2025+AHA心肺复苏与心血管急救指南-第9部分：成人高级生命支持

PREAMBLE

In the United States, cardiac arrest remains a significant public health challenge. The incidence of EMS-treated OHCA is 83.4 individuals per 100000 population an-nually.1 Despite advancements in resuscitation sci-ence, training, and systems of care, survival to hospital discharge after EMS-treated OHCA remains low, at approximately 10%. Immediate interventions, such as high-quality CPR and timely defibrillation, are crucial for improving outcomes.

In-hospital cardiac arrest(IHCA) occurs in approximately 1 in 100 hospitalized adults. Data indicates that about 72.2% of these patients achieve return of spontaneous circulation(ROSC), with survival to hospital discharge rates around 24.2%.Among those who survive to discharge, approximately 85% have favorable neurological outcomes. These statistics underscore the importance of ALS interventions, including advanced airway management, pharmacologic therapies, and coordinated postresuscitation care, in both prehospital and in-hospital settings.

The International Liaison Committee on Resuscitation(ILCOR) emphasizes the "Formula for Survival," which identifies 3 critical components for improved outcomes:guidelines based on sound science, effective educa-tion of resuscitation professionals, and well-functioning systems of care.2 The 2025 ALS guidelines build upon these principles by incorporating the latest evidence, pro-moting high-quality education for ALS professionals, and describing the critical decisions required to provide life-saving emergency cardiovascular care.

This document outlines the American Heart Association(AHA) recommendations for ALS interventions, drawing from rigorous evidence evaluation and expert consensus. Recom-mendations are tailored to the scope and practice of ALS

<EndOfPara>profession's, focusing on enhancing survival and functional recovery. The 2025 ALS guidelines aim to provide a frame-work for continued advancements in resuscitation science while highlighting areas for future research and innovation.

REFERENCES

1. Martin SS,Aday AW,Allen NB,Almarzoq ZI,Anderson CAM,Arora P,Avery CL,Baker-Smith CM, Bansal N,Beaton AZ,et al; American Heart Asso-ciation Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Committee. 2025 Heart disease and stroke statistics: a report of US and global data from the American Heart Association. Circula-tion.2025;151:e41-e660.doi:10.1161/CIR.0000000000001303

2.Soreide E, Morrison L, Hillman K, Monsieurs K, Sunde K, Zideman D, Eisenberg M, Sterz F, Nadckarni VM, Soar J, et al; Utstein Formula for Sur-vival Collaborators.The formula for survival in resuscitation. Resuscitation.2013;84:1487-1493.doi:10.1016/j.resuscitation.2013.07.020

INTRODUCTION TO THE 2025 ALS GUIDELINES

Scope of the Guidelines

The 2025 ALS guidelines provide evidence-based rec-ommendations for health care professionals managing adult cardiac arrest and life-threatening cardiovascular emergencies. These guidelines are tailored to profes-sionals with advanced training in resuscitation tech-niques, incorporating a wide range of pharmacologic and device-based therapies and critical interventions to opti-mize survival and neurological outcomes.

This document complements the separately published 2025 BLS guidelines, which address foundational resusci-tation practices for lay rescuers and BLS- and ALS-trained health care professionals. Importantly, the ALS guidelines address prehospital resuscucci, in-hospital resuscitation,and TOR recommendations when resuscitation has been unsuccessful. There is a recognition that in the literature there is differential use of the terms return of spontaneous circulation(ROSC) versus return of circulation. For the pur-poses of these guidelines, after CPR, when return of circu-lation is achieved by mechanical means(eg, extracorporeal membrane oxygenation), we use return of circulation; when due to cardiac function, we use ROSC. Specific recommen-dations about the training of ALS resuscitation professionals are provided in Part 12: Resuscitation Education Science,1 recommendations about incorporating ALS professionals or procedures into systems of care are provided in Part 4:Systems of Care,2 recommendations about caring for the adult patient following ROSCC are provided in Part 11: Post-Cardiac Arrest Care, ${}^{3}$ and recommendations about ethical considerations in delivering or withholding ALS care are pro-vided in Part 3: Ethical Considerations of Resuscitation. ${}^{4}$

Organization of the Writing Group

The ALS Writing Group included experts in emergency medicine, EMS, cardiology, critical care, public health, nurs-

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ing, and education, along with AHA staff and science editors. Members disclosed potential conflicts of interest before and every 90 days during appointment, aligning with the AHA's policies to ensure unbiased guideline development. Disclo-sure information for writing group members is in Appendix 1.

METHODOLOGY AND EVIDENCE REVIEW

These guidelines are based on evidence evaluation con-ducted by the ALS Writing Group.5 Evidence review process-es included systematic reviews, scoping reviews, and annual focused evidence updates, composed by ILCOR, affiliates,and individual Writing Group Members, to support robust and transparent guideline development. Each of these resulted in a description of the literature and exhaustive discussion among Writing Group members that facilitated guideline de-velopment. Details of evidence evaluation can be found in Part 2: Evidence Evaluation and Guidelines Development.6

Class of Recommendation and Level of Evidence

Each recommendation in the 2025 ALS guidelines is as-signed a Class of Recommendation(COR) to reflect its strength and a Level of Evidence (LOE). The LOE is based on the quality, quantity,relevance, and consistency of the available evidence. In determining the COR, the writing group considered the LOE and other factors, including systems is-sues, economic factors, and ethical factors such as equity,acceptability, and feasibility. Criteria for each COR and LOE are described in Table 1. For further explanation, refer to Part 2:Evidence Evaluation and Guidelines Development6

Guideline Structure

The 2025 ALS guidelines are organized into knowledge chunks, which are modular, and organized into sections addressing specific clinical topics.7 Each module includes a table of recommendations, a brief synopsis, supporting rationale, and references. Flow diagrams and tables clarify the cascade of clinical decision-making, and hyperlinked references provide access to studies and resources.

Document Review and Approval

Each section of the 2025 ALS guidelines underwent rigor-ous review by subject matter experts and independent peer reviewers. 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. Donoghue A,Auerbach M,Banerjee A,Blewer A,Cheng A,Kadlec K,Lin Y, Diederich E,Sawyer T, Stallings D, et al. Part 12: resuscitation educa

tion science: 2025 American Heart Association Guidelines for Cardio-

2. Dezufian C, Cabafas JG, Buckley JR, Cash RE, Crowe RP, Drennan IR,Mahgoub M, Mannarino CR, May T, Salcido DD, et al. Part 4: systems of care:2025 American Heart Association Guidelines for Cardiopulmonary Resus-citation and Emergency Cardiovascular Care. Circulation. 2025;152(suppl 2):S353-S384. doi:10.1161/CIR.000000000001378

3. Hirsch KG,Amorim E,Coppler PJ,Drennan IR,Elliott A,Gordon AJ,Jentzer JC,Johnson NJ,Moskowitz A,et al.Part 11:post-cardiac arrest care:2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation.2025;152(suppl 2):S718. doi:10.1161/CIR.00000000000001375

4. Elmer J, Atkins DL, Davisya MR, Del Rios M, Fry JT, Henderson CM,Lewis-Newby M, Madrigal VN, Marco CA, Ornato JP, et al. Part 3: ethics:2025 American Heart Association Guidelines for Cardiopulmonary Resus-citation and Emergency Cardiovascular Care. Circulation. 2025;152(suppl 2):S323-S325. doi: 10.1161/CIR.0000000000001371

5.Berg KM,Bray JE,Ng KC,Liley HG,Freif R,Carlson J,Norley PT,Drennan IR,Smyth M, Scholefield BR,et al; Collaborators.2023 International Consen-sus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Carecity With Treatment Recommendations: Summary From the Basic Life Support; Advanced Life Support; Pediatric Life Support; Neonatal Life Support; Education, Implementation, and Teams; and First Aid Task Forces. Cir-culation.2023;148:e187-e280. doi: 10.1161/CIR.000000000001179

6. Panchal AR, Bartos JA, Wyckoff MH, Drennan IR, Mahgoub M, Schexnayder SM, Rodriguez AJ, Sasson C, Wright JI, Brooks SC, et al. Part 2: evi-dence evaluation and guidelines development: 2025 American Heart As-sociation Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025;152(suppl 2):S313-S322. doi:10.1161/CIR0000000000000000000000000000000000000000000

7. Levine GN,O'Gara PT,Beckman JA, Al-Khatib SM, Birtcher KK, Cigarro AE, de las Fuentes L, Deswal A, Fleisher LA, Gentile F, et al. Recent In-novations, Modifications, and Evolution of ACC/AHA Clinical Practice Guidelines: An Update for Our Constituencies: A Report of the Ameri-can College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;139:8793-e886. doi: 10.1161/CIR.000000000000000651

DEFIBRILLATION

|Recommendations for Defibrillation Indication, Type, and Energy|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|B-NR|1. In adult patients with cardiac arrest, defibrillators (using biphasic or monophasic waveforms) are recommended to treat tachyarrhythmias requiring a shock such as ventricular fibrillation or pulseless ventricular tachycardia.|| |2a|B-R|2. Biphasic waveform defibrillation is preferred over monophasic waveform defibrillation for treatment of tachyarrhythmias in adult patients with cardiac arrest.|| |2a|B-NR|3. A single shock strategy is preferred to stacked shocks for defibrillation in adult patients with cardiac arrest.|| |2a|C-LD|4. It is reasonable that selection of fixed versus escalating energy levels for subsequent shocks for adults in cardiac arrest with presumed shock refractory arrhythmias be based on the specific manufacturer's instructions for that waveform.|| |2b|B-R|5. If using a defibrillator capable of escalating ener-gies, higher energy for second and subsequent shocks may be considered if the initial shock fails to restore a perfusing rhythm in adult patients with cardiac arrest.|| |2b|C-LD|6. In the absence of conclusive evidence that one bi- phasic waveform is superior to another in termina-tion of ventricular fibrillation, it may be reasonable close the manufacturer's recommended energy dose for the first shock in adult patients with car- diac arrest. If this is not known, defibrillation at the maximal dose may be considered.||

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Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care(updated December 2024)**

CLASS(STRENGTH) OF RECOMMENDATION

Class 1 (STRONG)

Benefit >>> Risk

Suggested phrases for writing recommendations:

• Is recommended

• Is indicated/useful/effective/beneficial

● Should be performed/administered/other

• Comparative-Effectiveness Phrases†:

- Treatment/strategy A is recommended/indicated in preference to treatment B

- Treatment A should be chosen over treatment B

Class 2a(MODERATE)

Benefit >> Risk

Suggested phrases for writing recommendations:

• Is reasonable

• Can be useful/effective/beneficial

• Comparative-Effectiveness Phrases $\dagger$

- Treatment/strategy A is probably recommended/indicated in preference to treatment B

It is reasonable to choose treatment A over treatment B

Class 2b (WEAK)

Benefit ≥ Risk

(Expert Opinion)

Suggested phrases for writing recommendations:

● May/might be reasonable

● May/might be considered

•Usefulness/effectiveness is unknown/unclear/uncertain or not well-established

Class 3: No Benefit(MODERATE)Benefit= Risk(Generally,LOE A or B use only)

Suggested phrases for writing recommendations:

• Is not recommended

• Is not indicated/useful/effective/beneficial

● Should not be performed/administered/other

Class 3: HARM(STRONG)

Risk > Benefit

Suggested phrases for writing recommendations:

• Potentially harmful

· Causes harm

$\bullet$ Associated with excess morbidity/mortality

$\dot{C}$ Should not be performed/administered/other

LEVEL(QUALITY) OF EVIDENCE#

Event A

•High-quality evidence\# from more than 1 RCT

•Meta-analyses of high-quality RCTs

•One or more RCTs corroborated by high-quality registry studies

Level B-R

(Randomized)

• Moderate-quality evidence $\neq$ from 1 or more RCTs

•Meta-analyses of moderate-quality RCTs

Level B-NR

(Nonrandomized)

•Moderate-quality evidence≠ from 1 or more well-designed, well-executed nonrandomized studies,observational studies, or registry studies

• Meta-analyses of such studies

(Limited Data)

Level C-LD

• Randomized or nonrandomized observational or registry studies with limitations of design or execution

•Meta-analyses of such studies

•Physiological or mechanistic studies in human subjects

Level C-EO

(Expert Opinion)

● Consensus of expert opinion based on clinical experience

COR 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.

* The outcome or result of the intervention should be specified (an improved clinical outcome or increased diagnostic accuracy or incremental prognostic information).

+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.

$\ddagger$ 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.

COR indicates Class of Recommendation; EO, expert opinion;LD, limited data; LOE, Level of Evidence; NR, nonrandomized;R,randomized; and RCT,randomized controlled trial.

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Synopsis

Along with CPR, early defibrillation is critical to survival when sudden cardiac arrest is caused by ventricular fi-brillation or pulseless ventricular tachycardia(VF/pVT).1,2 Defibrillation is most successful when administered as soon as possible after the onset of VF/pVT. Conversely,when VF/pVT is prolonged,depletion of the heart's ener-gy reserves can compromise the efficacy of defibrillation unless replenished by a prescribed period of CPR be-fore rhythm analysis. Figure 1 describes the algorithm for performing shocks and other ALS interventions. Minimiz-ing disruptions in CPR surrounding shock administration is a high priority. Currently marketed defibrillators use proprietary shock waveforms that differ in their electri-cal characteristics. These deliver different peak currents even at the same programmed energy setting, making comparisons of shock efficacy between devices chal-

lenging. Technologies have been developed to diagnose the underlying cardiac rhythm during CPR and to derive prognostic information from the ventricular waveform that may guide patient management. These technologies require further validation before routine use.

While investigations continue to evaluate the optimal waveform and current, escalating energy may also be effective in termination of VF or pVT. Furthermore, opti-mized pad placement for defibrillation is an important factor in shock success (see Recommendation-Specific Supportive Text, items 4 and 5, and the section Vector Change and Double Sequential Defibrillation).

Recommendation-Specific Supportive Text

1.Emergent electric defibrillation is highly effec-tive at terminating VF/pVT and other hemody-namic destabilizing tachyarrhythmias(please

 Figure 1. Adult Cardiac Arrest Circular Algorithm.

CPR indicates cardiopulmonary resuscitation; ET, endotracheal; IO, intraosseous; IV, intravenous pVT, pulseless ventricular tachycardia; and VF,ventricular fibrillation.

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see sections on wide-complex and narrow-complex tachycardias or atrial fibrillation/flutter as appropriate).

2. Biphasic waveform defibrillators(which deliver pulses of opposite polarity) expose patients to a much lower peak electric current with equiv-alent or greater efficacy for terminating atrial3 and ventricular tachyarrhythmias than mono-phasic(single polarity) defibrillators.4-10 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 were last commercially manufactured in the late 1990s, however, some may still be in use.

3.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 upon several con-siderations. 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,$11$ 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.12-14 It is unknown whether stacked shocks or single shocks are more effective in settings of a monitored witnessed arrest, spe-cifically, an in-patient cardiac arrest or cardiac arrest after cardiac surgery where the rhythm change is monitored in real time.(See the sec-tion on cardiac arrest after cardiac surgery in Part 10.15)

<BeginOfPara>4 and 5.Commercially available defibrillators either pro-vide fixed energy settings or allow for escalat-ing energy settings; both approaches are highly effective in terminating VF/pVT.16 An optimal energy setting for initial or subsequent bipha-sic defibrillation, whether fixed or escalating,has not been identified and is best deferred to the defibrillator's manufacturer. When a manu-facturer's specified setting is unknown, another approach is to apply the maximum dose setting for that device. A randomized trial comparing fixed 150 J biphasic defibrillation with escalat-ing higher shock energies(200-300-360 J)observed similar rates of successful defibril-lation 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. ${ }^{17}$ An observational study com-paring fixed 200 J biphasic defibrillation against escalating (2000-300-360 J) shocks had simi-lar findings. ${ }^{18}$ Different strategies to increase current delivery from biphasic waveform shock have been described, including optimizing pad-skin contact, applying manual pressure to pads during shock delivery (with appropriate self-protective insulation precautions), or vector change of pads. Vector change and double sequential defibrillation are described below. ${ }^{19}$

6. There is no conclusive evidence of superiority of one biphasic shock waveform over another for defibrillation.20 Given the variability in elec-tric characteristics between proprietary biphasic waveforms, energy settings are prespecified by the manufacturer for each specific device.

REFERENCES

1. Swor RA,Jackson RE,Cynar M, Sadler E,Basse E,Boji B,Rivera-Rivera EJ,Maher A,Grubb W,Jacobson R.Bustander 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)70207-5

2. Larsen MP, Eisenberg MS, Cummins RO, Hallstrom AP. Predicting surviv-al from out-of-hospital cardiac arrest: a graphic model. Ann Emerg Med.1993;22:1652-1658. doi: 10.1016/s0196-0644(05)81302-2

3.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. Resuscita-tion.2016;100:66-75. doi:10.1016/j.resuscitation.2015.12.009

4.White RD,Hankins DG,Bugliosi TF. Seven years' experience with early defi-brillation by police and paramamedics in an emergency medical services system.Resuscitation.1998;39:145-151.doi:10.1016/s0300-9572(98)00135-x

5. van Alem AP, Chapman FW, Lank P, Hart A, Koster RW. A prospective,randomised and blinded comparison of first shock success of monopha-sic and biphasic waveforms in out-of-hospital cardiac arrest. Resuscitation.2003;58:17-24. doi:10.1016/s0300-9572(03)00106-0

6.Schneider T, Martens PR, Paschen H, Kuisma M, Wolcke B, Gliner BE,Russell JK, Weaver WD, Bossaert L, Chamberlain D. Multicenter, random-ized, controlled trial of 150-J biphasic shocks compared with 200- to 360-J monphasic shocks in the resuscitation of out-of-hospital cardiac arrest vic-tims. Optimized Response to Cardiac Arrestic ORCA) Investigators. Circula-tion.2000;102:1780-1787. doi: 10.1161/01.cir.102.15.1780

7. Morrison LJ, Dorian P, Long J, Vermeulen M, Schwartz B, Sawadsky B,Frank J,Cameron B,Burgess R,Shield J,et al; Steering Committee,Central Vali-dation Committee, Safety and Efficacy Committee. Out-of-hospital cardiac arrest-restrectilinear biphasic to monophasic damped sine defibrillation wave-forms with advanced life support intervention trial(ORBIT). Resuscitation.2005;66:149-157. doi: 10.1016/j.resuscitation.2004.11.031

8. Leng CT, Paradis NA, Calkins H, Berger RD, Lardo AC, Rent KC, Halperin HR.Resuscitation after prolonged ventricular fibrillation with use of mono-phasic and biphasic waveform pulses for external defibrillation. Circulation.2000;101:2968-2974.doci:10.1161/01.cir.101.25968

9.Higgins SL, O'grady SG, Banville I, Chapman FW, Schmitt PW, Lank P,Walker RG, lina M. Efficiency of lower-energy biphasic shocks for trans-thoracic defibrillation: a follow-up clinical study. Prehosp Emerg Care.2004;8:262-267. doi: 10.1016/j.prehos.2004.02.002

10.Didon JP, Fontaine G, White RD, Jekova I, Schmid JJ, Cansell A. Clini-cal experience with a follow-energy pulsed biphasic waveform in out-of-hospital cardiac arrest. Resuscitation.2008;76:350-353. doi:10.1016/j.resuscitation.2007.08.010

11. Koster RW, Walker RG, Chapman FW. Recurrent ventricular fi-brillation during advanced life support care of patients with pre-hospital cardiac arrest. Resuscitation.2008;78:252-257. doi:10.1016/j.resuscitation.2008.03.231

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12. Rea TD, Helbock M, Perry S, Garcia M, Lloyd D, Becker L, Eisenberg M. In-creasing use of cardiopulmonary resuscitation during out-of-hostal expentric-ular fibrillation arrest: survival implications of guideline changes. Circulation.2006;114:2760-2765: doi:10.1016/CIRCULATIONAHA.106.654715

13. Jost D, Degrange H, Verret C, Hersan O, Berville IL, Chapman FW, Lankar P, Petit JL, Fuilla C, Migliar R, et al: DEFI 2005 Work Group. DEFI 2005: a randomized controlled trial of the effect of automated exter-nal defibrillator cardiopulmonary resuscitation on outcome from out-of-hospital cardiac arrest. Circulation. 2010;121:1614-1622. doi: 10.1161/CIRCULATIONAHA.107:887898

14. 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.299.10.1158

15. Cao D,Arens AM,Chow SL,Easter SR,Hoffman RS,Lagina AT,Lavonas EJ, Patil KD, Sutherland LD, Tsjissen JA, et al Part 10: adult and pe-diatric special circumstances of resuscitation: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergen-cy Cardiovascular Care. Circulation. 2025;152(suppl) 2:S578-S672. doi: 10.1161/CIR000000000000001378

16. Hess EP, Russell JK, Liu PY, White RD. A high peak current 150-J fixed-energy defibrillation protocol treats recurrent ventricular fibrilla-tion (VF) as effectively as initial VF. Resuscitation. 2008:79:28-33; doi: 10.1016/j.resuscitation.2008.04.028

17. Stiell IG, Walker RG, Nesbitt LP,Chapman FW, Cousineau D,Christenson J,Bradford P, Sookram, S Berringer R, Lank P et al. BlPHASIC trial: a random-ized 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.106.648204

18. Tang H,Wu R,Lin H,Wo J,Zhu J,HShengyong X,U.XeJ(Escalating vs fixed energy defibrillation in-out of hospital cardiac arrest ventricular fibrillation. JAMA Netw Open 2005;B-E285711.40,109.282045.7411

19.Deakin CD,Sado DM,Petley GW,Clewlow F. Determining the optimal pad-die force for external defibrillation. Am J Cardiol. 20029:812-813. doi: 10.1016/s0002-9149(02)02623-1

20. Morrison LJ,Henry RM,Ku V,Nolan JP,Morley P,Deakin CD.Single-shock defibration success in adult cardiac arrest: a systematic review. Resuscita-tion.2013;84:1480-1486. doi:10.1016/j.resuscitation.2013.07.008

ANCILLARY WAVEFORM TECHNOLOGY

|Recommendations for Ancillary Waveform Technology||| |---|---|---| |COR|LOE|Recommendations| |2b|C-LD|1. The effectiveness of artifact-filtering algorithms for analysis of electrocardiogram rhythms during chest compressions for adults in cardiac arrest has not been established.| |2b|L-D|2. The effectiveness of VF waveform analysis to guide the acute management of adults with car diac arrest has not been established.|

Synopsis

CPR obscures interpretation of the underlying rhythm because of the artifact created by chest compressions on the electrocardiogram. This makes it difficult to plan the next step of care and can potentially delay or even misdirect drug therapies if given empirically(blindly) on the basis of the patient's presumed, but not actual, under-lying rhythm.Time taken for rhythm analysis also disrupts CPR. Artifact-filtering and other innovative techniques to identify the underlying rhythm beneath ongoing CPR can surmount these challenges and minimize interruptions in chest compressions while offering a diagnostic advan-tage to better direct therapies.1-6 These still require fur-ther testing and validation before routine use.

Recommendation-Specific Supportive Text

1.Despite the theoretical advantages, no study has evaluated artifact-filtering technologies in a real-time clinical setting or validated their clini-cal effectiveness compared to current resuscita-tion strategies. At present, filtering algorithms are strictly used for visual(manual) rhythm interpreta-tion and not for automated VF/VT rhythm detec-tion in automated external defibrillators during ongoing CPR. Further investigation and clinical validation are necessary before these technologies are adopted into routine clinical practice. ${}^{7}$

2. The electric characteristics of the VF waveform are known to change over time.8 VF waveform analy-sis may be of value in predicting the success of defibrillation or other therapies during the course of resuscitation.9-11 The prospect of basing thera-pies 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 stan-dard shock-first protocol with a waveform analy-sis-guided shock algorithm was underpowered,however, observed no difference in ROSC.12 The consensus of the writing group is that there is cur-rently 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.

