1744LinkGoogle Scholar
8. Wenger TL, Butler VP, Haber E, Smith TW. Treatment of 63 severely digitalis-toxic patients with digoxin-specific antibody fragments.J Am Coll Cardiol. 1985; 5(suppl A):118A–123A. doi: 10.1016/s0735-1097(85)80471-xCrossrefMedlineGoogle Scholar
9. Hickey AR, Wenger TL, Carpenter VP, Tilson HH, Hlatky MA, Furberg CD, Kirkpatrick CH, Strauss HC, Smith TW. Digoxin Immune Fab therapy in the management of digitalis intoxication: safety and efficacy results of an observational surveillance study.J Am Coll Cardiol. 1991; 17:590–598. doi: 10.1016/s0735-1097(10)80170-6CrossrefMedlineGoogle Scholar
10. Hampson NB, Zmaeff JL. Outcome of patients experiencing cardiac arrest with carbon monoxide poisoning treated with hyperbaric oxygen.Ann Emerg Med. 2001; 38:36–41. doi: 10.1067/mem.2001.115532CrossrefMedlineGoogle Scholar
11. Sloan EP, Murphy DG, Hart R, Cooper MA, Turnbull T, Barreca RS, Ellerson B. Complications and protocol considerations in carbon monoxide-poisoned patients who require hyperbaric oxygen therapy: report from a ten-year experience.Ann Emerg Med. 1989; 18:629–634. doi: 10.1016/s0196-0644(89)80516-5CrossrefMedlineGoogle Scholar
12. Mumma BE, Shellenbarger D, Callaway CW, Katz KD, Guyette FX, Rittenberger JC. Neurologic recovery following cardiac arrest due to carbon monoxide poisoning.Resuscitation. 2009; 80:835. doi: 10.1016/j.resuscitation.2009.03.027CrossrefMedlineGoogle Scholar
13. Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning.Cochrane Database Syst Rev. 2011CD002041. doi: 10.1002/14651858.CD002041.pub3MedlineGoogle Scholar
14. American College of Emergency Physicians Clinical Policies Subcommittee on Carbon Monoxide Poisoning. Wolf SJ, Maloney GE, Shih RD, Shy BD, Brown MD. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute carbon monoxide poisoning.Ann Emerg Med. 2017; 69:98.e6–107.e6. doi: 10.1016/j.annemergmed.2016.11.003Google Scholar
15. Borron SW, Baud FJ, Barriot P, Imbert M, Bismuth C. Prospective study of hydroxocobalamin for acute cyanide poisoning in smoke inhalation.Ann Emerg Med. 2007; 49:794–801, 801.e1. doi: 10.1016/j.annemergmed.2007.01.026CrossrefMedlineGoogle Scholar
16. Fortin JL, Giocanti JP, Ruttimann M, Kowalski JJ. Prehospital administration of hydroxocobalamin for smoke inhalation-associated cyanide poisoning: 8 years of experience in the Paris Fire Brigade.Clin Toxicol (Phila). 2006; 44(suppl 1):37–44. doi: 10.1080/15563650600811870CrossrefMedlineGoogle Scholar
17. Borron SW, Baud FJ, Mégarbane B, Bismuth C. Hydroxocobalamin for severe acute cyanide poisoning by ingestion or inhalation.Am J Emerg Med. 2007; 25:551–558. doi: 10.1016/j.ajem.2006.10.010CrossrefMedlineGoogle Scholar
18. Houeto P, Hoffman JR, Imbert M, Levillain P, Baud FJ. Relation of blood cyanide to plasma cyanocobalamin concentration after a fixed dose of hydroxocobalamin in cyanide poisoning.Lancet. 1995; 346:605–608. doi: 10.1016/s0140-6736(95)91437-4CrossrefMedlineGoogle Scholar
19. Espinoza OB, Perez M, Ramirez MS. Bitter cassava poisoning in eight children: a case report.Vet Hum Toxicol. 1992; 34:65.MedlineGoogle Scholar
20. Hall AH, Rumack BH. Hydroxycobalamin/sodium thiosulfate as a cyanide antidote.J Emerg Med. 1987; 5:115–121. doi: 10.1016/0736-4679(87)90074-6CrossrefMedlineGoogle Scholar
21. Höbel M, Engeser P, Nemeth L, Pill J. The antidote effect of thiosulphate and hydroxocobalamin in formation of nitroprusside intoxication of rabbits.Arch Toxicol. 1980; 46:207–213. doi: 10.1007/BF00310436CrossrefMedlineGoogle Scholar
22. Mengel K, Krämer W, Isert B, Friedberg KD. Thiosulphate and hydroxocobalamin prophylaxis in progressive cyanide poisoning in guinea-pigs.Toxicology. 1989; 54:335–342. doi: 10.1016/0300-483x(89)90068-1CrossrefMedlineGoogle Scholar
23. Friedberg KD, Shukla UR. The efficiency of aquocobalamine as an antidote in cyanide poisoning when given alone or combined with sodium thiosulfate.Arch Toxicol. 1975; 33:103–113. doi: 10.1007/BF00353235CrossrefMedlineGoogle Scholar
24. Forsyth JC, Mueller PD, Becker CE, Osterloh J, Benowitz NL, Rumack BH, Hall AH. Hydroxocobalamin as a cyanide antidote: safety, efficacy and pharmacokinetics in heavily smoking normal volunteers.J Toxicol Clin Toxicol. 1993; 31:277–294. doi: 10.3109/15563659309000395CrossrefMedlineGoogle Scholar
25. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2010; 122(suppl 3):S829–S861. doi: 10.1161/CIRCULATIONAHA.110.971069LinkGoogle Scholar

