2025+AHA心肺复苏与心血管急救指南-第11部分：心脏骤停后护理

INTRODUCTION

# Scope of the Guidelines

This 2025 post-cardiac arrest care (PCAC) guideline from the American Heart Association (AHA) is based on the expert writing group review of the relevant Inter-national Liaison Committee on Resuscitation (ILCOR)Consensus on Science With Treatment Recommenda-tions (CoSTR) documents and the studies included in the systematic reviews as well as new evidence updates conducted by the writing group. The writing group dis-cussion and evidence reviews were conducted within the context of the clinical environments in which out-of-hospital and in-hospital resuscitations occur, with special consideration for the health care professionals who use these PCAC guidelines.

# Organization of the Writing Group

The PCAC Focused Update Writing Group includ-ed a diverse group of experts with backgrounds in

emergency medicine, neurocritical care, interventional and critical care care cardiology, psychology, and pulmo-nary critical care. Group members were appointed by the AHA Emergency Cardiovascular Care Science Subcommittee and approved by the AHA Manuscript Oversight Committee. Writing group members were selected to represent diverse backgrounds in clinical medicine and research expertise as well as to form a group that was institutionally diverse.

The AHA has rigorous conflict of interest poli-cies and procedures to minimize the risk of bias or improper influence during the development of guidelines. Before appointment, writing group mem-bers disclosed all relevant commercial relationships and other potential(including intellectual) conflicts.These procedures are described more fully in "Part 2:Evidence Evaluation and Guidelines Development" of the 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Car-diovascular Care.1 Appendix 1 of this document lists the writing group members' relevant relationships with industry.

# METHODOLOGY AND EVIDENCE REVIEW

The writing group members evaluated the current list of patient, intervention, comparison, and outcome ques-tions included in current PCAC guidelines. Patient,intervention, comparison, and outcome questions with novel evidence were revisited by the writing group. For each targeted patient, intervention, comparison, and outcome question, writing group members created a search strategy or utilized a previously created ILCOR search strategy when available. Search strategies were internally peer reviewed. This search was exe-cuted in Medine and Excerpta Medica Database using the Ovid search interface and in the Cochrane Central Register of Controlled Trials. Final searches were exe-cuted in November 2024.Search results were not lim-ited by language or year. Two writing group members performed dual screening of the titles and abstracts of all articles identified from each search and identified articles for full text review. Screening conflicts were resolved between the 2 writing group members and writing group leadership before full text review. Two writing group members reviewed the full text of all se-lected articles and applied the information contained to develop treatment recommendations appropriate for each clinical question. Each draft recommenda-tion was created by a group of 2 or 3 writing group members and then reviewed and refined by all writing group members during regular virtual meetings.The fi-nal manuscript was reviewed and approved by all writ-ing group members.

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Table 1. Applying American College of Cardiology/American Heart Association 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

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

● Associated with excess morbidity/mortality

● Should not be performed/administered/other

LEVEL(QUALITY) OF EVIDENCE#

Level 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\# from 1 or more RCTs

•Meta-analyses of moderate-quality RCTs

Level B-NR

(Nonrandomized)

• Moderate-quality evidence $\pm$ 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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Class of Recommendation and Level of Evidence

As with all AHA guidelines, each recommendation in this focused update is assigned a Class of Recommenda-tion (COR) based on the strength and consistency of the evidence, alternative treatment options, and the impact on patients and society (Table 1). The Level of Evidence(LOE) is based on the quality, quantity, relevance, and consistency of the available evidence. For each recom-mendation, the writing group discussed and approved specific recommendation wording and the COR and LOE assignments. In determining the COR, the writing group considered the LOE and other factors, including systems issues, economic factors, and ethical factors like equity,acceptability, and feasibility. These evidence-review meth-ods, including specific criteria used to determine COR and LOE, are described more fully in "Part 2: Evidence Evaluation and Guidelines Development" of the 2025 guidelines.1 The writing group members had final author-ity over and formally approved these recommendations.

Guideline Structure

The guidelines are organized into knowledge chunks,grouped into discrete modules of information on spe-cific topics or management issues. ${}^{2}$ Each modular knowledge chunk includes a table of recommenda-tions that uses standard AHA nomenclature of COR and LOE. A brief synopsis is provided to put the rec-ommendations into context with important background information and overarching management or treatment concepts. Recommendation-specific supportive text clarifies the rationale and key study data supporting the recommendations. When appropriate, additional tables are included.

This 2025 document updates the recommendations for the use of MCS, vasopressor choice, ventiolatory goals,coronary angiography and percutaneous coronary inter-vention(PCI), temperature control, seizure management(with a new section on postarrest myonclus), and survi-vorship after cardiac arrest(Figure 1). This 2025 update is based on the evidence identified in systematic reviews performed by ILCOR and this writing group address-ing novel data that has been published since the formal release of the 2020 AHA advanced life support guide-lines for cardiopulmonary resuscitation and the 2023 AHA Focused Update on Adult Advanced Cardiovascular Life Support. ${}^{1,3}$

Document Review and Approval

These guidelines were submitted for blinded peer review to 5 subject matter experts nominated by the AHA. Be-fore appointment, all peer reviewers were required to dis-close relationships with industry and any other conflicts

of interest, and all disclosures were reviewed by AHA staff. Peer reviewer feedback was provided for guidelines in draft format and again in final format. All guidelines were reviewed and approved for publication by the AHA Science Advisory and Coordinating Committee and the AHA Executive Committee. Comprehensive disclosure information for peer reviewers is listed in Appendix 2.

REFERENCES

1. Panchal AR, Bartos JA, Cababinas JG, Donnino MW, Drennan IR, Hirsch KG,Kudenchuk PJ, Kurz MC, Lavona 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-pulmonary Resuscitation and Emergency Cardiovascular Care. Circulation.2020;142:S366-S468. doi: 10.1161/CIR.0000000000000916

2.Levine GN,O'Gara PT,Beckman JA,Al-Khatib SM,Birtcher KK,Cigarroa JE, 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:e879-e886. doi:10.1161/CIR.00000000000000651

3.Perman SM,Elmer J, Maciel CB, Uzendu A, May T, Mumma BE, Bartos JA, Rodriguez AJ, Kurz MC, Panchal AR, Rittenberger JC; on behalf of the American Heart Association. 2023 American Heart Association focused update on adult advanced cardiovascular life support: an update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2024;149:e254-e273.doi: 10.1161/CIR.000000000000000000000000000000000000000

OYGENATION TARGETS IN ADULT PATIENTS AFTER CARDIAC ARREST

|Recommendations for Oxygenation Targets in Adult Patients After Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|B-R|1. The use of 100% inspired oxygen is recommended until the arterial oxygen saturation(Spo2) or the partial pressure of arterial oxygen(Pao2) can be reliably measured in adult patients after ROSC.|| |1|B-NR|2. Hypoxemia should be avoided in adult patients after ROSC.|| |2a|B-R|3. Once reliable measurement of oxygen saturation is available, it is reasonable to avoid hyperoxemia and hypoxemia by titrating the fraction of inspired oxygen(Fio2) to target oxygen saturation of 90% to 98%(PaO2, 60-105 mmHg) in adult patients after ROSC.|| |2b|C-LD|4. When relying relying on pulse oximetry, health care professionals should be aware of the increased risk of inaccuracy that may conceal hypoxemia in patients with darker skin pigmentation.||

Synopsis

Delivery of oxygen to the brain and other vital organs is critical in resuscitation. There are theoretical risks associated with both hyperoxemia and hypoxemia.1,2 Hyperoxemia may contribute to the development of reactive oxygen species in ischemic tissue, worsen-ing oxidative injury and cell death.3 Hypoxemia may

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Recommendation-Specific Supportive Text

1.In settings where accurate measures of Spo2 or Pao2 cannot be obtained, maintaining an Fio2 of 100% until a reliable measure of oxy-genation is obtained can help avoid hypoxemia.Administration of 100% oxygen immediately after ROSC until oxygen saturation can reli-ably be measured is supported by the EXACT(Reduction of Oxygen After Cardiac Arrest) ran-domized trial.5 This study found an increase in hypoxemic events in the prehospital setting when Fio2 was adjusted to maintain lower as compared to a higher Spo2 target.5

2. Hypoxia increases the risk of end-organ dam-age, and hypoxemia is a widely available surro-gate for hypoxia. Observational studies are mixed,with at least one study showing worse outcomes in patients experiencing post-ROSC hypoxemia.8 These observational data are supported by the EXACT randomized trial, which demonstrated that lower oxygen targets in the prehospital and emer-gency department setting led to more hypoxemic episodes and lower survival.5,9

3.Several clinical trials have compared different Spo2 and Pao2 targets after ROSC in a variety of clinical settings with no superior or inferior target identified.5,10,11 An Spo2 target of 90% to 98%(Pao2 target,60-105mmHg) reflects the ranges studied in key randomized trials. In a prespeci-fied subgroup of patients with hypoxic-ischemic encephalopathy in one clinical trial, patients ran-domized to a conservative oxygen therapy arm emphasizing protocolized reduction of Fio2 had better outcomes than those in a usual care arm.12 Observational studies have found an association between severe hyperoxemia(Pao2,>250 mmHg)and worse outcomes. ${}^{13}$

4. Patients with darker skin pigmentation may develop“ocult hypoxemia,” wherein the Spo ${}_{2}$ on pulse oximeter reads in the normal range but the Pao ${}_{2}$ is in the hypoxemic range. ${ }^{7,14-16}$

VENTILATION TARGETS IN ADULT PATIENTS AFTER CARDIAC ARREST

|Recommendations for Ventilation Targets in Adult Patients After Cardiac Arrest||| |---|---|---| |COR|LOE|Recommendations| |1|B-R|1. Arterial partial pressure of carbon dioxide(Paco$_{2}$) should be maintained within a normal physiologic range(generally 35-45 mmHg) in adult patients who remain comotast after ROSC| |2b|B-NR|2. It may be reasonable to obtain a blood gas measurement to assess $PaO_{2}$ in mechanically ventilated adult patients after ROSC|

Synopsis

Management of carbon dioxide during the postarrest phase is necessary given its role in regulating cerebral blood flow. Hypocapnia-induced vasoconstriction may lead to cerebral ischemia, while hypercapnia may exacerbate elevated intracranial pressure(ICP) through increased ce-rebral blood volume associated with vasodilation.

Recommendation-Specific Supportive Text

1. Although a strategy of mild permissive hypercap-nia(target Paco2, of 50-55 mmHg) might improve brain perfusion, observational studies have dem-onstrated mixed results on patient outcomes.8,17-19 The TAME(Targeted Therapeutic Mild Hypercapnia after Resuscitated Cardiac Arrest) randomized trial compared the maintenance of normocapnia(Paco2,35-45 mmHg) to mild hypercapnia(Paco2,50-55mmHg) for 24 hours in patients who remained comose after cardiac arrest and found no difference in neurologic outcome at 6 months or in other secondary outcomes.20 Although there was no outcome difference overall, the interven-tion in the TAME trial was stopped more often in the mild hypercapnia arm, possibly in response to severe acidemia because the protocol recom-mended suspending the intervention if pH<7.1 and base excess <-6 mmol/L. As a result, main-taining the Paco, within a normal physiologic range(generally,35-45 mmHg) is supported. Whether targets should be individualized based on individual patient physiology remains unknown.

2. The ability to measure Paco $_{2}$ after arrest is limited without blood gas measurement, and observational studies ${}^{21-24}$ suggest that end-tidal carbon dioxide levels may be falsely low and may not accurately reflect Paco $_{2}$ levels in post-cardiac arrest patients.

REFERENCES

1. Johnson NJ,Carlomb DJ, Gaieski DF. Ventilator Management and Respira-tory Care After Cardiac Arrest: Oxygenation, Ventilation, Infection, and Injury Chest.2018;153:1466-1477. doi: 10.1016/j.chest.2017.11.012

2. Bray J, Skrifvars MB, Bernard S. Oxygen targets after cardiac ar-rest: A narrative review. Resuscitation. 2023;189:109899. doi:10.1016/j.resuscitation.2023.109899

3. Litjos JF, Mira JP, Duranteau J, Cariou A. Hyperoxia toxicity after car-diac arrest: What is the evidence? Ann Intensive Care. 2016;6:23. doi:10.1186/s13613-016-0126-8

4. Robca B,Cadenes R,Battaglini D,Ball L,Sanfilippo F,Brunetti I,Jakobsen JC,Lija G,Friberg H,Wendel-garcia PD,et al;TTM2 Trial collaborators.Oxygen targets and 6-month outcome after out of hospital cardiac arrest:a pre-planned sub-analysis of the targeted hypothermia versus targeted normothermia after Out-of-Hospital Cardiac Arrest(TTM2) trial. Crit Care 2022;26:323. doi: 10.1186/s13054-022-04186-8

5.BernardSAB,BrayJE,SmithK,Stephenson,MFinn,JranthamH,HeinC,Masters,S,Stub D,Perkins GD,et al; EXACT Investigators.Effect of Lower vs Higher Oxygen Saturation Targets on Survival to Hospital Discharge Among Patients Resuscitated After Out-of-Hospital Cardiac Arrest: The EXACT Randomized Clinical Trial. JAMA 2022;2023:1818-1826. doi: 10.1001/jama.2022.17701

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6.Seitz KP,Wang L,Casey JD,Markus JA,Jackson KE,Qian ET,Self WH,Cire RW,Semmer WL,Py Oximetry and Race in Critically III Adults. Crit Care Explor:2022;4:e0758. doi: 10.1097/ CCE.00000000000000758

7. Spoding MW, Dickson RP, Ishyra NJ, Gay SE, Valley TS, Racial Bias in Pulse Oximetry Measurement. N Engl J Med. 2020;383:2477-2478. doi:10.1056/NEJMc2029240

8. Wang HE, Prince DK, Drnner, R.Nuangra, B. Carbony DJ, Johnson N,Hansen M, Elmer J, Christenson J, Kudenchuk P, et al.; Resuscitation Out-comes Consortium(ROC) Investigators. Post-resuscitation arterial oxygen and carbon dioxide and outcomes after cut-off-hospital cardiac arrest, re-suscitation.2017;120:113-118. doi: 10.1016/j.resuscitation.201708.244

9. Holmberg MJ, Ikeyama T, Garg R, Drrenan L, Iavones E, Bray J, Olasveeneng T, Berg KM, on behalf of the Advanced Life Support and Basic Life Sup-port Task Forces. Oxygenation and ventilation targets after cardiac arrest:an updated systematic review and meta-analysis.2023. Accessed March 21,2025. https://costil.org/corordic/document/oxygen-and-carbon-dioxide-targets-in-patients-with-return-of-spontaneous-circulation-after-cardiac-arest-als-rst.

10. Semier MW, Casey J, Lloyd BD, Hastings PG, Hays MA, Stollstijin JL, Buell KG, Brems JH, Qian ET, Seitz KP; et al. PILOT Investigators and the Prag-matic Critical Care Research Group. Oxygen-Saturation Targets for Critically III Adults Receiving Mechanical Ventilation. N Engl J Med.2022;387:1759-1769. doi:10.1065/NEJm208204815

11. Schmidt H, Kjaergard J, Hassager, C. Molstrom S, Grand J, Bororegaard B, Roelsgaard Obling Le V, Seno S, Sarkisian L, Mamaev de, et al. Oxygen Targets in Compositse Survivors of Cardiac Arrest. Nerg J Engl J Med 2022;387:1467-1476. doi:10.1056/NEMOa2208686

12. Mackle D, Bellomo R, Bailey M, Beasley R, Deane A, Eastwood G, Finfer S,Freebair R, King L, Vanke et al; IUC-ROV Investigators and the Austra-lian and New Zealand Intensive Care Society Clinical Trials Group. Conser-vative Oxygen Therapy during Mechanical Ventilation in the ICU. NEng J Med 2020;382:998-998.10.1056/NEJMoA 1903297

13. Holmberg MJ, Nicholson N, Nolan JP, Schexnery S, Reynolds J, Nation K, Westesford M, Morley P, Soar J, Berg KM; Adult Pediatric Advanced Life Support Task Forces at the International Liaison Committee on Resuscita-tion(ILCOR). Oxygenation and ventilation targets after cardiac arrest: a systematic review and meta-analysis. Resuscitation. 2020:152:107-115. doi:10.1016/j.resuscitation.2020.04.031

14. Fawzy A,Wu TD,Wang K,Robinson ML,Farha J,Bradke A,Golden SH,Xu Y,Garibbal RiT, Bacial and Ethnic Discrepancy in Pulse Oimetry and Delayed Identification of Treatment Eligibility Among Patients With COVID-19.JAMA Intem Med 2022;182:7830-738. doi 10.1001/10.0171amainmeder2022.1906

15. Jamali H, Castillo LT, Morgan CC, Coult J, Muhammad JJ, Osabino O,Parsons EC, Adamson R. Racial Disparity in Oxygen Saturation Measurements by Pulse Oximetry: Evidence and Implications. Ann Am Thorac: Soc.2022;19:1951-1964. doi: 10.1513/Annals302-2020-370CME

16. Wong Al, Charignon M, Kim H, Josef C, de Hond AAH, Fojas JJ,Tabaia A, Liu X. Mireles-Cabodevila E, Carvalho L, et al. Analysis of Discrepancies Between Pulse Oximetry and Arterial Oxygen Satura-tion Measurements by Race and Ethnicity and Association With Organ Dysfunction and mortality. JAMA Netw Open.2021;4:e2131674. doi:10.1001/jamanetworkopen.2021.31674

13. Schneider AG, Eastwood GM, Bellano R, Bailey M, Plicsey M, Picher D, Young P, Stow P, Santamaria J, Stachowski E, et al. Arterial car-don dioxide tension and outcome in patients admitted to the intensive care unit after cardiac arrest. Resuscitation. 2013;84:927-934. doi: 10.1016/j.resuscitation.2013.02.014