REFERENCES

1. Tan Q, Freeman GA, Geheb F, Bisera J. Electrocardiographic analy-sis during uninterrupted cardiopulmonary resuscitation. Crit Care Med.2008;36:S409-S412. doi: 10.1097/ccm.Ob013e31818a7fbf

2. 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.2011.2118755

3.Li Y,Bisera J,Tang W,Weil MH,Automatic detection of ventricular fibrilla-tion to guide cardiopulmonary resuscitation. Crit Pathw Cardiol.2007;6:131-134. doi: 10.1097/HPC.0b013e31813429b0

4.Hu Y,Tang H,Liu C,Jing D,Zhu H,Zhang Y,Yu X,Zhang G,Xu J.The perfor-mance of a new shock advisory algorithm to reduce interruptions during CPR.Resuscitation.2019;143:1-9. doi:10.1016/j.resuscitation.2019.07.026

5. Fumagalli F, Silver AE, Tan Q, Zaidi N, Ristagno G. Cardiac rhythm analy-sis during ongoing cardiopulmonary resuscitation using the Analysis Dur-ing Compressions with Fast Reconfirmation technology. Heart Rhythm 2018;15:248-255. doi: 10.1016/j.hrthm.201709.003

6. Babaeizadeh S, Froozabadi R, Han C, Helfenbein ED. Analyzing car-diac rhythm in the presence of chest compression artifact for au-tomated shock advisory. J Electrocardiol. 2014;47:798-803. doi:10.1016/j.jelectrocard.2014.07021

7. Berg KM, Soar J, Anderen LW, Bottiger BW, Cacciola S, Callaway CW,Couper K, Cronberg T, D'Arrigo S, Deakin CD, et al; Adult Advanced Life Support Collaborators. Adult Advanced Life Support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardio-vascular Care Science With Treatment Recommendations. Circulation 2020;142:S92-S139.doi: 10.1161/CIR.00000000000893

8. Asano Y, Davidenko JM, Baxter WT, Gray RA, Jalife J. Optical map-ping of drug-induced polymorphic arrhythmias and torsade de pointes

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in the isolated rabbit heart. J Am Coll Cardiol. 1997;29:831-842. doi:10.1016/s0735-109(96)0078-5088

9.Coult J, Kwok H, Sherman L, Blackwood J, Kudenchuk PJ, Rea TD. Ven-tricular fibrillation waveform measures combined with prior shock outcome predict defibrillation success during cardiopulmonary resuscitation. J Elec-trocardiol.2018;51:99-106. doi:10.1016/j.jielectrocard.2017.07:016

10.Couft J, Blackwood J, Sherman L, Rea TD, Kudenchuk PJ, Kwok H. Ventricular Bibrillation Waveform Analysis During Chest Comressions to Predict Survival From Cardiac Arrest. Circ Arrhythm Electrophysiol.2019;12:e006924. doi:10.1161/CIRCEP118.006924.

11. Callaway CW, Sherman LD, Mosesso VN Jr., Dietrich TJ, Holt E, Clarkson. SC, Scaling exponent predicts defibrillation success for out-of-hospital ventricular fibrillation cardiac arrest. Circulation.2001;103:1656-1661. doi: 10.1161/01.cir.103.12.1656

12. Ruggeri L, Fumagali F, Bemasconi F, Semeraro F, Meessen J, Blanda A,Migliari M, Magliocca A, Gordini G, Fumagali R, et al. Amplitude Spectrum Area of ventricular fibrillation to guide defibrillation: a small open-label,pseudo-randomized controlled multicenter trial. EBioMedicine 2023;90:104544. doi: 10.1016/j.ebiom.2023.104544

VECTOR CHANGE AND DOUBLE SEQUENTIAL DEFIBRILLATION

|Recommendations for Vector Change and Double Sequential Defibrillation|||| |---|---|---|---| |2B||LOE|Recommendations| |2b||B-R|1. The usefulness of vector change for adults in cardiac arrest with persisting VF/pT after≥3 con-secutive shocks has not been established.| |2b||B-R|2. The usefulness of double sequential defibrillation for adults in cardiac arrest with persisting VF/ pVT after≥3 consecutive shocks has not been established.|

Synopsis

Combined with CPR, successful defibrillation is essential to survival from cardiac arrest caused by VF/VT.12 Defi-brillation delivers shock energy(joules), creating a current across the thorax from pad-to-pad.3 Its success is influ-enced by a variety of factors independent of energy setting,including the electrical resistance of tissues encountered(typically highest at the skin-pad interface) that can dra-matically reduce current delivery,4-7 pad positions(and re-sulting shock“vector”) that encompass the heart anatomi-cally8-11 and concomitant high quality CPR. When these are all properly managed, biphasic shock can be highly ef-fective(>75% success) in terminating VF/pVT.12,13

“Shock-resistant” and“shock-refractory” are com-monly used to describe VF/pVT that continues to be seen on rhythm checks after repeated shocks. In some cases this is due to true failure of shock to terminate VF/pVT,resulting on ongoing, incessant VF/pVT. Causes of such shock failure can be related to correctable deficiencies in defibrillation technique that are best addressed before employing alternate shock strategies such as pad reposi-tioning(vector change) or double sequential defibrillation(DSD). Conversely, evidence indicates a far more com-mon mechanism for VF/pVT that continues to be seen on post-shock rhythm checks(≈80% of instances) is not due to shock failure, but rather to VF/pVT's recurrence

following successful termination by shock, an event that is obscured by the ensuing period of CPR. When CPR is later paused for rhythm/pulse checks, VF/pVT then seen is attributed to shock failure rather than to its recurrence after successful termination, which is more often the actual case.12,14,15 This distinction is impor-tant since recurrent VF/pVT may be better remedied by post-shock rhythm stabilization therapy rather than alter-ing an already successful defibrillation technique. Thus labels like“shock-refractory” can be misleading when they conflate different mechanisms for post-shock VF/pVT, for which different treatment strategies may be required. Accordingly, we propose using“persisting VF/pVT" in these guidelines for patients who remain in VF/pVT arrest after≥3 consecutive shocks, when its actual mechanism(issant VF/pVT due to true shock failure vs recurrent VF/pVT following successful termination by shock) is not known with certainty.

Recommendation-Specific Supportive Text

1 and 2. Prior systematic reviews of low-quality evidence have not reported benefit from DSD for persist-ing VF.16-20 Defibrillator pad relocation, called vector change(VC), an inherent feature of DSD,was evaluated in only one trial as a stand-alone measure. That trial(DOSE-VF), compared stan-dard defibrillation, VC, and DSD in patients with cardiac arrest in whom VF continued to be seen on rhythm checks after 3 standard shocks. It found significant improvement in survival at hospital dis-charge with VC and DSD compared to standard defibrillation by intention-to-treat, but notably not when trial findings were analyzed by the treatment strategy patients actually received.21 Furthermore,in a secondary exploratory analysis a significant survival benefit from DSD was only observed in the 17% of study patients in whom VF was incessant,and not in the vast majority (83\%) of patients in whom VF recurred after a successful shock.22 The interval between each sequential "double" shock required for successfully terminating VF has also been shown experimentally23,24 and demonstrated in DOSE-VF itself25 to require a level of precision(separated by milliseconds) unlikely to be con-sistently achievable by manual activation of two defibrillators. Based on its review, ILCOR's 2023 International Consensus on CPR and Emergency Cardiovascular Care Science With Treatment Recommendations(CoSTR) judged the overall supportive evidence as relatively weak when issu-ing "may be considered" recommendations for VC and DSD.26 The adoption of VC or DSD into routine clinical practice for persisting VF/pVT(by whatever mechanism) thus requires further inves-tigation, given its diagnostic and technological requirements.27 These include technologies that can reliably distinguish recurrent from incessant

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post-shock VF during ongoing CPR,28 provide the precise timing interval needed between shocks,and best direct if, how, when, and in whom such a strategy may be applicable.

REFERENCES

1. Swar RA,Jackson RE,Cynar M,Sadler E,Basse E,Boji B,Rivera-Riva 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)70207-5

2. 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/s10196-0644(95)81302-2

3. Kerber RE, Martins JB, Kienke MG, Constantin L, Olshansky B, Hopson R, Charbonnier F. Energy, current, and success in defibrillation and cardioversion: clinical studies using an automated impedance-based method of energy adjustment. Circulation. 1988;77:1038-1046. doi:10.1161/01/cir77.1038

4. Kerber RE, Kouba C, Martins J, Kelly K, Low R, Hoyt R, Ferguson D, Bailey L. Bennett P. Charbonnier F. Advance prediction of transthoracic impedance in human defibrillation and cardioversion: importance of impedance in deter-mining the success of low-energy shocks. Circulation. 1984;70:303-308. doi: 10.1161/01.jcr.702.203

5. Li W Li J, Wei L, Wang J, Peng L, Wang J, Yin C, Li Y. A framework of current based defibrillation improves defibrillation efficacy of biphasic truncated exponential waveform in rabbits. Sci Rep. 2021;1158:1968. doi: 10.1038/s41598-020-80521-9

6. Squara F, Ebaum C, Garrett R, Liprandi C, Dunset, SS Mossaz B,Rocher M, Bateau J, Mocer P, et al. Active compression versus standard anterior-posterior defibrillation for external cardioversion of atrial fibrillation: 201064246464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646464646

7. Sira SJ, Ferguson DW, Charbonnier F, Kerber RE. Factors affecting transthoracic impedance during electrical cardiovalliver. Amn J Cardiol.1988;62:1048-1052. doi:10.1016/0002-9149(88)90546-2

8. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Car-diovascular Care. Part 6: advanced cardiovascular life support: section 2:defibrillation. The American Heart Association in collaboration with the Inter-national License Committee on Resuscitation. Circulation: 2000;102:190-194.

9. Koster RW, Walker RG, Chapman FF. Current Ventricular fi-brillation during advanced life support care of patients with pre-hospital cardiac arrest. Resuscitation. 2008;78:252-957. doi:10.1016/j.resuscitation.2008.03.231

10.Esibov A, Chapman FW, Melnick SB, Sullivan JL, Walcott GP. Minor Varia-tions in Electrode Pad Placement Impact Defibrillation. Successov. Prehap Emerg Care.2016;20:292-298. doi: 10.3109/10903127.2015.1076095

11.Yeh KH,Chang HC,Lin J.PF. Paddle position and contact force: an important step to check when troubleshooting for refractory ven-tricular fibrillation. Hong Kong J Emerg Med.2016;23:289-292. doi:10.1177/102497016920300506

29. SpIMs, D. Kiekenap J, Rupp D, Betz S, Kill C, Sassen MC. Time to change the times? Time of recurrence of centrifibrular fibrillation during OHACR. Re-suscitation:2020157:219-224 doi:10.1016/j.resuscitation:202009.0299

13. Verkaik BJ, Walker RG,Taylor TG, Ekelk MM, Mar R,ystie R, Gelsin R, van Eeden VGM, Doeleman LC, Hulleman M, Chapman FW, et al. Defibrillation and refractory ventricular fibrillation. Eur Heart J. 2024;46:582-584. doi:10.1093/eurheart/ehae767

14. van Alem AP, Poster K. WRF 成r. WRF occurrence: characteristics and patient outcome in out-of-hospital cardiac arrest. Resuscitation.2003;59:181-188.doi:10.1016/s0300-9572(03)00208-9

15. Bhandari S, Doan J, Blackwood J., Cout J. Kudenchuk P, Sherman L.Rea T, Kwok H. Rhythmia prores and survival after out-of-hospital ven-tricular fibrillation cardiac arrest. Resuscitation. 2018;125:22-27. doi:10.1016/j.resuscitation.2018;0.01.037

16. Miraglia D, Ramzy M. Double external defibrillation for shock-refractory ventricular fibrillation cardiac arrest: A step towards standardization. Am J Emerg Med.2021;41:73-79. doi:10.1016/j.ajem.2020.12.031

17. Li Y, He X, Li Z, Li D, Yuan X, Yang J. Double sequential external defibrilla-tion versus standard defibrillation in refractory ventricular fibrillation: A sys-tematic review and meta-analysis. Front Cardiovasc Med. 2022;9:1017935. doi: 10.3389/fcvm.2022.1017935

18. Delorenzo A, Nehme Z, Yates J, Bernard S, Smith K. Double sequential extera defibrillation for refractory ventricular fibrillation out-of-hospital cardiac arrest: A systematic review and meta-analysis. Resuscitation.2019;135:124-129. doi:10.1016/j.resuscitation.2018.10.025

19. Deakin CD, Morley P, Soar J, Drennan IR. Double (dual) sequential defibril lation for refractory ventricular fibrillation cardiac arrest: A systematic review.Resuscitation:2020;155:24-31.doi:10.1016/j.resuscitation.2020.06.008

20.Abuelaz TM, Ghanem A, Katamesh BE, Hassan AR, Abdalshafy H, Seri AR, Awad AK, Abdelnabeloi M, Abdelazemee B. Defibrillation strategies for refractory ventricular fibrillation out- of-hospital cardiac arrest: A system-atic review and network meta-analysis. Ann Noninvasive Electrocardi.2023;28:e13075. doi: 10.1111/anec.13075

21. Cheskes S, Verbeek PR, Drennan IR, McLeod SL, Turner L, Pinto R, Feldman M,Davis M, Vaillancourt C, Morrison LJ,et al. Defibrillation Strategies for Re-fractory Ventricular Fibrillation. N Engl J Med.2022;387:1947-1956. doi:10.1056/NEMoo2207304

22. Cheskes S, Drenn IR, Turner L, Pandit SV, Dorian P. The impact of alternate defibrillation strategies on shock-refractory and recur-vent ventricular fibrillation: A secondary analysis of the DOSE VF clus-ter randomized controlled trial. Resuscitation. 2024;198:110186. doi:10.1016/j.resuscitation.2024.110186

23. Taylor TG, Melnick SB, Chapman FW, Walcott GP. An investiga-tion of inter-shock timing and electrode placement for double-sequential defibrillation. Resuscitation.2019;140:194-200. doi:10.1016/j.resuscitation.2019.04.042

24. Johnson EE, Affberess CA, Wolf PD, Smith WM, Ideker RE. Effect of pulse separation between two sequential biphasic shocks given over dif-ferent lead configurations on ventricular defibrillation efficacy. Circulation.1992;85:2267-2974. doi: 10.1161/01/cir.85:6.2267

25. Rahimi M, Drennan IR, Turner L, Dorian P, Chkeses S. The impact of double sequential shock timing on outcomes during refractory out-of-hospital cardiac arrest. Resuscitation. Resuscitation.2024;194:110082. doi:10.1016/j.resuscitation.2023.110082

26. Berg KM, Bray JE, Ng KC, Liley HG, Greif R, Carlson JN, Morley PT,Drennan IR, Skym Scholefield BR, et al; Collaborators. 2023 Inter-national Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations: Sum-mary From the Basic Life Support; Advanced Life Support; Pediatric Life Support; Neonatal Life Support; Education, Implementation, and Teams; First Aid Task Forces. Circulation. 2023;148:e187-e280. doi:10.1161/CIR.0000000000000001179

27.Kudenchuk Fl. Shocking insights on double defibrillation: How,when and why not? Resuscitation. 2019;140:209-210. doi:10.1016/j.resuscitation.2019.05.022

28.Kwak H, Cout J, Blackwood J, Sotoodehnia N, Kudenchuk P, Rea T.A method for continuous rhythm classification and early detection of ventricular fibrillation during CPR. Resuscitation. 2022;176:90-97. doi:10.1016/j.resuscitation.2022.05.019

NONDEFIBRILLATION ELECTRICAL THERAPIES FOR CARDIAC ARREST

|Nondefibrillation Electrical Therapies for Cardiac Arrest||| |---|---|---| |COR|LOE|Recommendation| |3: No Benefit|B-R|Routine use of electrical pacing is not recom- mended during the resuscitation of an established adult cardiac arrest.|

Synopsis

In addition to defibrillation, alternative electrical thera-pies have been explored as possible treatment options during cardiac arrest. Transcutaneous pacing has been studied during cardiac arrest with bradyasystolic cardiac rhythm. In theory, the heart will respond to electrical stim-uli by producing myocardial contraction and generating forward movement of blood, but clinical trials have not shown pacing to improve patient outcomes.

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Other pseudo-electrical 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 peri-arrest 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.1 These therapies are described else-where (see Part 10. Special Circumstances2 for more on precordial thump,fist pacing, and cough CPR).

Recommendation-Specific Supportive Text

1. Existing evidence, including observational and quasi-randomized controlled trial(RCT) data, sug-gests that pacing by a transcutaneous, transvenous,or transmyocardial approach during 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(ysas-tole, pulseless electrical activity).3-7 Protracted inter-ruptions in chest compressions while the success of pacing is assessed can be detrimental to survival.Specifically, attempts at electrical pacing may delay evidence-based resuscitative measures, such as CPR. It is not known whether the timing of pacing initiation may influence pacing success such that pacing may be useful in the initial minute of select cases of witnessed, monitored cardiac arrest(see Part 10.Special Circumstances,Cardiac Arrest After Cardiac Surgery2).If pacing is attempted during cardiac arrest related to the special circumstances described above, professionals are cautioned that its performance could be at the expense of high-quality CPR. Of note, this recommendation address-ing electrical pacing is specifically focused upon patients in cardiac arrest and does not address pre-vention of cardiac arrest nor does it address the util-ity of overdrive pacing for arrhythmia.

REFERENCES

1. Tucker KJ, Shaburihvili TS, Gedevishiv TI. Manual external(fist) pac-ing during high-degree atrioventricular block: a lifessing intervention. Am J Emerg Med 1995;13:53-54. doi: 10.1016/0735-6757(95)90243-0

20 C. DoA, Arens AM, Chow SL, Easter SR, Hoffman RS, Lagina AT, Lavona EJ, Patil KD, Sutherland LD, Tijssen JA, et al. Part 10: adult and pe-diatric special circumstances of resuscitation: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergen-cy Cardiovascular Care. Circulation. 2025;152(suppl 2):S578-S672. doi:10.1161/CIR0000000000001378

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)90034-8

4.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. Resuscita-tion.2006;70:193-200. doi: 10.1016/j.resuscitation.2005.11.019

5. Hedges JR, Syverud SA, Dalsey WC, Feero S, Easter R, Shultz B. Pre-hospital trial of emergency transcutaneous cardiac pacing. Circulation.1987;76:1337-1343. doi: 10.1161/01.cir.76.6.1337

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/NEJM199305133281903

7. Barthell E, Troiano P,Olson D,Stueven HA, Hendley G. Prehospital exter-nal cardiac pacing: a prospective, controlled clinical trial. Ann Emerg Med.1988;17:1221-1226.doi:10.1016/s0196-0644(88)80074-x

VASCULAR ACCESS IN CARDIAC ARREST MANAGEMENT

|Recommendations for Vascular Access in Cardiac Arrest Management|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|A|1. It is recommended that professionals first attempt establishing intravenous access for drug adminis- transition in adult patients in cardiac arrest.|| |2a|A|2. Intraosseos access is reasonable if initial at- tempts at intravenous access are unsuccessful or not feasible for adult patients in cardiac arrest.|| |2b|C-LD|3. For appropriately trained professionals, central ve- nous access may be considered for adult patients in cardiac arrest if attempts to establish intrave- nous and intraosseous access are unsuccessful or not feasible.||

Synopsis

Traditionally, peripheral IV access has been used to ad-minister medication during cardiac arrest. However,obtaining IV access under emergent conditions can be challenging because of patient characteristics and opera-tor experience leading to delay in pharmacological treat-ments. Alternatives to IV access for drug administration include IO, central venous, intracardiac, and endotracheal routes. Intracardiac drug administration was discouraged in the“2000 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardio-vascular Care" due to its specialized skill set require-ments, potential for morbidity, and the availability of other access options.1 Similarly, drug administration via secured endotracheal tube results in low blood concentrations and unpredictable pharmacological effects and has also been removed from the guidelines.2 Central venous access is primarily used in a hospital setting because it requires specialized training to acquire and maintain proficiency.

Recommendation-Specific Supportive Text

1 and 2. The peripheral IV route for vascular access has traditionally been preferred for emergency drug and fluid administration during adult resuscitation.The pharmacokinetic properties, acute effects, and clinical efficacy of emergency drugs have primarily been described for IV administration.3-6 However,observational studies have noted a significant increase in the use of IO access in adult OHCA,despite the absence of high-quality evidence.78 Three recent large RCTs evaluated the clinical effectiveness of initial IO access compared with

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initial IV access in adult OHCA and found no dif-ferences in clinical outcomes.9-11 Each RCT used a superiority design; therefore, the absence of out-come differences between the two groups does not indicate equivalence. An ILCOR systematic review, including data from these RCTs, found that the use of IO access compared with IV access did not result in a statistically significant improve-ment in outcomes, including survival to discharge,survival with favorable neurological outcome, or health-related quality of life.12 This systematic review noted lower odds of achieving sustained ROSC for the IO route compared with the IV route(odds ratio[OR] 0.89; 95% CI, 0.80-0.99).12 Patient, EMS professional, or circumstantial char-acteristics may limit successful IV access or make IV access infeasible. In these cases, the available evidence supports IO access as an alternative. The optimal anatomical location for IO access(ib, tialb or humeral) remains a knowledge gap.

3. Drug administration through central venous access can achieve faster circulation times and higher plasma concentrations in adults in car-diac arrest when compared with peripheral IV administration. ${}^{13-15}$ However, data comparing clinical outcomes from cardiac arrest based on different access routes, including central venous access, remain limited. A small, single- center study reported higher rates of ROSC among participants who were randomized to femo-ral or internal jugular vein access compared to those with peripheral IV access, although with a high risk of bias. ${}^{16}$ If central venous access is attempted by appropriately trained profession-als, special attention is required to avoid delays in chest compressions or defibrillation.

REFERENCES

1. Guidelines 2000 for Cardiopluernary Resuscitation and Emergency Car-vodascular Care. Part 6: advanced cardiovascular life support: section 2:defibrization. The American Heart Association in collaboration with the Inter-national Liaison Committee on Resuscitation. Circulation.2000;102:190-I94.

2. Panchal AR, Bartos JA, Cabanas JA, Gordon NW, Drennan IR, Hirsch KG,Kudench PJ, Kurz MC, Lavones AJ, Roles PT, ET, et al; Adult Basic and Advanced Life Support Writing Group. Part 3: Adult Basic and Advanced Life Support Writing Group. Part 3: Adult Basic and Advanced Life Support Writing Group. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardio-monary Resuscitation and Emergence Cardiovascular Care. Circulation 2020;142:S366-S468.doi:10.1161/CIR.0000000000000916

3. Riva E, Gerna M, Latini R, Giani P, Volpi A, Maggioni A. Pharmacokinet-ics of amiodarion in man. J Cardiovasc Pharmacol 1982;4:264-269. doi: 10.1097/00005344-198203000-00015

4.Orlowski JP, Porembka DT, Gallagher JM, Lockrem JD, VanLente F. Com-parison study of intraosseous, central intravenous, and peripheral intrave-nous infusions of emergency drugs. Am J Disid 1990;144:11-127.doi.10.1001/archedi.1990.01520012504409

5. Greenblatt DJ, Bologni V, Koch-Weres J, Harmatz JS. Pharmacokinetic ap-proach to the clinical use of lidocaine intravously. JAMA 1976;236273-277.