Knowledge Gaps and Priorities of Research

As part of the overall work for development of these guidelines, the writing group was able to review a large amount of literature concerning the management of adult cardiac arrest. One expected challenge faced through this process was the lack of data in many areas of cardiac arrest research. This challenge was faced in both the 2010 Guidelines and 2015 Guidelines Update processes, where only a small percent of guideline recommendations (1%) were based on high-grade LOE (A) and nearly three quarters were based on low-grade LOE (C).1

Similar challenges were faced in the 2020 Guidelines process, where a number of critical knowledge gaps were identified in adult cardiac arrest management. These topics were identified as not only areas where no information was identified but also where the results of ongoing research could impact the recommendation directly. Throughout the recommendation-specific text, the need for specific research is identified to facilitate the next steps in the evolution of these questions.

Critical knowledge gaps are summarized in Table 4.

Table 4. 2020 Adult Guidelines Critical Knowledge Gaps

Sequence of Resuscitation
Initiation of resuscitation	What are optimal strategies to enhance lay rescuer performance of CPR?
Metrics for high-quality CPR	What is optimal for the CPR duty cycle (the proportion of time spent in compression relative to the total time of the compression-plus-decompression cycle)?
Metrics for high-quality CPR	What is the validity and reliability of ETCO2 in nonintubated patients?
Metrics for high-quality CPR	For patients with an arterial line in place, does targeting CPR to a particular blood pressure improve outcomes?
Metrics for high-quality CPR	How does integrated team performance, as opposed to performance on individual resuscitation skills, affect resuscitation outcomes?
Defibrillation	Is there an ideal time in the CPR cycle for defibrillator charging?
Defibrillation	Can artifact-filtering algorithms for analysis of ECG rhythms during CPR in a real-time clinical setting decrease pauses in chest compressions and improve outcomes?
Defibrillation	Does preshock waveform analysis lead to improved outcome?
Defibrillation	Do double sequential defibrillation and/or alternative defibrillator pad positioning affect outcome in cardiac arrest with shockable rhythm?
Vascular access	Is the IO route of drug administration safe and efficacious in cardiac arrest, and does efficacy vary by IO site?
Vasopressor medications during cardiac arrest	Does epinephrine, when administered early after cardiac arrest, improve survival with favorable neurological outcome?
Nonvasopressor medications during cardiac arrest	Do antiarrhythmic drugs, when given in combination for cardiac arrest, improve outcomes from cardiac arrest with shockable rhythm?
Nonvasopressor medications during cardiac arrest	Do prophylactic antiarrhythmic medications on ROSC after successful defibrillation decrease arrhythmia recurrence and improve outcome?
Nonvasopressor medications during cardiac arrest	Do steroids improve shock or other outcomes in patients who remain hypotensive after ROSC?
Adjuncts to CPR	Does the use of point-of-care cardiac ultrasound during cardiac arrest improve outcomes?
Adjuncts to CPR	Is targeting a specific ETCO2 value during CPR beneficial, and what degree of rise in ETCO2 indicates ROSC?
Termination of resuscitation	Can ETCO2 be used for intra-arrest prognostication, in combination with other metrics?
Termination of resuscitation	Can point-of-care cardiac ultrasound, in conjunction with other factors, inform termination of resuscitation?
Advanced Techniques and Devices for Resuscitation
Advanced airway placement	What is the optimal approach to advanced airway management for IHCA?
Advanced airway placement	There is a need for further research specifically on the interface between patient factors and the experience, training, tools, and skills of the provider when choosing an approach to airway management.
Advanced airway placement	What is the specific type, amount, and interval between airway management training experiences to maintain proficiency?
Alternative CPR techniques and devices	Which populations are most likely to benefit from ECPR?
Specific Arrhythmia Management
Atrial fibrillation or flutter with rapid ventricular response	What is the optimal energy needed for cardioversion of atrial fibrillation and atrial flutter?
Bradycardia	What is the optimal approach, vasopressor or transcutaneous pacing, in managing symptomatic bradycardia?
Care After ROSC
Postresuscitation care	Does avoidance of hyperoxia in the postarrest period lead to improved outcomes?
Postresuscitation care	What is the effect of hypocarbia or hypercarbia on outcome after cardiac arrest?
Postresuscitation care	Does the treatment of nonconvulsive seizures, common in postarrest patients, improve patient outcomes?
Postresuscitation care	What are the optimal pharmacological treatment regimens for the management of postarrest seizures?
Postresuscitation care	Do neuroprotective agents improve favorable neurological outcome after arrest?