18. Roberts BW,Kilgannon JH, Chansky ME, Trzeziak S. Association between initial prescribed minute ventilation and post-resuscitation partial pressure of arterial carbon dioxide in patients with post-cardiac arrest syndrome. Ann Intensive Care 2014:4.9: doi:10.1186/2110-5820-4-9

19. Tolins ML,Henning DJ,Gaieski F,Gosresseuer AV,Jaworski A,Johnson NJ. Initial arterial carbon dioxide tension is associated with neurological out-come after resuscitation from cardiac arrest. Resuscitation:2017;11:63-58. doi:10.1016/j.resuscitation.2017.03.006

20.Eastwood G,Nichol AD,Hodgson C,Parke RL,McGuinness S,Nielsen N,Bernard S, Skrifvars ML, Subd Taccos F,et al; TAME Study Investiga-tors,Mild Hypercapria or Normocanna after Out-of-Hospital Cardiac Ar-rest. N Engl J Med.2023;389:45-57. doi:10.1056/NEJMo22+214552

21. Moon Lee, SWi CH, Hong YS, Kim SJ, Kim NH. Arterial minus end-tidal CO2 as a prognostic factor of hospital survival in patients re-suscitated from cardiac arrest. Resuscitation: 20077:219-925: doi:10.1016/j.resuscitation.2006.06.034

22.Mueller M.,Jankow E.,Grafener J., Schergoenfero C., Poppe M., Schriefl C.,Clodi C.,Koch M.,Eft H: Hozer M.,et al.The difference between arterial

pCO(2) and etCO(2) after cardiac arrest- Outcome predictor or marker of unfavorable resuscitation circumstances? Am J Emerg Med.2022;61:120-126. doi: 10.1016/j.ajem.2022.08.058

23.Abrahawomicz AA, Counts CR, Danielson KR, Bulger NE, Maynard C,Caribdom DJ, Swenson ER, Latimer AJ, Yang B, Sayre MR, et al. The asso-ciation between arterial-end-tidal carbon dioxide difference and outcomes after out-of-hospital cardiac arrest. Resuscitation. 2022;181:3-9. doi: 10.1016/j.resuscitation.2022.09.019

24. Kim YW,Hwang SO, Kang HS,Cha KC.The gradient between arterial and end-tidal carbon dioxide predicts in-hospital mortality in post-cardiac arrest patient.Am J Emerg Med.2019;37:1-4.doi:10.1016/j.ajem.2018.04.025

BLOOD PRESSURE TARGETS IN ADULTS AFTER CARDIAC ARREST

|Recommendation for Blood Pressure Targets in Adults After Cardiac Arrest||| |---|---|---| |COR|LOE|Recommendation| |1|B-R|1. Hypotension should be avoided in adults after ROSC by maintaining a minimum MAP of at least 65 mmHg.|

Synopsis

Adequate blood pressure is important after cardiac arrest to maintain end-organ perfusion, including to the brain and heart. Determining the optimal blood pressure for an individual patient can be influenced by characteristics like the degree of myocardial dysfunction, the prearrest baseline blood pressure, the cause of hypotension, and the degree of neurologic injury.1 The physiologic rationale for considering a higher MAP after cardiac arrest relates to impaired cerebral blood flow autoregulation, which can potentially impair the ability of the brain to maintain per-fusion, even at normal MAP.

Recommendation-Specific Supportive Text

1. Hypotension and shock occur in at least two thirds of patients after cardiac arrest. Observational stud-ies have associated hypotension with worse over-all survival and lower rates of favorable neurologic outcome after cardiac arrest.2-6 Four randomized trials including over 1000 patients compared lower(a cutoff of≥70 mmHg) to higher(≥71 mmHg)MAP targets after out-of-hospital cardiac arrest(OHCA).7-10 These studies did not demonstrate better overall survival or favorable neurologic out-mately 65 mmHg, which is the standard minimum MAP recommendation of lower MAP arms was approxi-ness, including CS and sepsis. Collectively, these trials do not provide evidence for a different MAP goal in patients after cardiac arrest.11-13 The safety of a lower MAP target(eg, 60-65 mmHg) has not been evaluated in post-cardiac arrest patients.14 It is also unknown if a higher MAP target(eg,80-100 mmHg) may be beneficial for some

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patients. Because the referenced trials used MAP targets and not systolic blood pressure, the recom-mendation is updated to remove a previous systolic blood pressure target.

REFERENCES

1. Hirsch KG, Abella BS, Amorim E, Bader MK, Barletta JF, Berg K, Callaway CW,Friberg H,Gilmore EJ,Gremer DM,Kern KB,Livesay S,May TL,Neumar RW,Nolan JP,Odd P,Meberdy MA,Poloyac SM,Seder,SDA tore Fcoss,Fuzendu A, Walsh B,Zimmerman JL,Geocadin RG; on behalf of the Ameri-can Heart Association and Neurocritical Care Society. Critical care man-agement of patients after cardiac arrest: a scientific statement from the American Heart Association and Neurocritical Care Society. Circulation.2024;149e168-e200.doi:10116/C0000000000001163

2.Bhate TD, McDonald B, Sekhon MS, Griesdale DE. Associa-tion between blood pressure and outcomes in patients after car-diac arrest A systematic review. Resuscitation. 2015/97:1-6. doi: 10.1016/j.resuscitation.2015.08.023

3. Laurikkala J, Wilkman E, Pettilla V, Kurola J, Reinikainen M, Hoppu S,Ale-Koktok T, Tallgren M, Tieren A, Vaahersalo J, et al; FINNRESUSCI Study Group. Mean arterial pressure and vasopressor load after out-of-hospital cardiac arrest: Associations with one-year neurologic outcome, re-suscitation.2016;105:112-126. doi:10.1016/j.resuscitation.2016.05.026

4. Tabi M, Burstein BJ, Ahmed A, Dezufian C, Kashani KB, Jentzer JC. Shock Severity and Hospital Mortality In Out of Hospital Cardiac Arrest patients Treated With Targeted Temperature Management. Shock.2021;55:48-54.doi: 10.1097/SHK.00000000000001600

5. Jenter JC, Henry TD, Barsarky GW Menon, Baran DA, Van Depen S. Influence of cardiac arrest and ASCI shock stage. Cancer unit care mortality. Catheter Cardiovasc Interv. 2020;96:1350-1359. doi: 10.1002/ccd.28854

6. Roberts BW,Kilgannon JH, Hunter BR, Puskarich MA, Shea L, Donnino M,Jones C,Fuller BM,Kline JA,Jones AE,et al.Association Between Elevated Mean Arterial Blood Pressure and Neurologic Outcome After Resuscitation from Cardiac Arrest. Results From a Multicenter Prospective Cohort Study.Crt Care Med.2019;47:93-100, doi:10.1097/CCM.000000000000474

7.Jakkula P, Pettilla V, Hastabko L, Baoka Jiu, Painen 3, Wilkman E,Poppila J, Koske T, Bendel S, et al: COMACARE study group. Targeting low-normal or high-normal mean arterial pressure after cardiac arrest and resuscitation: a randomised pilot trial. Intensive Care Med. 2018;44:2091-2101. doi:10.1007/s00134-018-5448-8.

8.Amelot K, Deeyne C, Eermart V, Ferdinande B, Dupont M, Palmers PJ,Pettit T,Nuyens P, Maeremans J, Vundelinck J, et al.Early goal-directed haemodynamic optimization of cerebral oxygenation in comatose survivors after cardiac arrest: Neurotheoptoid postcard arrest trial. Eur Heart J.2019;40:1804-1814. doi: 10.1093/eurheart/ehz120

9. Grand M. Meyer AS, Kjaergaard J, Wberg S, Thomsen JH, Fryland M,OstrowsR, Schwarsson P, Hassager C. A randomised double-blind pilot trial comparing a mean arterial pressure target of 65 mm Hg versus 72 mm Hg after of-out-hospital cardiac arrest. Eur J Heart J. 2020;9:S100-S109. doi: 10.1177/2048872619900095

10. Kjaergaard J, Meller JE, Schmidt H, Grand Meltren S, Boregaard E,Vene S, Sarkis M, Laaema D, Wenjek L, et al. Blood-Pressure Targets in Comatose Survivors of Cardiac Arrest. N Engl J Med. 2022;387:1456-1466. doi: 10.1056/NEJMoA20206887

11. Nemella V,Siddiqui F,Amelok T, Reiainoni M, Grand J., Hastbach J, Hassager, C Kjaergaard J, Aneman A, Tiainen M, et al. Higher versus lower blood pressure targets after cardiac arrest: Systematic review with individual patient data meta-analysis. Resuscitation.2023;189:109862.doi:10.1016/j.resuscitation.2023.109862

12. Evans L, Rhoden A, Alhaznani W, Antonelli O,Spercomith CM. French C, Machado FR, Mclntyre L, Ostermann M, Prescott HC, et al. Surviving Sepsis: Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021;49:e1063-e1143. doi:10.1097/CCM.0000000000005337

13. van Diepen S, Katz JN, Albert Nm-Tendy J, Jacobs AK, Kapur NK, Kilic A, Menon V, Ohman EM, Sweitzer NK, Thieh Z, Hamash JB, Cohen MG; on behalf of the American Heart Association Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Quality of Care and Outcomes Research; and Mission: Lifeline. Contem-porary management of cardiogenic shock: a scientific statement from

the American Heart Association. Circulation. 2017;136:e232-e268. doi: 10.1161/C.I.CR.00000000000000525

14. Lamontagne F, Richards-Belle A, Thomas K, Harrison DA, Sadique MZ,Grieve RD,Camsookai J,Darnell R,Gordon AC,Henry D,et al;65 trial inves-tigators. Effect of Reduced Exposure to Vasopressors on 90-Day Mortality in Older Critically III Patients With Vasodilatory Hypotension: A Randomized Clinical Trial. JAMA 2020;323:938-949. doi: 10.1001/jama.2020.0930

DIAGNOSTIC STUDIES FOR ADULTS AFTER CARDIAC ARREST

Recommendations for Diagnostic Studies for Adults After Cardiac Arrest

|COR|LOE|Recommendations for Diagnostic Studies for Adults After Cardiac Arrest| |---|---|---| |COR|LOE|Recommendations| |1|B-NR|1. A 12-2 lead electrocardiogram(ECG) should be obtained as soon as feasible for all adult patients after ROSC.42-lead electrocardiogram(ECG) should be obtained as soon as feasible for all adult patients after ROSC.42-lead electrocardiogram(ECG) should be obtained as soon as feasible for all adult patients after ROSC.42-lead electrocardiogram(ECG) should be obtained as soon as feasible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as feasible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as feasible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as possible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as possible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as possible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as possible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as possible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as possible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as possible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as possible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as possible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as possible for all adult patients after ROSC.42-lead electrocardiogram(ECG). should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients after ROSC. should be obtained as soon as possible for all adult patients|

Synopsis

Diagnosis and treatment of the underlying cause of cardiac arrest as well as identification and treatment of complications from cardiac arrest and cardiopulmo-nary resuscitation(CPR) are important considerations in postrestare care. Twelve-lead ECG, echocardiography,point-of-care cardiac ultrasound, and CT imaging are used in postrestare patients to identify clinically significant diagnoses requiring intervention. These diagnostic mo-dalities are complementary, with patients often receiving multiple studies. While the majority of patients resuscitat-ed from cardiac arrest and patient have abnormal findings on these studies, these are not always diagnostic for the specific etiology of cardiac arrest and may not change clinical management.1-7 The performance,timing, and interpreta-tion of each study is guided by the clinical context. It is also important to note that the considerations regarding diagnostic imaging for an in-hospital cardiac arrest may differ from those in OHCA and that most of the available literature focuses on OHCA.

Recommendation-Specific Supportive Text

1. A 12-lead ECG obtained after ROSC can iden-tify arrhythmia, ST-segment elevation myocar-dial infarction(STEMI), and other diagnoses associated with cardiac arrest for which treat-ment or monitoring is indicated. While the ECG is critical in identifying patients with STEMI or STEMI-equivalent patterns,8,9 its accuracy for these diagnoses in the immediate post-ROSC period has limitations.1,10-14 Electrocardiograms

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Post-Cardiac Arrest Care: 2025 AHA Guidelines for CPR and ECC

performed within the first 8 minutes following ROSC have been shown to have higher false positive rates for STEMI than those performed later.1,10 In one study, approximately two thirds of STEMI patterns on the immediate post-ROSC ECG evolved to non-STEMI patterns on repeat ECG performed a median of 30 minutes later.10 Optimal timing of an initial and repeat ECG fol-lowing ROSC are not well defined. Furthermore,the absence of ST-segment elevation does not rule out an intervenable coronary lesion.11,15-18

2.Full body CT scan (ie, head to pelvis) can diagnose pathologies contributing to cardiac arrest, includ-ing but not limited to intracerebral hemorrhage, pulmonary embolism, cardiac tamponade, aortic dissection, and pneumothorax. A 2019 systematic review evaluating post-cardiac arrest imaging to determine arrest etiology included 17 observa-tional studies and found that, despite heterogene-ity in the CT protocols, the diagnostic yield of CT scans for clinically significant diagnoses and inju-ries ranges from 8% to 54%,3 with several stud-ies indicating an approximate yield of 30%.7 This review was limited by the small number of patients included in the individual studies and the fact that few studies are prospective and that none were randomized.

CT imaging can also identify complications of car-diac arrest or resuscitation, such as fractures, aspi-ration, pulmonary contusions, pneumothorax, and hemorrhage, which may inform subsequent medi-cal interventions. ${}^{3-7,19,20}$ Small observational studies showed that patients resuscitated from OHCA may have CPR injuries identifiable by $CT^{21-23}$ including a small proportion of time-critical injuries, such as liver/splenic lacerations and pneumothorases. ${ }^{6}$

CT imaging carries risks such as contrast-associ-ated nephropathy. Transporting critically ill patients also carries the risks of hemodynamic instabil-ity, dislodging medical equipment, and delaying other interventions ${}^{24,25}$ that are weighed against the benefits of obtaining additional diagnostic information. ${}^{3-7}$

Head CT for neuroprognostication is discussed elsewhere.

3.Echocardiography and point-of-care cardiac ultrasound have been studied in the intra-rest setting for a variety of purposes, including iden-tification of a reversible cause for cardiac arrest.Available data suggest that these modalities can also contribute to elucidating the etiology of car-diac arrest in the postarest setting. Diagnoses that have been evaluated with echocardiography or point-of-care ultrasound include pericardial effusion, pericardial tamponade, right ventricular dilation suggestive of pulmonary embolism, aortic

$\text{dissection, cardiac regional wall motion abnor-}$malities suggestive of myocardial infarction, car-diomyopathy, and hypovolemia.3,26-35 An important limitation of most studies is that echocardiogra-phy or point-of-care ultrasound diagnoses were not compared to a reference standard ${}^{32}$ ; thus, the accuracy of these studies for most diagnoses can-not be quantified.3,36 Data are limited on whether cardiac regional wall motion abnormalities have an additional benefit when ECG and cardiac troponin results are considered.29,37 Noncardiac point-of-care ultrasound protocols have been described,but limited data are available on their yield and accuracy.38-40 The optimal time frame, operator,and technique for performing ECG or point-of-care cardiac ultrasound following ROSC remain uncertain.36 Ultrasound is operator dependent,and recommendations for sonographer train-ing and competencies are available from other organizations.41-43

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2. Ramjee V, Grossestreuer Av, Yao Y, Perman SM, Leary M, Kirkpatrick JN,Foria PR, Kolansky DM, Abella BS, Gaieski DF, Right ventricular dysfunc-tion after resuscitation predicts poor outcomes in cardiac arrest patients independent of left ventricular function. Resuscitation. 2015;96:186-191.doi: 10.1016/j.resuscitation.2015.08.008

3. Petek BJ, Erley CL, Kudenchuk PJ, Carlomb D, Strote J, Gatewood MO,Shuman WP, Hira RS, Gunn ML, Maynard C, et al. Diagnostic yield of non-invasive imaging in patients following non-traumatic out-of-hospital sudden cardiac arrest: A systematic review. Resuscitation. 2019;135:183-190. doi:10.1016/j.resuscitation.2018.09.004

4. Branch KRH, Gatewood MO, Kudenchuk PJ, Maynard C, Sayre MR,Carboml DJ, Edwards RM, Counts CR, Probstfield JL, Brusen R, et al. Di-agnostic yield, safety, and outcomes of Head-to-pelvis sudden death CT imaging in post arrest care: The CT FIRST cohort study. Resuscitation.2023;188:109785. doi: 10.1016/j.resuscitation.2023.109785

5. Tam J, Souferli C, Ratay C, Frisch A, Elmer J, Case N, Flickinger KL,Callaway CW, Coppler RJ; University of Pittsburgh Post-Cardiac Arrest Service. Diagnostic yield of computed tomography after non-traumatic out-of-hospital cardiac arrest. Resuscitation.2023;189:109898. doi:10.1016/j.resuscitation.2023.109898

6. Karatasakis A, Sarikaya B, Liu L, Gunn ML, Kudenchuk RJ, Gatewood MO, Maynard C, Sayre MR, Counts CR, CarlbOM DJ, et al. Prevalence and Patterns of Resuscitation-Associated Injury Detected by Head-to-Pelvis Computed Tomography After Successful Out-of-Hospital Car-diac Arrest Resuscitation. J Am Heart Assoc. 2022;11:e023949. doi: 10.1161/JAHA.121.023949

7. Branch KR, Nguyen ML, Kudenchuk RJ, Johnson NJ. Head-to-pelvis CT imaging after sudden cardiac arrest: Current sta-tus and future directions. Resuscitation. Resuscitation. 2023;191:109916. doi: 10.1016/j.resuscitation.2023.109916

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Disposition of Acute Chest Pain in the Emergency Department: A Report of the American College of Cardiology Solution Set Oversight Committee.J.Am Coll Cardiol.2022;80:1925-1960. doi:10.1016/j/ajcc.2022.08.750