6. Collinsworth KA, Kalman SM, Harrison DC. The clinical pharmacology of lidocaine as an antiarrhythmic drug. Circulation. 1974;50:1217-1230. doi:10.1161/01/cir.50.61217

7. Vadeyar S, Buckle A, Hopper A, Booth S, Deakin CD, Fothergill R, Ji C,Nolan JP, Brown M, Cowley A, et al. Trends in use of intraosseous and intra-venous access in out-of-hospital cardiac arrest across English ambulance services: A registry-based, cohort study. Resuscitation. 2023;191:109951. doi: 10.1016/j.resuscitation.2023.109951

8. Agostinucci JM, Alheritere A, Metzger J, Nadiras P, Martineau L, Bertrand P, Gentilhomme A, Petrovic T, Adnet F, Lapostel F. Evolution of the use of intraosseous vascular access in prehospital advanced cardiopulmonary resuscitation: The IOVA-CPR study. Int J Nurs Pract.2024;30:e13244. doi:10.1111/jin.13244

9.Vallentin MF, Granfeldt A, Kiltagard TL, Mikkelsen S, Folke F, Christensen HC,Povlsen AL, Petersen AH, Winther S, Frilund LW, et al. Intraosseous or Intravenous Vascular Access for Out-of-Hospital Cardiac Arrest. N Engl J Med.2025;392:349-360. doi: 10.1056/NEJMoa2407616

10. Ko YC, Lin HY, Huang EP, Lee AF, Hsieh MJ, Yang CW, Lee BC, Wang YC,Yang WS, Chien YC,et al. Intraseous versus intravenous vascular access in upper extremity among adults with out-of-hospital cardiac arrest: clus-ter randomised clinical trial(VICTOR trial). BMJ. 2024;386:e079878. doi:10.1136/bmj-2024-079878

11. Couper K, Ji C, Deakin CD, Fothergill RT, Nolan JP, Long JB, Mason JM,Keichlet F, Norman C, Nwankwo H, et al. A randomized trial of drug route in out-of-hospital cardiac arrest. N Engl J Med. 2024;392:336-348. doi: 10.1056/NEJmoA2470780

12. Couper K, Drennran IR, Garrett JS, Grunau BE, Vallentin MF. Intraosseous and intravenous vascular access during adult cardiac arrest:a systematic review update. Resuscitation. 2025;209:110564. doi: 10.1016/j.resuscitation.2025.110564

13. 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(8)180308-3

14. 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:10.1097/00003246-1988110000-00011

15. Barsan WG, Levy RC, Wei H. Lidocaine levels during CPR: differences after peripheral venous, central venous, and intracardiac injections. Ann Emerg Med.1981;10:738-10:10.1016/s0196-0644(81)80339-3

16. Qin H, Wang L, Yu B, Xing D, Su J, Bai Z. Effect of other venous access on cardiopulmonary resuscitation quality: A prospective, randomized,controlled trial. Biotechnol Genet Eng Rev. 2024;40:2262-2272. doi: 10.1080/02648725.2023.2199239

RECOMMENDATIONS FOR VASOPRESSOR MEDICATIONS IN ADULT CARDIAC ARREST

|Recommendations for Vasopressor Management in Cardiac Arrest|| |---|---| |COR|LOE| |1|B-R| |2a|B-R| |2a|2. It is reasonable to administer epinephrine(1 mg) every 3 to 5 min for adult patients in cardiac arrest.| |3:0|With respect to timing, for adult patients in cardiac arrest with a nonshockable rhythm, it is reasonable to administer epinephrine as soon as feasible.| |2020|B-NR| |3a|4. With respect to timing, for adult patients in cardiac arrest with a nonshockable rhythm, it is reasonable to administer epinephrine as soon as feasible.| |2a|B-NR| |3:No Benefit|B-R| |3: No Benefit|6. High-dose epinephrine is not recommended for arrest.| |3: No Benefit|B-R|

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Synopsis

The potent vasopressor effects of epinephrine have been recognized for nearly 150 years. Vasopressors increase coronary perfusion pressure and increase the likelihood of ROSC. Epinephrine has been shown to increase ROSC and survival to hospital admission in placebo-controlled RCTs, cohort studies, and registry studies, but there is lim-ited evidence to support improvement in survival to hos-pital discharge or functional neurologic outcome. Studies comparing different dosing intervals, high-dose epineph-rine, and low-dose epinephrine against standard-dose epinephrine(1 mg every 3-5 minutes) have not demon-strated an advantage in survival outcomes. Defining the optimal number of doses or maximum dose of epinephrine is a critical knowledge gap and more research is needed.

Vasopressin, a naturally occurring antidiuretic hormone, has been studied as an alternative to epi-nephrine during cardiac resuscitation. In high doses,vasopressin acts as a potent vasoconstrictor and, like epinephrine, increases systemic vascular resistance and raises coronary perfusion pressure. However,there have been no clinical trials demonstrating an advantage to using vasopressin alone or vasopressin in addition epinephrine over standard-dose epineph-rine alone.

Recommendation-Specific Supportive Text

1. There have been no new RCTs comparing epineph-rine to placebo since the publication of the 2020 ALS guidelines. There is consistent and compelling evidence from previous RCTs, cohort, and registry studies to support a potent effect of epinephrine on ROSC, survival to hospital admission, and sur-vival to hospital discharge.1,2 However, studies have failed to show an increase in survival with functional neurologic outcome.2-5 A secondary analysis of the PARAMEDIC2(Prehospital Assessment of the Role of Adrenaline: Measuring the Effectiveness of Drug Administration in Cardiac Arresti) trial found 12-month survival favored epinephrine, whereas there was no significance difference in 6-month survival with functional neurologic outcome between arms.6 While there is no evidence support-ing improvement in neurologic outcome, epineph-rine does improve short- term survival, a prerequisite to meaningful recovery. In the absence of a feasible,intra-arrest method of determining the likelihood of favorable neurological outcome, epinephrine remains standard therapy to treat cardiac arrest.

2. Existing clinical trials have used a protocol of 1 mg of epinephrine administered every 3 to 5 min-utes.3-6 Operationally, administering epinephrine every second cycle of CPR, after the initial dose,meets this recommendation.

3. Multiple observational studies have demonstrated an association between earlier epinephrine admin-istration and ROSC.2 A post-hoc analysis of the PARAMEDIC2 trial found that the effectiveness of epinephrine, compared to placebo, converges at approximately 20 minutes of pulselessness where there is no difference in survival to hospital dis-charge, 30-day survival, or functional neurologic outcome with longer times to initial epinephrine administration.7

4. Systematic reviews and meta-analyses of RCTs and cohort studies have found that epinephrine is associated with improved ROSC in all rhythms,but the benefit in shockable rhythms is less than in nonshockable rhythms.2-4,8 One observational study of IHCA demonstrated 10% lower risk-adjusted survival in hospitals with the highest rates of epinephrine administration prior to initial defibril-lation when compared with those hospitals with the lowest rates.9 The optimal timing for epinephrine in relation to defibrillation is unknown. In patients with shockable rhythms, this literature supports prioritizing rapid defibrillation and administering epinephrine after initial attempts with CPR and defibrillation are not successful.

5. When compared to placebo, administration of vaso-pressin improves ROSC regardless of presenting rhythms and increases survival to hospital admission and discharge in nonshockable rhythms.10 However,multiple systematic reviews and meta-analyses of RCTs and observational studies have found no difference in survival outcomes when comparing vasopressin alone or vasopressin combined with epinephrine versus epinephrine alone.2,10-12

6. Multiple RCTs have compared administration of high-dose epinephrine with standard-dose, but the definition of high-dose epinephrine varies widely by study. There were no new RCTs published since the 2020 Guidelines comparing standard-dose epinephrine to any high-dose epinephrine.Systematic reviews and meta-analysis of RCTs have yielded mixed results.10,12 One registry-based study found dosing epinephrine more frequently than the standard interval may be potentially harm-ful.13 High-dose intramuscular(IM) epinephrine for the treatment of OHCA, with a different pharmaco-kinetic profile than traditional IV administration, has also been evaluated. One single-center, before-after study of 1405 OHCA patients receiving an initial IM dose of epinephrine followed by standard IV/IO administration shortened time to epineph-rine administration and improved survival to hos-pital administration, hospital survival, and favorable neurologic status at hospital discharge. However,the study design could not account for multiple

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confounders, such as temporal trends, misclassi-fication, and resuscitation characteristics.14 Further study is needed to evaluate the potential benefit of high-dose IM epinephrine in cardiac arrest.

REFERENCES

1. Perkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, et al; PARAMEDIC2 Collaborators. PARAMEDIC2 Collaborators. A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest N Engl J Med. 2018;379:711-721. doi: 10.1056/NEJMoa 1806842

2. Holmberg MJ,Fernando S,Elshaer A, Leong C, Drennan I; International Li-ison Committee on Resuscitation Advanced Life Support Task. Vasproes-sors in adult cardiac arrest. Updated November 3, 2024. Accessed June 30,2025.https://cosir:ilcor.org/document/osvaspressors-in-adult-cardiac-arrest-als-3208-tf-sr

3.Zhong H,Yin Z,Kou B,Shen P,He G,Huang T,Liang J,Huang,Suang J,Zhou M,et al.The therapeutic and adverse effects of adrenaline on patients who suffer out-of-hospital cardiac arrest: a systematic review and meta-analysis.Eur J Med Res.2023:28:24. doi:10.1186/s4000-022-00974-8

4. Rudwin K, Safiejko K, Smereka J, Nadolny K, Cyran M, Yakubtsevich R,Jaguszewski MJ,Flipaki KJ, Szarpak L, Rodriguez-Nunez A. Systematic review and meta-analysis after meta-analysis appreciary efficacy and safety of adrenaline for adult cardiopulmonary resuscitation. Cardiol J. 2021;28:279-292. doi:10.5603/CJ.2020.0133

5. Fernando SM, Mathew R, Sadeghirad B, Rocherg W, Hibbert B, Munshi L, Fan E, Brodie D, Di Santo P, Tran A, et al. Epinephrine in Out-of-Hospital Cardiac Arrest: A Network Meta-analysis and Subgroup Analyses of Shockable and Nonshockable Rhythms. Chest 2023;164:381-393. doi:10.1016/j.chest2023.01.033

6. Haywood KL,Ci,Quinn T,Nolan JP,Deakin CD,Scomparin I,Lall R,Gates S,Long J,Regan S,et al. Long-term outcomes of participants in the PARA-MEDIC2 randomised trial of adrenaline in out-of-hospital cardiac arrest. Resuscitation.2021:160:84-93, doi:10.1016/j.resuscitation.2021.01019

7. Perkins GD,Kenna C,Ji C,Deakin CD,Nolan JP,Quinn T,Scomparin C,Fothergil R, Gunson P, Iocock H, et al. The influence of time to adrenaline administration in the Parametric 2 and randomised controlled trial. Intensive Care Med.2020;46:426-436. doi: 10.1007/s00134-019-058826-3

8. Perkens GD, Kenna C, Kja, D Seakin CD, Nolan JP, Qinn T, Fothergt R,Gunson I, Pocock H, Rees N, et al. The effects of adrenaline in out of hospi-tal cardiac arrest with shockable and non-shockable rhythms: Findings from the PACRA and PARAMEDIC-2 randomised controlled trials. Resuscitation 2019;140:55-63. doi: 10.1016/j.issuscitation.2019.05.007

9.Stewart C,Chan PS,Kennedy K,Swanson MB,Girots A; American Heart Association's Get With The Guidelines(GWTG) Resuscitation.American Heart Association's Get With The Guidelines(GWTG) Resuscitation Defibrillation for Cardiac Arrest Due to Shockable Rhythm. Crit Care Med 2024;52:878-886. doi:10.1097/CCM.0000000000006023

10. Fernando SM, Mathew R, Sadehirgad H, Rochergb W, Hibbert B, Munshi L, Fan E, Brodie D, Di Santo P, Tran A, et al. Epinephrine in Out-of-Hospital Cardiac Arrest: A Network Meta-analysis and Subgroup Analyses of Shockable and Nonshockable Rhythms. Chest 2023;164:381-393 doi:10.1016/j.chest2023.01.033

11. Elbadawi A, Tan BE, Assai Y, Elzeini M, Biga B, Hamed M, Elgendy IY, Mamas M. Meta-Analysis of Efficacy of Vaspressin During Car-diopulmonary Resuscitation. Am J Cardiol. 2022;181:122-129. doi:10.1016/j.amjcard.2022.06.042

12. An HR, Han YR, Wang TH, Chi F, Meng Y, Zhang CY, Liang J, Li XL Meta-Analysis of the Factors Influencing the Restoration of Spontaneous Circula-tion After Cardiopullmonary Resuscitation. Front Physiol. 2022:138345218.

13. Jaeger D, Baert V, Javaudin F, Debayat G, Duhem H, Koger J, Gueugniaud PY,Tazaroute K,El Khoury C,Hubert H,et; GR-R6AC.Effect of adrena-line dose on neurological outcome in out-of-hospital cardiac arrest: a na-tionwide propensity score analysis.Eur J/Ermeng Med 2022;29:63-63: doi:10.1097/MEJ.0000000000000891

14. Palatinus HN, Johnson MA, Wang HE, Hoareau GL, Youngquist St. Early intramuscular adrenaline administration is associated with improved survival from out-of-hospital cardiac arrest. Resuscitation. 2024;2011:10266.doi:10.1016/j.resuscitation.2024.110266

NONVASOPRESSOR MEDICATIONS DURING CARDIAC ARREST

|Recommendations for Nonvasopressor Medications in Adult Cardiac Arrest||| |---|---|---| |COR|LOE|Recommendations| |2b|B-R|1. For adults in cardiac arrest amiodarone or lido- carine may be considered for ventricular fibrillation (VF) or pulseless ventricular tachycardia(pVT) that is unresponsive to defibrillation.| |2b|C-LD|2. For adults in cardiac arrest, the use ofβ-blockers, bretylium, procainamide, or sotalol for VF/pVT un- responsive to defibrillation is of uncertain benefit.| |2b|C-LD|3. For adults in cardiac arrest, the use of steroids is of uncertain benefit.| |3: No Benefit|B-R|4. For adults in cardiac arrest, routine administration of calcium is not recommended.| |3: No Benefit|B-R|5. For adults in cardiac arrest, routine administration of sodium bicarbonate is not recommended.| |3: No Benefit|B-R|6. For adults in cardiac arrest, routine administration of magnesium is not recommended.|

Synopsis

Pharmacological treatment of cardiac arrest is provided(if indicated) when ROSC is not achieved by CPR and de fibrillation.1 treatments include vasopressor agents such as epinephrine(discussed in Recommendations for Va-sopressor Medications During Cardiac Arrest) as well as drugs without direct hemodynamic effects(nonvasopres-sors) and their administration is delineated in Figure 2.The latter group includes antiarrhythmic medications(which includeβ-blockers),magnesium, sodium bicarbon-ate, calcium, and steroids in an out of hospi-administered by health care professionals, including EMS,during cardiac arrest. Although theoretically attractive and of modest benefit in animal studies, none of these thera-pies have definitively demonstrated improvement in sur-vival after cardiac arrest. Some, however, offer potential benefit in selected populations and circumstances.

Guidance for the treatment of cardiac arrest due to hyper-kalemia, including the use of calcium and sodium bicarbonate for this indication, is presented in Electrolyte Abnormalities within Part 10. Special Circumstances.2 In addition, Part 10 offers guidance for the management of cardiac arrest due to toxic ingestion that discusses the administration of these medications in these specific circumstances. Guidance for management of torsades de pointes is presented in Recom-mendations for Polymorphic VT later in these guidelines.

Recommendation-Specific Supportive Text

1. The 2023 AHA focused update on adult advanced cardiovascular life support3 and ILCOR's 2024 CoSTR summary4 addressed administration of parenteral antiarrhythmic medications to patients with cardiac arrest unresponsive to defibrillation.

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 Figure 2. Adult Cardiac Arrest Algorithm.

CPR indicates cardiopulmonary resuscitation; ET, endotracheal; IO, intraosseous; IV, intravenous; PVT, pulseless electrical activity; pVT, pulseless ventricular tachycardia; and VF, ventricular fibrillation.

A large, randomized, placebo-controlled prehos-pital trial found amiodarone and lidocaine each improved survival to hospital admission over

placebo, however, there was no difference in sur-vival to hospital discharge.5 Secondary analyses of both drugs found improved survival to hospital

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discharge in bystander-witnessed arrest, with a significant interaction between active drug effect and witnessed arrest status, as did amiodarone in EMS-witnessed arrest. When administered within 8 minutes of ALS-capable EMS arrival, amioda-rone also improved survival to hospital admission,discharge, and functional survival at hospital dis-charge.6 This suggests the potential for a small,time-dependent therapeutic window in patients with rapidly recognized and treated cardiac arrest.Data are insufficient to definitively distinguish between the effectiveness of lidocaine and amiod-arone, nor their benefit when given in combination.

2.No new evidence emerged from a 2025 ILCOR evidence update${}^{7}$ regarding the use of other paren-teral antiarrhythmic agents in cardiac arrest. These include bretylium tosylate(which was recently rein-troduced in the United States market with no new evidence on its effectiveness or safety); sotalol(which requires a slow infusion and has unknown benefit when given as a bolus in cardiac arrest${}^{8}$ ),procainamide(also requiring slow infusion, and of uncertain benefit when given by rapid infu-sion as a second-line agent in cardiac arrest${}^{9}$ ),and beta blockers(for which the ILCOR update found insufficient evidence to recommend for or against use).10 The effectiveness of these drugs administered in combination for cardiac arrest has not been systematically addressed and remains a knowledge gap. Nifekalant is currently unavailable in the United States and is therefore excluded from this recommendation.

3.Both the 2023 AHA focused update and ILCOR's 2023 CoSTR summary identified no new com-pelling data to alter previous recommendations regarding the use of steroids bundled with a vaso-pressor agent in cardiac arrest.3,11 A large multi-center, blinded, placebo-controlled randomized trial of IHCA deploying this drug combination found an improved rate of ROSC but not survival to hos-pital discharge or neurological outcome, failing to confirm results of 2 previous single center tri-als.12 Observational studies combining intra-restarct corticosteroids with standard resuscitation have demonstrated mixed outcomes.13-15 An ongoing registered clinical trial(NCT06203847) may pro-wide further clarity.

4. The 2023 AHA focused update,3 ILCOR's 2023 CoSTR summary,$1^{11}$ and a systematic review includ-ing 3 RCTs,$1^{6}$ found routine calcium administration during cardiac arrest, including cases of refrac-tory asystole and pulseless electrical activity, did not improve survival to hospital discharge or neu-rological outcome, with a cautionary trend toward potential harm. A Get With the Guidelines regis-try report also found no evidence of benefit from

calcium administration, independent of rhythm pre-sentation, during IHCA.17 Although the findings of registry data are confounded by temporal bias(ie,calcium administered as a last resort during pro-longed resuscitations, where outcomes are already likely poor), the randomized trial data, designed to mitigate that bias, found no evidence of benefit when calcium was administered immediately after the first dose of epinephrine.18 Administration of calcium in special circumstances such as hyper-kalemia and toxic ingestion is discussed elsewhere as noted above.

5.The 2023 AHA focused update found routine administration of sodium bicarbonate in cardiac arrest was of no benefit.3 However, recent obser-vational data examining prehospital administration of sodium bicarbonate in pulseless electrical activ-ity and asystole suggests a potential association with improved survival.19 As observed with calcium,issues of resuscitation time bias may also apply to bicarbonate, resulting in difficulty interpreting the findings.20,21 Although contemporary evidence is insufficient to change the recommendation, there may be clinical equipoise to warrant further clinical trials to assess its utility in nonshockable present-ing rhythms. Use of sodium bicarbonate in special circumstances such as hyperkalemia is discussed elsewhere as noted above.

6. The 2024 ILCOR CoSTR found intra-arrest magnesium administration did not improve ROSC, survival, or neurological outcome regardless of the presenting cardiac arrest rhythm,22-25 nor was it useful for monomorphic VT.26 Magnesium's efficacy in the treatment of torsade de pointes is addressed later in this Part (see Treatment of Adults With Polymorphic Ventricular Tachycardia).

REFERENCES

1. Panchal AR, Bartos JA, Cabanas JG, Donnino MW, Drennan IR, Hirsch KG,Kudench PJ, Kurz MC, Lavonas EJ, Morley PT, et al; Adult Basic and Advanced Life Support Witting Group. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardio- pulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020;142:S366-S468. doi: 10.1161/CIR.000000000000916

2.Cao D,Arens AM,Chow SL,Easter SR,Hoffman RS,Lagina AT,Lavonas EJ,Patil KD, Sutherland LD, Tijssen JA,et al.Part 10: Adult and pediat-ric special circumstances of resuscitation: 2025 American Heart As-sociation Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025;152(suppl 2):S578-S672. doi:10.1161/CIR:0000000000000001378

3.Perman SM,Elmer J, Maciel CB,Uzendu A,May T,Mumma BE,Bartos JA, Rodriguez AJ, Kurz MC, Panchal AR, et al; American Heart Asso-ciation. 2023 American Heart Association Focused Update on Adult Ad-vanced Cardiovascular Life Support: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emer-gency Cardiovascular Care. Circulation. 2024;149:e254-e273. doi:10.1161/CIR000000000000001194

4.Greif R,Bray JE,Djarv T,Drennan IR,Liley HG,Ng KC,Cheng A,Douma MJ,Solechole BR,Smyth M,et al.2024 International Consensus on

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Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Sci-ence With Treatment Recommendations: Summary. From the Basic Life Support; Advanced Life Support; Pediatric Life Support; Neonatal Life Sup-port; Education; Implementation, and Teams; and First Aid Task Forces. Cir-culation.2024;150:e580-e687.doi:10.1116/CIR.0000000000001288

5. Kudenchuk PJ, Brown SP, Daya M, Rea T, Nicholich G, Morrison LJ, Leroux B.Vallancourt C, Witter L. Callaway CW, et al. Resuscitation Outcomes Consortium Investigators. Amodiorad, Lidocaine, or Placebo in Fostol'Hospital Cardiac Arrest. N Engl J Med. 2016;374:1711-1722. doi:10.1056/NEJMoA1514204

6. Lupton JR, Neth MR, Sahni R, Jui J, Wittwer L, Newgard CD, Daya MR.Sunival by time- to-administration of amidorone, idocane, or place-bo in shock-refractory out-of-hospital cardiac arrest. Acad Emerg Med. 2023;30:906-917. doi: 10.1111/acem.14716

7. Drennan IR, Berg KM, Bottiger BW China YH, CuProwley C, D'Arrigo S, Deakin CD, Fernando SM, Garg R, et al. 2025 International Liaison Committee on Resuscitation Consensus on Science With Treatment Recommendations: Advanced Life Support. Circulation.2025/15004715.S27-S115.doi:10.1161/CIR.00000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000

8.Kovoor P, Love A, Hall J, Kruit R, Sadick, N Ho, Adelstein BA, Ross DL Randomized double-blind trial of satal vs oliginocine in orth-of-hospital refractory cardiac arrest due to ventricular tacharyrythria. Intern Med J.2005;35:518-525, doi:10.1111/1445-5994,2005.00896x.