Postresuscitation care	What is the most efficacious management approach for postarrest cardiogenic shock, including pharmacological, catheter intervention, or implantable device?
Postresuscitation care	Is there a role for prophylactic antiarrhythmics after ROSC?
Targeted temperature management	Does targeted temperature management, compared to strict normothermia, improve outcomes?
Targeted temperature management	What is the optimal temperature goal for targeted temperature management?
Targeted temperature management	What is the optimal duration for targeted temperature management before rewarming?
Targeted temperature management	What is the best approach to rewarming postarrest patients after treatment with targeted temperature management?
PCI after cardiac arrest	Does emergent PCI for patients with ROSC after VF/VT cardiac arrest and no STEMI but with signs of shock or electric instability improve outcomes?
Neuroprognostication	What is the interrater agreement for physical examination findings such as pupillary light reflex, corneal reflex, and myoclonus/status myoclonus?
Neuroprognostication	Can we identify consistent NSE and S100B thresholds for predicting poor neurological outcome after cardiac arrest?
Neuroprognostication	Are NSE and S100B helpful when checked later than 72 h after ROSC?
Neuroprognostication	Are glial fibrillary acidic protein, serum tau protein, and neurofilament light chain valuable for neuroprognostication?
Neuroprognostication	More uniform definitions for status epilepticus, malignant EEG patterns, and other EEG patterns are needed to be able to compare prognostic values across studies.
Neuroprognostication	What is the optimal timing for head CT for prognostication?
Neuroprognostication	Is there a consistent threshold value for prognostication for GWR or ADC?
Neuroprognostication	Standardization of methods for quantifying GWR and ADC would be useful.
Recovery
Recovery and survivorship after cardiac arrest	What do survivor-derived outcome measures of the impact of cardiac arrest survival look like, and how do they differ from current generic or clinician-derived measures?
Recovery and survivorship after cardiac arrest	Are there in-hospital interventions that can reduce or prevent physical impairment after cardiac arrest?
Recovery and survivorship after cardiac arrest	Which patients develop affective/psychological disorders of well-being after cardiac arrest, and are they treatable/preventable/recoverable?
Recovery and survivorship after cardiac arrest	Does hospital-based protocolized discharge planning for cardiac arrest survivors improve access to/referral to rehabilitation services or patient outcomes?
Special Circumstances of Resuscitation
Accidental hypothermia	What combination of features can identify patients with no chance of survival, even if rewarmed?
Accidental hypothermia	Should severely hypothermic patients receive intubation and mechanical ventilation or simply warm humidified oxygen?
Accidental hypothermia	Should severely hypothermic patients in VF who fail an initial defibrillation attempt receive additional defibrillation?
Accidental hypothermia	Should severely hypothermic patients in cardiac arrest receive epinephrine or other resuscitation medications? If so, what dose and schedule should be used?
Drowning	In what situations is attempted resuscitation of the drowning victim futile?
Drowning	How long after mild drowning events should patients be observed for late-onset respiratory effects?
Electrolyte abnormalities	What is the optimal treatment for hyperkalemia with life-threatening arrhythmia or cardiac arrest?
Opioid overdose	What is the minimum safe observation period after reversal of respiratory depression from opioid overdose with naloxone? Does this vary based on the opioid involved?
Opioid overdose	Is there benefit to naloxone administration in patients with opioid-associated cardiac arrest who are receiving CPR with ventilation?
Opioid overdose	What is the ideal initial dose of naloxone in a setting where fentanyl and fentanyl analogues are responsible for a large proportion of opioid overdose?
Opioid overdose	In cases of suspected opioid overdose managed by a non–healthcare provider who is not capable of reliably checking a pulse, is initiation of CPR beneficial?
Pregnancy	What is the ideal timing of PMCD for a pregnant woman in cardiac arrest?
Pulmonary embolism	Which patients with cardiac arrest due to “suspected” pulmonary embolism benefit from emergency thrombolysis during resuscitation?
Toxicity: β-adrenergic blockers and calcium channel blockers	What is the ideal sequencing of modalities (traditional vasopressors, calcium, glucagon, high-dose insulin) for refractory shock due to β-adrenergic blocker or calcium channel blocker overdose?
Toxicity: local anesthetics	What are the ideal dose and formulation of IV lipid emulsion therapy?
Toxicity: carbon monoxide, digoxin, and cyanide	Which patients with cyanide poisoning benefit from antidotal therapy?
Toxicity: carbon monoxide, digoxin, and cyanide	Does sodium thiosulfate provide additional benefit to patients with cyanide poisoning who are treated with hydroxocobalamin?