0. Alundeharefe EL-TPeng EL 9,Shadéalpha,WGutterman DD,Weston BWPE PE, Baker JE,Labinski J,Debated G,Tang L,et al:echange in out-of-hospital 12-lead ECG diagnostic classification following resuscitation from cardiac arrest.Resuscitation:2021;169:45:52. doi:10.1016/j.resuscitation.2021.10.012

11. Salam I, Hassager, C Thomsen JH, Langkjaer S, Soholm H, Bro-Jeppesen J, Bang L, Holmvang L, Eringe D, Wanscher M, et al. Editor's Choice-Is pre-hospital ECG after out-of-hospital cardiac arrest accurate for the diag-nosis of ST-elevation myocardial infarction? Eur Heart J Acute Cardiovasc Care 2016;5:317-326. doi:10.1177/2048872615585519

12. McFadden P, Reynolds JC, Mader RD, Brown M. Diagnostic test accu-racy of the initial electrocardiogram after resuscitation from cardiac ar-rest to indicate invasive coronary angiographic findings and attempted revascularization: A systematic review and meta-analysis. Resuscitation 2021;160:20-36. doi:10.1016/j.resuscitation.2020.11.039

13. Sharma A. Miranda, FDMon R.,Dofin B, Bart BA, SMon S, Shroff GR. Interob-server variability among experienced electrocardiogram readers to diagnose acute thrombotic coronary occlusion in patients with out of hospital cardiac arrest: Impact of metabolic silica and angiographic culprit. Resuscitation 2022;172:24-31. doi:10.1016/j.resuscitation.2022.01.005

14. Yoshimura S,Gukchiz T, Isurta Y, Yamada T, Yoshiya K, Park C, Nishimura T, Ishibe K, Kobata H, Kishimoto M, et al. Diagnostic test accuracy of life-threatening electrocardiographic findings(ST-elevation myocardial infarc-tion equivalents) for acute coronary syndrome after out-of-hospital cardiac arrest without ST-segment elevation. Resuscitation. 2023;184:109700. doi:10.1016/j.resuscitation.2023.109700

15.Saier-Jensson H,NakastED R,Emosang E,Arisland E,Jraangni T,Jacobsen D,SundeK,Andersen G.Post-Resuscitation ECG for Selection of Pa-tients for immediate Coronary Angiography in Out-of-Hospital Cardiac Arrest. Circudos Incavert.2015:8:10.1161/circinatory 11.057284

12. Zanutti D, Armellini, I Nucifora G, Grillo MT, Morcogiti L, Carchetti E, Trillo G, Spedicator L, Bernard G, Proclemer A. Predictive value of electorac-diogram in diagnosing acute coronary artery lesions among patients with out-of-hospital-cardiac-arrest. Resuscitation. 2013;84:1250-1254. doi:10.1016/j.resuscitation.2013;03:04.023

17. Sideris G, Voicu S, Dillinger JG, Stratiev V, Logeart D, Broche C, Vivien B, Brun PY, Deyne N, Capan D, et al. Value of post-resuscitation electro-cardiogram in the diagnosis of acute myocardial infarction in out-of-hospital cardiac arrest patients. Resuscitation. 2011:82:1148-1153. doi:10.1016/j.resuscitation.2011:04.023

18. Millin AG, Com AC Njob, Johnston JW, Boltman N, Levne MJ,Seaman KG, Hirshom JM. Patients without ST elevation after return of spontaneous circulation may benefit from emergent percutaneous interven-tion: A systematic review and meta-analysis. Resuscitation. 2016;108:54-60. doi:10.1016/j.resuscitation.2016.09.004

19. Ratay C.;Eleram J,Callaway FC,WJinger KL,Coppler PJ: University of Pitts-burgh Post-Cardiac Arrest Service. Brain computed tomography after resus-citation from in-hospital cardiac arrest. Resuscitation. 2024:198110181.

20. Lee KY, So WZ, Ho JSY, Guo L, Shi Z, Yuh T, Hiao L, Ho AFW. Prevalence of intracranial hemorrhage amongst patients presenting with ou-hol'hospital cardiac arrest: A systematic review and meta-analysis. Resuscitation 2022;20216:136-149. doi:10.1016/j.resuscitation.2022.05.001

21. Champignele B.,Harelun PA,Plimacho R.,Dumas F,Geri G,Annout P,Paul M, Pene F, Mira JP, Bougouin W, et al. Major traumatic complications after out-of-hospital cardiac arrest: Insights from the Parisian registry. Resuscitation 2018;128:70-75. doi:10.1016/j.resuscitation.2018.04.022

22. Kashiwagi Y, Sasakawa T, Tampo A, Kawata D, Nishiwa T, Kokita N, Iwasiak H, Fujita S. Computed tomography findings of complications resulting from cardiopulmonary resuscitation. Resuscitation.2015;88:86-91. doi:10.1016/j.resuscitation.2014.12.022

23. Karasek J, Slezak J, Steela T, Ropinka H, Markovka B, Doubovskia T, Pisatova T, Nahalka D, Bartes T, Hladik J, et al. CPR-related injuries after non-traumatic out-of-hospital cardiac arrest: survivors versus non-survivors.Resuscitation:20221:170-95: doi:10.1016/j.resuscitation:2021.12036

24. Murata M, Nakagawa N, Kawasaki T, Yasuo S, Yoshida T, Ando K, Okamori S, Okada Y. Adverse events during intrahospital transport of critically ill patients: A systematic review and meta-analysis. Am J Emerg Med 2022;52:13-19. doi:10.1016/j.ajem.2021.11.021

25.Schweibel C.,Clech M.,Sinelet M.,Canirano-Ouraleas M.,Bonadona A,Dunamen J, Samali S, Kallel H, Goldran-Toledano D, et al; OUTCOMEREA Study Group. Safety of intrahastpi transport in ventilated critically ill pa

tients: a multicenter cohort study'. Crit Care Med.2013;41:1919-1928.doi:10.1097/C0C.0M13e031828a3bbd

2.6. Elfvén L,Hildebrand K,Schierbeck S,Sundqvist M,Ringh M,Claesson A,Olsson J,Nordberg P.Focused cardiac ultrasound after return of spontane-ous circulation in cardiac-arrest patients. Resuscitation.2019;142:16-22.doi:10.1016/j.resuscitation.2019.06.282

27. Breitkreiz R, Price S, Steiger HV, Seeger FH, Ilper H, Ackermann H,Rudolph M, Uddin S, Weigand MA, Müller E, et al; Emergency Ultrasound Working Group of the John Wolfgang Goethe-University Hospital, Frank-turl main Am. Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients: a prospective trial. Resuscitation.2010:81:1577-1553. doi:10.1016/j.resuscitation.2010.07.013

28. Chardoli M, Heidari F, Rabiee H, Sharif-Alhoseini M, Shokoohii H, Rahiml-Movavah V. Echocardiography integrated ACLS protocol versus conventional cardiopulmonary resuscitation in patients with pulseless elec-trical activity cardiac activity. Chin J Traumatol.2012;15:284-287.

29. Kim J, Cho YS, Lee BK, Lee DH, Jung E, Moon JM, Chun BJ. Diagnostic value of transthoracic echocardiography compared to electrocardiogram in predicting coronary artery stenosis among patients after cardiac arrest. Am J Emerg Med.2021;46:97-101. doi:10.1016/j.ajem.2021.02.053

30. Kim YW, Jung WJ, Cha R, Roh YI, Kim YS, Kim OH, Cha YS, Kim H, Lee KH,Hwang SO. Diagnosis of aortic dissection by transesophageal echo-cardiography during cardiopulmonary resuscitation. Am J Emerg Med.2021;39:92-95. doi:10.1016/j.ajem.2020.01.026

31. Lien WC,Hsu SH,Chong KM,Sim SS,Wu MC,Chang WT,Fang CC,Ma MH,Chen SC,Chen WU.CS-CAB protocol for ultrasonographic evaluation during cardiopulmonary Resuscitation: Validation and potential impact.Re-suscitation.2018;127:125-131. doi: 10.1016/j.resuscitation.2018.01.051

32. Hoy L, Sung W Chen YC, Lien WC, Chang WT, Huang CH. Performance of Intra-arest Echocardiography: A Systematic Review. West J Emerg Med.2024;156-174. doi:10.5811/westjem.18440

33.Hafner C,Manschein V,Klaus DA,Schaubmayr W,Tiboldi A,Scharner V,Gleiss A,Thal B,Krammel M,Ham T,et al.Live stream of prehospital point-of-care ultrasound during cardiopulmonary resuscitation- A feasibility trial. Resusciti-tation.2024;194:110089. doi:10.1016/j.resuscitation.2023.110089

34. Jung WJ, Cha KC, Kim YW, Kim YS, Roh YI, Kim SJ, Kim HS,Hwang SO. Intra-estret anosophageal echocardiographic find-utions and reuscitation. Resuscitation. 2020;154:31-37. doi: 10.1016/j.resuscitation.2020.06.035

35. Marstrand P, Correll P, Henriksen FL, Pehrson S, Bundgaard H, Theilade J.Clinical evaluation of unselected cardiac arrest survivors in a tertiary center over a 1-year period(the LAZARUZ study). J Electrocardi. 2016;49:707-713. doi: 10.1016/j.jelectrocard.2016.05.008

36. Liu L, Karatasakis A, Kukenchuk PJ, Kirkpatrick JN, Sayre MR, Carlomb DJ, Johnson NJ, Kolfabthel, Counts, C Branch KRH. Scoping review of echocardiographic parameters associated with diagnosis and prognosis after rescussited subcardi cardiac arrest. Resuscitation. 2023;184:109719.doi:10.1016/j.resuscitation.2023.109719

37. Lee SE, Uhm JS, Kim JY, Pak HN, Lee MH, Joung B. Combined ECG,Echocardiographic, and Biomarker Criteria for Diagnosing Acute Myocar-dial Infration of Out-of-Hospital Cardiac Arrest Patients. Yonsei Med J.2015;56:887-894. doi:10.3349/ymj.2015.56.4.887

38. Magon F, Longhtano Y, Savioli G, Picioni A, Tesauro M, Del Duca F,Denotano G, Volnonino G, Maiese A, La Russa R, et al. Point-of-Care Ultrasound(POCUS) in Adult Cardiac Arrest: Clinical Review. Diagnostics(Based) 2024:1443 doi: 10.3390/diagnostics 14040434

19. Hernandez, S. Chuler H., Hannan H., Sonyika C, Likourezos A, Marshall J.C.A.S.E. Cardiac arrest ultra-sound exam-a better approach to manag-ing patients in primary non-arrhythmogenic cardiac arrest. Resuscitation.2008;76:198-206. doi:10.1016/j.resuscitation.2007.06.033

40. Corbett SW OCallaghan T. Detection of traumatic complications of car-dipulmonary reuscitation by ultrasound. Ann Emerg Med.1997;29:317-21; discussion 322. doi:10.1016/s0196-0644(97)70342-1. discussion 322

41. Frankel HL, Kirkpatrick AW, Elbarbary M, Blaivas M, Desai H, Evans D,Summerfield DT, Slonim A, Breitkreutz R, Price S, et al. Guidelines for the Appropriate Use of Bedside General and Cardiac Ultrasonography in the Evaluation of Critically III Patients-Part I: General Ultrasonography. Crit Care Med.2015;43:2479-2502. doi:10.1097/CCM.0000000000001216

42. Levitov A, Frankel HL, Blaibava M, Kirkpatrick AW, Su E, Evans D,Summerfield DT, Slonim A, Breitkreutz R, Price S, et al. Guidelines for the Appropriate Use of Bedside General and Cardiac Ultrasonography in the Evaluation of Critically III Patients-Part II: Cardiac Ultrasonography. Crit Care Med.2016;44:1206-1227. doi:10.1097/CCM.0000000000001847

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43. American College of Emergency Physicians. Ultrasound guidelines:emer-gency, point-of-care, and clinical ultrasound guidelines in medicine. 2023.Accessed March 21, 2025. https://www.acep.org/siteassets/new-pdfs/policy-statements/ultrasound-guidelines-emergency-point-of-care-and-clinical-ultrasound-guidelines-in-medicine.pdf

TEMPERATURE CONTROL AFTER CARDIAC ARREST IN ADULTS

|Recommendations for Temperature Control After Cardiac Arrest in Adults|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|B-R|1. A deliberate, protocolized strategy of temperature control is recommended for all adults who are unresponsive to verbal commands after ROSC, irrespective of arrest location or presenting rhythm.|| |1|B-R|2. Maintaining a temperature between 32°C and 37.53°C in patients unresponsive to verbal commands after ROSC is recommended for adults.|| |2a|B-R|3. It is reasonable that temperature control be maintained for at least 36 h in adult patients who remain unresponsive to verbal commands after ROSC.|| |2b|B-R|4. The benefit of strategies other than rapid infusion of cold intravenous fluids for prehospital cooling is unclear.|| |2b|B-R|5. It may be reasonable to avoid rapid(faster than 0.5°C/h) rewarming in adult patients who have spontaneous hypothermia after ROSC or who are warming after hypothermic temperature control.|| |2b|B-NR|6. It is unclear if maintenance of a specific temperature(hypothermia versus normothermia) improves outcomes in subgroups of adult patients with higher illness severity.|| |3: No Benefit|B-R|7. Routine rapid infusion of intravenous fluids for prehospital hypothermic temperature control in adult patients after ROSC is not recommended.||

Synopsis

Temperature control has been a focus of PCAC for several decades, reflecting strong physiologic ra-tionale, evidence of benefit from preclinical and ob-servational studies, and benefit in some randomized trials. ${}^{1-4}$ In 2023, the AHA published a focused update on temperature control that revised recommendations based upon newly published clinical trial data includ-ing the TTM2(Targeted Temperature Management 2)trial and the CAPITAL CHILL(Moderate vs Mild Thera-peutic Hypothermia in Comatose Survivors of OHCA)trial. 5-7 A recent systematic review and meta-analysis published in 2023 summarizes the multiple random-ized trials conducted in various domains of temperature control. ${}^{8}$

Temperature control refers to the period of active tem-perature management to a hypothermic target or to a normothermic target. In settings in which a hypothermic target is used, a period of fever prevention or temper-ature control to a normothermic target may follow the hypothermic period. The entire duration of active temper-ature management is considered temperature control.

Recommendation-Specific Supportive Text

1. Multiple randomized trials have tested various approaches to temperature control after cardiac arrest, including surface, intravascular, and intrana-sal cooling. Most of these trials specified deliberate temperature control strategies in both the inter-vention and control arms.67,9-11

2. A 2023 updated ILCOR systematic review8 incor-porates 6 additional randomized trials published between 2021 and 2023. All trial arms controlled temperature to between 31°C and 37.7°C. In the meta-analysis, there was no difference in survival when applying temperature control at 32°C to 34°C versus 36°C or normothermia; however, the confidence intervals did not exclude a potential beneficial effect of temperature control at colder temperatures.8 None of the included trials found worse outcomes with lower temperature goals.Observational studies have found that adopt-ing higher temperature targets may result in an increased risk of fever and potentially worse out-comes, though confounders are likely present.12-14

3.The optimal overall duration of temperature control, including hypothermic temperature con-trol(32°C-34°C) and normothermic or fever- prevention temperature control(36°C-37.5°C), is an important area of ongoing investigation. In one randomized trial, there was no difference in out-comes comparing hypothermic temperature con-trol for 24 versus 48 hours, although the trial may have been underpowered and effect estimates favored longer temperature control durations. ${}^{10}$ In another recent randomized trial, there was no dif-ference in outcomes comparing a period of device-based fever prevention of 12 versus 48 hours after an initial 24-hour period of temperature control to 36°C(ie,36 versus 72 total hours of temperature control, respectively). ${}^{15}$ The 2 large TTM random-ized trials protocolized patients to 72 hours of total temperature control. ${}^{69}$ Recognizing evolution of evidence and definitions with respect to tempera-ture control, 36 hours of total temperature control is the shortest recommended duration. Multiple observational studies have found strong associa-tions between post-cardiac arrest fever and poor outcomes, including for fevers occurring after an initial 24-hour period of temperature control. ${}^{16-19}$ Results of the ICECAP(Influence of Cooling Duration on Efficacy in Cardiac Arrest Patients)trial, which aimed to identify the optimal duration of hypothermic temperature control for patients with both shockable and nonshockable rhythms,are pending after the study was stopped in June 2025.20

4. A randomized trial measured the impact of pre-hospital transnasal evaporative intra-arrest cooling

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versus postadmission temperature control on sur-vival in 671 patients and found no difference in the primary outcome of neurologically favorable survival at 90 days(16.6% in the treatment group and 13.5% in the control group).21 The ongoing PRINCESS-2 trial aims to study a similar approach in patients with shockable rhythm, a subgroup of interest in earlier trials.22 Cooling through surface or intravascular methods are reasonable alternatives.

5.In one small, randomized trial, there was no differ-ence in the primary outcome of interleukin-6 level or other outcomes comparing rewarming or temperature control at 33°C at a rate of 0.25°C per hour as compared to 0.5°C per hour.23 Recent randomized trials of temperature control used rewarming rates ranging from 0.25°C to 0.5°C per hour when transitioning out of temperature control to colder target temperatures.6,79-11 Patients pre-senting with spontaneous hypothermia after ROSC may have more severe neurologic injury and be more susceptible to secondary injury with rewarm-ing. In these cases, it is unclear whether passive,uncontrolled rewarming(potentially at rates above 0.5°C per hour) results in worse outcomes as com-pared to slow, controlled rewarming. Approaches to warming of patients presenting at temperatures below target in randomized trials have varied from allowing either active or passive warming ${}^{6}$ to active control,controlled warming at 0.25°C to 0.5°C per hour.