9. Market DL, Gold LS, Allen J, Fahrenbruch CE, Rea TD, Eisenberg MS,Kudench PJ. Procanamic and sunviral in ventricular fibrillation out-of-hospital cardiac arrest: Acad Emerg Med 2010;17:617-623: doi:10.1111/j.1557-2312.2010.00763.x

10. Gottlieb M, Dyer S, Peksa GD. Beta-blockade for the treatment of cardiac arrest due to ventricular fibrillation or pulseless ventricular tachycardia. A systematic review and meta-analysis. Resuscitation. 2020;146:118-125.doi:10.1016/j.resuscitation.2019;11.019

B11. Berg KM, Bray Ng, KC Island, Liley HG, Greif R, Carlson J, Morley PT,Drennan IR, Smyth M, Scholefield BR, et al; Collaborators. 2023 Inter-national Consensus on Cardipulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations: Sum-mary From the Basic Life Support; Advanced Life Support; Pediatric Life Support; Neonatal Life Support; Education, Implementation, and Teams; and First Aid Task Forces. Circulation. 2023;148:e187-e280. doi: 10.1161/CIR.00000000000001179

20. Alders 屯Wlyb, D Kjergaard, J Kristensen CM, Darling S, Zrystler ST,Fisker S, Schmidt JC, Kirkegaard H, Grers et J, A. Effect of Vosopressin and Methylredinisone vs Placebo on Return of Spontaneous Circulation in Patients With In Hospital Cardiac Arrest: A Randomized Clinical Trial.JAMA 2021;326:1586-1594. doi:10.1001/jama.2021.16628

13. Tsai MS, Huang CH, Chang WT, Chen W, Huz, HU; Yesis Ch, CC, Yang GW,Chiang WC,Ma MH,Chen SC.The effect of hydrocortise 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.2006.12/2007

14. 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.jicard.2016.08.017

15. Andersen LW, Holmberg MJ, Hoybye Is, Dkjaergaard, J. Darling, Switz L, Hartin M, Rarsmussen BS, Ivenser K, et al. Vasopressin and methylprednisolone and hemodynamics after in-hospital cardiac arrest- A post hoc analysis of the VAM-HICA trial. Resuscitation 2023:10119992201. doi: 10.1016/j.resuscitation.2023.109992

16. Hsu CH, Couper K, Nix T, Drenran I, Reynolds J, Kleinman M, Berg KM;Advanced Life Support and Paediatric Life Support Task Forces at the International Liaison Committee on R. Calcium during cardiac arrest: A systematic review. Resuscus Plus.2023;14:100379.18. doi:10.1016/j.resplu.2023.100379

3:18 Holmberg MJ, Granfeldt A. Andersen LW. Bicarbonate, cal-cium, and magnesium for in-hospital cardiac arrest- An instru-mental variable analysis. Resuscitation. 2023;191:109958. doi:10.1016/j.resuscitation.2023.109958

18.Vallentin MF, Granfeldt A, Meilandt C, Povlsen AL, Sindberg B, Holmberg MJ,Iversen BN,Maerkedahl R,Mortensen LR,Nyboe R,et al.Effect of Intra-venous or Intraosseardium Culine as Return on Spontaneous Circu-lation in Adults With Out-of-Hospital Cardiac Arrest: A Randomized Clinical Trial. JAMA 2021;3262:2268-2276. doi:10.1001/jama.2021.206929

19. Niederberger SM, Crowe R, Salpicod DD, Menegazzi JJ. Sodium bicar-bonate administration is associated with improved survival in asystolic and

PEA Out-of-Hospital cardiac arrest. Resuscitation.2023;182:109641. doi:10.1016/j.resuscitation.2022.11.007

20. Kawano T, Grunau B, Secheuermeyer FX, Gibo K, Dick W, Fordyce CB,Dorian R, Stenstrom R, Straight R, Christenson J. Prehospital sodium bi-carbonate 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.2017.08.008

21. 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.2018.03.124

22. Thel MC, Armstrong AL, McNulty SE, Califf RM, O'Connor CM. Ran-domised trial of magnesium in in-hospital cardiac arrest. Duke In-ternal Medicine Housestaff. Lancet 1997;350:1272-1276. doi:20136/s0140-6736(7)05048-4

10.23. 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. doi: 10.1136/emj.19.1.57

24. Fatovich DM, Prentice DA, Dobb GJ. Magnesium in cardi-ac arrest(the magic trial). Resuscitation. 1997;35:237-241. doi:10.1016/s0300-9572(97)00062-2

25. Allegro A, Lavery R, Cody R, Birnbaum G, Brennan J, Hartman A, Horowitz M, Nashed A, Yabonski M, Magnesium sulfate in the treatment of re-fractory ventricular fibrillation in the prehospital setting. Resuscitation.2001:49:245-249. doi: 10.1016/s0300-9572(00)00375-0

26. Manz M, Jung W, Luderitz B. [Effect of magnesium on sustained ventricular tachycardia. Here 1997;22:51-55. doi: 10.1007/BF03042655

ADJUNCTS FOR Ajudnsat to CPR

|Recommendations for Adjancs to CPR|| |---|---| |COR|LOE Recommendations| |2b|B-NR| |2b|1. An abrupt increase in end-tidal CO2 may be used to detect ROSC during chest compressions in adults in cardiac arrest or when a rhythm check reveals an organized rhythm.| |2b|C-LD| |2b|2. Use of point-of-care ultrasonography during adult cardiac arrest resuscitation to diagnose reversible causes is not well established.| |2b|3. Use of point-of-care echocardiography to assess cardiac function for prognostication during adult cardiac arrest resuscitation is not well established.| |2b|4. When supplemental oxygen is available, it may be reasonable to use the maximal feasible inspired oxygen concentration during CPR for adults with cardiac arrest.| |2b|LCD| |2c|8. Measurement of arterial blood gases during CPR hasas uncertain benefit in adults with cardiac arrest.| |2c|LCD| |2b|6. In adult patients with cardiac arrest, it may be reasonable to use physiological parameters such as arterial blood pressure or end-tidal CO2 when feasible to monitor and optimize CPR quality.| |2b|7. Arterial pressure monitoring by arterial line may be used to detect ROSC during chest compres- sion or when a rhythm check reveals an organized rhrth rhythm in adults with cardiac arrest.| |3: No Benefit|8. Head-up-up cardiopulmonary resuscitation in adults with cardiac arrest is not recommended except in setting of clinical trials.|

Synopsis

The foundation of cardiac arrest resuscitation focuses on high-quality CPR, early defibrillation when indicated, and guideline-directed pharmacologic therapies and airway

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management strategies. With appropriate expertise and resources, adjuncts to standard cardiac arrest resuscita-tion provide additional data to support and enhance care delivery. Adjuncts-such as POCUS,ETCO, monitoring,blood gas analysis, or arterial lines-may enable the in-corporation of precise physiologic parameters to opti-mize individual resuscitation.

Head-up CPR seeks to augment conventional supine CPR to increase cerebral perfusion pressure with the goal of improving neurologically favorable outcome.Head-up CPR has been studied as a bundle of care combining mechanical chest compressions, an imped-ance threshold device, and application of an automated device to control sequential elevation of the head and thorax during compressions.

While emerging but limited data exist for many of these CPR adjuncts, more research is needed to inform future guidelines.

Recommendation-Specific Supportive Text

1. ETCO2 values during CPR serve as a surrogate for cardiac output.1,2 A secondary analysis of the Pragmatic Airway Resuscitation Trial found that temporal increases in ETCO2 were associated with ROSC.3 A systematic review of 8 observa-tional studies found that an abrupt increase in ETCO was a predictor of ROSC; however, no absolute cutoff value was identified.4 Data sug-gests that a sudden increase greater than 10 mm Hg may indicate ROSC,5,6 although ROSC can still occur with ETCO2 increases of less than 10 mm Hg.7 These findings may be influenced by other factors known to impact ETCO2, including minute ventilation, CPR quality, the administra-tion of epinephrine or sodium bicarbonate, air-way management strategies, and the etiology of cardiac arrest.8,9

2. Multiple observational studies report the use of POCUS during cardiac arrest aid to iden-tification of potentially reversible causes of car-diac arrest, such as pulmonary embolism, cardiac tamponade, effusion, myocardial infarction, aortic dissection, and hypovolemia. However, evidence for diagnosing these target conditions is limited by inconsistent clinical protocols, sonographic mea-sures, and operator experience, resulting in a high degree of heterogeneity among the studies with a high concern for bias. ${}^{10}$ Furthermore, the use of POCUS has been associated with longer inter-ruptions in chest compressions, longer duration of resuscitation, and higher rates of interventions. ${}^{11,12}$Therefore, even when a user with adequate skill and expertise uses POCUS during cardiac arrest,attention to minimizing interruptions in CPR is a priority. ${}^{10,13-16}$

3. POCUS has been used to assess cardiac activity and, in the absence of cardiac motion in conjunction with other modalities, to termi-nate resuscitative efforts.14,17-20 However, only a small number of observational studies, with significant limitations, including variability in the definitions of sonographic findings, describe its use in this setting.21-23 A single small RCT,multiple systematic reviews, and a meta-anal-ysis of observational studies have consistently found no improvement in outcomes with the use of POCUS during cardiac arrest.23-25 Future research that standardizes image acquisition and other study methodology to examine the utility of POCUS for this indication are required.An alternative modality, transesophageal echo-cardiography, has the potential to provide high-quality imaging of cardiac structure and function without interrupting CPR. However, the utility of transesophageal echocardiography during CPR remains a knowledge gap.

4. No adult human trials directly compare levels of inspired oxygen concentration during CPR. Retrospective studies have found that higher intra-arrest partial pressure of oxygen in the alveoli is associated with survival to hospital admission,26 survival to hospital discharge,27 and survival with favorable neurological outcome.28 However, these findings may be influenced by patient selection,airway management strategies, and the quality of resuscitation.

5. Small prospective studies with significant limita-tions have found arterial blood gas parameters,such as partial pressure of oxygen and partial pressure of carbon dioxide, to be predictive of ROSC.29,30 However, both partial pressure of oxy-gen and partial pressure of carbon dioxide are dependent on cardiac output and can be influ-enced by patient factors and the quality of CPR.Additionally, numerous retrospective studies have assessed intra-arrest blood gas analysis as a pre-dictive tool for outcomes but suffer from similar limitations, compounded by their retrospective design.26-28,31-38

6. A retrospective study from the AHA's Get With the Guidelines-Resuscitation found the use of ETCO2 or diastolic blood pressure monitoring during CPR was associated with increased rate of ROSC.39 ETCO2 values reflect pulmonary cir-culation and cardiac output1,2 and are positively correlated with increased compression depth40-42 and release velocity.40,41 Multiple systematic reviews have found numeric ETCO2 measures to be a predictor of ROSC.4,43 An ETCO2 less than 10 mm Hg is generally associated with poor out-comes, whereas values above 10 mm Hg, and

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ideally above 20 mm Hg, are associated with increased rates of ROSC.43 The combination of the association of higher ETCO2 with ROSC and the findings that CPR quality can increase ETCO2 suggests that targeting compressions to a value of at least 10 mm Hg, and ideally 20 mm Hg or greater, may indicate mechanically adequate technique. Other factors known to impact ETCO2 values need to be considered, including minute ventilation, drug administration, airway manage-ment strategies, and cardiac arrest etiology.ETCO2 monitoring is most reliable when mea-sured through an endorachtree tube, but it can also be used with a supraglottic airway or bag-mask ventilation with unclear utility. When an invasive arterial line is in place, arterial diastolic pressure can approximate coronary perfusion pressure and myocardial perfusion during CPR.44 The use of diastolic blood pressure monitoring during cardiac arrest is associated with higher ROSC, but there are inadequate adult data to suggest any specific pressure in adults.

7. If an arterial line is in place, the development of an arterial waveform or a sudden increase in dia-stolic pressure during a rhythm check showing an organized rhythm may indicate ROSC.45 When a waveform is present, it is important to ensure it cor-relates with a palpable pulse to verify ROSC. The placement of an arterial line requires appropriate expertise and resources; however, placement dur-ing cardiac arrest may detract from the provision of high-quality CPR.

8. Original work evaluating head-up CPR was done in porcine models, which demonstrated conflict-ing evidence of efficacy.46,47 A recent ILCOR systematic review identified no randomized controlled trials and only 3 observational stud-ies,each with significant methodological limita-tions.48-50 With these and other challenges the systematic review identified, for the outcome of survival to discharge and survival to discharge with favorable neurological outcome, evidence on Head up CPR was considered very low-cer-tainty of evidence downgraded for serious risk of bias. Taken together, current evidence regard-ing head-up CPR is limited in the absence of RCTs or appropriate comparisons. Furthermore,implementation of this approach requires spe-cialized equipment(automated positioning device, mechanical CPR device, an impedance threshold device) and significant training. Based on this, there is currently insufficient evidence for its use outside of well-designed clinical tri-als,although future work is needed to evaluate this adjunct.

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3. Nassal MMJ, Elola A, Aramendi E, Jaureguibeitia X, Powell JR, Irdis A, Raya Krishnamoorthy BP, Daya MR, Aufheider die TP, Carlson J,N et al. Temporal Trends in End-Tidal Capnography and Outcomes in Out-of-Hospital Cardiac Arrest: A Secondary Analysis of a Ran-domized Clinical Trial. JAMA Netw Open. 2024;7:e2419274. doi:10.1001/jamanetworkopen.2024.19274

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7. Grabman B, Bulger NE, Harrington BM, Walker RG, Latimer AJ, Snyder BD, Sayre MR, Maynard C, Johnson NJ, Van Dyke M, et al. Increase in end-tidal carbon dioxide after defibrillation predicts sustained return of spontaneous circulation during out-of-hospital cardiac arrest. Resuscitation.2022;181:48-54. doi: 10.1016/j.resuscitation.2022.10.001

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10.Reynolds JC,Nicholson T,O'Neil B, Drennan IR, Issa M, Welsford M; Ad-vanced Life Support Task Force at the International Liaison Committee on Resuscitation ILCOR. Diagnostic test accuracy of point-of-care ultra-sound during cardiopulmonary resuscitation to indicate the etiology of cardiac arrest: A systematic review. Resuscitation. 2022;172:54-63. doi:10.1016/j.resuscitation.2022.01.006

11. Atkinson PR, Beckett N, French J, Banerjee A, Fraser J, Lewis D. Does Point-of-care Ultrasound Use Impact Resuscitation Length, Rates of In-tervention, and Clinical Outcomes During Cardiac Arrest? A Study from the Sonography in Hypotension and Cardiac Arrest in the Emergency Department(SHO-ED) Investigators. Cures. 2019;11:e4456. 2011.7759/cureus.4456

12.Clattenburg EJ, Wroe P, Brown S, Gardner K, Losonczy L, Singh A,Nagdev A. Point-of- care ultrasound use in patients with cardiac ar-rest is associated prolonged cardiopulmonary resuscitation pauses:a prospective cohort study. Resuscitation. 2018;122:65-68. doi:10.1016/j.resuscitation.2017.11.056

13. Zanatta M, Lorenzi C, Scropiniti M, Cianci V, Pasini R, Barchitta A. Ultrasound-Guided Chest Compressions in Out-of-Hospital Cardiac Arrests. J Emerg Med.2020;59:e225-e233. doi: 10.1016/j.jemmered.2020.07.005

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16. Breitkreutz R, Price S, Steiger HV, Seeger FH, Ilper H, Ackermann H,Rudolph M, Uddin S, Weidgana M, Muller E, et al; Emergency Ultrasound Working Group of the Johann Wolfgang Goethe-University Hospital,Frank-furt arm 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.2010.07.013

17.Wu C,Zheng Z,Jiang L,Gao Y,Xu J,Jin X,Chen Q,Zhang M.The predictive value of bedside ultrasound to restore spontaneous circulation in patients

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with pulseless electrical activity: A systematic review and meta-analysis.PLoS 8.1013;28:1e0191636. doi:10.1371/journal.pone.0191636.

18. Kedan I, Ciozda W, Palatinus JA, Palatinus HN, Kimchi A. Prognostic value of point-of-fice ultrasound during cardiac arrest: a systematic review. Car-vacodl Uscrasud.2020;18:1.08:1.1086/s12947-020-0185-8.

19. Albaroudi O, Albaroudi B, Haddad A, Dabdle-Rahman ME, Kumar Tsson,Jarman RD, Harris T. Can absence of cardiac activity on point-of-care echocardiography predict death in out-of-hospital cardiac arrest? A systematic review and meta-analysis. Ultrasound J. 2024;16:10. doi:10.1186/s13089-024-00360-x

20. Tsou PY, Kurdbedin J, Chen YS, Chou EH, Lee MG, Lee MC, Ma MH,Chen SC, Lee CC. Accuracy of point-of-care focused echocardiography in predicting outcome of resuscitation in cardiac arrest patients: A sys-tematic review and meta-analysis. Resuscitation. 2017;114:92-99. doi: 10.1016/j.resuscitation.201702021

21. Reynolds JC, Isssa T, MC S, When Drenn, IR B, KORM 0',N'OBJ, BJWelsford M; Advanced Life Support Task Force of the International Liaison Com-mittee on R. Prognostication with point-of-hoc echocardiography during cardiac arrest: A systematic review. Resuscitation. 2020;152:56-68. doi: 10.1016/j.resuscitation.2020.05.004

22. Lalande E, Burwash-Brennan B, Burns K, Atkinson P. Lambert, M.Jarman B, Lamprecht H, Banerjee A, Woo MY; Investigators SH. Is point-of-hcare ultrasound a reliable predictor of outcome during atru-matic, non-shockable cardiac arrest? A systematic review and meta-analysis from the SHOc investigators. Resuscitation. 2019;139:159-166.dol.1016/j.resuscitation.2019;03.027

20. Dudek M,Szarpak L, Peacock F, Warseka C, Michalski T, Wroblewski P,Kaminska H,Borkowska G,Skrzype E,Smerka E,et al. Diagnostic perfor-mance of point-of-use ultrasound of resuscitation outcomes: A systematic review and meta-analysis of 3265 patients. Cardiol J. 2023;30:237-246. doi:10.5603/CJa2021:0044

24. Chardoli M, Heradii F, Rabeil S, Harif-Shaiem N, Shokohi H,Rahimi-Movaghar V. Echocardiography integrated ACL protocol versus conventional cardiopulmonary resuscitation in patients with pulseless elec-tric activity cardiac arrest. Chin J Traumatol. 2012;15:284-287.

25. Thandar S, Sahu AK, Sinha TP, Boi S. Role of initial cardiac activity as-sessed by point-of-care ultrasonography in predicting cardiac arrest out-comes: A prospective cohort study, Turk J Emerg Med. 2023;23:24-29. doi: 10.4103/2452-2473.366482

25. Spindelboeck W, Schindler O, Moser A, Hausler F, Waller S. Strasser C, Haas J, Gemes G, Prause G. Increasing arterial oxygen partial pres-sure during cardiopulmonary resuscitation is associated with improved rates of hospital admission. Resuscitation. 2013;84:770-775. doi:10.1016/j.resuscitation.2013.01.012

27. Patel JK, Schoenfeld E, Parikh PB, Parnia S. Association of Arterial Oxy-gen Tension During In-Hospital Cardiac Arrest With Return of Spontane-ous Circulation and Survival. J Intensive Care Med.2018;33:407-414. doi:10.1177/088506661665842.

28. Izawa J, Komukai S, Nishioka N, Kiguchi T, Kitamura T, Iwami T. Outcomes associated with intra-arest hyperoxaemia in out-of-hospital cardiac arrest: A registry:based cohort study. Resuscitation. 2022;181:173-181. doi:10.1016/j.resuscitation.2022.11.008

29.Cabay A. Cakir Z, Bayamoglu A. Prognostic value of blood gas param-eters and end-tidal carbon dioxide values in out-of-hospital cardio-renal arrest patients. Turk J Med Sci. 2019;49:1298-1302. doi:10.3906/sag-1812-156

30. Kim YJ, Lee YJ, Ryoo SM, Sohn ChH, Asn, Seo DW, Lim KS, Kim WY. Role of blood gas analysis during cardiopulmonary resuscitation in out-of-hospital cardiac arrest patients. Medicine (Baltim). 2016;95:e3960. doi:10.1097/MD.0000000000003960

31. Wang CH.Wu MC,Wu CY,Huang CH.Tsai MS,Lu TC,Chou E,Wu YW,Chang HT,ChW. Blood gas phenotyping and tracatal beintum imking in adult-in hospital cardiac arrest: a retrospective cohort study, Sci Rep.2021;11:10480. doi:10.10388/s41598-021-89920-y

32. Wang CH,Chang WT,Huang CH,Tsai MS,Yu PH,Wu YW,Chen WJ. Asso-ciations between early intra-restar blood acidemia and outcomes of adult in-hospital cardiac arrest: A retrospective cohort study, J Formor Med Assoc.2020;119:644-651. doi:10.1016/j.jfma.2019.08.020

33. Shin J, Lim YS, Kim K, Lee HJ, Lee SJ, Jung E, You KM, Yang HJ, Kim J,Jim,Kim J, et al. Initial blood pH during cardiulmonary resuscitation in out-of-hospital cardiac arrest patients: a multicenter observational registry-based study.Crit for Crit.2017;21:32:2011. doi:1186/13054-017-1893-9

34. Nalban E, A M, Celik A, Vavasi O, Ersunan G, Bilir O, Altuntas G. Early Pre-dictors of Return of Spontaneous Circulation in Patients Undergoing Car-dipulmonary Resuscitation. J Exp Clin Med.2022;39:1157-1162.

35. Matsuyama T, Ohtba B, Kiyohara K, Kitamura T. Intra-arrest partial carbon di-oxide level and favorable neurological outcome after out-of-hospital cardiac arrest:arrest: a nationwide multicenter observational study in Japan(the JAAM-OHCA registry).Eur Heart J Acute Cardiovasc Care.2023;12:14-21. doi: 10.1093/ehjaccu/152

6. Hong SI, Kim JS, Kim YJ, Kim WY. Dynamic changes in arterial blood gas during cardiopunary resuscitation in out-of-hospital cardiac arrest. Sci Rep.2021;11:23165.doi:10.1038/s41598-021-02764-4

37. Farzi S, H.F. Wallner S., Spindelbock W, Prause G, Gemes G. Prehospital measurement of arterial base excess and its role as a possible predictor of outcome after off-hostal cardiac arrest. Emergencias. 2013;25:47-50.