References

1. Morrison LJ, Gent LM, Lang E, Nunnally ME, Parker MJ, Callaway CW, Nadkarni VM, Fernandez AR, Billi JE, Egan JR, et al.. Part 2: evidence evaluation and management of conflicts of interest: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Circulation. 2015; 132(suppl 2):S368–S382. doi: 10.1161/CIR.0000000000000253LinkGoogle Scholar

Article Information

The American Heart Association requests that this document be cited as follows: Panchal AR, Bartos JA, Cabañas JG, Donnino MW, Drennan IR, Hirsch KG, Kudenchuk PJ, Kurz MC, Lavonas EJ, Morley PT, O’Neil BJ, Peberdy MA, Rittenberger JC, Rodriguez AJ, Sawyer KN, Berg KM; on behalf of the Adult Basic and Advanced Life Support Writing Group. Part 3: adult basic and advanced life support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020;142(suppl 2):S366–S468. doi: 10.1161/CIR.0000000000000916

Acknowledgments

The writing group acknowledges the following contributors: Julie Arafeh, RN, MSN; Justin L. Benoit, MD, MS; Maureen Chase; MD, MPH; Antonio Fernandez; Edison Ferreira de Paiva, MD, PhD; Bryan L. Fischberg, NRP; Gustavo E. Flores, MD, EMT-P; Peter Fromm, MPH, RN; Raul Gazmuri, MD, PhD; Blayke Courtney Gibson, MD; Theresa Hoadley, MD, PhD; Cindy H. Hsu, MD, PhD; Mahmoud Issa, MD; Adam Kessler, DO; Mark S. Link, MD; David J. Magid, MD, MPH; Keith Marrill, MD; Tonia Nicholson, MBBS; Joseph P. Ornato, MD; Garrett Pacheco, MD; Michael Parr, MB; Rahul Pawar, MBBS, MD; James Jaxton, MD; Sarah M. Perman, MD, MSCE; James Pribble, MD; Derek Robinett, MD; Daniel Rolston, MD; Comilla Sasson, MD, PhD; Sree Veena Satyapriya, MD; Travis Sharkey, MD, PhD; Jasmeet Soar, MA, MB, BChir; Deb Torman, MBA, MEd, AT, ATC, EMT-P; Benjamin Von Schweinitz; Anezi Uzendu, MD; and Carolyn M. Zelop, MD.

The writing group would also like to acknowledge the outstanding contributions of David J. Magid, MD, MPH.