6. Most patients enrolled in temperature control tri-als had shockable rhythms with primary cardiac causes of arrest, despite eligibility criteria including both shockable and nonshockable rhythms.67,10, A patient level meta-analysis including patients with nonshockable rhythms from the TTM2 and HYPERION trials found no difference between hypothermic and normothermic temperature con-trol.24 Patients who do not meet eligibility criteria for randomized trials or who suffer cardiac arrest in the United States as compared to other parts of the world may have differences in important char-acteristics like arrest etiology, initial rhythm, witness status, bystander CPR, and downtime.26,26 Some observational studies suggest benefit with tem-perature control to lower temperatures for patients with higher illness and brain injury severity.27,28

7.There was no clear benefit to prehospital initiation of temperature control with cold intravenous fluids and signals of potential harm in one large random-ized clinical trial. ${}^{29}$

REFERENCES

1. Arrich J, Herkner H, Müllner D, Behringer W. Targeted tempera-ture management after cardiac arrest. A systematic review and meta-analysis of animal studies. Resuscitation. 2021;162:47-55. doi:10.1016/j.resuscitation.2021.02.002

2. Yenari MA, Han HS. Neuroprotective mechanisms of hypothermia in brain ischaemia. Nat Rev Neurosci.2012;13:267-278. doi:10.1038/nrn3174

3.Yanagawa Y, Ishihara S, Norio H, Takino M, Kawakami M, Takasu A, Okamoto K, Kaneko N, Terai C, Okada Y. Preliminary clinical outcome study of mild resuscitative hypothermia after out-of-hospital cardiopulmonary arrest. Re-suscitation.1998;39:61-66. doi:10.1016/s0300-9572(98)00118-x

4.Granfeldt A, Holmberg MJ, Nolan JP, Soar J, Andersen LW; International Liaison Committee on Resuscitation(ILCOR) Advanced Life Support Task Force. Targeted temperature management in adult cardiac arrest: Sys-tematic review and meta-analysis. Resuscitation. 2021;167:160-172. doi: 10.1016/j.resuscitation.2021.08.040

5. Perman SM,Elmer J, Maclic EB, Uzendu A, May T, Mumma BE, Bartos JA, Rodriguez AJ, Kurz MC, Panchal AR, Rittenberger JC; on behalf of the American Heart Association. 2023 American Heart Association focused up-date on adult advanced cardiovascular life support: an update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2024;149:e254-e273.doi:10.1161/CIR.000000000000000000000000000000000

6. Dankiewicz J, Cronberg T, Lilja G, Jakobsen JC, Levin H, Ullien S, Rylander C,Wise MP,ODdo M, Caniou A,et al; TTM2 Trial Investigators. Hypothermia versus Normothermia after Out-of-Hospital Cardiac Arrest. N Engl J Med.2021;384:2283-2294. doi: 10.1056/NEJMoa2100591

7.Le May M, Osborne C, Russo J, So D, Chong AY, Dick A, Froeschl M, Glover C, Hibbert B, Marquis JF, et al. Effect of Moderate vs Mild Therapeutic Hy-pothermia on Mortality and Neurologic Outcomes in Comatose Survivors of Out-of-Hospital Cardiac Arrest. The CAPITAL CHILL Randomized Clinical Trial. JAMA 2021;326:1494-1503. doi: 10.1001/jama.2021.15703

8. Granfeld A, Holmberg MJ, Nolan JP, Soar J, Andersen LW; International Liaison Committee on Resuscitation ILCOR Advanced Life Support Task Force. Temperature control after adult cardiac arrest: An updated sys-tematic review and meta-analysis. Resuscitation 2023;1911:109928. doi: 10.1016/j.resuscitation.2023.109928

9.Nielsen N, Wetterslev, J.Cronberg T,Erlinge D, Gasche Y, Hassager C, Horn J, Hovdenes J, Kjaergaard J, Kuiper M, et al; TTM Trial Investigators. Tar-geted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med.2013;369:2197-2206. doi: 10.1056/NEJMoa1310519

10.Kirkegaard S.Horede E, de Haas I, Pettila V, Taccone FS, Arus U, Storm C,Hassager C,Nielsen JF,Sorensen CA,et al.Targeted Temperature Manage-ment for 48 vs 24 Hours and Neurologic Outcome After Out-of-Hospital Cardiac Arest: A Randomized Clinical Trial. JAMA 2017;318:341-350.doi:10.1001/jama.2018.7978B

11.Lassarob JA,Lerdji H,Le Gouge A,Colin G,Grillet G, Girardy P,Coupez E,Dequin PF,Cariou A,Boulain T,et al;CRICS-TRIGGERSEP Group.Targeted Temperature Management for Cardiac Arrest with Nonshockable Rhythm.N Engl J Med.2019;381237-2337. doi: 10.1056/NEJMoa1906661

12.Bray JE, Stub D, Bloom JE, Segan L, Mitra B, Smith K, Finn J, Bernard S.Changing target temperature from 33°C to 36°C in the ICU management of out-of-hospital cardiac arrest: A before and after study. Resuscitation.2017;113:39-43. doi: 10.1016/j.resuscitation.2017.01.016

13.Johnson NJ, Danielson KR, Counts CR, Ruark K, Scruggs S, Hough CL,Maynard C, Sayre MR, Carlob DJ. Targeted Temperature Management at 33 Versus 36 Degrees: A Retrospective Cohort Study. Crit Care Med.2020;48:362-369. doi:10.1097/CCM.0000000000004159

14.Salter R, Bailey M, Bellon R, Eastwood G, Goodwin A, Nielsen N, Pilcher D,Nichol A,Saxena M, Shehabi Y,et al; Australian and New Zealand Inten-sive Care Society Centre for Outcome and Resource Evaluation(ANZICS-CORE). Changes in Temperature Management of Cardiac Arrest Patients Following Publication of the Target Temperature Management Trial. Crit Care Med.2018;46:1722-1730. doi: 10.1097/CCM.000000000003339

15. Hassager C, Schmidt H, Møller JE, Grand J, Molstrom S, Beske RP,Boesgaard S, Borregaard B, Bekker-Jensen D, Dahl JS, et al. Duration of Device-Based Fever Prevention after Cardiac Arrest. N Engl J Med.2022;3888-889-897. doi:10.1056/NEJMoa2212528

16. Bro-Jeppesen J., Hassager C, Wanscher M, Soholm H, Thomsen JH, Lippert FK,Moller JE,Kober L,Kjaergaard J. Post-hypothermia fever is associated with increased mortality after out-of-hospital cardiac arrest. Resuscitation.2013;84:1734-1740.doi:10.1016/j.resuscitation.2013.07.023

17. Grossestreuer AV, Gaieski DF, Donnino MW, Wiebe DJ, Abella BS. Magni-tude of temperature elevation is associated with neurologic and survival out-comes in resuscitated cardiac arrest patients with postwarming pyrexia. J Crit Care.2017;38:78-83. doi:10.1016/j.crc.2016.11.003

18.Picett E, Antonini MV, Bartolini Y, DeAngelis A, Delaj L, Florindo I, Villani F, Caspani ML. Delayed Fever and Neurological Outcome after Cardiac Ar-rest: A Retrospective Clinical Study. Neurocrit Care.2016;24:163-171. doi:10.1007/s12028-016-251-0

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19. Gebhardt K, Guyette FX, Doshi AA; Callaway W, Rittenberger JC; Post Cardiac Arrest Service. Prevalence and effect of fever on outcome following resuscitation from cardiac arrest. Resuscitation.2013;84:1062-1067. doi: 10.1016/j.resuscitation.2013;03:03038

20. Meuer WJ, Schmitzberger FF, Yeatts S, Ramakrishnan V, Abella B, Aufderheide T, Barsan W, Benoit J, Berry S, Black J, et al; ICECAP trial investigators. Influence of Cooling duration on Efficacy in Cardiac Arrest Patients[ICECAP): study protocol for a multicenter, random-ized, adaptive allocation clinical trial to identify the optimal duration of induced hypothermia for neuroprotection in comatose, adult survi-vors of after out-of-hospital cardiac arrest. Trials. 2024;25:502. doi:10.1186/s13063-024-08280-w

21. Nordberg T, Paccos F, Truhlar A, Forsberg S, Hollenberg J, Jonsson M, Cuny J, Goldstein P, Vermeersch N, Higuet A, et al. Effect of Trans-Nasal Evaporative Intra-arest Cooling on Functional Neurologic Outcome in Out-of-Hospital Cardiac Arrest: The PRINCESS Randomized Clinical Trial. JAMA 2019;321:1677-1685. doi: 10.1001/jama.2019.4149

22. Dillenbeck E, Hollenberg J, Holzer M, Busch HJ, Nichol G, Radsel P,Belohlavex J, Torres EC, López-de-Sa E, Rosel F, et al. The design of the PRINCESS 2 trial: A randomized trial to study the impact of ultrafast hy-potherm on complete neurologic recovery after ooh-tospital cardiac arrest with initial shockable rhythm. Am Heart J. 2024;271:97-108. doi: 10.1016/jahj.2024.02020

23. Lassarou JB, Guichard E, Reignier J, Le Gouge A, Pouplet C, Martin S,Lacherade JC, Colin G. Impact of rewarming rate on interleukin-6 levels in patients with shockable cardiac arrest receiving targeted temperature management at 33°C: the ISOCRATE pilot randomized controlled trial. Crit Care.2021;25:434. doi: 10.1186/s13054-021-03842-9

24. Cassore FBosckiew Z, Cariou A, Lijia G, Asfa P, Belohlavek J, Boulain T,Colin G, Cronberg T, Frat JP, et al. Hypothermia vs Normothermia in Patients With Cardiac Arrest and Nonshockable Rhythm: A Meta-Analysis. JAMA Neurol. 2024;81-126.138: 10.001/1001.01/1002.283.428.

25. Nishiyama C, Kiguchi T, Okubo M, Alihodiz H, Al-Araji R, Bald E, Beganton F,Booth S,Bray J,Christensen E,et al.Three-year trends in ouf-hospital cardiac arrest across the world: Second report from the International Liaison Committee on Resuscitation(ILCOR). Resuscitation.2023;186:109757. doi:10.1016/j.resuscitation.2023109757

26. Axelsson C, Axelsson AB, Svensson L, Herlitz J. Characteristics and out-come among patients suffering from out-of-hospital cardiac arrest with the emphasis on availability for intervention trials. Resuscitation.2007;75:460-468. doi: 10.1016/j.resuscitation.2007.05.018

27. Callaway CW, Coppler PJ, Faro J, Puyana JS, Solanki P, Dezifian L, Coshi AA,Elmer J, Frisch A, Guyette FX,et al.Association of Initial Ilness Se-verity and Outcomes After Cardiac Arrest With Targeted Temperature Management at 36°C or 33°C. JAMA Netw Open.2020;3:e8208215. doi: 10.1010/jametworkopen.2020.8215

28. Nutma S, Tjepkema-Cloostermans MC, Rujter BJ, Tromp SC,van den Bergh WM, Foudraine NA, Kornips FHM, Drost G, Scholten E,Strang A,et al.Effects of targeted temperature management at 33℃'s.36℃ on comatose patients after cardiac arrest stratified by the severity of encephalopathy. Resuscitation. 2022;173:147-153. doi:10.1016/j.resuscitation.2022.01.026

29. Kim F,Nichol G,Maynard C,Hallstrom A,Kudenchuk PJ,Rea T,Copass MK,Carlbom D,Deem S,Longstreth WT Jr,et al.Effect of prehospital induc-tion of mild hypothermia on survival and neurological status among adults with cardiac arrest and randomized clinical trial. JAMA 2014;311:45-52. doi:10.1001/jama.2013.282173

ADDITIONAL TREATMENTS IN ADULTS AFTER CARDIAC ARREST

|Recommendations for Additional Treatments in Adults After Cardiac Arrest||| |---|---|---| |COR|LOE|Recommendations| |2b|B-R|1. The routine use of prophylactic antibiotics in adult patients after ROSC is of uncertain benefit.| |2b|B-R|2. The effectiveness of agents to mitigate neurological injury in adult patients who remain comatose after ROSC is uncertain.|

|Recommendations for Additional Treatments in Adults After Cardiac Arrest (Continued)|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|B-R|3.The routine use of steroids for adult patients with shock after ROSC is of uncertain value.|| |2b|B-NR|4. In adult patients with ROSC after cardiac arrest, it may be reasonable to avoid hypoglycemia (glucose<70 mg/dL) as well as hyperglycemia (glucose>180 mg/dL).||

Synopsis

Patients with cardiac arrest often remain critically ill in the immediate post-cardiac arrest period, though treat-ments for general critical care populations may not be universally applicable to the post-cardiac arrest patient population. One important area in post-cardiac arrest therapies where new observational data have emerged is glucose control for post-cardiac arrest patients, and this has also been studied more extensively in general critical care populations. Patients are at risk of develop-ing pneumonia after cardiac arrest, which is often caused by aspiration during the cardiac arrest and resuscitation.Thus, there is rationale to evaluate whether empiric anti-biotic treatment can improve outcomes. Steroids are also of physiologic interest in patients after cardiac arrest due to their broad effects, including reducing inflammation and possibly supporting hemodynamics. Similarly, neuro-protective agents that act through a broad range of pos-sible mechanisms continue to be an area of clinical and research interest.

Recommendation-Specific Supportive Text

1. A 2020 ILCOR systematic review1 identified 2 randomized controlled trials(RCTs) that found no difference in survival or neurological outcome23 in patients treated with early prophylactic antibiotics after cardiac arrest. One RCT2 did find lower inci-dence of early pneumonia in those who received prophylactic antibiotics, but this did not translate to a difference in other outcomes. Since then,one observational study similarly demonstrated a reduction of early ventilator-associated pneumonia with prophylactic antibiotics4 but no differences in other patient-oriented outcomes(ie, short-term mortality, duration of mechanical ventilation, or intensive care unit length of stay). Given the need for general antibiotic stewardship and the findings of the above studies, there is insufficient evidence to suggest the use of antibiotics routinely after car-diac arrest.

2. A recent systematic review ${}^{5}$ evaluated neuropro-tective drugs and their effect on mortality and functional outcome. Nineteen RCTs of drugs cat-egorized as neuroprotective agents and 16 stud-ies of drugs categorized as anti-inflammatory

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or antioxidant were included. Multiple agents,including magnesium, nimodipine, inhaled gases(hydrogen, nitric oxide, and xenon), coenzyme Q10(ubiquinol), thiamine, and others, were evalu-ated. Most studies were single-center trials with low numbers of participants. The heterogeneity of intervention agents and trial designs limited the ability to perform meta-analyses, and there was overall low certainty of evidence, thus, limiting the ability to recommend any specific agent.

3.One small RCT including 50 patients compared steroids to placebo for post-cardiac arrest shock.6 Time to shock reversal and other outcomes did not differ between groups. A large retrospective obser-vational study found that steroid use after cardiac arrest was associated with survival.7 A recent sys-tematic review evaluating drug therapy compared with placebo included 2 RCTs using hydrocorti-sone after arrest as part of a multigraph protocol.8.9 There was insufficient evidence to perform a meta-analysis for steroids after ROSC and insuf-ficient evidence to recommend any specific drug treatment after ROSC.This topic does not address intra-artra arrest's steroids.

4.One small RCT evaluating strict versus moder-ate glucose control in patients resuscitated from cardiac arrest due to ventricular fibrillation(VF)10 found no difference in survival, though the thera-peutic ranges for their control and experimental arms are no longer congruent with current critical care management. Many subsequent observational studies have demonstrated an association between hyperglycemia or hypoglycemia in the post-cardiac arrest period and worse neurological outcomes and mortality, though these were not evaluating active glucose management interventions.11-16 While no RCTs have evaluated glucose targets in broad pop-ulations of post-cardiac arrest patients, treatment of blood glucose using insulin in the general critical care population improves mortality and is recom-mended in other guidelines, acknowledging risks of hypoglycemia when lower blood glucose ranges are targeted.17-19 Given the observational findings in post-cardiac arrest patients, the RCT findings in general critical care populations, and that post-cardiac arrest patients are often critically ill, this recommendation is updated to address avoidance of hypoglycemia and hyperglycemia without giving a specific target glucose range.