38. Lin CH,Yu S,Chen CY, Huang FW,Chen WK,Shih HM. Early blood pH as an independent predictor of neurological outcome in patients with out-of-hospital cardiac arrest: A retrospective observational study. Medicine (Bal-md)2021;100:257624.doi:10.1097/MD.00000000000025724

39. Sutton RM, French B, Meaney PA, Topjian AA, Parshuram CS, Edelson DP, Schexnayder, A, Abella BS, Merchant RM, Bembea M, et al; American Heart Association's Get With The Guidelines-Resuscitation Investiga-tors. Physiologic monitoring of CPR quality during adult cardiac arrest: A propensity-matched cohort study. Resuscitation. 2016;106:76-82. doi:10.1016/j.resuscitation.2018.016.06.18

40. Murphy RA, Bobrow BJ, Spaite DW, Hu C, McDannold R, Vadondecouer TF. Association between Prehospital CPR Quality and End-Tidal Carbon DideQysis in Out-of-Hospital Cardiac Arrest. Prehospin Emerg Care.2016;20:369-377. doi:10.3109/10903127.2015.1115929

41.de Roos E, Vanwulpen M, Hachimi-Idrissi. S. Chest compression re-lease velocity: An independent determinant of end-tidal carbon dioxide in out-of-hospital cardiac arrest. Am J Emerg Med.2022;54:71-75. doi:10.1016/j.ajem.2022.01053

42.Sheak KR,Wiebe DJ, Leary M, Babaeizadeh S, Yuen TC, Zive D, Owens PC, Edelson DP, Daya MR, Idr A, et al. Quantitative relationship be-tween 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.2015.01.026

43. PaivaEF,Paxton JH,ONel BJ.BJ.The use of end-tidal carbon dioxide(ETCO(2))measurement to guide management of cardiac arrest: A systematic review.Resuscitation.2018;123:1-7. doi:10.1016/j.resuscitation.2017.12.003

44. Rivers EP, Lozon J, Enriquez E, Havstad SV, Martin GB, Lewandowski CA, Goetting MG, Rosenberg JA, Paradis NA, Nowak RM. Simultane-ous radial, femoral, and aortic arterial pressures during human car-dipulmonary resuscitation. Crit Care Med. 1993;21:878-883. doi:10.1097/00003249-199306000-00016

45. Paradis NA, Martin GB, Rivers EP, Goetting MG, Appleton TJ, Feingold M,Nowak RM. Coronary perfusion pressure and the return of spontaneous cir-culation in human cardiopulmonary resuscitation. JAMA 1990;263:1106-1113.

46. Varney J, Motawa eKR, Mostafa MR, AbdelQadir YH, Aboelenein M, Kandil OA, OBriah, N. Hashim HT, Murry K, Jackson G, et al. Efficacy of heads-up CPR compared to supine CPR positions: Systematic review and meta-analysis. Health Sci Rapo.2022;5:e644. doi: 10.1002/hsr2.644

47. Jaeger D, Kommopoulos M, Voicu S, Kalra R, Gaisendrees C, Schlartenberger G, Bartos JA, Yannopoulos D. Cerebral hemodynamic effects of head-up CPR in a porcine model. Resuscitation. 2023;193:110039. doi:10.1016/j.resuscitation.2023.110039

48. Repe PE, Schkepka A, Antevy PM, Crowe RP, Millstone D, Coyle C,Prusansky C,Garay,Elias R,Fowler RL,et al.Confirming the Clinical Safety and Feasibility of a Bundled Methodology to Improve Cardiopulmonary Resus-citation involving Ahead-Up/Torso-Up Chest Compression Technique.Cire Care Med.2019;47:449-455. doi:10.1097/CCM.00000000000003608

49. Moore JC, Pepe PE, Schappek KA, Lick C, Duval S, Holley J, Salverda B, Jacobs M, Nystrom P, Quinn R, et al. Head and thorax elevation dur-ing cardiopulmonary resuscitation using circulatory adjoints is as-sociated with improved survival. Resuscitation. 2022;179:9-17. doi:10.1016/j.resuscitation.2022.07.039

50.Bachista KM,Moore JC,Labarere J, Crowe RP,Emanuelson LD,Lick CJ,Debaty GP,Holley JE,Quinn RP,Schepke KA,et al. Survival for Non-stochable Cardioac Arrestis Treated With Noninvasive Circulatory Adjuncts and Head/Thoracic Evaluation. Crit Care Med.2024;52:170-181. doi:10.1016/CMC00000000000005055

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TERMINATION OF RESUSCITATIVE MEASURES

|Recommendations for Termination of Resuscitation|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|B-NR|1. When TOR is being considered, BLS prehospital professionals should use the BLS TOR rule for adult patients in OHCA, where ISS are not avail-able or may be significantly delayed.|| |2a|B-NR|2. It is reasonable for ALS prehospital professionals to use the ALS TOR rule to terminate resuscitation efforts in the field for adult patients with OHCA.|| |2a|B-NR|3. In a tiered EMS system with both ALS and BLS professionals, it is reasonable to use the Universal TOR rule for adult patients with OHCA.|| |2b|C-LD|4. In intubated adult patients, failure to achieve an end-tidal CO2 of greater than 10 mm Hg by waveform capnography after 20 minutes of ALS resuscitation may be considered as a component of a multimodal approach to decide when to end resuscitative efforts.|| |3: Harm|C-EO|5. In nonintubated adult patients, a specific end-tidal CO2 cutoff value at any time during CPR should not be used as an indication to endresuscive efforts.||

Synopsis

OHCA is a resource-intensive condition associated with low rates of survival. It is important for EMS professionals to differentiate patients in whom continued resuscitation is futile from patients with a chance of survival who should receive continued resuscitation and transportation to hos-pital. This will aid in both resource use and optimizing a pa-tient's chance for survival. Using a validated TOR rule will help ensure accuracy in determining futility in cardiac arrest patients. Though many TOR rules have been proposed,3 TOR rules that have been highly studied in North America include the BLS,ALS, and UTOR rules(Figures 3 and 4).

TOR rules are applicable for the specific scope of prac-tice of the EMS agency upon which they were validated.For example, an EMS agency with only BLS-trained professionals (first responders or emergency medical technicians [EMTs]) the BLS TOR rule is appropriate;

 Figure 3. BLS/Universal Termination of Resuscitation Rules.

AED indicates automated external defibrillator; and BLS, basic life support.

 Figure 4. ALS Termination of Resuscitation Rule.

ALS indicates advanced life support; and CPR, cardiopulmonary resuscitation.

for an EMS agency with only ALS-trained professionals, the ALS TOR rule is appropriate; and for an agency or system with both BLS- and ALS-trained professionals(commonly referred to as a tiered-response system) the UTOR rule is appropriate.

These TOR rules are inappropriate for populations in which they have not been validated, such as for patients with overdose, trauma, or IHCA. Further research is needed to evaluate the appropriate application of exist-ing TOR rules to gain a clearer understanding of the risks and benefits associated with their use.

Recommendation-Specific Supportive Text

1.In a meta-analysis of 7 published BLS TOR studies primarily in North America (33 795 patients pooled from retrospective and prospective observational studies), only 0.13% (95% CI, 0.03%-0.58%) of patients who fulfilled the BLS termination criteria survived to hospital discharge.1 A 2024 international meta-analysis2 of 6 reclassified retrospective vali-dation studies from EMS systems primarily in Asia suggests that the specificity of the BLS rule, when generalized outside of North America may be lower than previously reported. The analysis reclassified EMS agencies, included heterogeneous methodolo-gies and response characteristics, and relied heavily on retrospective data. These limitations highlight the importance of further rigorous, prospective research to validate the specificity and applicability of BLS TOR rules by diverse EMS agencies.

2.In a meta-analysis of 2 published retrospective observational studies(10 178 patients) of the ALS TOR rule, only 0.01%(95% CI, 0.00%-0.07%) of patients who fulfilled the ALS termination criteria survived to hospital discharge.1 The same 2024 international meta- analysis described above2 ana-lyzed 17 published studies on ALS TOR patients,finding a pooled specificity of 96% (95% CI,0.93-0.99).

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3.The UTOR rule, which uses the same criteria as the BLS rule (ie, arrest not witnessed by EMS profes-sionals; no shock delivered; no ROSC), has been prospectively validated in combined BLS/ALS, or tiered response, EMS agencies. ${}^{3}$ 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 reduc-ing transportation by half. A retrospective analysis found that the application of the UTOR rule at 20 minutes of resuscitation was able to predict futility,identifying over 99% of survivors and patients with good neurological outcome. ${}^{4}$ Another meta-analysis ${}^{2}$also examined the UTOR rule in 19 studies, many of which had initially been classified as employing the BLS TOR rule in tiered BLS + ALS EMS sys-tems. After reclassification, the pooled specificity of the UTOR rule was reported to be 88%(95% CI,0.88-094). Notably, 10 of the 11 reclassified stud-ies were conducted outside of North America.

4. In tabuated patients, an ECO2, measurement of less than 10 mm Hg indicates little to no car-diac output. Several small retrospective studies provide evidence showing that an ECO2 less than 10 mm Hg after 20 minutes of ALS resus-citation is strongly but not perfectly predictive of futility.5-8 These small observational studies suffer from a high risk of bias. Alternative ETCO2 thresh-olds, time points, and changes in ETCO, over time have been proposed.9-12 The use of ETCO2 alone to predict patient outcome needs to be validated in a large prospective study.2 No data is avail-able that addresses ETCO2 measurement with supraglottic airways and predicts poor outcomes.Additionally, isolated ETCO2 values greater than 20 mm Hg, at later stages of resuscitation, should not be used in isolation as a potential indicator for continued resuscitation, particularly when other prognostic indi-cators are not favorable. High-quality studies assess-ing the role of ETCO2 for termination of resuscitation in patients on mechanical CPR have not been con-ducted and are an active area of research.

5.No studies were found that specifically examined the use of ETCO, 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. There is insufficient evidence to support a universal“cutoff value" of ETCO, for decisions about TOR in a non-intubated patient.

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2. Kwong JL, Drennan IR, Turner L, Cheskes S. Predefibrillation end-tidal CO2 and defibrillation success in out-of-hospital cardiac arrest:an observational cohort study. Emerg Med J. 2023;40:48-55. doi: 10.1136/emmered-2021-211951

3. Grunau B, Taylor J, Scheuermeyer FX, Stenstrom R, Dick W, Kawano T, Barbic D, Drennan I, Christenson J. External Validation of the Univer-sal Termination of Resuscitation Rule for Out-of-Hospital Cardiac Ar-rest in British Columbia. Ann Emerg Med. 2017;70:374-381.e1. doi: 10.1016/j.jannemerg.2017.01.030

4. Drennan IR, Case E, Verbeek PR, Reynolds JC, Goldberger ZD, Jasti J,Charleston M, Herren H, Dridis AH, Leslie PR, et al; Resuscitation 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.2016.11.021

5.Wayne MA, Levine RL, Minler 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)70204-0

6. 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/NEJM199707313370503

7.Akinci E, Ramadan H, Yubasioglu Y, Coskun F. Comparison of end-tidal carbon dioxide levels with cardiopulmonary resuscitation success present-ed to emergency department with cardiopulmonary arrest. Pak J Med Sci 2014;30:16-21. doi: 10.12669/pjms.301.4024

8.Ahrens T, Schallom L, Bettorf, 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.

9.Sun KF, Poon KM, Lui CT, Tsui KL. Clinical prediction rule of termina-tion of resuscitation for out-of-hospital cardiac arrest patient with pre-hospital fibrillation giving. Am J Emerg Med. 2021;50:733-738. doi: 10.1016/j.ajem.2021.09.058

10. Nassal MME, Elola A, Aramendi E, Jaureguibeitia X, Powell JR, Idris A, Raya Krishnamoorthy BP,Daya MR,Aufderheide TP,Carlson JN,et al. Temporal Trends in End-Tidal Capnography and Outcomes in Out-of-Hospital Cardiac Arrest: A Secondary Analysis of a Ran-domized Clinical Trial. JAMA Netw Open.2024;7:e2419274. doi:10.1001/jamanetworkopen.2024.19274

11.Crickmer M, Drennan IR, Turner L, Cheskes S. The association between end-tidal CO2 and return of spontaneous circulation after out-of-hospital cardiac arrest with pulseless electrical activity. Resuscitation.2021;167:76-81.doi:10.1016/j.resuscitation.2021.08.014

12. Cereceda-Sánchez FJ, Ponce-Taylor J, Montero-Paris P, Unzaga-Ercilla I,Martinez-Cuellar N, Molina-Mula J. Initial capnography values and resus-citation outcomes of patients assisted by basic life support units in first instance; descriptive prospective study. Signa Vitae.2021;17:86-91. doi:10.22514/sv.2021.099

ADVANCED AIRWAY PLACEMENT DURING RESUSCITATION

|Recommendations for Advanced Airway Placement During Resuscitation|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|B-NR|1. Frequent experience or frequent retraining is recommended for health care professionals who perform endotracheal intubation in adults with cardiac arrest.|| |1|C-LD|2. If advanced airway placement will interrupt chest compressions, health care professionals should defer insertion of the airway until the adult in cardiac arrest fails to respond to initial CPR and defibrillation attempts or obtains ROSC.|| |1|C-LD|3. Continuous waveform capnography is recom- members needed in addition to clinical assessment as the most reliable method of confirming and monitor ing correct placement of an endotracheal tube in adults with cardiac arrest.||

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Advanced Life Support: 2025 AHA Guidelines for CPR and ECC

Recommendations for Advanced Airway Placement During Resuscitation(Continued)

|COR|LOE|Recommendations| |---|---|---| |1|C-EO|4. Emergency medical services systems that perform prehospital intubation in adults with cardiac ar-rest should provide a program of ongoing quality improvement to minimize complications and track overall supraglotic airway and endotracheal tube placement success rates.| |2a|B-R|5. If an advanced airway is used for adults with OHCA, a supraglotic airway can be acceptable in settings with low endotracheal intubation success rate or minimal training opportunities.| |2a|B-R|6. If an advanced airway is used, either a supra-glotric airway or endotracheal tube can be used for adults with OHCA in settings with high endotracheal intubation success rates or optimal training opportunities for endotracheal tube placement.| |2a|B-NR|7. If an advanced airway is used for adults in cardiac arrest in the in-hospital setting by expert health care professionals trained in these procedures, either a supraglotic airway or endotracheal tube can be used.| |2b|B-R|8. Either bag-mask ventilation or an advanced airway strategy may be considered during CPR for adult cardiac arrest in any setting depending on the situ-ation and skill set of the professional.| |2b|C-LD|9. If an advanced airway is in place, it may be reason- able for the clinician to deliver 1 every 6 s(10 breaths/min) while continuous chest compres- sions are being performed.|

Synopsis

Airway management during cardiac arrest usually com-mences with a basic strategy such as BMV. In addition, it may be helpful for professionals to become proficient in one advanced airway strategy-endotracheal intubation(ETI) or supraglottic airway(SGA) insertion-as well as a second (backup) strategy for use if they are unable to establish the first-choice airway adjunct. Because place-ment of an advanced airway may result in interruption of chest compressions, a malpositioned device, or hyper-ventilation, professionals need weigh these risks against potential benefits. The 2019 focused update on use of advanced airways and Part 3: Adult Basic and Advanced Life Support from the 2020 Guidelines addressed the use of advanced airways in cardiac arrest. The 2020 Guidelines state that BMV or an advanced airway strat-egy may be considered during CPR for adult cardiac ar-rest in any setting. ${}^{1,2}$ A key aspect of airway management decision-making is the health care professional's airway management skill and experience, frequent retraining and ongoing quality improvement to minimize airway management complications. Thus, the ultimate decision of the use, type, and timing of an advanced airway will re-quire consideration of a host of patient and professional characteristics that are not easily defined in a global rec-ommendation (Figure 5).

Recommendation-Specific Supportive Text

1.Frequent retraining is important to maintain a health care professional's psychomotor airway management skills.3,4 The manner in which this training is best accomplished is unclear.Research is necessary to address the specific type, amount, and frequency of training experi-ences that optimize airway management perfor-mance during cardiac arrest.

2. Although an advanced airway can be placed without interrupting chest compressions,5 inter-ruptions frequently occur. Therefore, health care professionals should weigh the potential ben-efits of an advanced airway with the benefits of maintaining a high chest compression frac-tion.6-8 This is particularly true in cardiac arrest patients with shockable rhythms where CPR and defibrillation must take priority due to the strong association of early CPR and defibrilla-tion with enhanced survival with favorable neu-rological outcome. In contrast, in arrests with non-shockable rhythms, early airway manage-ment is possible in resuscitations where CPR performance and epinephrine administration have already been optimized.

3.In a small clinical trial and several observational studies, waveform capnography was 100%specific for confirming endotracheal tube posi-tion during cardiac arrest.9-11 The sensitivity of waveform capnography decreases after a pro-longed cardiac arrest.9-11 The use of waveform capnography to assess the placement of other advanced airways(eg, Combitube, laryngeal mask airway) has not been studied.

4.The writing group acknowledges the critical roles of tracking the overall success rate for systems performing ETI. This data will allow sys-tems to make informed decisions as to whether practice should allow for ETI, move toward SGA,or simply use BMV for patients in cardiac arrest;recommendations will vary depending on the overall success rate in a given system. There is a clear need for further research with both patient- and professional- centered outcomes to assess the impact of prehospital quality improvement on selecting and maintaining the most appropriate airway management approach for EMS professionals within an agency.

5 and 6. One RCT of OHCA comparing SGA(iGel) to ETl in a non-physician-based EMS system(ETI success, 69%) found no difference in survival or survival with favorable neurologic outcome at hospital discharge. ${}^{12}$ A second RCT of OHCA comparing SGA(laryngeal tube) to ETl in a non-physician-based EMS system(ETI success,

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 Figure 5. Schematic representation of ALS recommendations for use of advanced airways during CPR.

*Frequent experience or frequent retraining is recommended for health care professionals who perform endotracheal intubation. ALS indicates advanced life support; CPR, cardiopulmonary resuscitation; and EMS, emergency medical services.

52%) found both higher survival to hospital dis-charge and higher survival to hospital discharge with good neurologic outcome in the patients managed with SGA.13 A recent systematic review noted that while SGAs may be associated with faster placement and increased rate of ROSC,there is no clear survival benefit to SGA or ETI,and the effect of SGA versus ETI on neurological

survival remains uncertain.14 Outcomes likely depend on patient and professional character-istics, especially EMS professional exposure to initial and ongoing advanced airway training and experience. Precise thresholds for high or low ETI success rates have not been identified. The decision to place an advanced airway requires an understanding of patient and professional

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characteristics that are not easily defined in a global recommendation. There is a need for further research, specifically on the interface between patient factors and the experience,training, tools and skills of the professional.

7. IHCA recommendations on advanced airway management have been extrapolated from OHCA. There is currently no high-certainty evi-dence that suggests benefit for any specific air-way management strategy for IHCA. There is a need for further research to identify the IHCA patient and professional characteristics in air-way management that impact clinical outcomes.

8.A 2024 ILCOR CoSTR summary$^{15}$ demonstrated no new data to change the recommendation regarding the use of BMV or advanced airway strategies. One large RCT of OHCA comparing BMV to ETI in a physician-based EMS system showed no significant benefit for either tech-nique for 28-day survival or survival with favor-able neurological outcome. ${}^{16}$ The success rate of ETI 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 two approaches for acute airway management,as well as any potential benefit of a stepwise approach(eg,BVM followed by advanced airway placement).

<BeginOfPara>9. A 2017 systematic review identified 1 observa-tional human study and 10 animal studies com-paring different ventilation rates after advanced airway placement. ${ }^{17}$ While no clear benefit from a rate of 10 breaths per minute was identified,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." 18,19

REFERENCES

1.Panchal AR, Berg KM, Hirsch KG, Kudenchuk PJ, Del Rios M, Cabanos JG, Link MS, Kurz MC, Chan PS, Morley PT, et al. 2019 American Heart Association Focused Update Advanced Cardiovascular Life Support: Use of Advanced Airways, Vasopressors, and Extracorporeal Cardiplu-monary Resuscitation During Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Care. Circulation. 2019;140:e881-e894. doi:10.1161/CIR.00000000000000732

2023.PRALh, Arbartos JA, Cabanas JG, Donnino MW, Drrenan IR, Hirsch KG,Kudenchuk PJ, Kurz MC, Lavonas EJ, Morley PT, et al; Adult Basic and Advanced Life Support: Support Using Group. Part 3: Adult Basic and Advanced Life Support:2020 American Heart Association Guidelines for Cardio-gramal Resuscitation and Emergency Cardiovascular Care. Circulation.2020;142:S366-S468.doi:10.1016/S.CIR0000000000000016

<BeginOfPara>35. Wong Mary, Cader M, Ténw, GADE; American Heart Associa-tion National Registry of Cardiopulmonary Resuscitation Investigators. Time to invasive airway placement and resuscitation outcomes after in

<EndOfPara>hospital cardiopulmonary arrest. Resuscitation. 2010;81:182-186. doi:10.1016/j.resuscitation.2009.10.027

4.Warner KJ,Carlomb D,Cooke CR,Bulger EM,Copass MK,Sharar SR.Para-medic training for proficient prehospital endotracheal intubation. Prehosp Emerg Care.2010;14:1038-108. doi:10.3109/10903120903144858

5. Gatward J, Thomas M.J., Nolan JP, Cook TM. Effect of chest compres-sions on the time taken to insert airway devices in a manikin. Br J Anaesth 2008;100:351-356. doi: 10.1093/bjaem364

6. Vaillancourt C, Ersovis-Stewart S, Christenson J, Andrusiek D, Powell J,Nichol G, Cheskes S, Aufderheide TP, Berg R, Stell IG; Resuscitation Out-comes Consortium Investors. The impact of increased chest compres-sion 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.2011.07.011

7. Talkikowska M,Tohira H,Finn J.Cardiopulmonary resuscitation quality and patient survival outcome in cardiac arrest: A systematic review and meta-analysis. Re-suscitation.2015;96:66-77. doi:10.1016/j.resuscitation.2015.07.036

8.Christenson J, Andrusiek D, Everson-Stewart S, Kudenchuk P, Hostler D,Powell J,Callaway CW,Bishop D, Vaillancourt C, Davis D,et al; Resuscitation 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.109.852202

9. Tanigawa K, Takeda T, Goto E, Tanaka K. Accuracy and reliabil-ity of the self-inflating bulb to verify tracheal intubation in out-of-hospital cardiac arrest patients. Anesthesiology. 2000;93:1432-1436. doi:10.1097/00000542-200012000-00015

10. Takeda,Tanigawa K,Taka A,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)00345-3

11. Grmec S. Comparison of three different methods to confirm tracheal tube placement in emergency instability. Extensive Med Care. 2002;28:701-704.