Disclosures

Appendix 1. Writing Group Disclosures

Writing Group MemberEmploymentResearch GrantOther Research SupportSpeakers’ Bureau/HonorariaExpert WitnessOwnership InterestConsultant/Advisory BoardOther

Ashish R. Panchal	The Ohio State University	None	None	None	None	None	None	None
Katherine M. Berg	Beth Israel Deaconess Medical Center	NHLBI Grant K23 HL128814†	None	None	None	None	None	None
Jason A. Bartos	University of Minnesota	None	None	None	None	None	None	Abbott Labs; Biotronik Inc; Edwards Lifesciences Corp; Inari Medical, Inc; Maquet Cardiovascular US Sales, LLC; Stryker Corp; Zoll Circulation, Inc*
José G. Cabañas	Wake County Emergency Medical Services	None	None	None	None	None	None	None
Michael W. Donnino	Beth Israel Deaconess Med Center	NIH†; General Electric; Kaneka (Investigator-initiated)	None	Speaking engagements with respect to cardiac arrest topics*	None	None	None	None
Ian R. Drennan	Sunnybrook Health Sciences Center (Canada)	None	None	None	None	None	None	None
Karen G. Hirsch	Stanford University	NIH (Salary support for research activities in cardiac arrest); AHA (Salary support for research related to cardiac arrest)	None	None	None	None	None	None
Peter J. Kudenchuk	University of Washington	NIH (PI at my institution for the SIREN Network)†	None	None	None	None	None	None
Michael C. Kurz	University of Alabama at Birmingham	DOD (DSMB member for PACT trial); NIH (CO-I for R21 examining mast cell degranulation in OHCA)	None	Zoll Medical Corp*	None	None	Zoll Circulation, Inc†	Zoll Circulation, Inc†
Eric J. Lavonas	Denver Health Emergency Medicine	BTG Pharmaceuticals (Denver Health (Dr Lavonas’ employer) has research, call center, consulting, and teaching agreements with BTG Pharmaceuticals. BTG manufactures the digoxin antidote, DigiFab. Dr Lavonas does not receive bonus or incentive compensation, and these agreements involve an unrelated product. When these guidelines were developed, Dr Lavonas recused from discussions related to digoxin poisoning.)†	None	None	None	None	None	American Heart Association (Senior Science Editor)†
Peter T. Morley	University of Melbourne, Royal Melbourne Hospital (Australia)	None	None	None	None	None	None	None
Brian J. O’Neil	Wayne State University	SIREN Network (Clinical trial network through NHLBI)*	None	Zoll circulation; Genentech	None	None	None	None
Mary Ann Peberdy	Virginia Commonwealth University	None	None	None	None	None	None	None
Jon C. Rittenberger	Guthrie Medical Center	NIH- SIREN (ICECAP Trial); AHA (Grant In Aid)	None	None	Bailey Glasser*	None	Hibernaid, LLC*	None
Amber J. Rodriguez	American Heart Association	None	None	None	None	None	None	None
Kelly N. Sawyer	University of Pittsburgh	None	None	None	None	None	None	None

Appendix 2. Reviewer Disclosures

ReviewerEmploymentResearch GrantOther Research SupportSpeakers’ Bureau/HonorariaExpert WitnessOwnership InterestConsultant/Advisory BoardOther

Clifton Callaway	University of Pittsburgh	NIH (Grants to study emergency care, including treatment of cardiac arrest and cardiac emergencies)†	None	None	None	None	None	None
Alix Carter	Dalhousie University (Canada)	Maritime Heart (descriptive factors survival ohca)*	None	None	None	None	None	None
Henry Halperin	Johns Hopkins University	Zoll Circulation (CPR research)†; NIH (CPR research)†	None	None	None	None	None	None
Timothy Henry	The Christ Hospital	None	None	None	None	None	None	None
Jonathan Jui	Oregon Health and Science University	NIH (HL 126938)*	None	None	None	None	None	None
Tommaso Pellis	AAS 5 Friuli Occidentale (Italy)	None	None	None	None	None	None	None
Fred Severyn	Denver Health and Hospital Authority; University of Colorado Anschutz Medical Campus; University of Arkansas for Medical Sciences	None	None	None	None	None	None	None
Andrew H. Travers	Emergency Health Services, Nova Scotia (Canada)	None	None	None	None	None	None	None

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Is a CPR card the same as BLS?

What's the Difference Between BLS and CPR Certification? CPR is taught in BLS certification classes, but since BLS certification is intended for healthcare professionals, the class is more in-depth than traditional CPR training.

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Upon completion of all course requirements, participants receive a BLS Provider Course Completion Card which is valid for two years.

What is a BLS eCard?

The BLS Provider eCard is the electronic equivalent of the BLS Provider printed course completion card and can be provided to students as an alternative to a printed card. It certifies that the student has successfully completed the BLS course. Issued according to AHA ECC Guidelines.