REFERENCES

1. Berg KM, Soar J, Andersen LW B, Bottiger W, Bcacciola 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 Diopmonary Uressuscitation and Emergency Cardio-vascular Care Science With Treatment Recommendations. Circulation.2020;142:S92-S139.doi: 10.1161/CIR000000000000893

2. Francois B, Cariou A, Ciere-Jehl R, Dequin PF, Renon-Carron F, Daix T,Güton C, Deye N, Legriel S, Plantefeve G, et al; CRICS-TRIGGERSEP Network and the ANTHARTIC Study Group. Prevention of Early Ventilator Associated Pheumonia after Cardiac Arrest. N ENgJ Med.2019;381:1831-1842. doi: 10.1056/NEJMoA1812379

3. Ribaric SF, Turel M, Knafelj R, Gorjup V, Stanic R, Gradisek P, Cerovic O, Mirkovic T, Noc M. Prophylactic versus clinically-driven anti-biotics in comatose survivors of out-of-hospital cardiac arrest-a Randomized pilot study. Resuscitation. 2017;111:103-109. doi: 10.1016/j.resuscitation.2016.11.025

4. Harmon MBA, Hodiamond CJ, Dankiewicz J, Nielsen N, Schultz MJ, Horn J, Friberg H, Juffermans NP. Microbiological profile of nosocomial in fections following cardiac arrest: Insights from the targeted tempera-ture management (TTM) trial. Resuscitation. 2020;148:227-233. doi: 10.1016/j.resuscitation.2019.11.033

5. McGuigan RJ, Pauley E, Eastwood G, Hays LMC, Jakobsen JC,Moseby-Knappe M, Nicholas AD, Nielsen N, Skrifvars MB, Blackwood B,et al. Drug therapy versus placebo or usual care for comatose survivors of cardiac arrest; a systematic review with meta-analysis. Resuscitation.2024;205:110431. doi: 10.1016/j.resuscitation.2024.110431

6. Donnino MW, Andersen LW, Berg KM, Chase, Mher, Sherwin R, Smithline H,Carney E, Ngo L, Patel PV, Liu X, et al; Collaborating Authors from the Beth Israel Deaconess Medical Center's Center for Resuscitation Science Research Group. Corticoseroid therapy in refractory shock following car-diac arrest: a randomized, double-blind, placebo-controlled, trial. Crit Care 2016:20:82. doi: 10.1186/s13054-016-1257-x

7. Tsai MS, Chuang PY, Huang CH, Tang CH, Yu PH, Chang WT,Chen WJ. Postarrest Steroid Use May Improve Outcomes of Car-diac Arrest Survivors. Crit Care Med. 2019;47:167-175. doi:10.1097/CCM.000000000000003468

8. Mentelopoulos SD, Malachias S,Chamos C, Konstantopoulos D, Ntaidou T,Papastylianou A, Kolliantzaki I,Theodoriidi M,Ischaki H,Makris D,et al.Vaso pressin,steroids,and epinephrine and neurologically favorable survival after in-hospital cardiac arrest: a randomized clinical trial. JAMA 2013;310:270-279. doi: 10.1001/jama.2013.7832

9.Mentelopoulos SD, Zaktinhinos SG, Tzoufi M, Katsios N, Papastylianou A,Gkisiot S, Stathopoulos A, Kollintza A, Somataki E, Roussos C. Vasopres-sin, epinephrine, and corticosteroids for in-hospital cardiac arrest. Arch In-tern Med.2009;169:15-24. doi:10.1001/archintermed.2008.509

10. Oksanen T, Skrifvars MB, Varpula T, Kuitunen A, Pettila V, Nurmi J,Castrén M. Strict versus moderate glucose control after resuscitation from ventricular fibrillation. Intensive Care Med.2007;33:2093-2100. doi:10.1007/s00134-007-0876-8

11. Borgquist O, Wise MP, Nielsen N, Al-Subaei N, Cranshaw J, Cronberg T, Glover G, Hassager C, Kjaergaard J, Kuiper M, et al; TTM-Trial Inves-tigators. Dysglycemia, Glycemic Variability, and Outcome After Cardiac Arrest and Temperature Management at 33°C and 36°C. Crit Care Med.2017;45:1337-1343.doi: 10.1097/CCM.000000000002367

12.Davidau F, Dumas F, Demars N, Geri G, Bouglé A, Morichau-Beauchant T, Nguyen LY, Bougouin W, Pène F, Charpentier J, et al. Blood glucose level and outcome after cardiac arrest: insights from a large regis-try in the hypothermia era. Intensive Care Med. 2014;40:855-862. doi:10.1007/s00134-014-3269-9

13. Russo JJ,James TE, Hibbert B, Ramirez FD, Simard T, Osborne C, Bernick J,Wells GA, Le May MR; CAPITAL Investigators. Hyperglycaemia in coma-tosev survives of out-of-hospital cardiac arrest. Eur Heart J Acute Cardiovasc Care.2018;7:442-449. doi:10.1177/2048872616684685

14. Nurmi J, Boyd J, Antalitaen N, Westerbacka J, Kuisma M. Early increase in blood glucose in patients resuscitated from out-of-hospital ventricular fibrillation predicts poor outcome. Diabetes Care. 2012;35:510-512. doi:10.2337/dc11-1478

15. Bang HJ, Youn CS, Park KN, Oh SH, Kim HJ, Kim SH, Park SH. Glu-cose control and outcomes in diabetic and nondiabetic patients treated with targeted temperature management after cardiac arrest. PLoS One.2024;19:e0298632 doi: 10.1371/journal.pone.0298632

16.Zhou D,Li Z,Shi G,Zhou J. Proportion of time spent in blood glucose range 70 to 140 mg/dL is associated with increased survival in patients admit to ICU after cardiac arrest: A multicenter observational study. Medicine(Baltimore) 2020;99:e21728. doi: 10.1097/MD.00000000000021728

17. Finfer S, Chittola DR, Su SY, Blair D, Foster D, Dhingra V, Bellomo R, Cook D, Dodek P, Henderson WR, et al; NICE-SUGAR Study Investigators. In-tensive versus conventional glucose control in critically ill patients. N Engl J Med.2009;360:1283-1297. doi: 10.1056/NEJMoa0810625

18.Draznin B, Aroda VR, Bakris G,Benson G,Brown FM,Freeman R,Green J,Huang E,Isaacs, D.Kahan S,et al. Diabetes Care in the Hospital: Standards

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of Medical Care in Diabetes-2022. Diabetes Care. 2022:45:S244-s253.doi: 10.2337/dc22-S016

19.Honarmand K, Sirmaturos M, Hirshberg EL, Bircher NG, Agus MSD,Carpenter DL, Downs CR, Farrington EA, Freire AX, Grow A, et al. Soci-ety of Critical Care Medicine Guidelines on Glycemic Control for Critically III Children and Adults 2024. Crit Care Med. 2024;52:e161-e181. doi: 10.1097/CCM.00000000000006174

USE OF VASOPRESSORS IN ADULTS AFTER CARDIAC ARREST

Recommendation for Use of Vasopressors in Adults After Cardiac Arrest

|COR|LOE|Recommendation| |---|---|---| |2b|B-NR|1. There is insufficient evidence to recommend a specific vasopressor to treat low blood pressure in adult patients after cardiac arrest.|

Synopsis

Hypotension requiring vasopressors occurs in up to 75% of post-cardiac arrest patients.1,2 After cardiac ar-rest, shock is often caused by multiple etiologies, and the shock phenotype may evolve from initial low-output CS from post-cardiac arrest myocardial dysfunction to a later vasodilatory shock from inflammatory vasopleslegia.2 Vasopressors are commonly used to support blood pres-sure and cardiac output in the setting of hypotension after cardiac arrest. Vasopressors have dose-dependent differences in cardiac(inotropic), vascular (vasoconstric-tive), and adverse (tissue ischemia, cardiac arrhythmia)effects, which influence their efficacy and safety across individuals.3

Recommendation-Specific Supportive Text

1.No large-scale RCTs have compared clinical out-comes between different vasopressors in post-cardiac arrest patients. ${ }^{4}$ A small prehospital RCT(n=40) comparing epinephrine and norepinephrine and norepinephrine and norepinephrine in observational studies with a high risk of bias and residual confounding have suggested worse out-comes in postarrest patients who received epi-nephrine versus norepinephrine. ${ }^{4,6}$ In patients with CS, many of whom had cardiac arrest, epineph-rine and dopamine have been associated with a less favorable safety profile and potentially worse outcomes than norepinephrine; the presence of cardiac arrest did not influence this effect in one meta-analysis comparing epinephrine to other drug regimens. ${ }^{7-9}$ In non-cardiac arrest patients with vasodilatory or septic shock, epinephrine was associated with more arrhythmias and meta-bolic abnormalities but similar survival while dopa-mine was associated with worse outcomes. ${ }^{10}$

Accordingly, norepinephrine is suggested as the first-line vasopressor for patients with CS or septic shock, but whether this recommendation applies to undifferentiated post-cardiac arrest patients remains unproven. ${ }^{11-13}$

REFERENCES

1.Bhate TD, McDonald B, Sekhon MS, Griesdale DE. Association between blood pressure and outcomes in patients after cardiac arrest: A systematic re-view.Resuscitation.2015;97:1-6.doi:10.1016/j.resuscitation.2015.08.023

2.Jentzer JC, Chonde MD, Dezfulian C. Myocardial Dysfunction and Shock after Cardiac Arrest. Biomed Res Int. 2015;2015:314796. doi:10.1155/2015/314796.

3.Jentzer JC, Hollenberg SM. Vasopressor and Inotrope Therapy in Cardiac Critical Care. J Intensive Care Med. 2021;36:843-856. doi: 10.1155/2015/314796.17630

4.Lawson CK, Faine BA, Rech MA, Childs CA, Brown CS, Slocum GW,Acquisto NM, Ray L; PEMHARM-NET Study Group. Norepinephrine versus epinephrine for hemodynamic support in post-cardiac arrest shock: A systematic review. Am J Emerg Med. 2024;77:158-163. doi: 10.1016/j.ajem.2023.12.031

5.Pansiritanot W,Vathanavalun O, Chakorn T.Early post-resuscitation outcomes in patients receiving norepinephrine versus epinephrine for post-resuscitation shock in a non-trauma emergency department: A parallel-group, open-label, feasibility randomized controlled trial. Resusc 4.Plus.2024;17:100551.doi:10.1016/j.resplu.2024.100551

6.Drennan IR,Berg KM,Bottiger BW,Chia YW,Couper K,Crowley C,D'Arrigo S,Deakin CD,Fernando SM,Garg R,Granfeldt A, Grunau B, Hirsch KG,Holmberg MJ, Kudenchuk PJ, Lavones OJ, Leong CK-L, Vok N, Morley PT, Moskowitz A, Neumar RW, Nicholson TC, Nikolaou NI, Nolan JP,ON'Neil BJ, Ohshimo S, Parr M, Pocock H, Sandroni C, Scquizzato T, Soar J,Welsford M, Zelop CM, Skrifvaris MB; on behalf of the Advanced Life Sup-port Task Force Collaborators. Advanced life support: 2025 International Liaison Committee on Resuscitation Consensus on Science with Treat-ment Recommendations. Circulation. 2025;152(suppl 1):S72-S115. doi:10.1161/CIR.00000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000

7.Rui Q, Jiang Y, Chen M, Zhang N, Yang H, Zhou Y. Dopamine ver-sus norepinephrine in the treatment of cardiogenic shock: A PRISMA-compliant meta-analysis. Medicine (Baltim). 2017;96:e8402. doi: 10.1097/MD.000000000000008402

8.Léopold V,Gayat E,Pirrachio R,Spinar J,Apenarica J,Tarvasmaki T,Lassus J,Harjola VP,Champion S,Zannad F,et al.Epinephrine and short-term sur-vival in cardiogenic shock:an individual data meta-analysis of 2583 patients.Intensive Care Med.2018;44:847-856.doi:10.1007/s00134-018-5222-9

9.Levy B, Clere-Jehl R, Legras A, Morichau-Beauchant T, Leone M,Frederique G, Quenot JP, Kimmoun A, Cariou A, Lassus J, et al; Collabo-rators. Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction. J Am Coll Cardiol. 2018;72:173-182. doi:10.1016/j.jacc.2018.04.051

10.Jia L, Wang P, Li C, Xie J. THE EFFICACY AND SAFETY OF VASO-PRESSORS FOR SEPTIC SHOCK PATIENTS: A SYSTEMIC REVIEW AND NETWORK META-ANALYSIS. Shock. 2023;60:746-752. doi:10.1097/SHK.0000000000000002193

11. Evans L, Rhodes A, Ahlazzani W, Antonelli M, Coopersmith CM, French C, Machado FR, McIntyre L, Ostermann M, Prescott HC, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021;49:e1063-e1143. doi: 10.1097/CCM.000000000000000000000000000000000000000

12. van Diepen S, Katz JN, Albert NM,Henry TD, Jacobs AK, Kapur NK, Kilic A, Menon V, Ohman EM, Sweitzer NK, Thiele H, Washam JB, Cohen MG; on behalf of the American Heart Association Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Quality Care and Outcomes Research; and Mission: Lifetime. Contem-porary management of cardiogenic shock: a scientific statement from the American Heart Association. Circulation. 2017;136:e232-e268. doi:10.1161/CIR.0000000000000000000000000000000000000000000000000000000000000000000000000000000

13.Chioncel O,Parisis J, Mebazaza A, Thiele H, Desch S, Bauersachs J, Harjola VP, Antohi EL, Arrigo M, Ben Gal T, et al. Epidemiology, pathophysiology and contemporary management of cardiogenic shock- a position statement from the Heart Failure Association of the European Society of Cardiology.Eur J Heart Fail.2020;22:1315-1341.doi:10.1002/ejhf.1922

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PERCUTANEOUS CORONARY INTERVENTION IN ADULTS AFTER CARDIAC ARREST

|COR|LOE|Recommendations| |---|---|---| |1|B-NR|1. Coronary angiography should be performed emergently after cardiac arrest for all patients with suspected cardiac cause of arrest and persistent ST-segment elevation on ECG, regardless of the presence of coma.| |1|B-NR|2. Coronary angiography is recommended prior to hospital discharge in adult cardiac arrest survivors with suspected cardiac etiology, particularly in the presence of an initial shockable rhythm, unexplained left ventricular systolic dysfunction, or evidence of severe myocardial ischemia.| |2a|B-NR|3. Emergency coronary angiography is reasonable for selected adult patients after cardiac arrest with suspected cardiac etiology without ST-segment elevation on ECG in the presence of CS, recurrent ventricular arrhythmias, or evidence of significant ongoing myocardial ischemia, regardless of the presence of coma.| |3: No Benefit|B-R|4. In adult comatose patients with ROSC after cardiac arrest, emergency coronary angiography is not recommended over a delayed or selective strategy in the absence of ST-segment elevation, shock, electrical instability, or evidence of significant ongoing myocardial ischemia.| |3: No Benefit|B-R|5. In the setting of multivessel coronary artery disease(CAD) in adult patients with shock after cardiac arrest, immediate revascularization of non-infarct-related coronary lesions is not recommended over initial revascularization of only the infarct-related artery.|

Synopsis

Coronary artery disease is identified in up to two thirds1 of patients with OHCA from a presumed cardiac etiol-ogy who undergo invasive coronary angiography, includ-ing acute culprit lesions in one third of these patients;the prevalence is higher in patients with VF, particularly refractory VF receiving extracorporeal CPR(ECPR).2 ldentifying and treating unstable CAD has been shown to improve outcomes by stabilizing hemodynamics, pre-venting recurrent arrhythmias, and preserving myocardial function.3 The ILCOR CoSTR4 and the 2023 AHA Fo-cused Update5 on this topic were reviewed, and an inde-pendent literature search undertaken.

Observational studies have demonstrated higher overall and favorable neurologic outcome among OHCA patients who receive invasive coronary angiography with PCI performed within 24 hours of admission, recogniz-ing that selection bias and confounding by indication can magnify this effect. Evidence regarding the optimal timing of coronary angiography after OHCA comes from multiple RCTs enrolling 1590 comatose hemodynami-cally stable OHCA patients without STEMI, the majority having a shockable rhythm.6-12 Therefore, the certainty

of data is limited for types of cardiac arrest patients excluded from these trials. Randomized data are also lacking for patients with ST-segment elevation or cohorts permitted to cross over in RCTs because of the presence of CS, signs of significant myocardial damage, electrical instability, or ongoing ischemia. A key challenge is the competing risk of poor outcome due to hypoxic-ischemic brain injury in patients who had cardiac arrest compared to those who have acute coronary syndromes but did not have cardiac arrest. Poor outcome due to the brain injury may mitigate and confound the potential benefit of coro-nary revascularization in this population. ${}^{13}$

Recommendation-Specific Supportive Text

1. The presence of STEMI or STEMI-equivalent pat-tern on ECG after cardiac arrest implies transmural myocardial ischemia and a high probability of acute coronary occlusion, which can result in worsening cardiovascular instability if not promptly revascular ized.14 Multiple observational studies have demon-strated improved neurologically favorable survival when early coronary angiography is performed fol-lowed by PCI in patients with cardiac arrest who have STEMI.15 This recommendation mirrors global recommendations for all patients with STEMI.Randomized controlled trials examining the optimal timing of coronary angiography after OHCA sys-tematically excluded patients with STEMI.

2.Evaluating for CAD prior to hospital discharge with invasive coronary angiography in cardiac arrest survivors with a presumed cardiac etiology is sup-ported by other cardiology-focused guidelines and scientific statements.3,16-18 Randomized controlled trials examining the timing of coronary angiography after OHCA etiol. All 3,16-18 Randomized controlled trials examining the timing of coronary angiography after OHCA etiol. All 3,16-18 Randomized controlled trials examining the timing of coronary angiography after OHCA etiol. All 3,16-18 Randomized controlled trials examining the timing of coronary angiography after OHCA etiol. All 3,16-18 Randomized controlled trials examining the timing of coronary angiography after OHCA etiol. All 3,16-18 Randomized controlled trials examining the timing of coronary angiography after OHCA etiol. All 3,16-18 Randomized controlled trials examining the timing of coronary angiography after OHCA in comatose patients with isolated crossover to the emergent timing arm for

3. Cardiogenic shock(hemodynamic instability) or recurrent ventricular arrhythmias(electrical instabil-ity) after cardiac arrest can be caused by severe myocardial ischemia. Patients with these unstable cardiovascular conditions are at high risk of rearrest if myocardial ischemia goes untreated. Randomized controlled trials examining the timing of coronary angiography after OHCA in comatose patients allowed crossover to the emergent timing arm for shock, recurrent VF, or evidence of severe myocar-dial ischemia. Elevated serum troponin levels ${}^{19-29}$and ischemic ECG abnormalities(other than STEMI)630-34 are common after OHCA but have inadequate sensitivity or specificity for unstable CAD and do not predict the benefit of invasive coronary angiography. This makes the optimal definition of severe myocardial ischemia uncertain, although the TOMAAWHK(Angiography After Out-of-Hospital Cardiac Arrest Without ST-Segment Elevation) trial

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Post-Cardiac Arrest Care: 2025 AHA Guidelines for CPR and ECC

used a serum troponin cut-off 70 times the upper reference limit. Patients with OHCCA with refractory VF from a presumed cardiac etiology who receive ECPR have a high prevalence of unstable CAD, and early invasive coronary angiography was part of the ECPR bundle in RCTs.2,35-37

4. In multiple RCTs of stable comatose OHCA patients without STEMI, there was no evidence of improved overall survival or favorable neuro-logic outcome with early invasive coronary angi-ography(eg, within 2 hours) versus delayed or selective invasive coronary angiography(eg,after awakening), with some studies suggesting poten-tial harm with early angiography.38 In the delayed angiography group, up to 40% of patients did not receive invasive coronary angiography due to lack of awakening12 and up to 17% crossed over to early intervention8 due to hemodynamic or electrical instability or severe myocardial ischemia. Invasive coronary angiography can be safely deferred until after neurological awakening in comatose OHCA patients without any of the following: STEMI or STEMI-equivalent patterns,CS,recurrent ventricular arrhythmias, or evidence of significant myocardial ischemia. Cardiac arrest patients without coma were excluded from these RCTs.