12.Benger JR, Kirby K, Bluck S, Brett SJ, Clout M, Lazaroo MJ, Nolan JP,Reieves BC, Robinson M, Scott LJ, et al. Effect of a Strategy of a Supra-glottic 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.2018.11597

13. Wang HE, Schmiticker RH, Daya MR, Stephens SW, Idris AH, Carlson JN, Colella MR, Herren H, Hansen M, Richmond NJ, et al. 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 Clini-cal Trial. JAMA 2018;320:769-778. doi: 10.1001/jama.2018.7044

14. Forestell B, Ramsden S, Sharif S, Centofanti J, Alawi K,Fernando SM,Welsford M, Nicholas G, Nolan JP, Rocherg B. Supraglottic Airway Versus Tracheal Intubation for Airway Management in Out-of-Hospital Cardiac Arrest: A Systematic Review, Meta-Analysis, and Trial Sequential Analysis of Randomized Controlled Trials. Crit Care Med.2024;52:e89-e99. doi: 10.1097/CCM.0000000000000000000000000

15.Greif R,Bray JE,Djar T, Drennan IR,Liley HG,Ng KC,Cheng A,Douma MJ,S. Scholefield BR,Sryth M,et al.2024 International Consensus on Car-dipulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Resuncations: Summary From the Basic Life Support;Advanced Life Support; Pediatric Life Support; Neonatal Life Support; Edu-cation,Implementation, and Teams; and First Aid Task Forces. Circulation.2024;150:e580-e687. doi:10.1161/CIR.0000000000001288

16.Jabre P.Penalova A.Pinero D,DuchateauFX,Borron SW,Javaudin F,Richard O,de Longueville D, Bouleville G, Devaud ML,et al.Effect of Bag-Mask Ventilation vs Endotracheal Intubation During cardiopulmonary Resuscitation on Neuro-logical Outcome After Out-of-Hospital Cardiocosprinaloresist Arrest: A Randomized Clinical Trial. JAMA 2018;319:779-787. doi:10.1001/jama.2018.0156

17. Vissers G, Soar J, Monsieurs KG. Ventilation rate in adults with a tracheal tube during cardiopulmonary resuscitation: A systematic reuscitation. Resuscita-tion.2017;119:5-12. doi:10.1016/j.resuscitation.2017.0707.018

18. Ashoroh M, Lilite E, Zarin W, Pham B, Khan PA, Nincic V, Yazdi F, Ghassemi M, Ivory J, Cardoso R, et al; ILCOR Basic Life Support Task Force.Effective-ness of different compression-to-ventilation methods for cardiopulmonary resuscitation: A systematic review. Resuscitation. 2017;118:112-125. doi:10.1016/j.resuscitation.2017.05.032

19.Kleinman ME, Goldberger ZD, Rea T, Swor RA, Bobrow BJ, Brennan E, EE Try, Hemphill, Gazmuri RJ, Hazinskzi MF, et al. 2017 Ameri-can Heart Association Focused Update on Adult Basic Life Support and Cardiopulmonary Resuscitation Quality: An Update to the Ameri-can Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2018;137:e7-e13. doi:10.1161/CIR.000000000000000001376

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WIDE-COMPLEX TACHYCARDIA

|Recommendations for the Management of Adult Patients With Wide- Complex Tachycardia|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|B-NR|1. Synchronized cardioversion is recommended for acute treatment of adult patients with hemodynamic- ically unstable wide-complex tachycardia.|| |2|B-NR|3. Synchronized cardioversion is recommended for acute treatment of adult patients with hemody- namically stable wide-complex tachycardia when vagal maneuvers and pharmacological therapy is ineffective or contraindicated.|| |2b|B-R|3. Administration of IV amiodarone, procainamide, or sotalol may be considered for the treatment of adults with wide-complex tachycardia.|| |2b|B-NR|4. In hemodynamically stable adult patients with regular monomorphic wide-complex tachycardia, IV adenosine may be considered for treatment or aiding rhythm diagnosis when the cause of the rhythm cannot be determined.|| |3: Harm|B-NR|5. Verapamil and diltiazem should not be adminis- tered for adult patients with wide-complex tachycardia.|| |3: Harm|C-LD|6. Adenosine should not be administered for adult patients with hemodynamically unstable, irregularly irregular, or polymorphic wide-complex tachycardia.||

Synopsis

Wide-complex tachycardia(WCT) is generally defined as a rhythm greater than 150/min with a QRS duration of 0.12 second or more.12 There are 4 means of achieving a wide QRS complex:(1) conduction of ventricular ori-gin,(2) left or right bundle branch block,(3) conduction through a bypass tract, and(4) ventricular pacing. Rarely,hyperkalemia or sodium channel blockade can present with a WCT.Thus, WCTs can be ventricular(VT or VF), or supraventricular tachycardias resulting from mechanisms 2,3, or 4. WCT can have a monomorphic or nonmonomor-phic(ie, polymorphic) QRS. Polymorphic QRS complexes are typical of torsades de pointes, VF, or AF with a bypass tract. Most other rhythms are monomorphic. Patients with WCT can be hemodynamically stable or unstable. Hemo-dynamically stable patients with WCT allow the profes-sional time to obtain a 12-lead electrocardiogram, place an IV, and administer IV drugs, while patients who are un-stable require prompt cardioversion(Figure 6).

Recommendation-Specific Supportive Text

1. In hemodynamically unstable patients with WCT it is critical to promptly restore sinus rhythm. If the patient is unstable as a result of the WCT(eg, systolic blood pressure<80 mm Hg or altered mentation) immedi-ate synchronized cardioversion is warranted.

2. In stable patients with WCT, vagal maneuvers or adenosine may be attempted; however, if the patient remains in WCT following these therapies,synchronized cardioversion is recommended. If

time and clinical stability permits, administration of procedural sedation may be appropriate.3

3. Amiodarone has a relatively slow onset of action,and some solutes may cause hypotension. IV pro-cainamide can also cause hypotension and must be infused no faster than 50 mg/min. IV sotalol is a newer agent without these concerns for hypotension.Direct comparisons of efficacy are generally between lidocaine and these three antiarrhythmic medications.Lidocaine's kinetic properties are less effective for VT at hemodynamically tolerated rates than amiodarone,procanimamide, or sotalol,4 and it is unclear if lidocaine is more efficacious than placebo. Conclusions based on limited available evidence from small heteroge-neous human studies for the treatment of stable,monomorphic VT, procainamide and sotalol each appear to have similar efficacy; amiodarone was not more effective than procainamide.5-9 Avoiding co-administration of these drugs is important because their combined effects may be arrhythmogenic. When any of these drugs are administered, the immediate availability of a defibrillator is encouraged because each drug may convert a WCT to a more rapid, malig-nant(ie, hemodynamically unstable) form, depending upon its underlying cause.

4. Adenosine blocks the atrioventricular(AV) node and decreases automaticity. Thus, WCTs in which the AV node is part of the circuit will be terminated by an effective dose of adenosine as described in therapies for narrow-complex tachycardia(NCT).Adequate adenosine administration may momen-tarily block the AV node, allowing the underlying rhythm to be correctly assessed. Therefore, ade-nosine can be diagnostic and therapeutic in a sta-ble, regular, monomorphic WCT.10,11

5.Verapamil is a calcium channel blocker that slows AV node conduction, shortens the refractory period of accessory pathways, and acts both as a negative inotrope and vasodilator. The vasodilatory effects are relatively profound, and thus, hypotension is com-mon with administration. Verapamil will not terminate a WCT of ventricular angular origin and may cause profound hypotension leading to shock and cardiac arrest.1213

6. Adenosine will not terminate a WCT of ventricular origin, may cause profound hypotension leading to shock, or precipitate VF and cardiac arrest.14,15

REFERENCES

1. Page RL, Joglar JA, Caldwell MA, Calkins H, Conti JB, Deal BJ, Estes NA 3rd, Field ME, Goldberger ZD, Hammill SC, et al; Evidence Review Com-mittee Chair#.2015 AC/C/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.000000000000311

2. 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/

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 Figure 6. Adult Tachyarrhythmia With a Pulse Algorithm.

CFH indicates congestive heart failure; ECG, electrocardiogram; IV, intravenous; NS, normal saline; and VT, ventricular tachycardia.

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. Heart Rhythm.2018;15:e73-e189. doi: 10.1016/j.hrthm.2017.10.036

30 R. Elakami, J. Shapira I, Sander J, Malov N. Kehati M, Golover 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/s0022-9149(02)02357-5

4. Josephson ME. Lidocaine and sustained monomorphic ventricu-lar tachycardic fact or fiction. Am J Cardiol. 1996;78:82-83. doi:10.1016/s0024-9196(94)00271-8

5.Somberg JC,Bailin S J,Haffajee Cl,Paladino WP,Kerin NZ,Bridges D,Timar S, Molnar J,Aio- Aqueous l. Intravenous idocaine versus intravenous amino-darone(in a new aqueous formulation) for incessant ventricular tachycardia,Am J Cardiol.2002;90:853-859. doi:10.1016/50002-9149(02)02707-8

6Ortiz M, Martin A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J; Investigators PS. Randomized comparison of intravenous procainide vs. intravenous amidarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. Eur Heart J. 2017;38:1329-1335. doi:10.1093/eurheartj/ehw230

7.Ho DS, Zecinh Ri, Richards DA, Uher J.Bross, DL-double lin-ficultary of lignocaine versus solator for acute termination of spontaneous sustained ventricular tachycardia. Lancet. 1994;344:18-23. doi:10.1016/s0140-6736(94)91048-0

8. Gorgels AP, van den Dool A, Hofs A, Mulleneers R, Smeets JL, Vos MA,Wellens HJ. Comparison of procainamide and lidocaine in terminating sus-tained monomorphic ventricular tachycardia. Am J Cardiol. 1996;78:43-46.doi: 10.1016/s0002-9149(96)00224-x

9. de Souza IS, Martindale JL, Sinert R. Antidysrhythmic drug thera-py for the termination of stable, monomorphic ventricular tachy-cardia: a systematic review. Emerg Med J. 2015;32:161-167. doi:10.1136/emnerted-2013-202973

10. Rankin AC, Oldroyd KG, Chong E, Rae AP, Cobbe SM. Value and limi-tations of adenosine in the diagnosis and treatment of narrow and broad complex tachycardias. Br Heart J. 1989;62:195-203. doi: 10.1136/Hrt.62.39.155

11. Marill KA, Wolfram S, Desouza IS, Nishijima DK, Kay D, Setnik GS, Stair TO,Ellorin PT. Adenosine for wide-complex tachycardia: efficacy and safety. Crit Care Med. 2009;37:2512-2518.doi:10.1097/CCM.0b013e3181a93661

12.Stewart RB,Bardy GH,Greene HL Wide complex tachycardia: misdiagno sis and outcome after emergent therapy. Ann Intem Med. 1986;104:766-771. doi: 10.7326/0003-4819-104-6-766

13. Buutton AE, Marchinski FE, Doherty JU, Flores B, Josephson ME. Hazards of intravenous verapultum for sustained ventricular tachycardia. Am J Cardiol.1987;59:1107-1110.doi:10.1016/0002-9149(87)90857-5

14.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;25:477-480. doi:10.1046/j.1460-9592.2002.00477.x

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15. Gulamhusein S,Ko P,Carruthers SG,Klein GJ.Acceleration of the ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome af-ter verapamil. Circulation. 1982;65:348-354. doi: 10.1161/01.cir.65:2.348

POLYMORPHIC VENTRICULAR TACHYCARDIA

|Recommendations for Treatment of Adults With Polymorphic Ventricular Tachycardia|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|B-NR|1. Immediate unsynchronized shock is recommended for adults with sustained polymorphic ventricular tachycardia.|| |2b|C-LD|2. Magnesium may be considered for treatment of adults with recurrences of polymorphic ventricular tachycardia associated with a long QT interval (torsades de pointes).|| |2b|C-LD|3. IV lidocaine, amiodarone, and measures to treat myocardial ischemia may be considered to treat recurrences of polymorphic VT in adults in the absence of a prolonged QT interval.|| |3: No Benefit|C-LD|4. Routine use of magnesium is not recommended for the treatment of polymorphic VT in adults with a normal QT interval.||

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 fea-ture in the diagnosis and treatment of polymorphic VT is not the morphology of the rhythm but rather what is known(or suspected) about the patient's underlying QT interval. It is often difficult to know whether the tachycardia is pVT or ven-tricular fibrillation(VF). Most VF begins with pVT and if pVT is prolonged it will usually degenerate into VF(Figure 6).

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 cor-rected QT interval is greater than 500 milliseconds and accompanied by bradycardia.1 Torsades can be due to an inherited genetic abnormality2 or can be caused by drugs and electrolyte imbalances that lengthen 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 poly-morphic VT, a genetic abnormality in which polymorphic VT is provoked by exercise or emotion6;“short QT” syn-drome, a form of polymorphic VT associated with an unusually short QT interval(correct OT interval less than 330-370 milliseconds)78; idiopathic right ventricular outflow tract polymorphic VT; and bidirectional VT seen in digitalis toxicity in which the axis of alternate QRS com-plexes shifts by 180°9. There are no RCTs examining the acute pharmacological treatment of polymorphic VT. Sup-portive data, with and without long corrected QT interval,are largely based on case reports and case series.

Recommendation-Specific Supportive Text

1. Regardless of the underlying QT interval, all forms of polymorphic VT are considered hemodynamically and electrically unstable. Episodes of polymorphic VT may repeatedly recur and remit spontaneously, become sustained, or degenerate to VF. When the QRS com-plex of a VT is of uniform morphology, electric cardio-version synchronized to the QRS complex minimizes the risk of provoking VF during the vulnerable period of the cardiac cycle(T wave). In contrast, polymor-phic VT cannot be synchronized reliably because of the differing characteristics of each QRS complex and requires high-energy (maximum manufacturer's setting) unsynchronized shock. Assessment of a patient's mental status is important when the appro-priateness of sedation is considered before defibril-lation. While effective in terminating polymorphic VT,defibrillation may not prevent its recurrence, for which pharmacological therapies are often required and the primary focus of subsequent recommendations.

2. Torsades de pointes typically presents in a recur-ring pattern of self-terminating, hemodynamically unstable polymorphic VT in context of a known or suspected long QT abnormality, often with an associated bradycardia. Termination of torsades by defibrillation may not prevent its recurrence, which requires additional pharmacological interventions.In small case series, IV magnesium has been effec-tive in suppressing and preventing recurrences. ${}^{10-13}$ Magnesium is believed to suppress fluctuations in the myocardial action potential that can trigger tor-sades. ${}^{14}$ Correcting electrolyte abnormalities, par-ticularly hypokalemia, is also advisable.

Treatment of torsades with antiarrhythmic med-ications may 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 bradycar-dia or pause-prepipitated torsades, expert consul-tation is best sought for additional measures such as overdrive packing or isoproterenol.15 There is lit-erature to support instances of medication induced torsades, so prevention of drug induced prolonged QT is an important priority for professionals.

3. Polymorphic VT that is clearly not associated with QT prolongation, is most often triggered by acute myocardial ischemia or infarction and often rapidly degenerates into VF.3,5 Polymorphic VT may be diffi-cult to differentiate from VF initially, but, as with other ventricular arrhythmias(VT and VF), is terminated with immediate defibrillation. However, termination of polymorphic VT with defibrillation may not prevent its recurrence, requiring additional pharmacological measures. No RCTs have been performed to deter-mine the optimal pharmacological management of

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polymorphic VT. Treatment of causative myocardial ischemia(eg,β-adrenergic blockers or emergent coronary intervention) as well as lidocaine and amidorone,16-22 in concert with fibrillation, may be synergetic when the arrhythmia is sustained.β-Adrenergic blockers have also been shown to reduce the incidence of ventricular arrhythmias in acute coronary syndromes.23,24

Expert consultation is advisable when alterna-tive causes of polymorphic VT are suspected, for whichβ-adrenergic blockers and antiarrhythmics may also have efficacy.6.25 Since the 2018 AHA Focused Update on Advanced Cardiovascular Life Support Use of Antiarrhythmic Drugs During and Immediately After Cardiac Arrest,26 no new evidence has been identified.

4. In the absence of long QT, magnesium has not been shown to be effective in the treatment of polymor-phic VT10 or other ventricular tachyarrhythmias.12 A single case series with 5 patients showed no ben-efit of magnesium administration for polymorphic VT with normal QT. Since the 2018 AHA focused update on antiarrhythmic drugs during and imme-diately after cardiac arrest no new evidence has been identified.

REFERENCES

1. Chan A, Isbister GK, Kirkpatrick CM, Dufful SB. Drug-induced QT of longration and sades de pointes: evaluation of a QT onogram Q.M.Q 2007;100-869-615. doi:10.1039/qmed/hcm72

2.Saprunungang A, Khongphathanthayoxin A, Mauleukoonphairo J, Wandee P,Kanjanauthi S, Bhuiyan ZA, Wilde A M, Poovoranov Y. Genotype and clinical characteristics of congenial long QT syndrome in Thailand. Indian Pacing Electrophysiol.J.2018;18:165-171. doi:10.1016/j.ijpe.2018.07.007

3. Drew BJ, Ackerman MJ, Fukman, Gibler WB, Kildgari P. Menon V. Philipseg J, Roden DM, Zareba W; American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology. 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.2010.01.001

4.Wolfe CL,Nibley C, Bhandari A, Chatterjee K, Scheinman M. Polymorphous ventricular tachycardia associated with acute myocardial infarction. Circula-tion.1991;84:1543-1551. doi:10.1161/01/cir.84:1543.1543

V.goploss Mar,CPB. Electrophysiologic mechanisms underlying arrhythmias-mias due to reperfusion of ischemic myocardium. Circulation. 1987;76:404-426. doi:10.1011/61c/172.26404

6. Liu N,Ru,YPNari P.Sior C.Cathelorganiclymporphic ventricular tachycar-dia. Prog Cardiovasc Dis.2008;51:23-30. doi:10.1016/j.pcad.2007.1005

7. Golomb M, Redpath CJ, Roberts. JD The short QT syndrome: pro-posed diagnostic criteria. J Am Coll Cardiol. 2011;57:802-812. doi: 10.1016/j.jacc.2010.09.048

8. Cross B, Homoud M, Link M, Foote C, Garlitski AC, Weinstock J,Estes NA 3rd. The short QT syndrome. J Interv Card Electrophysiol, 2011;31:25-31.doi:107004/s10840-011-9666-0

Chapman M, Hargmeaves S, Schneider H, Royle M. Bidirectional ventricular tachycardia associated with digoxin toxicity and with normal digoxin levels.Heart Hhythm 2014;11:1122-1225. doi:10.1016/j.ithrdn2014;030.050

10. Tizvoni D,Keren A, Cohen A, MInel B, Zahavi I, Chenzbraun A, Stern S.Magnesium therapy for torsades de pointes. Am J Cardiol. 1984;53:528-530. doi:10.1016/0000-9149(88)4002-05

11. Zivoni D, Baniai 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:10.1011/cir.172.392.

12. Manz M, Jung W, Luderitz B.[Effect of magnesium on sustained ventricular tachycardia]. Herz 1997:2251-55: doi:10.1007/BF03042655

13. Hoshino K, Ogawa K, Hishitani T, Isobe T, Etoh Y. Successful uses of mag-nesium 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.x

14. Baker WL. Treating arrhythmias with adjunctive magnesium: identify-ing future research directions. Eur Heart J Cardiovasc Pharmacother.2017;3:108-117. doi:10.1093/ehjcpv/pvw028

15.DiSegni E,KeinHO,David D,Libhaber C, Kaplinsky E. Overdrive pacing in quinidine syncope and other long QT-interval syndromes. Arch Intern Med.1980;140:1036-1040.

16. 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 Palacyl Oloumoc Czech Repub.2013;157:114-124. doi:10.5507/bp.2013.030

17. Steg PG,James SK,Atar D,Badano LP,Blomstrom-Lundqvist C, Borger MA,Di Mario C, Dickstein K, Ducroqc G,et al.; Task Force on the man-agement of STseamiotETSO C.ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J.2013;23:3569-2619. doi:10.1093/eurheart/ehs215

18. Nalliah CJ, Zaman S, Narayan A, Sullivan J, Koorov P. Coronary artery re-perfusion 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/eut307

19.Brady W, Meldon S, DeBehnke D, Comparison of prehospital mono-morphic and polymorphic ventricular tachycardia: prevalence, re-sponse to therapy, and outcome. Ann Emerg Med. 1995;25:64-70. doi:10.1016/s0196-0644(9)70357-8

20.Brady WJ, DeBehnke DJ, Laudrie 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.x

21. Gorenek B, Lundqvist CB, Terradellas JB, Camm AJ, Hindricks G, Huber K, Kirchhof P, Kuck KH, Kudaiberdieva G, Lin T, et al. 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:10.1177/2048872614550583

22. Luqman S, Nung RJ, Wang CL, Kuo CT. Myocardial ischemia and ven-tricular fibrillation:pathology and clinical implications. Int J Cardiol.2007;119:283-290. doi:10.1016/j.jicard.2006.09.016

23. AlKhatib 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 guidelines 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. Heart Rhythm. 2018;15:e73-e1897. doi:10.1016/j.17hrrm.2017.10.036

24. Chatterjee S, Chaudhuri D, Vedanthan R, Fuster V, Ibanez B, Bangalore S, Mulichene 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.jicard.2012.10.050

52. Van Houzen HE, Shealskin-Ali AA, Garlitski AC, Homoud MK, Weinstock J,Link MS,Estes NA 3rd. Short QT syndrome review. J Interv Card Electro-physiol 2008:231-5. doi: 10.1007/s10840-008-9201-x

20. Canchal AR, Berg K, KM, Jendukchuj PJ, Del Rios M, Hirsch KG, Link MS, Kurz MC, Chan P, Cabasji J, G, Morley PT,et al. 2018 American Heart Associa-tion Focused Update on Advanced Cardiovascular Life Support Use of An-tiarthrycugs During During and Immediately After Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resus-citation and Emergency Cardiovascular Care. Circulation. 2018;138:e740-e749. doi:10.1016/C1R.00000000000000613

REGULAR NARROW-COMPLEX TACHYCARDIA

|Recommendations for the Treatment of Regular Narrow-Complex Tachycardia in Adults||| |---|---|---| |COR|LOE|Recommendations| |1|B-R|Arolus maneuvers are recommended for acute treatment of adult patients with regular narrow complex tachycardias.|

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|Recommendations for the Treatment of Regular Narrow-Complex Tachycardia in Adults(Continued)|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|B-R|2. Adenosine is recommended for acute treatment of adult patients with regular narrow-complex tachycardias.|| |1|B-NR|3. Synchronized cardioversion is recommended for acute treatment of adult patients with hemodynamic-ically unstable narrow-complex tachycardias.|| |2|B-NR|4. Synchronized cardioversion is recommended for acute treatment of adult patients with hemodynam-ically stable narrow-complex tachycardias when vagal maneuvers and pharmacological therapy is ineffective or contraindicated.|| |2a|B-R|5. Intravenous diltiazem or verapamil can be effective for acute treatment of adult patients with hemody- namely stable narrow-complex tachycardias that are regular.|| |2a|C-LD|6. Intravenous β-adrenergic blockers are reasonable for acute treatment of adult patients with hemody- namely stable narrow-complex tachycardias that are regular.||

Synopsis

In most patients narrow-complex tachycardias(NCTs),which include sinus tachycardia, atrial flutter, AV nodal reen-trant tachycardia, AV reentrant tachycardia, and other atrial tachycardia, and previously referred to imprecisely as supra-ventricular tachycardia, generally are not hemodynamically unstable, and health care professionals have an opportunity to attempt vagal maneuvers. Adenosine may also be effec-tive in terminating arrhythmias in these patients.

For hemodynamically unstable patients with NCTs,electrical therapies are warranted(Figure 6). However,there must be a reasonable expectation that the NCT is causing instability rather than being a manifestation of instability caused by another clinical diagnosis(eg, sep-sis). Hemodynamically unstable patients with NCT may have hypotension, acutely altered mental status, signs of shock, chest pain, or acute heart failure. Most patients with NCTs have conversion success rates of up to 98% with vagal maneuvers, pharmacological management, or both,described below(eg, adenosine, diltiazem, verapamil).

If nasally administered calcium channel blockers become available in the future, they will be evaluated for their effi-cacy and safety and considered for inclusion in these guide-lines and the corresponding treatment algorithm.1-3

These recommendations are supported by the 2015 American College of Cardiology,AHA,and Heart Rhythm Society Guidelines for the Management of Adult Patients With Supraventricular Tachycardia and a 2025 evidence update.

Recommendation-Specific Supportive Text

1. The Valsalva maneuver is effective in terminating 20 to 30% of NCTs.4.5 With modified techniques, termi-nation improves to up to 50%.6-9 Vagal maneuvers

include having the patient blow into a 10 cc syringe,baring down, and carotid massage. However, more effective approaches have been described, such as passive leg raise, supine repositioning, and passive leg elevation immediately after Valsalva, blowing into a syringe attached to a sphygmomanometer,and pressing the epigastric region 10 seconds after Valsalva. When performing carotid massage, caution is advised because the technique can precipitate a stroke in patients with carotid atherosclerosis.