5.There is substantial overlap between the OHCA and CS populations, as acute myocardial infarc-tion is often the underlying pathophysiology in both.339 Multivessel CAD is identified in up to 50%of patients receiving invasive coronary angiogra-phy after OHCA, as in patients with CS from acute myocardial infarction.40,41 No RCTs have examined the optimal revascularization approach for patients with cardiac arrest and multivessel CAD, and RCTs examining multivessel revascularization in patients with STEMI have excluded patients with cardiac arrest.42 The CULPRIT-SHOCK(Culprit Lesion Only PCI Versus Multivessel PCI in Cardiogenic Shock) trial41 randomized patients with CS from acute myocardial infarction(including 55% OHCA patients) who had multivessel CAD and underwent culprit vessel PCI to either immediate multivessel PCI or delayed selective multivessel PCI. Patients randomized to immediate multivessel PCI had higher mortality and more complications, with simi-lar findings of harm with initial multivessel PCI in the subgroup of patients with cardiac arrest.43 Thus,immediate revascularization of nonculprit coronary lesions is not recommended over initial culpritly-revascularization in patients with multivessel CAD and shock after cardiac arrest and is supported by the 2021 AHA/ACC/SCAl Guideline for coronary revascularization and 2025 AHA/ACC Guideline for acute coronary syndromes.14,44

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TEMPORARY MCS FOR ADULTS AFTER CARDIAC ARREST

|Recommendations for Temporary MCS for Adults After Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-EO|1. In adult patients with cardiac arrest who have been placed on MCS, appropriate monitoring and management by a team with experience managing the device(s) and the potential associated complications is recommended.|| |2b|B-NR|2. In highly selected adult patients with refractory CS after cardiac arrest and ROSC, temporary MCS may be considered.|| |3: No Benefit|B-R|3. In adult patients with CS after cardiac arrest and ROSC, should not be routinely used.||

Synopsis

Cardiogenic shock commonly occurs as either a cause or consequence of cardiac arrest.1 Patients with CS are usually managed with vasopressors and inotropes, but treatment failures and drug toxicity are common with these therapies.1 Temporary MCS devices have been de-veloped to increase blood pressure and cardiac output in patients with CS as an alternative or adjunct to vasoac-tive drug therapy. These devices include the intra-aortic balloon pump, percutaneous ventricular assist devices(including the Impella and TandemHeart families of devic-es), and extracorporeal membrane oxygen(ECMO).Temporary MCS devices can provide hemodynamic sta-bilization in refractory CS, allowing time for neuroprog-nostication and potential cardiac recovery. Balancing the aforementioned benefits with associated increased risk of bleeding and ischemic complications observed with percutaneous ventricular assist devices and ECMO is important. Temporary MCS is becoming more commonly used as a rescue strategy for patients with refractory CS despite initial vasoactive drug therapy. While few trials of temporary MCS have exclusively included cardiac arrest patients, many of the CS patients enrolled in clinical trials of temporary MCS had cardiac arrest. Accordingly, the evidence guiding the use of temporary MCS in CS more broadly may apply to patients with cardiac arrest in the

absence of studies showing differential benefits in the cardiac arrest subgroup specifically.

Recommendation-Specific Supportive Text

1. Management of temporary MCS is nuanced and requires specific knowledge. Balancing hemody-namic needs with device management is often chal-lenging because responses to interventions can be paradoxical or counterintuitive during MCS. Given these challenges, optimizing outcomes necessi-tates a team experienced in MCS management.Although specific team composition and training are not well defined, a volume-outcome relation-ship has been noted with the use of advanced tem-porary MCS devices whereby centers with higher volume have better patient survival, suggesting that greater familiarity with these devices may result in improved outcomes.2,3

2,3.Temporary MCS devices, including intra-aortic bal-loon pump, percutaneous ventricular assist devices,and ECMO, can potentially improve hemodynam-ics for patients with CS refractory to vasopressor and inotrope therapy. No large-scale RCTs have specifically evaluated patient-centered outcomes with early routine use of MCS devices in cardiac arrest patients. One small(n=60) RCT showed no difference in mortality with early routine intra-aortic balloon pump in patients with acute coronary syndrome who had suffered an in-hospital cardiac arrest with ROSC.4 Patients with cardiac arrest made up the majority(64%) of patients included in RCTs assessing MCS in CS, though the subgroup of patients with cardiac arrest ranged from<20%to>90% across studies.4-18

In a meta-analysis of 14 trials, there was no differ-ence in survival for CS patients treated with routine MCS compared to standard of care(OR,1.17;95%CI,0.97-1.42[ILCOR meta-analysis]). A patient-level meta-analysis of 9 RCTs in acute myocardial infarction CS(n=1114) found no survival benefit for early routine use of percutaneous ventricular assist devices or ECMO in the 51.6% with prior cardiac arrest(HR, 0.91; 0.71-1.15).19 Patient-level subgroup analysis of 816 resuscitated car-diac arrest patients from 11 RCTs(n=816) found no difference in survival with MCS(OR,1.21;95%CI,0.91-1.60[ILCOR meta-analysis]). The singu-lar RCT that showed survival benefit with routine use of MCS in CS patients included 20% car-diac arrest survivors but systematically excluded OHCA patients who were comatose after ROSC.16 Importantly, individual RCTs and meta-analyses demonstrate increased harm, including severe bleeding and ischemic vascular events, with the routine use of MCS.13,15,16,18,19 Accordingly, routine

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use of MCS in cardiac arrest patients with CS is not likely to improve survival, however, selective use of MCS in cardiac arrest patients with refractory CS may be considered, particularly for those who are not comatose and have STEMI as represented in the DanGer Shock (Danish-German Cardiogenic Shock) trial.16,20

REFERENCES

1. van Diepen S, Katz JN, Albert NM,Henry D, Jacobs AK, Kapur NK, Kilic A. Menon V, Ohman EM, Sweitzer NK, Thiele H, Washian JB, Cohen MG; on behalf of the American Heart Association Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Quality of Care and Outcomes Research; and Mission: Lifeline. Contem-pary management of cardiogenic shock: a scientific statement from the American Heart Association. Circulation 2017;136:e232-e268.doi:10.1161/CIR0000000000000525

2. Watanabe A, Miyamoto Y, Ueyama HA, Gotanda H, Jenter JC,AKapur NK, Jorde US, Kojett 2018;Circ. Derance W, Kuroa 2017; Impacts of Hospital Vol-ume and Patient-Hospital Distances on Outcomes of Older Adults Receiving Percutaneous Microaxial Ventricular Assisties for Cardiogenic Shock. Circ. Cardiovasc Interast. 2024;17:e014738. doi:10.1161/CIRCINTERVENTIONS.124.014738.

3.O'Neill WW, Grines C, Schreiber T, Moses J, Maini B, Dixon SR, Ohman EM. Analysis of outcomes for 15,259 US patients with acute myocardial infarction cardiogenic shock(AMICS) supported with the Impella device. Am Heart J.2018;2023:33-38. doi:10.1016/j.ahj.2018.03.024

4Drair F. Uini宇, Yiadriantor H, Boom E, Harimurt K, Romondi R,Kusmana D. Early insertion of intra- bolical bumpal operation cardiac art-rest on acute coronary syndrome patients: a randomized clinical trial. Cardol Cardiovasc Med.2019;3:193-203. doi: 10.26502/fccm.92920067

5. Ohman EM,Nanas J, Stomel RJ, Leesar MA,Nielsen DW,O'Dea D,Rogers F,Harber D,Hudson MP,Frano EloE; et al: TACTICS Trial. Thrombolysis and counterpulsation to improve survival in myocardial infarction compli-cated by hypotension and suspected cardiogenic shock or heart failure:results of the TACTICS Trial. J Thromb Thrombolysis.2005;19:33-39. doi:10.1007/s11239-005-0938-0

6.Thiele H, Sick R, Poubri D. Eiederich W, KMBOhrat R, Esnerau J.,Schuler G. Randomized comparison of intra- aortic balloon support with a percutaneous left ventricular assist device in patients with revascularized acute myocardial infarction complicated by cardiogenic shock. Eur Heart J.2005;26:1276-1283. doi: 10.1093/eurheart/ehi161

7. Ouwenel DM,Eriksen E,Sjauk WD, van Dongen IM, Hirsch A, Packer EJ,Vis MM, Wykrzykowska J.Jk, Koch BAan J, et al. Percutaneous Mechanical Circulatory Support Versus Intra-Aortic Balloon Pump in Cardiogenic Shock After Acute Myocardial Infarction, J Am Coll Cardiol 2017;69:278-287: doi:10.1016/j.jacc.2016.10.022

8.Burkhoff D, Cohen H, Brunchorkost C, O'Enill WW. A randomized multicenter clinical study to evaluate the safety and efficacy of the Tandemir-per cutaneous ventricular assist device versus conventional therapy with in-traotic balloon pumping for treatment of cardiogenic shock. Am Heart J.2006;152:469e-1.469e.8.doi:10.1016/j.ajh.2006.05031

9.Seyfarth M, Sibbing D, Bauer F, Rohfich G, Bott-Filgel L, Byrne R,Dirschinger J, Kastrai A, Schmidig A. A randomized clinical trial to evaluate the safety and efficacy of a percutaneous left ventricular assist device versus intra-ortic balloon pumping for treatment of cardiogenic shock caused by myocardial infarction. J Am Coll Cardiol 2008;52:1684-1588.

10.Thiele H, Zeymer U, Neumann FJ, Ferenc, M Olbrich HG, Hausleiter J,Richardh G, Hennerford S, Empen K, Fuengrau U, et al; IBP-SHOCK II Treat lnvestigators. Intraaortic balloon support for myocardial infarct with cardiogenic shock. N Engl J Med. 2012;367:1287-1296. doi:10.1056/NEmJoA20148

11. Brunner S, Guenhier SPW, Lackermair K, Petersse S, Orban M, Boulesteix Al,Michel S, Hussteler J, Massberg S, Hagci C. Extracorporeal Life Support in Cardiac Shock Complicating Acute Myocardial Infarction. J Am Coll Cardiol.2019;73:2355-2357. doi:10.1016/j.jacc.2019.02.044

12.Bochaton T, Huolt E,Blaiz M, Delmas C, Aissoui N, Farhat F, Newton N,Bonefry E; IMPELTA-STIC investigators. Mechanical circulatory sup-port and the Impella® LP5.0 pump and an intra-aortic balloon pump

<EndOfPara>for cardiogenic shock in acute myocardial infarction: The IMPELLA-STIC randomized study. Arch Cardiovasc Dis. 2020;113:237-243. doi: 10.1016/j.jacvd.2019.10.005

13. Banning AS, Sabaté M, Orban M, Gracey J, López-Sobrino T, Massberg S, Kastrati B, Aogaerts K, Adriaenssens T, Berry C, et al. Venoarterial ex-tracorporeal membrane oxygenation or standard care in patients with car-dogenic shock complicating acute myocardial infarction: the multicentre,randomised EURO SHOCK trial. Eurontervention.2023;19:482-492. doi:10.4244/EJ/D-23-00204

14. Ostadal P, Roktya R, Karasek J, Kruger A, Vondrakova D, Janotka M, Naar J, Smalcova J, Hubatova M, Hromadka M, et al; ECMO-CS Investigators.Extracorporal Membrane de Oxygenation in the Therapy of Cardiogenic Shock: Results of the ECMO-CS Randomized Clinical Trial. Circulation.2023;147:454-464. doi: 10.1161/CIRCULATIONAHA.122.062949

15. Thiele H, Zeymer U, Akin I, Behnes M, Rassaf T, Mahabadi AA, Lehmann E, Ritel I, Gel T, Seidler, T et al; ELS-SHOCK Investigators. Extracor-poral Life Support in Infarct-Related Cardiogenic Shock. N Engl J Med.2023;389-1268-1297.doi:10.1056/NEJMoa2307227

16. Meller JE, Engstrom T, Jensen LO, Eiskjaer H, Mangner N, Polzin A,Schulze PC, Skurk C, Norbeck P, Clemmensen P, et al; DanGer Shock Investigators. Microxial Flow Pump or Standard Care in Infarct-Related Cardiogenic Shock. N Engl J Med.10.1065/NEJMost 215727.

17. Prondzinsky R, Lemh S. Wyterman, Wegener N, Unverzagt S, Carter JM,Russ M, Schlitt A, Buerke U, Christoph A, et al. Intra-aortic balloon counter-pulsation in patients with acute myocardial infarction complicated by cardio-genic shock: the prospective, randomized IABP SHOCK Trial for attenuation of multiorgan dysfunction syndrome. Crit Care Med.2010;38:152-160. doi:10.1097/CCM.0b013e3181b78671

18.Drennan IR,Berg KM,Bottiger BW,Chia YW,Couper K,Crowley C,D'Arrigo S,Deakin CD,Cfernando SM,Garg R,et al. Advanced life support: 2025 International Liaison Committee on Resuscitation Consensus on Science With Treatment Recommendations. Circulation. 2025;152(suppl 1):S72-S115. doi: 10.1161/CIR/0000000000001360

19.Thiele H, Moller J, HErques Jques, Bogger M, Seyfarth M, Burkhoff D,Ostadal P, Roktya R, Belohlavek J, Massberg S, et al; MCS Collaborator Scientific Group. Temporary mechanical circulatory support in infarct-related cardiogenic shock: an individual patient data meta-analysis of ran-domised trials with 6-month follow-up. Lancet 2024;404:1019-1028. doi: 10.1016/S0140-6736(24)01448-X

20. Rao SV, O'Donoghue M L, Ruel M, Rab T, Tamis-Holland JE, Alexander JH, Baber U, Baker H, Cohen MG, Cruz-Ruiz M, Davis LL, de Lemos JA, DeWald TA, Elgendy IY, Feldman DN, Goyal A, Isiadin I, Menon V,Morrow DA,Mukherje D,Platz E, Promes SB,Sandner S,Sandoval Y,Schunder R, Shah B, Stopyra JP, Talbot AW, Taub PR, Williams MS.20252 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the manage-ment of patients with acute coronary syndromes: a report of the Ameri-can College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2025;151:e771-e862. doi:10.1161/CIR:00000000000000000000000

ADVANCED NEUROMITORING IN ADULTS AFTER CARDIAC ARREST

|Recommendation for Advanced Neuromonitoring in Adults After||| |---|---|---| |CorR|LOE|Recommendation for Advanced Neuromonitoring in Adults After| |COR|LOE|Recommendation for| |2b|C-LD|1. The usefulness of monitoring ICP, cerebral blood flow, brain tissue oxygenation, or jugular venous oxygen saturation in adults after cardiac arrest is not well established.|

Synopsis

Hypoxic-ischemic brain injury causes imbalance in physiological processes involved in cerebral homeosta-sis. These disruptions place patients at risk for sec-ondary brain injury, which may contribute to mortality

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and unfavorable neurologic outcomes. Causes of sec-ondary brain injury are heterogeneous and vary tem-porally and between patients but include inadequate cerebral perfusion, oxygenation, and mismatch in metabolic supply and demand.2 Conventional patient monitoring by clinical examination and vital signs can be insensitive to detecting secondary brain injury.3,4 Advanced neuromonitoring refers to placing probes into or adjacent to brain tissue through a cranial burr hole or through jugular vein cannulation. These probes permit direct and frequent measurement of ICP, cere-bral blood flow, brain tissue oxygen saturation (Pbto2),jugular venous oxygen saturation, and neurophysiology(electrocorticography).5,6 They also allow for sampling of the interstitial space (microdialysis) and calculation of cerebral autoregulation indices, such as pressure re-activity index and optimal cerebral perfusion pressure.These measurements can provide additional informa-tion about cerebral physiology and facilitate targeted interventions. While these techniques have been used in other types of acute brain injury populations, there has been limited investigation in hypoxic-ischemic brain injury. Limitations of previous studies in cardiac arrest populations include their observational nature;highly selected subpopulations; variability in the timing,duration, and methods of monitoring; and thresholds used to prompt interventions.

Recommendation-Specific Supportive Text

1.There are no RCTs comparing invasive neuro-monitoring to no invasive neuroimonitoring after cardiac arrest. Eleven nonrandomized observa-tional studies ${}^{7-17}$ evaluated ICP monitoring. Five studies found an association between ICP eleva-tion or lower intracranial compliance with poor functional outcomes. ${}^{7,10,13,16,17}$ Three observational studies using intracranial ICP monitoring evalu-ated cerebral autoregulation using pressure reac-tivity index. ${}^{8,13,18}$ The pressure reactivity index is a measure of cerebral autoregulation derived from the correlation of ICP and MAP. Two of these stud-ies measured deviations from the optimal cerebral perfusion pressure, which was associated with mortality and lower Pbto ${}^{8,18}$ Of 5 nonrandom-ized studies, 2 showed that cerebral hypoxia mea-sured using Pbto ${}^{2}$ or arterio-jugular differences of oxygen was more common in patients with poor functional outcomes. ${}^{8,13-16}$ One single-center pro-spective nonrandomized interventional study eval-uated functional outcomes with care guided by monitoring of ICP, Pbto ${}^{2}$ and jugular venous oxy-gen saturation. ${}^{8}$ The invasive monitoring group had superior functional outcomes at 6 months com-pared to a historical matched comparison group.All findings for ICP, cerebral autoregulation, Pbto ${}^{2}$

and jugular venous oxygen saturation were incon-sistent across studies, and there was overall high risk of bias.

REFERENCES

1.Perkins GD, Callaway CW, Haywood K, Neumar RW, Lilja G, Rowland MJ,Sawyer KN, Skrifars MB, Nolan JP. Brain injury after cardiac arrest. Lancet.2021;398:1269-1278.doi: 10.1016/S0140-6736(21)00953-3

2. Sandroni C, Cronberg T, Sekhon M. Brain injury after cardiac arrest: patho-physiology, treatment, and prognosis. Intensive Care Med. 2021;47:1393-1414. doi: 10.1007/s00134-021-06548-2

3. Mansour A, Fuhrman JD, Ammar FE, Loggini A, Davis J, Lazaridis C,Kramer C, Goldenberg FD, Giger ML. Machine Learning for Early Detec-tion of Hypoxic-ischemic Brain Injury After Cardiac Arrest. Neurocrit Care 2022;36:974-982. doi: 10.1007/s12028-021-01405-y

4. Peluso L, Oddo M, Minini A, Citerio G, Horn J, Di Bernardini E,Rundgren M, Cariou A, Payen JF, Storm C, et al. Neurological pupil in dex and its association with other prognostic tools after cardiac ar-rest: A post hoc analysis. Resuscitation. 2022;179:259-266. doi:10.1016/j.resuscitation.2022.07.030

5. Hirsch KG, Abella BS, Amorim E, Bader MK, Barletta JF, Berg K,Callaway CW, Friberg H, Gilmore EJ, Greer DM, Kern KB, Livesay S,May TL, Neumar RW, Nolan JP, Oddo M, Peberdy MA, Poloyac SM,Seder D, Taccone FS, Uzendu A, Walsh B, Zimmerman JL, Geocadin RG; on behalf of the American Heart Association and Neurocritical Care Society. Critical Care management of patients after cardiac ar-rest: a scientific statement from the American Heart Association and Neurocritical Care Society. Circulation. 2024;149:e168-e200. doi: 10.1161/CIR.00000000000001163

6. Lindblad C, Raj R, Zeiler FA, Thelin EP. Current state of high-fidelity multimodal monitoring in traumatic brain injury. Acta Neurochir(Wien).2022;164:3091-3100.doi:10.1007/s00701-022-05383-8

7.Sekhon MS,Griesdale DE,Ainslie PN,Goodherm A,Poster F,Dczosnyka M,Robba C,Cardim D. Intraecial pressure and compliance in hypoxic isch-emic brain injury patients after cardiac arrest. Resuscitation.2019;141:96-103. doi: 10.1016/j.resuscitation.2019.05.036

8.Sekhon MS, Gooderham P, Menon DK, Brasher PMA, Foster D, Cardim D,Czosnyka M,Smielewski P,Gupta AK,Ainslie PN,et al.The Burden of Brain Hypoxia and Optimal Mean Arterial Pressure in Patients With Hypoxic Isch-emic Brain Injury After Cardiac Arrest. Crit Care Med.2019;47:960-969.doi: 10.1097/CCM.00000000003745

9.Sakabe T, Tateishi A, Myauchi Y, Maekawa T, Matsumoto M, Tsutsui T,Takeshita H. Intracranial pressure following cardiopulmonary resuscitation.Intensive Care Med.1987;13:256-259. doi:10.1007/BF00265114

10. Gueugniaud PY, Garcia-Darennes F, Gaussorgues P, Bancalari G, Petit P,Robert D. Prognostic significance of early intracranial and cerebral per-fusion pressures in post-cardiac cardiac arrest anoxic coma. Intensive Care Med.1991;17:392-398.doi:10.1007/BF01720676

11. Naito H, Isotani E, Callaway CW, Hagioka S, Morimoto N. Intracranial Pressure Increases During Rewarming Period after Mild Therapeutic Hy-pothermia in Postcardiac Arrest Patients. Ther Hypothermia Temp Manag.2016;6:189-193. doi: 10.1089/ther.2016.0009

12.Cardim D, Griesdale DE Ainsie PN, Robba C, Calviello L, Czosnyka M,Smielewski P, Sekhmon MS. A comparison of non-invasive versus in-vasive measures of intracranial pressure in hypoxic ischaemic brain injury after cardiac arrest. Resuscitation. 2019;137:221-228. doi:10.1016/j.resuscitation.2019.01.002

13. Balu R, Rajagopalan S, Baghshomali S, Kirschen M, Murthur A,Kofke WA, Abella BS. Cerebrovascular pressure reactivity and in-tracranial pressure are associated with neurologic outcome after hypoxic-ischemic brain injury. Resuscitation. 2021;164:114-121. doi:10.1016/j.resuscitation.2021.04.023

14. Ferguson NA, Holland RL, Thara S, Foster D, Gooderham P, Rikhraj K,Grunau B, Christenson J, Ainslie P, Griesdale DEG, et al. Goal-Directed Care Using Invasive Neuromonitoring Versus Standard of Care After Car-diac Arrest: A Matched Cohort Study. Crit Care Med.2021;49:1333-1346.

doi:10.1097/CCM.0000000000000

15. Richter J, Sklienka P, Sestra AE, Zahorec R, Das S, Chatterjee N. Is jugu-lar bubital acetast monitoring associated with outcome in out of hospi-tal cardiac arrest patients? J Clin Monit Comput 2021;35:741-748. doi:10.1007/s10877-020-00530-x

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16. Chae MK, Lee SE, Kang SY, Sim MS. Monitoring of Cerebral Metabolism in Postcardiac Arrest Patients: A Pilot Study. Ther Hypothermia Temp Manag.2018;8:234-238. doi: 10.1089/ther:2018.0018

17. Hifumi T, Kawakita K, Yoda T, Okazaki T, Kuroda Y. Association of brain metabolites with blood lactate and glucose levels with respect to neurological outcomes after out-of-hospital cardiac arrest: A pre-liminary microdialysis study. Resuscitation. 2017;110:26-31. doi: 10.1016/j.resuscitation.2016.10.1013

18. Kirsch MP, Majmudar T, Diaz-Arastria R, Berg R, Abella BS, Topjian A,Balu R. Deviations from PRx-derived optimal blood pressure are associ-ated with mortality after cardiac arrest. Resuscitation. 2022;175:81-87. doi: 10.1016/j.resuscitation.2022.03.003

SEIZURES, MYOCLONUS, AND OTHER EPILEPTIFORM ACTIVITY

Diagnosis and Management of Seizure and Other Epileptiform Activity in Adults After Cardiac Arrest

|Recommendations for Diagnosis and Management of Seizure and Other Epileptiform Activity in Adults After Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-LD|1. We recommend promptly performing and interpreting EEG for the diagnosis of seizures in adult patients who do not follow commands after ROSC.|| |2|C-LD|2. We recommend treatment of clinically apparent seizures in adult patients after ROSC.|| |2a|B-R|3. Treatment of nonconvulsive seizures (ie, diagnosed by EEG only) is reasonable in adult patients after ROSC.|| |2a|C-LD|4. Monitoring EEG repeatedly or continuously is reasonable for adult patients who do not follow commands after ROSC.|| |2b|C-LD|5. The same antiseurization medications used for treatment of seizures caused by other etiologies may be considered for seizures in adult patients after ROSC.|| |2b|C-EO|6. A therapeutic trial of a nonsating antiseizure medication may be reasonable in adult patients who do not follow commands after ROSC with EEG patterns on the itcital-intercital continuum.|| |3: No Benefit|B-R|7. Routine seizure prophylaxis in adult patients who do not follow commands after ROSC is not recommended.||

Synopsis

Seizures and status epilepticus are common acute neu-rologic complications in the post-cardiac arrest period,occurring in 10% to 35% of patients who do not follow commands after ROSC.1-6 Cerebral hyperexcitability after cardiac arrest may exacerbate a mismatch between neu-ronal bioenergetic supply and demand, thereby contribut-ing to secondary brain injury.5 Post-cardiac arrest hyper-excitability can manifest as a wide range of electroclinical findings, from seizures with overt clinical manifestations,such as convulsions to periodic or rhythmic discharges on EEG and other abnormal EEG patterns.7 Clinical or electrographic findings can manifest with or without

$\text{impairment of consciousness and may or may not reach}$$\text{the criteria for seizures or status epilepticus(Table 2).}^{8}$

The indications for and intensity of antiseizure medi-cations vary in clinical practice and across studies.Although the occurrence of status epilepticus in post-cardiac arrest patients has been associated with poor outcomes in observational studies,2,9,10 some patients survive with recovery of functional independence. Myoc-lonus is covered in a separate section because only a subset of patients with post-cardiac arrest myoclonus meets criteria for electroclinical seizures or status epi-lepticus. Marked heterogeneity in the definitions of sei-zures and status epilepticus across studies challenges the interpretation of available data.

Recommendation-Specific Supportive Text

1. In patients who are unable to follow commands after cardiac arrest, EEG can detect nonconvulsive seizures and status epilepticus(Table 3).11-13 This recommendation is informed by the high preva-lence of nonconvulsive seizures and other epilep-tiform activity in cardiac arrest survivors.5 However,there is no direct evidence that detection of non-convulsive seizures with EEG improves outcomes.An ILCOR systematic review from 2023 did not specifically address the timing and method of EEG monitoring in this setting.14

2. There are no nonrandomized trials or RCTs com-paring the effect of treating clinical seizures versus no seizure treatment. ${}^{14}$ There is no widely accepted definition for clinically apparent seizure or status epilepticus after cardiac arrest, and previous litera-ture has used a variety of clinical and EEG clas-sifications. It remains unclear which seizures or status epilepticus represent an epiphenomenon of severe brain injury or treatment-responsive tar-gets to prevent secondary brain injury. Despite the lack of high-certainty evidence, untreated clinically apparent seizure activity is thought to be poten-tially harmful to the brain; therefore, treatment of seizures or status epilepticus is recommended. ${}^{15}$

3.Seizures or status epilepticus that have no clearly apparent clinical correlate,(ie,electrographic or non-convulsive seizures or status epilepticus), emerge in 1% to 20% of post-cardiac arrest patients. ${}^{16}$ The American Clinical Neurophysiology Society(ACNS)has developed specific criteria for electrographic or nonconvulsive seizures or status epilepticus for critically ill patients(Table 2), though prior studies have used varying definitions. Given the limited evidence to support withholding treatment of non-convulsive seizures after arrest, a similar approach to nonconvulsive seizure treatment for other eti-ologies is reasonable. The TELSTAR(Treatment of Electroencephalographic Status Epilepticus after

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Table 2. American Clinical Neurophysiology Society Criteria for Electrographic Seizures, Status Epilepticus, and Ictal-Interictal Continuum

|Hyperexcitable phenomenon|Diagnostic criteria| |---|---| |Electrographic seizure|1. Epileptiform discharges averaging>2.5 Hz for ≥10 s* or 2. Any pattern with definite evolution lasting≥10 s*| |Electrographic status epilepticus|1. Any pattern qualifying for electrographic seizure for≥10 continuous min# or for a total duration of≥20% of any 60-min# period of monitoring| |Ictal-interictal continuum (ie, possible electrographic status epilepticus; if an unequivocal electrographic and clinical response is seen following therapeutic trial, that is diagnostic for electroclinical status epilepticus)|1. Any periodic discharges or spike/sharp-wave pattern averaging>1.0 and ≤2.5 Hz over 10 s or 2. Any periodic discharges or spike/sharp-wave pattern averaging≥0.5 Hz and ≤1.0 Hz over 10 s with either a plus modifier$ or fluctuationl or| ||3. Any lateralized rhythmic delta activity averaging>1 Hz over 10 s with either a plus modifierS or fluctuationl|

*The minimum duration of 10 s does not apply if a consistent clinical correlate is in lockstep to the electrographic pattern (ie, electroclinical seizure).

tEvolution:At least 2 unequivocal, sequential changes in frequency,morphology,or location

The minimum duration for bilateral motor activity with an electrographic correlate is 5 continuous minutes(ie, electroclinical convulsive status epilepticus).

$Plus$ modifier: Additional feature that renders the pattern more ital in appearance $(+F$ [superimposed fast activity], $+R$ [superimposed rhythmic activity], $+S$ [super-imposed sharp waves or spikes, or sharply contoured])

IFluctuation:≥3 changes, all within 1 min in frequency, morphology, or location but not qualifying as evolution

Data from Hirsch LJ et al(2021).8

Cardiopulmonary Resuscitation) trial17 is the first RCT of protocolized tiered treatment targeting sup-pression of electrographic seizures, status epilep-ticus, or interictal patterns detected on continuous EEG in adults after arrest compared with standard care(Table 2). The trial randomized 172 subjects and the use of antiseizure medication was allowed but discouraged in the standard care group. The rate of unfavorable neurological outcome(defined as Cerebral Performance Category score of 3-5)did not differ at 3 months, but only 10% of patients in both treatment groups had electrographic sei-zures (the rate of clinically apparent and electroclin-ical seizures were not reported). Although the trial was not powered for subgroup analyses, patients with electrographic seizures(ie, periodic discharge frequencies surpassing 2.5 Hz), evolving patterns,or those with nongeneralized periodic discharges between 0.5 and 2.5 Hz had better outcomes with protocolized, tiered antisure treatment than stan-dard care alone.

4. There are several approaches to EEG monitor-ing that vary in duration(ie, from short 20- to 40-minute recordings to continuous monitoring for several days) and electrode arrangement(ie, from full 21 electrodes to simplified 6-10 electrode montages). Seizures, epileptiform abnormalities,and clinical myoclonus may occur immediately after ROSC or emerge several days after initial resusci-tation.7,12,18 Continuous EEG after cardiac arrest,although more costly and labor intensive, increases sensitivity for seizures, status epilepticus, and epi-leptiform activity detection when compared with brief intermittent recordings given the variability in the timing these patterns occur and frequent lack of clinical correlation. However, use of continuous

EEG was not associated with improvement in sur-vival or functional outcome in observational cardiac arrest studies19,20 or the CERTA(Continuous EEG Randomized Trial in Adults) trial,21 a multicenter pragmatic study involving critically ill patients with impaired consciousness, of whom nearly one-third had been post-cardiac arrest patients.

5. Cardiac arrest as the etiology of seizures and status epilepticus has been an exclusion criterion in RCTs specific to status epilepticus22,23; conse-quently, therapeutic algorithms are extrapolated from other settings, including guidelines for gen-eralized convulsive status epilepticus. The 2023 ILCOR CoSTR summary14 recommended that seizures be treated when diagnosed in postar-rest patients. No specific antiseizure medications were recommended.

6. The ACNS defines the ictal-interictal continuum as rhythmic or periodic patterns that may be consistent with possible nonconvulsive seizures or status epi-lepticus even without fulfilling strict electrographic criteria(Table 2).8 Patients with patterns on the ictal-interictal continuum who exhibit both electro-graphic and clinical response to a therapeutic trial with a loading dose of a nonsedating antiseizure medication (ie, not benzodiazepines) are consid-ered to have electroclinical status epilepticus; thus,therapeutic trials of antiseizure medication may be considered for interictal findings. Clinical response to a therapeutic trial may not be apparent on bed-side examination in patients who are unresponsive to commands after ROSC, therefore, determination of an electroclinical response to a therapeutic trial may be challenging.

7.No new studies were identified in the updated ILCOR CoSTR summary from 2023.14 Seizure

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prophylaxis did not improve outcomes after car-diac arrest in 2 prospective RCTs$^{24,25}$ and 1 non-randomized prospective clinical trial with historical controls.26 Prophylaxis was also not effective in preventing subsequent seizures in the post-car-diac arrest period.24-26 However, these studies lacked systematic diagnosis of seizures with EEG monitoring, seizures reported were abstracted from clinical documentation, and the sample size was insufficiently powered for this outcome.Additionally, these studies were designed as ther-apeutic trials of neuroprotection with thiopental,magnesium and diazepam, or diazepam alone,with the primary outcome being functional neu-rologic outcome with the Cerebral Performance Category scale. Therefore, their study designs are inadequate to provide definitive evidence on the role of seizure prophylaxis in the prevention of acute symptomatic seizures and later devel-opment of epilepsy following cardiac arrest.Furthermore, the chosen therapeutic agents in these studies24-26 are not commonly used as sei-zure prophylaxis in clinical practice in the current era, thus, precluding extrapolation of findings on seizure prophylaxis with other agents that might have a more favorable side effect profile with fewer sedating effects.