2. Adenosine has demonstrated very high rates of con-version of AV nodal reentrant tachycardia, AV reen-trant tachycardia, and many atrial tachycardias. ${}^{10}$It also blocks the AV node, confirming a diagnosis of atrial flutter or fibrillation. Adenosine has a very short half-life and may be less effective if infused in a peripheral vein. Adequate dosing is assured by alteration of the NCT, including termination or the patient's symptoms of flushing and a feeling of dread. Adenosine may have profound effects in patients with central lines or post-heart transplant patients; 1 mg IV may be adequate to terminate the NCT. Adenosine can cause severe bronchospasm in patients with asthma, and thus, is contraindicated.

3. In hemodynamically unstable patients with NCT, it is critical to promptly restore sinus rhythm. If unsta-ble, immediate cardioversion is warranted. ${}^{11}$

4. Cardioversion can be used to treat stable patients with NCT not responsive to vagal maneuvers and pharmacological therapy. ${}^{11}$ Assessment of a patient's mental status and clinical stability is important when the appropriateness of sedation is considered before cardioversion.

5. IV diltiazem and verapamil convert NCT to normal sinus rhythm in 64% to 98% of patients. The effi-cacy of verapamil is similar to adenosine but with significant concerns for inducing hypotension. ${}^{12-18}$ Diltiazem and verapamil are particularly useful in patients with recurrent supraventricular tachycardia after treatment with adenosine because they are longer acting. Hypotension is a common side effect,and these medications must be infused slowly. ${}^{19}$ For patients with NCT and suspicion of systolic heart failure, diltiazem and verapamil are best avoided.

6.Intravenous$\beta$ -adrenergic blockers are gener-ally safe and have been shown to terminate NCT in adult patients with hemodynamically stable narrow-complex tachycardias that are regular.

REFERENCES

1.Ip JE,Couut B,Bennett MT,Pandey AS,Stambler BS,Sager P,Chen M,Shardonofsky S,Plat F,Camm AJ.Etripamil Nasal Spray for Conversion of Repeated Spontaneous Episodes of Paroxysmal Supraventricular Tachycar-dia During Long-Term Follow-Up: Results From the NODE-302 Study.J.Am Heart Assoc.2023;12:e028227. doi: 10.1161/JAHA.122.028227

2.Stambler BS,Camm AJ,Allings M,Dorian P,Heidbuchel H,Houtgraaf J,Kowey PR,Merino JL,Mondesert B, Piccini JP,et al; RAPID Investigators.Self-

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administered intranasal peritamil using a symptom-prompted, repeat-dose regimen for atriventricular-nodal-dependent supraventricular tachycardia(RAPID): a multicentre, randomised trial. Lancet 2023;402:118-128. doi: 10.1016/S0140-6736(20)00776-6

3. Stambler BS, Plat F, Sager PT, Shardonsfsky S, Wight D, Potvin D, Pandey AS, lp JE, Cuteu B, Mondesert B, et al. First Randomized, Multicenter,Placebo-Controlled Study of Self-Adminer intranasal Etripani for Acute Conversion of Spontaneous Paroxysmal Supraventricular Tachy-cardia(NODE-301). Circ Arrhythm Electrophysiol. 2022;15:e010915. doi:10.1161/CIRCEP12:0201095.

4. Lim SH,Anantharaman V, Teo WS, Goh PP, Tan AT. Comparison of treatment of supraventricular tachycarda by Valsava maneuver and carotid sinus mas-sage. Ann Emerg Med.1998;31:30-35.

5. Smith GD, Fry MM, Taylor D, Morgans A, Cantwell K. Effectiveness of the Valsalva Manoeure for reversion of supraventricular tachy-cardia. Cochrane Database Syst Rev. 2015;2015;CD009502. doi:10.1002/14651858.CD009502.pub3

6. Appelboam A, Reuben A, Mann C, Gagg J, Ewing PJ, Barton A, Layer D, Vicky J, Benger J, REVERT trial collaborators. Postural modifi-cation to the standard Valsalva manoeuvre for emergency treatment of su-preventricular tachycardias(REVERT): a randomised controlled trial. Lancet 2015;386:1747-1753. doi:10.1016/S0140-6736(15)61485-4

7. Chen C,Tam TK,Sun S,Guo Y,Teng P,Jin D,Xu L,Liu X,Aulticenter ran-domized controlled trial of a modified Valsalva maneuver for cardioversion of supraventricular tachycardias. Am J Emerg Med.2020;38:1077-1081.doi:10.1016/j.ajem.2019.188371

8. Corbaccioglu Sk, Aenciki E, Veyik Y, Atyar H, Oncul MV, Akkan S,Uuzanosomoglu H. Comparing the success rates of standard and modified Valsalva maneuvers to terminate PSVT: A randomized controlled trial. Am J Emerg Med.2017;35:1662-1665. doi: 10.1016/j.ajem.2017.05.034

9. Lan Q, Han B, Wu F, Peng Y, Zhang Z. Modified Valsana maneuver for treat-ment of supraventricular tachycardias: A Meta-analysis, Am J Emerg Med.2017;50:507-512. doi:10.1016/j.ajem.2021.08.067

10. DiMarco JP, Sellers D, Beme RW, West GA, Belendini A. Adenosine:electrophysiologic effects and therapeutic use for terminating paroxys-mal supraventricular tachycardia. Circulation. 1983;68:1254-1263. doi:10.1161/01.61c86.1254

11. Roth A, Elkeyam I, Shapira I, Sander J, Malov N, Kehati M, Golover M. Effectiveness of prehital synchronous direct-coumentary cardioversion for supraventricular tachycardia causing unsuperventricular harmodynamic, states.Am J Cardiol.2003;91:489-491. doi:10.1016/s0002-9149(02)03257-5

12. Ahmad Fu Sebnein S. Patel RS, Rohit Reddy S. Lukiman A, Hashin A,Daddon DR, Gordon K. In The Line of Treatment: A Systematic Revaluation of Paroxysmal Supraventricular Tachycardia. Cureus.2021;13:e15502.doi:107.7556/cusus.15502

13. Alabad S, Sabouni A, Providencia R, Atallah E, Qintar M, Chico TJ. Ade-nosine versus intravenous calcium channel antagonists for supraventricu-lar tachycardia. Cochane Database Syst Rev. 2017:10:CD005154. doi:10.1002/14651858.CD005154.pub4

14. Delaney Boy L, Kelly J, Kelly Fm. The relative efficacy of adenosine versus a-pamil for the treatment of stable poroxysmal supraventricular tachycar-dia in adults: a meta-analysis. Eur J Emerg Med.2011;18:148-152. doi:10.1097/MEJ01b03e283400ba2

15.Dimar COPs, Mak I, Wafkar M, Milstein S, Sharma AD, Platia E,McGovern B, Scheinman MM, Govier WC. Adenosine for paroxysmal supraventricular tachycardia: dose ranging and comparison with versa-pamil. Assessment in placebo-controlled, multicenter trials. The Adenos-ine for PSVT Study Group. Ann Intem Med. 1990;113:104-110. doi:10.7326/0003-4819-113-2-104

16. Lim SH,Anantharaman V, Teo WS. Slow-infusion of calcium channel block-ers in the emergency management of supraventricular tachycardia. Resusculi-tation.2002;52:167-174. doi:10.1016/s0300-9572(01)00459-2

17. 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)70179-6.

18. Pachutspulka VH, Paudel Y, Patel A, Najam B, Desai HN, Ilnoan J,Seffah KD, Kumar M, Naveen N, Khan S. Efficacy of Adenosine Versus Verapamil in Terminating Acute Attacks of Paroxysmal Surpraventricu-lar Tachycardia: A Systematic Review. Cureus. 2023;15:e45946. doi:10.7759/cureus.45946

19. Lim SH,Anantharaman V, Teo WS, Chan YH. Slow infusion of calcium chan-nel blockers compared with intravenous adenosine in the emergency treat-ment of supraventricular tachycardia. Resuscitation. 2009;80:523-528. doi:10.1016/j.resuscitation.2009;0.1017

ARIAL FIBRILLATION OR FLUTTER WITH RAPID VENTRICULAR RESPONSE: PART 1 ELECTRICAL THERAPIES

|COR|LOE|Recommendations| |---|---|---| |1|1. In adult patients with hemodynamic instability at- tributable to atrial fibrillation or atrial flutter with rapid ventricular rates, immediate electrical car- diversion should be performed to restore sinus rhythm.|| |2|1. Urgent direct-current cardioversion of new onset atrial fibrillation or atrial flutter with rapid ventricular rates in the setting of acute coronary syndrome is recommended for adult patients with hemodynam- ic compromise, ongoing ischemia, or inadequate rate control.|| |2a|B-R|3. For synchronized cardioversion of atrial fibrillation in adults using any currently US-approved bipha- sic waveform defibrillator, an initial energy setting at least 200 J is reasonable and incremented in the event of shock failure, depending on the bipha- sic defibrillator used.| |2b|B-R|4. The usefulness of double synchronized cardiover- sion of atrial fibrillation in adults as an initial treat- rystalline strategy is uncertain.| |2b|2b|5. For synchronized cardioversion of atrial flutter in adults, an initial energy setting of 200 J may be reasonable and incremented in the event of shock failure, depending on the biphasic defibrillator 2| |2b|2b|6. The usefulness of double synchronized cardiover- failure, depending on the biphasic defibrillator 2| |2b|2b|6. The usefulness of double synchronized cardiover- as a rescue treatment for shock-refractory atrial fibrillation in adults is uncertain.| |2b|2b|6. The usefulness of double synchronized cardiover- as a rescue treatment for shock-refractory atrial fibrillation in adults is uncertain.| |2b|2b|6. The usefulness of double synchronized cardiover- as a rescue treatment for shock-refractory atrial fibrillation in adults is uncertain.| |2b|2b|6. The usefulness of double synchronized cardiover- as a rescue treatment for shock-refractory atrial fibrillation in adults is uncertain.|

Synopsis

Atrial fibrillation(AF) is a disorganized atrial rhythm due to multiple reentry(reself-circulating) circuits throughout atrial myocardium. Atrial flutter is a more organized tachyrrhythmias caused by a single macroreentrant atrial circuit. The two arrhythmias are common, often co-exist, and are treated similarly. Treating AF/flutter with rapid ventricular rates depends on hemodynamic stability. Unstable patients and those with rate-related ischemia often need urgent electrical cardioversion(Figure 7). Stable patients can be treated pharmaco-logically to achieve rate or rhythm control. Conversion of AF/flutter greater than 48 hours in nonanticoagu-lated patients risks thromboembolic events. For acute AF/flutter assessed as less than 48 hours, decision-making is more nuanced, requiring expert consultation unless emergent cardioversion is needed. Pre-excited AF/flutter (Wolff-Parkinson-White) is covered under Wide-Complex Tachycardias.

Electrical cardioversion is influenced by many factors. Technical features(beyond energy setting)affecting shock success include pad dimensions,pad location, minimizing impedance barriers, shock waveform, and timing(proper electrocardiogram

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Notes

*Effective regimens have included a sedative(eg, diazepam) with or without an analgesic agent(eg, fentanyl). Many experts recommend anesthesia if service is readily available.

†Note possible need to resynchronize after each cardioversion.

l#f delays in synchronization occur and clinical condition is critical, go immediately to unsynchronized shocks.

©2025 American Heart Association

synchronization).2,3 Clinical factors influencing cardio-version outcome include body habitus, cardiac status(ventricular function, atrial size), rhythm duration, and concomitant medication use. Any of these, alone or together, can affect outcome as much or more than the energy setting itself.4, Apart from energy, electrical cardioversion requires regard for the details of how the procedure itself is conducted and the characteristics of the patient in whom it is performed.6

These recommendations are supported by the "2023 ACC/AHA/ACCP/HRS Guideline for the Management of Atrial Fibrillation" and a 2025 evidence update.

Recommendation-Specific Supportive Text

1 and 2. Uncontrolled tachycardia may impair ventricular filling, cardiac output, and coronary perfusion while increasing myocardial oxygen demand.

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While an expeditious trial of medications, intrave-nous fluids, or both may be appropriate in some cases, unstable patients or patients with ongo-ing cardiac ischemia caused or exacerbated by atrial fibrillation/flutter require prompt cardio-version. ${}^{7-9}$ One should also consider whether the arrhythmia is causative or secondary to a rapid ventricular response driven by underly-ing factors (eg, sepsis), as this may guide initial pharmacologic strategies for hemodynamic sta-bilization. Limited data exist on these strategies in hemodynamically unstable patients; however,the hemodynamic benefits of successful car-dioversion have been documented. ${}^{10,11}$ In addi-tion, risk of hypotension and hypoperfusion with negative inotropes has been demonstrated even in normotensive patients. ${}^{12-14}$

Hemodynamically unstable patients and those with ongoing cardiac ischemia are likely to benefit from improved hemodynamic status from immediate restoration of sinus rhythm and avoidance of hypotension caused by pharma-cological therapies. Depending on the clinical scenario, patients cardioverted from atrial fibril-lation/flutter of greater than 48 hours' duration are candidates for anticoagulation. Appropriate selection of patients and medications for antico-agulation are addressed elsewhere and beyond the scope of these guidelines.1

3.Guidance for monophasic waveform car-dioversion of AF/flutter is found in previous guidelines, ${ }^{15}$ displaced by biphasic waveforms due to their greater efficacy. Given propri-etary differences in electrical characteristics,guidelines previously deferred biphasic car-dioversion energy settings to manufacturer specifications. ${ }^{16}$ However, interim randomized head-to-head trials together with a network meta-analysis involving $>3000$ AF patients found that 200-J shocks achieved greater than 90% cumulative cardioversion success across all 3 biphasic platforms currently available in the United States. ${ }^{6,17-21}$

Previous guidelines advocated lower energy settings over concerns that higher energies posed greater risk for cardiac injury and com-plications. ${}^{18,22-25}$ Subsequent clinical studies observed no association between starting biphasic shock energies of up to 360 J with energy-associated elevations in cardiac-spe-cific enzymes, postcardioversion arrhythmias,cardiac dysfunction, or other sequelae.26-28 Notably, low-energy monophasic shocks were significantly more likely to provoke VF when cardioverting AF, and AF when cardioverting atrial flutter than a 200-J or greater setting.29

This observation is consistent with the upper limit of vulnerability principle: that an energy threshold exists above which a shock will not induce fibrillation.30,31 A higher starting energy was also found to be more efficient than“starting low, titrating higher” approaches,achieved greater first-shock cardioversion suc-cess, required fewer overall shocks, and could shorten the period of anesthesia needed for serial shock attempts.18,22

Considering efficacy, safety, efficiency,simplicity, and consistency with other profes-sional guidelines, evidence supports a starting energy of 200 J. ${}^{16-21}$ Regardless of energy setting, appropriate sedation for cardioversion is advisable in awake patients, given shock is a painful procedure.

4.One approach to synchronized cardioover-sion is double synchronized cardioversion.Administering 2 simultaneously-synchronized high-energy shocks from separate defibrilla-tors and pads has been described anecdotally,in small case series, and a single randomized trial. As an“initial” cardioversion strategy, a mod-estly-sized randomized trial comprised of class II obesity patients(39% had prior cardioversion attempts) found first shock efficacy improved with 400 J double synchronized cardioversion versus 200 J synchronized cardioversion(98%versus 87%, p=0.002).32 Although not consis-tently reported, double synchronized cardioover-sion has not been associated with proarrhythmia,hemodynamic complications, cardiac-specific enzyme elevation,28 or postprocedure discom-fort but has caused defibrillator damage.33

A concern in all studies has been the vagueness of procedural specifications, par-ticularly how 2 independently-initiated shocks from separate defibrillators being reliably simultaneously-synchronized was assured.34 Given the high success of optimal synchronized cardioversion using biphasic waveforms, the incremental benefit from double synchronized cardioversion is modest.

5. Organized rhythms like atrial flutter, caused by a discrete reentry circuit, require less energy for termination than AF, whose multiple reentry circuits broadly engulf the atrial myocardium.35 However, periodic transitions between the two arrhythmias are common. Distinguishing AF from flutter in an emergent setting with only sin-gle-lead monitoring can be challenging. Studies evaluating rectilinear and truncated exponen-tial biphasic waveforms available in the United States, while indirect and fewer in number than for AF, have shown comparable cumulative

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cardioversion success for atrial flutter between these waveforms at the same energy settings,ranging from 50% to 75% at 50 J, improv-ing to 85% to 90% at 100 J, and approach-ing 100% at 200 J.23,28,36-38 Using a higher(200 J) initial energy setting for flutter cardio-version also affords shorter procedural times without causing cardiac injury or compromising safety,23,26,36-38 accompanied by a lower risk of provoking AF or undertreating AF if mistaken as flutterer of flutter.27,36 The likelihood of greater efficacy, effi-ciency, and simplicity, without safety concerns,supports a starting energy of 200 J for flutter cardioversion using any currently US-marketed biphasic defibrillator; incremented in the event of shock failure, depending on the defibrillator's features.23,28,36,37

6. Shock-refractory AF, defined as AF that remains incessant after maximum-energy shocks, is relatively uncommon with bipha-sic shock waveforms and distinguished from recurrent AF, which returns after an initially successful shock. As in many situations, shock success can be optimized by minimizing trans-thoracic impedance3 by improving pad-skin contact and applying pad pressure; relocating pads to redirect the shock vector; or adding antiarthymic drugs to alter the defibrillation threshold.2,5,6,39,40

Another possibility is the use of dou-ble synchronized cardioversion.41 Data on this approach are limited, including proce-dural uncertainties described above (item 4). Observational studies found double-synchronized cardioversion to be successful in 75% to 100% of patients who had previously failed standard cardioversion.41-43 Alternatively,a large prospective observational study evaluated a systematic approach to shock-refractical AF. It found applied pad pressure improved synchronized cardioversion success from 87% to 93% and with pad repositioning to 96%, after which the added increment from double-synchronized cardioversion only mod-estly improved to 98%.2

REFERENCES

1. Joglar JA, Chung MK, Armbruster AL, Benjamin EJ, Chuyou JY, Cronin EM, Deswal E, Eckhardt LL, Goldberger ZD, Gopinathanhar R, et al; Peer Review Committee Members. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Com-mittee on Clinical Practice Guidelines. Circulation.2024;149:e1-e156.doi: 10.1161/CIR:000000000001193.

2.Darrat Y,Leung S, Elayl L, Parrott K, Ogunbayo G, Kotsher J, Sorrell V,Gupta V,Anaya P, Morales G, et al. A stepwise external cardioversion protocol for atrial fibrillation to maximize acute success rate. Europe. 2023;25:828-834. doi: 10.1093/europace/euud00

3. Sadek MM, Chaugai V, Cleland MJ, Zakutney TJ, Birnie DH, Ramirez FD.Association between transthoracic impedance and electrical cardioversion success with biphasic fibrillators: An analysis of 1055 shocks for atrial fi-brillation and flutter. Clin Cardiol. 2018;41:666-670. doi: 10.1002/ccl.22947

4. Brandes A, Crijns H, Rienstra M, Kirchhof P, Grove EL, Pedersen KB,Van Gelder IC. Cardioversion of atrial fibrillation and atrial flutter revisited:current evidence and practical guidance for a common procedure. Europe.2020;22:1149-1161.doi:10.1093/europace/euaa057

5.Kukendrarajah K,Ahmad M,Carrington M,loannou A,Taylor J,Razvi Y,Papageorgiou N,Mead GE, Nevis IF,D'Ascenzo F,et al. External electri-cal and pharmacological cardioversion for atrial fibrillation, atrial flutter or atrial tachyldiac: a network meta-analysis. Cochrane Database Syst Rev.2024;6:CD013255.doi:10.1002/14651858.CD013255.pub2

6. Nguyen ST, Belley-Cote E P, Ibrahim O, Um KJ, Lengyel A, Adli T, Qiu Y,Wong S,Mibilio S, Benz AP, et al. Techniques improving electrical cardioversion success for patients with atrial fibrillation: a systematic review and meta-analysis.Europace.2023;25:318-330. doi: 10.1093/europe/aceu199

7.January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC Jr., Conti JB, Ellinor PT, Ezekowitz MD, Field ME, et al; ACC/AHA Task Force Members. 2014 AHA/ACC/HRS guideline for the management of patients with fibrillation: a report of the American College of Car-diology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Stochastic. Circulation. 2014;130:e199-e267. doi: 10.1161/CIR.0000000000000000000041

8.January CT, Wann LS, Calkins H, Chen LY,Cigararro JE, Cleveland JC Ellinor PT, Ezekowitz MD, Field ME, Furie KL, et al. 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 Surgons. Circulation. 2019;140:e125-e151. doi: 10.1161/CIR.00000000000000665

9.McMurray J, Kober 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 Car-1.2005;45:525-530. doi: 10.1016/j.jacc.2004.09.076

10. DeMaria AN, Lies JE, King JF, Miller RR, Amsterdam EA, Mason DT. Echo-graphic assessment of atrial transport, mitral movement, and ventricular performance following electroversion of supraventricular arrhythmias. Cir-culation.1975;51:273-282. doi: 10.1161/01.cir.51:2.273

11. Raymond RJ, Lee AJ, Messinoe FC, Manning MJ, Silverman DI. Cardiac performance early after cardioversion from atrial fibrillation. Am Heart J.1998;136:435-442. doi: 10.1016/s0002-8703(98)70217-0

12.Delle Karth G, Geppert A, Neunteufi T, Priglinger U, Haumer M,Schgwandner M, Siostrzonek P, Heinz G. Amodiorare versus diltiazem for rate control in critically ill patients with atrial tachyarrhythmias. Crit Care Med.2001;29:1149-1153.doi:10.1097/00003246-200106000-00011

13.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-s

14. Platia EV, Michelson EL, Porter field JK, Das G. Esmolol ver verapamil in the acute treatment of atrial fibrillation or atrial flutter. Am J Cardiol.1989;63:925-929. doi: 10.1016/0002-9149(89)90141-0

15.Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Car-diovascular Care. Part 6: advanced cardiovascular life support: section 2:defibrillation. The American Heart Association in collaboration with the In-ternational Liaison Committee on Resuscitation. Circulation.2000;102:190-194.

16. Panchal AR, Bartos JA, Cabanas JG, Donnino MW, Drennan IR, Hirsch KG,Kudenchuk PJ, Kurz MC, Lavonas EJ, Morley PT, et al; Adult Basic and Advanced Life Support Writing Group. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardio-2020;142:S366-S468. doi: 10.1161/CIR.0000000000000916

17.Nal Se, N. Ngarmukos T. Lessard D, Rosenthal L. Comparison of the effica-cy and safety of two biphasic defibrillator waveforms for the conversion of atrial fibrillation to sinus rhythm. Am J Cardiol. 2003;92:810-814. doi: 10.1016/s0002-9149(03)0088-9

18. Kim ML,Kim SG,Park DS,Gross JN,Ferrick KJ,Palma EC,Fisher JD.Com-parison of rectilinear biphasic waveform energy versus truncated exponential biphasic waveform energy for transthoracic cardioversion of atrial fibrillation. A 2003;25:828-134. doi: 10.1016/j.amidol.2004;94:148-1440. doi: 10.1016/j.amjcard.2004.07.149

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19. Inacio JF, da Rosa Mdos S, Shah J, Rosario J, Vissocar, JR. Manica AL,Rodrigues CG. Monophasic and biphasic shock for transthoracic conversion of atrial fibrillation: Systematic review and network meta-analysis. Resuscita-tion:2016;1006;76-85. doi:10.1016/j.resuscitation.2015.12.009

20. Deakin CD, Connelly S, Wharton R, Yuen HM. A comparison of rectilinear and truncated exponential biphasic waveforms in elective cardioversion of atrial fibrillation: a prospective randomized controlled trial. Resuscitation 2013;84:286-291. doi:10.1016/j.resuscitation.2012.07010

21. Alatafi W, Gurevitz O, White RD, Amasmich NM, Malouf JF, Bruce CJ, Moon BS, Rosales AG, Hodge D, Hamill SC et al. Prospective, randomized comparison of two biphasic waveforms for the efficacy and safety of transthoracic biphasic cardioversion of atrial fibrillation. Heart Rhythm 2005;282-387. doi:10.1016/j.rthm.2004.12.024

22. Resnekov L, McDonald L. Complications in 220 patients with cardiac dys-rhythmias treated by phased direct current shock, and indications for elec-troconversion. Br Heart J. 1967;29:926-936: doi: 10.1136/189t.269.926

23. Mortensen K, Risius T, Schwemfer TF, Ayadin M, Koster, R Klemu H, Lutomsky B, Reinertz T, Verartura R, Wlemis S, Bphasic versus monophasic shock for external cardioversion of atrial flatter: a prospective, randomized trial. Cardiology.2008;111:57-62. doi:10.159/0000113429

24. DiCola FC, Freedman GS, Downing SE, Zerret BL. Mycrosyl uptake of turchennet-99m stannous pyrophosphate following direct current transthoracic countershock.Circulation 1976;54:5980-986. doi:10.1161/071.c54:6980

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26. Schmidt AS, Lauridens KG, Torp P, Bach LF, Rickers H, Lofgren B.Maximum-Mixed energy shocks for cardiovascular fibrillation. Eur Heart J.2020;41:626-631. doi: 10.1093/eurheart/ehz585

27. Lobo R,White RD,White LD.,Oleunwkes AM, Kelley BR,Melduni RM,Jaffe AS Absence of significant myocardial injury following effective direct current cardioversion for atrial fibrillation. Heart Rhythm 02,2023:4:180-186. doi:10.1016/j.1hoo.2022.12.004

20. Lobo R, Jaffe AS, Cahill C, Blake O, Abbas S, Meany TB, Hennessy T,Kiernan TJ. Significance of High-Sensitivity Protontr T by Effective Exterral: N al直 Current Cardioversion for Atrial Fibrillation or Atrial Flutter. Am J Cardiol.2018;121:188-192. doi:10.1016/j.jamcard.2017.10.009

29. Gallagher MM, Yap YG, Padula M, Ward DE, Rowland E, Camm AJ. Arrhythmic complications of electrical cardioversion: rel-tionship to shock energy. Int J Cardiol. 2008;123:307-312. doi:10.1016/j.jcard.2006.12.014

30. Swiderlow CD, Martin DJ, Kass RM, Davie S, Mandel WJ, Gang ES, Chen PS.The zone of vulnerability to T wave shocks in humans. J Cardiovasc Elec-trophysiol.1997;8:145-154. doi:10.1111/1540-81671997765.

31. Swerdlow CD, Martin DJ, Kass RM, Davie S, Mandel WJ, Gang ES, Chen PS.The zone of vulnerability to T wave shocks in humans. J Cardiovasc Elec-phrodystory 1:978:145-154. doi:10.1111/1540-8167199776x

32. Aymond JD, Sanchez AM, Castine MR, Bernard ML, Khatib S, Hiltbold AE, Polin GM, Rogers PA, Dominic, NSis Velcc-Gonzalez C, et al.Dual vs Single Adoversion Atrial Fibrillation in Patients With Obe-sity: A Randomized Clinical Trial. JAMA Cardiol. 2024;9:641-648. doi:10.1010/jamcardio.2024.1091

38. Gerstein NS, McLean AR, Stecker EC, Schulman P. Exter-nal Defibrillator Damage Associated With attempted Synchronized Dual-Dose Cardovision. Ann Emerg Med. 2018;711-109-112. doi:10.1016/j.annemerged.2017.04.005

34. Bjerregard P,El-Shafei A, Janoski DL, Schiller L, Quattromani A. Double external direct-current shocks for refractory atrial fibrillation. Am J Cardiol.1999;83:972-4,A10. doi:10.1016/s0002-9149(98)0148-0

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37. Reisinger J,Scstein W,Crestin T,Zeindhoeflner,Hollinger K,Mori M,Schiller A,Winter A,Geiger H,Siostrzonek P.Optimization of initial energy for car-domovision of atrial tachyarrhythmias with biphasic shocks. Am J Emerg Med 2010;28:159-165. doi:10.1016/jajem.2008.10.028

38. Mortensen K, Aydin MA, Schwener T, Ventura R, Reppel M, Bode F,Metıko R, Schunkert R, Hisert Rus. Low energy biphasic cardioversion of atrial flutter: results from a pilot trial. Int J Cardiol. 2010;145:368-370. doi:10.1016/j.jicard.2010.02.042

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ATRIAL FIBRILLATION AND FLUTTER WITH RAPID VENTRICULAR RESPONSE: PART 2 MEDICAL THERAPIES

|Recommendations for Medical Therapies for Atrial Fibrillation/Flutter|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|B-NR|1. AV administration of aβ-adrenergic blocker or nondiabrydropyridine calcium channel antagonist is recommended to slow the ventricular heart rate in acute setting in adult patients with atrial fibrilla- tion or atrial flutter with rapid ventricular response without preexcitation.|| |2a|B-NR|2. Animodarone can be useful for rate control in typically ill adult patients with atrial fibrillation with rapid ventricular response without preexcitation.|| |3: Harm|C-LD|3. In adult patients with preexcitation atrial fibrillation or atrial flatter, DCl- and atrial flutter, digoxin, nondihydropyridine calcium channel antagonists,β-adrenergic blockers, and IV theymodon should not be administered because may increase the ventricular response and result in VF.|| |3: Harm|C-EO|4. Nondihydropyridine calcium channel antagonists in and IVβ-adrenergic blockers should not be used in adult patients with left ventricular systolic function and decompensated heart failure because these may lead to further hemodynamic compromise.||

Synopsis

Control of rapid heart rates in the emergency setting are achievable using an intravenous nondihydropyridine calcium channel antanistagonist(eg, diltiazem, verapamil) orβ-adrenergic blocker(eg, metoprolol, esmolol). Pharma-cologic rhythm control(chemical cardioversion) employs intravenous drugs such as amiodarone, procanamide, or sotalol to convert AF/flutter to sinus rhythm and prevent its recurrence. Amiodarone is unique in that it can also be used for rate control in patients with heart failure in

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whom calcium channel orβ-adrenergic blockers may not be tolerated.

These recommendations are supported by the"2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation" and a 2025 evidence update. ${}^{1}$

Recommendation-Specific Supportive Text

1. Clinical trial evidence shows that nondihydropyri-dine calcium channel antagonists(eg, diltiazem,verapamil) andβ-adrenergic blockers(eg, meta-prool, esmolol, propranolol), are effective for rate control in patients with atrial fibrillation/flutter.2-9 Systematic reviews show that IV diltiazem improves heart rate control in atrial fibrillation/flutter without preexcitation with rapid ventricular response when compared to IV metoprolol.10-18 However, most of the included studies were limited by small sample size, retrospective data, and many did not report relevant clinical outcomes and comorbidities.Randomized clinical trials examining verapamil are lacking, thus, diltiazem is generally preferred.

2.Amiodarone is effective for rate control in patients with atrial fibrillation/flutter without preexcitation in patients with contraindications for nondihydropyri-dine calcium channel antagonists orβ-adrenergic blockers.2-9 Digoxin is less commonly used in the acute setting because of the slow onset of effect.19-21 In an observational study, the optimal amiodarone dosing for heart rate control(<115-80/min) was examined in 80 critically ill patients,most with cardiogenic shock or sepsis.22 The dose needed to achieve heart rate control was nearly twice as high in patients with persistent versus paroxysmal atrial arrhythmias, but patients who

were taking amiodarone prior to intensive care unit admission required lower doses.

3.Based on limited case reports and small case series, there is concern that patients with con-comitant 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, nondihydro-pyridine calcium channel antagonists,β-adrenergic blockers, or IV amiodarone.23-26 In this setting, car-diversion is recommended as the most appropri-ate management.

4.Because of their negative inotropic effect, non-dihydropyridine calcium channel antagonists(eg,diltiazem, verapamil) may further decompensate patients with left ventricular systolic dysfunction and symptomatic heart failure.7 Patients with heart failure with preserved ejection fraction may tolerate better nondihydropyridine calcium channel antago-nists. Whileβ-blockers can be safe in patients with cardiomyopathy, they can be harmful in patients who are decompensated.20,27,27 Limited evidence suggests that intravenous diltiazem may cause increased risk of decompensation compared to intravenous $\beta$ -adrenergic blockers, but more data are needed to support preferential use. ${ }^{28}$ Multiple studies have demonstrated $\beta$ -adrenergic blockers are safe for use in patients with chronic obstructive pulmonary disease. ${ }^{29}$ Refer to Table 2.

REFERENCES

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Table 2. IV Medications Commonly Used for Acute Rate Control in Atrial Fibrillation and Atrial Flutter

|Medication|Bolus dose|Infusion rate|Notes| |---|---|---|---| |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, and acute coronary syndromes| |$\beta$ -Adrenergic blockers|||| |Metoprolol|2.5-5 mg over 2 min, up to 3 doses||Avoid in decompensated heart failure| |Esmolol|500 mcg/kg IV over 1 min|50-300 mcg/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|Other medications|Other medications|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|

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29. Salpeter S, Ormiston T, Salpeter E. Cardioselective beta-blockers for chronic obstructive pulmonary disease. Cochrane Database Syst Rev.2005;2005;C005:3566.doi:10.1002/14651858.CD003566.pub2

INITIAL MANAGEMENT OF BRADYCARDIA

|Recommendations for Initial Management of Bradycardia|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-EO|1. In adult patients presenting with acute symp- tomatic bradycardia, evaluation and treatment of revir-versible causes are recommended.|| |2a|B-NR|2. In adult patients with acute bradycardia associated with hemodynamic compromise, administration of atropine is reasonable to increase heart rate.|| |2a|B-NR|3. In adult patients with persistent hemodynamically unstable bradycardia refractory to medical therapy, temporary transvenous pacing is reasonable to increase heart rate and improve symptoms.|| |2b|C-LD|4. If bradycardia is unresponsive to atropine, IV adrenergic agonists with rate-accelerating effects(eginephrine, dopamine) or transcutaneous pacing may be effective while the adult patient is prepared for emergent transvenous temporary pacing if required.|| |2b|2c-EO|5. Immediate pacing might be considered in unstable adult patients with high-degree AV block when IV/ IO access is not available.||

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Synopsis

Bradycardia has historically been defined as a ventricu-lar heart rate of less than 60/min. However, the "2018 ACC/AHA/HRS Guideline on the Evaluation and Man-agement of Patients With Bradycardia and Cardiac Con-duction Delay" adopted a lower threshold of less than 50/min, reflecting population studies that commonly use this lower cutoff.1 Bradycardia can be a normal finding in healthy adults, athletes, or during sleep.1 The clinical manifestation of bradycardia ranges from stable (asymp-tomatic) through symptomatic to unstable (symptomatic and associated with signs of poor perfusion). Patients with symptomatic bradycardia can present with dizziness or light-headedness, acute altered mental status, isch-emic chest discomfort, acute heart failure, hypotension, or syncope due to decreased cardiac output and tissue hy-perfusion. Clinicians must evaluate bradycardia within the clinical context to determine whether it is a manifesta-tion of another underlying disease process (eg, myocar-dial ischemia, hypoxia, electrolyte disturbance, acidosis,hypothermia) or the primary driver of the clinical presen-tation. Immediate treatment of symptomatic bradycardia as described in Figure 8 is focused on both supporting perfusion and identifying and reversing the underlying cause(s). The 2018 ACC/AHA/HRS Guideline provides comprehensive recommendations on the evaluation and management of chronic stable and unstable bradycardia.

These recommendations remain supported by the 2018 ACC/AHA/HRS Guideline and a 2025 evidence update.

Recommendation-Specific Supportive Text

1. Symptomatic bradycardia may be caused by a number of potentially reversible or treatable causes,including myocardial ischemia, hypoxemia,hypothyroidism,infections,structural heart disease,increased vagal tone, metabolic derangement,electrolyte abnormalities, or medications/toxins.1 Bradycardia may be difficult to resolve without addressing the underlying cause(s), underscoring the importance of evaluating potential etiologies while simultaneously initiating emergstabili-zation measures. A large retrospective review of prehospital patients undergoing transcutaneous pacing identified hypoxia and initial nonbradycardic rhythms as factors associated with pacing failure and increased mortality, emphasizing the critical need to address underlying causes alongside sta-bilization efforts.2

2.$\text{Atropine has been shown to be effective for the}$treatment of symptomatic bradycardia in observa-tional studies.$^{3-7}$ In a study in patients with OHCA and a nonshockable heart rhythm (asystole or pulseless electrical activity), the addition of atropine following epinephrine was a predictor of survival to

hospital admission. ${ }^{8}$ In a study among patients with IHCA, the administration of atropine for nonshock-able heart rhythms did not improve survival.

3.When symptomatic bradycardia is refractory to medical management, cardiac pacing is a reason-able alternative. Transcutaneous pacing is nonin-vasive, can be performed quickly at bedside, and is typically used as a bridge to placement of a tempo-rary transvenous pacing catheter. Transcutaneous pacing is often painful in the conscious patient and procedural tolerance may necessitate seda-tion. Evidence for transvenous pacing consists of limited observational studies, many of which have focused on indications and the relatively high com-plication rate(including bloodstream infections and pneumothorax, among others).10-13 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.

4.If atropine is ineffective, alternative agents to increase heart rate and blood pressure or trans-cutaneous pacing are reasonable alternatives. For medical management of a periarrest patient, epi-nephrine has gained popularity, including IV infu-sion and use of“push-dose” administration for acute bradycardia and hypotension. Studies on push-dose epinephrine for bradycardia specifi-cally are lacking, although limited data support its use for hypotension.14,15 Use of push-dose vaso-pressors require careful attention to correct dos-ing. Medication errors and adverse hemodynamic effects have been reported.16 Dopamine infusion can also increase heart rate.17 There are limited studies comparing medications to transcutaneous pacing for the treatment of bradycardia. A random-ized feasibility study in patients failing atropine compared dopamine to transcutaneous pacing and found no difference in survival to discharge.17 Whether to trial transcutaneous pacing, epineph-rine, dopamine, or other vasoactive agent will likely,therefore, depend on clinician experience and resources available.

5.For severe symptomatic bradycardia causing shock, if no IV or IO access is available, immedi-ate transcutaneous pacing while access is being pursued may be undertaken. A 2006 systematic review involving seven studies of transcutaneous pacing for symptomatic bradycardia and bradya-systolic cardiac arrest in the prehospital setting did not find a benefit from pacing compared with standard ALS, although a subgroup analysis from a single trial suggested a possible benefit in patients with symptomatic bradycardia.18 More recent stud-ies have underscored persistent challenges for

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Advanced Life Support:2025 AHA Guidelines for CPR and ECC

 Figure 8. Adult Bradycardia With a Pulse Algorithm.

clinicians in achieving and maintaining both elec-trical and mechanical capture during pacing.19,20 These difficulties may limit patient benefit in cer-tain scenarios, emphasizing the need for improved methods to distinguish true electrical capture from false capture. Future research is needed to deter-mine optimal pad placement and develop reliable methods for confirming initial and sustained cap-ture, such as the practicality and preferred location of pulse palpation, hemodynamic findings, pulse

oximetry characteristics, continuous ETCO2 moni-toring, and ultrasound.

REFERENCES

1.Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenogen KA,Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Pa-tients 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.0000000000000628

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Advanced Life Support: 2025 AHA Guidelines for CPR and ECC

2. Smida T, Voges L, Crowe R, Scheider J, Bardres J. Prehospital Transcutane-ous Cardiac Pacing in the United States: Treatment Epidemiology, Pricd-tors of Treatment Failure, and Associated Outcomes. Prehosp Emerg Care.2024;29:578-588: doi:10.1080/109031272024393768

3. Swart G, Brady WJ Jr, DeBehnke DJ, Ma OJ, Aufdeheride TP. Acute myocardial infarction complicated by hemodynamically unstable bradyar-rhythmia: prehospital and ED treatment with abproine. Am J Emerg Med 1999;17:647-652. doi: 10.1016/s0735-6757(99)90151-1

4. Smith I, Monk TG, White PF. Comparison of transesophageal atrial pacing with anticholinergic drugs for the treatment of in-traoperative bradycardia. Anesth Analg. 1994;78:245-252. doi:10.1213/00000539-199402000-00009

5. Chadda KD, Lichstein E, Gupta K, Kurpostis E. Effects of atropine in patients with bradyarrythmia complicating myocardial infarction. Usefulness of an optimum dose for overdrive. Am J Med 1977;53:03-510. doi:1016/0.00023433(77)90194-2

6. Chadda KD, Lichstein E, Gupta PK, Choy R. Bradycardia-hypotension syndrome in acute myocardial infarction. Repraspraisal of the overdrive effects of atropine. Am J Med. 1977;59:158-164. doi:10.1016/0002-9343(75)90349-6

7. Brady WJ, Swart G, DeBehnke DJ, Ma SJ, OAl, Aufherdehe TP. The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrio-ventricular block: prehoshal and emergency department considerations.Resuscitation.1999;41:47-55. doi:10.1016/s0305-9757(99)00032-5

8. Yano T, Kawana R, Yamauchi K, Endo G. Nagylation Y. The Additive Effect of Attopine Sulfate during Cardiopulmonary Resuscitation in Ou-oh-spatial non-traumatic Cardiac Arrest patients with Non-shocable Rhythm. Intern Med 2019;58:1713-1721. doi:10.2169/internalmedic.1932-18

9. Holmberg MJ, Moskowitz A. Wiberg S. Grosseestearu AV. Yankama T,Witten L, Perman SM, Donnino MW, Andersen LW; American Heart Association's Get With The Guidelines®-Rossuscitation Investigators. Guideline removal of tropine and survival after adult in hospital cardiac arrest with a non-shockable rhythm. Resuscitation. 2019;137:69-77. doi:10.1016/j.resuscitation.2019;0.02.002

10. McCann P. A review of temporary cardiac pacing wires. Indian Pacing Elec-trophysiol.2007;7:40-49.

11. JouY LH, Hu HP,Tuan TC, Wang KL, Lin YL, Lo LW HY, FKong 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.1540-8159.20.02893.x

12. Ferguson JD, Banning AP, Bashir Y. Randomised trial of temporary car-diac pacing with semirgid and balloon-flotation electrode catheters. Lancet 1997;349:1883. doi: 10.1016/S0140-6736(97)24026-2

13. Sofi NU, Sinha SK, Ali A, Samrat R, Sazi MM, Sharma AK, Sachan M,Pandey U, Thakur R. Unguided temporary pacing via jugular/subclavian

Disclosures

Appendix 1. Writing Group Disclosures

|Writing Group Member|Employment|Research Grant|Other Research Support|Speakers’ Bureau/ Honoraria|Experistes|Ownership Interest|Consultant/ Advisory Board|Other| |---|---|---|---|---|---|---|---|---| |Michael C. Kurz|University of Chicago|None|None|None|None|None|None|None| |Jane G. Wigginton|UT Dallas|None|None|None|None|None|None|None| |Sachin Agarwal|Columbia University Irving Medical Center|NIHt|None|None|None|None|None|None| |Jason A. Bartos|University of Minnesota|None|None|None|None|None|None|None| |Ryan A. Coute|University of Alabama at Birmingham|NIHt;AHA*;NIH*; Zoll Foundation*|None|None|None|None|None|None| |lan R. Drennan|University of Toronto; Orgen Critical Care and Transport Medicine; Sunnybrook Health Sciences(Canada)|None|None|ZOLL Medicalt|None|None|None|None| |Amea Haamid|University of Chicago|None|None|None|None|None|None|None| |Peter J. Kudenchuk|University of Washington Medical Center|NIH/NINDtS|None|None|None|None|None|None|

(Continued)

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Appendix 1. Continued

|Writing Group Member|Employment|Research Grant|Other Research Support|Speakers Bureau/ Honoraria|Expert Witness|Ownership Interest|Consultant/ Advisory Board|Other| |---|---|---|---|---|---|---|---|---| |Mark S. Link|UT Southwestern Medical Center|None|None|None|None|None|None|None| |Ashish R. Panchal|The Ohio State University Wexner Medical Center|None|None|None|None|None|None|None| |Michele M. Pelter|UCSF Physiological Nursing|NIHt; UCSF*|None|None|None|None|Cardinal Health*|None| |Marina Del Rios|The University of Chicago Medicine|NIH*|None|None|None|None|None|None| |Amber J. Rodriguez|American Heart Association National Center|None|None|None|None|None|None|None| |Sarah M. Perman|Yale School of Medicine|NIH/NHLBlt|None|None|None|None|None|None| |Stephen Sanko|Keck School of Medicine of USC|None|None|None|None|None|None|None| |Pavitra Kotini-Shah|UIC Emergency Medicine|NIH K awardt; Zoll Foundation*; WorldPoint*|None|None|None|None|Worldpoint*|Illinois Heart Rescue*|

This table represents the relationships of writing group members that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure Questionnaire, which all members of the writing group are required to complete and submit. A relationship is considered to be"significant" if(a) the person receives$5000 or more during any 12-month period, or 5% or more of the person's gross income; or(b) the person owns 5% or more of the voting stock or share of the entity, or owns$5000 or more of the fair market value of the entity. A relationship is considered to be"modest" if it is less than"significant" under the preceding definition.*Modest.

*Modest.

tSignificant.

Appendix 2. Reviewer Disclosures

||||Other Research Support|Speakers & Honoraria|Expert Witness|Ownership Interest|Consultant/Advisory Board|Other| |---|---|---|---|---|---|---|---|---| |William Brady|University of Virginia|None|None|None|None|None|None|None| |Daniel Davis|Logan Health|None|None|None|None|None|Philips Healthcare*|None| |Michael W. Donnino|Beth Israel Deaconess Med Center|NIH(Consultant on NIH funded study on supraglotic airway versus intubation)t|None|None|None|None|None|None| |Bryan McNally|Emory University School of Medicine|CDC CARES Expansion and Modernization Grant (Funding for the Cardiac Arrest Registry to Enhance Survival(CARES))t|None|None|None|None|Qilu Hospital; St Lukes Hospital; Duke University*; Cedars Sinai Hospital*|None| |Robert W. Neumar|University of Michigan|NIH(Research Grants)t; AHA (Research Grant)t; Laerdal Foundation(Research Grant)*|None|None|None|None|None|None| |Robert A. Swor|William Beaumont Foundation(Research Grant)*|None|None|None|None|None|None|None|

This table represents the relationships of reviewers that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure Ques-tionnaire, which all reviewers are required to complete and submit. A relationship is considered to be“significant” if(a) the person receives$5000 or more during any 12-month period, or 5% or more of the person's gross income; or(b) the person owns 5% or more of the voting stock or share of the entity, or owns$5000 or more of the fair market value of the entity. A relationship is considered to be“modest” if it is less than“significant” under the preceding definition.

*Modest.

tSignificant.