REFERENCES

1. Rittenberger JC, Popescu A, Brenner RP, Guyette FX, Callaway CW.Frequency and timing of nonconvulsive status epilepticus in comatose post-cardiac arrest subjects with hypothermia. Neurocrift Care.2012;16:114-122.doi:10.1007/s12028-011-95650-6

2. Legrénl S, Havygrin J. Seres-Rigon M, Merceron S, Piotneau J,Henny-Lagarrigue M, Bruneel F, Nguyen A, Guezennepec N, Proch T6, G et al.Prognostic value of electrographic postanostatic status epilepticus in coma-tose cardiac-arest survivors in the therapeutic hypothermia era. Resuscita-tion.2013;84:343-350. doi:10.1016/j.resuscitation.2012.11.001

3.Draganance L, Backman S, Westell F, Undergra M, Fibren G, Bronberg T. Outcome following postanoxic status epilepticus in patients with tar-get temperature management after cardiac arrest. Epilepsy Behav.2015;49:173-117. doi:10.1016/j.yebh2015.04.043

4. Ruijter BJ, van Putten MJ, Hofmeijer J. Generalized epileptiform discharges in postanonic enepphalopathy: Quutitative characterization in relation to outcome. Epilepsia 2015:56:1845-1854. doi: 10.1111/epi.13202

5.Lybeck A, Fiberg H, Aneman A, Hassager C, Horn J, Kjergaard J,Kuiper M, Nielsen N, Uilén S, Wise MP, et al; TMT-trial Investigators.Prognostic significance of clinical seizures after cardiac arrest and tar-get temperature management Resuscitation. 2017;114:146-151. doi:10.1016/resuscitation.2017;01017

68. Beretta S, Coppo A, Bianchi E, Zanchi C, Carone D, Stabile A, Padovano G, Sulmina E, Grassi A, Bogliu G, et al. Neurologic outcome of postan-oxic roactivity status epliectus after aggressive treatment. Neurology.2018;91:e2153-e2162. doi:10.1212/WNL/10000000000006615

7.Barbella G, Lee JW, Alvarez V, Novy J, Oddo M, Beers L, Rossettl. AO prediction of regaining consciousness despite an early epilept-form EEG after cardiac arrest. Neurology. 2020;94:e1675-e1683. doi:10.1212/WNL000000000009283

8. Hirsch L.J. Wong MW, Leitner Moche, S. Beniczyk, S. Abend NS, Lee WJ, Wusthoff J.CHah CD, Westover MB, et al. American Clinical Neurophysiology Society's Standardized Critical Care EEG Terminology: 2021 Version. J Clin Neurophysiol. 2021;38:1-29. doi:10.1097/WNP0000000000000806

9.Rossetti AQ, Logroscino G, Liaudet L, Ruffieux C, Ribordy V, Schaller MD, Despland PA, Oddo M. Status epilepticus: an independent out-come predictor after cerebral anoxia. Neurology. 2007;69:255-260. doi:10.1212/01.011/0000265819.36639.e0

10. Lamartine Monteiro M, Taccone FS, Depondt C, Lamanna I, Gaspard N,Ligot M, Navoudakis N, Naeje G, Vincent JL, Legros B. The Prog-nostic Value of 48-h Continuous EEG During Therapeutic Hypother-mia After Cardiac Arrest. Neurocrit Care. 2016;24:153-162. doi: 10.1007/s12028-015-0215-9

11.Elmer J,Rittenberger JC,Faro J,Molyneaux BJ,Popescu A,Callaway CW,Baldwin M; Pittsburgh Post-Cardiac Arrest Service. Clinically distinct elec-troencephalographic phenotypes of early myoclonus after cardiac arrest.Ann Neurol.2016;80:175-184. doi:10.1002/ana.24697

12.Reynolds AS, Rohaut B, Holmes MG, Robinson D, Roth W, Velazquez A,Couch CK, Presciutt A, Brodie D, Moitra VK, et al. Early myoclonol for lowing anoxic brain injury. Neurol Clin Pract. 2018;8:249-256. doi:10.1212/CRJ00000000000000466

13. Caviness JN, Brown P. Myoclonus: current concepts and recent advances.Lancet Neurol.2004;3:598-607. doi:10.1016/S1474-4422(04)00880-4

14. Greif R, Bray JE, Djvar T, Drennan IR, Liley HG, Ng KC, Cheng A,Douma MJ, Scholefield BR, Smyth M, et al. 2024 International Con-sensus on Cardiopulmonary Resuscitation and Emergency Cardiovas-cular Care Science With Treatment Recommendations: Summary From the Basic Life Support; Advanced Life Support; Pediatric Life Sup-port; Neonatal Life Support; Education, Implementation, and Teams;and First Aid Task Forces. Circulation. 2024;150:e580-e687. doi: 10.1161/CIR.00000000000000001288

15. Glauser T, Shinnar S, Gloss D, Alldredge B, Arya R, Bainbridge J, Bare M,Bleck T, Dodson WE, Garity L, et al. Evidence-Based Guideline: Treat-ment of Convulsive Status Epilepticus in Children and Adults: Report of the Guideline Committee of the American Epilepsy Society. Epilepsy Curr.2016;16:48-61. doi: 10.5698/1535-7597-16.148

16.De Stefano P, Kaplan PW, Quintard H, Seeck M, Sutter R. Non-convulsive status epilepticus following cardiac arrest: overlooked,$19958-5

17. Rujiter BJ, Keijzer HM, Tjepkema-Cloostermans MC, Blans MJ, Beishuizen A, Tromp SC, Scholten E, Horn J, van Rootselara AF, Admirala MM, et al;TELSTAR Investigators. Treating Rhythmic and Periodic EEG Patterns in Comotose Survivors of Cardiac Arrest. N Engl J Med. 2022;386:724-734.

18.Westallhan E,Rosén L,Rundgren M, Bro-Jeppesen J, Kjaergaard J,Hassager C, Lindehamar H, Horn J, Ullén S, Nielsen N, et al. Time to epileptiform activity and EEG background recovery are independent pre-dictors after cardiac arrest. Clin Neurophysiol. 2018;129:1660-1668. doi: 10.1016/j.clinph.2018.05.016

19. Crepeau AZ, Fugeate JE, Mandrekar J, White RD, Wijdicks EF, Rabinstein AA, Britton JW. Value analysis of continuous EEG in patients during thera-peutic hypothermia after cardiac arrest. Resuscitation. 2014;85:785-789.doi:10.1016/j.resuscitation.2014.01.019

20.Fatuzzo D,Beuchat I,Alvarez V,Novy J,Oddo M,Rossetti AO.Does continu-ous EEG influence prognosis in patients after cardiac arrest? Resuscitation.2018:132:929-32. doi: 10.1016/j.resuscitation.2018.08.023

21.Rosetti AO, Schindler K, Sutter R, Rüegg S, Zubler F, Novy J, Oddo M, Warpelin-Decrausaz L, Alvarez V. Continuous vs Routine Electroen-cephalogram in Critically III Adults With Altered Consciousness and No Recent Seizure: A Multicenter Randomized Clinical Trial. JAMA Neurol.2020;77:1225-1232.doi: 10.1001/jamaneurol.2020.2264

22.Rosenthal ES, Claissen J, Wainwright MS, Husain AM, Vaitkevicius H,Raines S, Hoffmann E, Colquhoun H, Doherty JJ, Kanes SJ. Brexanolone as adjunctive therapy in super-refractory status epilepticus. Ann Neurol.2017;82:342-352. doi: 10.1002/ana.25008

23. Kapur J, Elm J, Chamberlain JM, Barsan W, Cloyd J, Lowenstein D,Shinar S, Convit R, Menzer C, Cock H, et al; NETT and PECARN In-vestor determinators. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus. N Engl J Med. 2019;381:2103-2113. doi:10.1056/NEiMoal 2005795

24. Brain Resuscitation Clinical Trial I Study Group. Randomized clinical study of thiopental loading in comatose survivors of cardiac arrest. N Engl J Med.1986;314:397-403. doi:10.1056/nejm198602133140701

25.Longrestth WT F Jr.,Fahnbruch CE, Olsufka M, Walsh TR, Copass MK,Cobb LA. Randomized clinical of magnesium, diazepam, or both af-ter off-thosolid cardiac arrest. Neurology. 2002;59:506-514. doi:10.1212/wml.59.4.506

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26. Monsalve F, Rucabad L, Ruano M, Cuat J, Lacueva V, Vinuales A. The neurologic effects of thiopental therapy after cardiac arrest. Intensive Care Med.1987;13:244-248.doi:10.1007/BF00265112

Diagnosis and Management of Myoclonus in Adults After Cardiac Arrest

|Recommendations for the Diagnosis and Management of Myoclonus in Adults After Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-LD|1. We recommend promptly performing and interpreting EEG for the diagnosis of seizures in adult patients with myoclonus after ROSC.|| |3: No Benefit|C-LD|2. Treatment to suppress myoclonus without an EEG correlate is not recommended in adult survivors of cardiac arrest.||

Synopsis

Myoclonus is a common clinical manifestation of hypoxic-ischemic brain injury, being observed in approximate-ly 18% to 34% of post-cardiac arrest patients.1-5 Myoclonus can present as diffuse or multifocal muscle jerks or more subtle focal motor movement involving the face and limbs.6,7 Up to half of patients with myoclonus are found to have elec-trographic seizures or status epilepticus, and the clinical exam alone is insufficient to predict which patients are having elec-trographic seizures.8-10 Myoclonus with a time-locked EEG correlate is a seizure(Table 2), although it is controversial whether this is an epiphenomenon of hypoxic-ischemic brain injury or if it is a seizure pattern that should be treated to pre-vent secondary brain injury.8,10,11 Independent of the presence of a time-locked EEG correlate, myoclonus may interfere with supportive care and ventilatory mechanics.12,13

Post-cardiac arrest studies are limited by substan-tial heterogeneity in definitions and terminology used for describing and classifying myoclonus and its asso-ciated EEG findings, including the presence of electro-graphic seizures and status epilepticus or epileptiform discharges or other electrographic events time locked to the myoclonus8,11,14-16(Table 3).

Recommendation-Specific Supportive Text

1.There is no specific clinical exam pattern, timing of occurrence, or myoclonus pattern that is reliably associated with the presence or absence of seizures or status epilepticus on EEG after cardiac arrest.4,6-8 Therefore, prompt EEG monitoring is necessary to diagnose whether myoclonus is associated with sei-zures, status epilepticus, or the presence of other EEG correlates(Table 3).16 Back averaging of EEG and electromyography signals may be neces-sary to determine the precise relationship between EEG events(eg, spikes, bursts) and myoclonus.8,17 Myoclonus can cause significant muscle artifact on EEG, which can be overcome with neuromuscular blockade under close monitoring.

2.There is no randomized or nonrandomized study evaluating the role of pharmacologic interventions for the management of myoclonus without an EEG correlate after cardiac arrest. Similarly, there is no evidence implicating myoclonus without an EEG correlate in the pathogenesis of secondary brain injury after cardiac arrest.18 Myoclonus after car-diac arrest is often refractory to treatment, and mul-tiple antiseizure medications or anesthetic agents may be needed for myoclonus control.2,5,7,8,13,18-24 High risk of bias related to patient selection and confounding effects and inconsistent reporting of myoclonus and EEG characteristics in the literature preclude a specific treatment recommendation for myoclonus without an EEG correlate.14 The risk of cardiovascular, neurological, and other medication side effects outweighs the unknown benefit of suppressing myoclonus without an EEG correlate on patient outcomes.

REFERENCES

1. Lybeck A, Friberg H, Aneman A, Hassager C, Horn J, Kjergagaard J, Kuiper M, Nielsen N, Ullén S, Wise MP, et al; TTM-trial Investigators. Prog-nostic significance of clinical seizures after cardiac arrest and target

Table 3. Commonly Used Terms and Definitions for Myoclonic Activity After Cardiac Arrest

|Terminology|Definition|Note| |---|---|---| |Status myoclonus|Repetitive myoclonic jerks that are diffuse or generalized,focal,or multifocal,occurring once every 10 s for at least 10 min or at least once every min for at least 30 min|Clinical diagnosis that is made without EEG evaluation Status myoclonus cannot be differentiated from myoclonic seizures without an EEG.| |Electroclinical myoclonic seizure/ status epilepticus|Clinical manifestation of myoclonic jerks with a consistent and unequivocal EEG correlate that is not confounded by muscle artifact on EEG|No definite distinguishable features on clinical exam May require back averaging EEG-EMG for confirmation Distinct electroclinical phenotypes have been identified, which may carry different prognostic implications.| |Subcortical myoclonus Myoclonus without EEG correlate|Clinical manifestation of myoclonic jerks without EEG correlate|No definite distinguishable features on clinical exam Ascertaining lack of EEG correlate can be challenging in clinical practice and may be aided by use of neuromuscular blockade.|

EEG indicates electroencephalography; and EMG, electromyography.

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temperature management. Resuscitation. 2017;114:146-151. doi:10.1016/j.resuscitation.2017.01017

2. Bouwaves A, van Poppelen D, Koelman JH, Kuiper MA, Zandstra DF, Weinstein HC., Tromp S, Zcandergen EG, Tjssen MA, Horn J. Acute hypostphic my-oclonus after cardiopulmonary resuscitation. BMC Neurol. 2012;12:63. doi:10.1186/1471-2377-12-63

3.Breachner A, Lindholin P, Jensen MJ, Toft P, Henriksen FL, Lassen JF,Mikkelsen S. Post-Hypoxic Myoclonus Status following Out-of-Hospital Cardiac Arrest- Does It still Predict a Poor Outcome? A Retrospective Study.Healthare(Basel).2021;10:41. doi:10.3390/healthcare 10010041

4.Chakraborty T, Braksick S, Rabinstein A, Wijdicks E. Status Myoclonus with Post-cardiac-astreson: Implications: Implications of Prognostication. Neurocrft Care 2022;36:387-394. doi:10.1007/s12028-021-01344-8

5.Seder DB,Sunde K, Rubertsson S, Mooney M, Stammet P, Riker RR, Kern KB, Unger B, Cronberg T, Dziotzi J, et J.; Intemational Cardiac Arrest Registry. Neurologic outcomes and postscustication care of patients with myoplus following cardiac arrest. Crit Care Med. 2015;43:965-972. doi:10.1097/CC00000000000000000000000000000000000000000000000

6. Mikhaeil-Demo Y, Gawala JR, Bellinski II, Macker MP, Narechiaani A,Templer JW, VanHaerents S, Schulee SU, Gerard EE. Clinical classifica-tion of post anoxic myoclinic status. Resuscitation. 2017;119:76-80. doi:101016/j.resuscitation.2017.07,035

7. Dhakar MB, Svaraju A, Macbiat CN, Youst G, Sanderg N, Gremer D, Hirsch L, Gilm E. Electro-clinical characteristics and prognostic signifi-cance of post anoxic myoclonus. Resuscitation. 2018;13:111-120. doi:10.1016/j.resuscitation.2018;06:030.03

8. Reynolds AS, Rohat B, Holmes MG, Robinson D, Roth V, Velazquez A.Couch CK, Presciuti A, Brodie, Moirtra VK, et al. Early myoclonal fol-lowing anoxic brain injury. Neurol Clact 2018:849-256. doi:10.1012/CFJ.00000000000000466

9. Orav K, Bosque Varela P, Priwasser T, Machegger L, Letinger M, Trinka E, Kuchukhid G. Post-hypoxic status epilepticus - A distinct subtype of status epilepticus with poor prognosis. Epilectic Disord. 2023;25:823-832.dol.1002/7epd2.20164

10.5094. Nüttser BJ, Beishuizen A, Tromp SC, Scholten E, Horn J,van den Bergh WM, van Kranen-Mastenbroek VH, Thomeer EC, Moudrous W,et al.TELSTAR Investigators. Myclonus in comatose patients with elec-trographic status epilepticus after cardiac arrest:Corresponding EEG pat-terns, effects of treatment and outcomes. Resuscitation. 2023;186:109745.$\dot{0}$ doi:10.1016/j.resuscitation.2023.109745.

11. Elmer J, Rittenberger JC, Faro J, Molyneaux BJ, Popescu A, Callaway CW,Baldwin M; Pittsburgh Post-Cardiac Arrest Service. Clinically distinct elec-troencephalographic phenotypes of early myoclonus after cardiac arrest Ann Neurol.2016;80:175-184. doi: 10.1002/ana.24697

12.Dalic L.J.,Fennyess,G.Edmonds M.Camery P,Opdam H,Archer J.Ear elec-troencephalogram does not reliably differentiate outcomes in post-hypoxic myoclonus. Criti Care Resusc.2019;21:45-52.

13. van Zijl JC, Beudel M, de Jong BM, van der Naalt J, Zutt R, Large F,van den Bergh WM,Elting JJ,Tjissen MAJ.The interrelation between clinici-cal presentation and neurophysiology of postphytic myoclonus. Ann Clin Transl/Neur 2018;5:386-396. doi:10.1002/acn3.514

14.De Stefano P, Leitinger M, Misrocichi F, Quintard H, Degano G, Trinka E.Myoclonus After Cardiac Aren Need: For standardization-A Systematic Re-view and Research Proposal in Termonology: Crit Care Med 2025;53:e410-e423. doi: 10.1097/CCM.00000000000006521

15.Hirsh KG,Abella BS,Amorin E,Bader MK,Barletta JF,Berg K,Callaywe,CW/Rberg, H Filmore JG, Eregran M, KDm, K BLYesay S, May TL, Neumarz RW, Nolan JP, Oddo M, Peberdy MA, Polyacow SM, Seder D, Tache Fosc,Uzendu A, Walsh, Zimmerman JL, Geocadrgn R; http of behalf of the Ameri-can Heart Association and Neurocritical Care Society. Critical care man-agement of patients after cardiac arrest: a scientific statement from the American Heart Association and Neurocritical Care Society. Circulation 2024;149:e168-e200. doi: 10.1161/CIR.00000000000001163

16. Caviness JN, Brown P. Myoylus: current concepts and recent advances-Lancet Neurol.2004;3:598-607. doi:10.1016/S1474-4420(04)00880-4

17. Shibasaki H, Hallett M. Electrophysiological studies of myoclonus. Muscle Neveus.2005;31:157-174. doi:10.1002/us2034

18. Young GB, Gilbert JJ, Zochodne DW. The significance of myoclonic sta-tus lepticus in postcanonic coma. Neurology; 1990;40:1843-1848.doi:10.1211:40.124.183

19.Aicua Rapun I, Novoy J, Solari D, Oddo M, Rossetti AO. Early Lance-Adams syndrome after cardiac arrest: Prevalence, time to return to awareness,and outcome in a large cohort. Resuscitation. 2017;115:169-172. doi:10.1016/j.resuscitation.2017.03.020

20. Kouroumanidis M, Sakelariou D. Low frequency nonevolving generalized periodic epileptiform discharges and the borderland of hypoxic nonconvul-sive status epilepticus in comatose patients after cardiac arrest. Epilepsy Behav.2015;49:255-262. doi: 10.1016/j.yebeh.2015.04.060

21. Scheibe F, Neumann WJ, Lange C, Scheel M, Furth C, Kohnlein M,Mergenthaler P, Schultze-Amberger J, Triebkorn P, Ritter P, et al. Movement disorders after hypoxic brain injury following cardiac arrest in adults. Eur J Neurol. 2020;27:1937-1947. doi: 10.1111/ene.14326

22.Beretta S, Coppo A, Bianchi E, Zanchi C, Carone D, Stabile A, Padovano G, Sulmina E, Grassi A, Bogliun G, et al. Neurologic outcome of postan-oxic refractory status epilepticus after aggressive treatment. Neurology.2018:91:e2153-e2162.doi: 10.1212/WNL000000000006615

23. Thoméke F, Weilemann S.L. Poor prognosis despite successful treatment of postan-ponatoxic generalized myonoclus. Neurology.2010;74:1392-1394. doi:10.1212/WNL018d5b9

24. van Zjj JC, Beudel M, vdno Huen, Lange F, Tijssen MA, Eltting JW. Elec-troencephalographic Findings in Posthypothoxic Myoclonus. J Intensive Care Med 2016;31:270-275. doi: 10.1177/0885066615571533

NEUROPROGNOSTICATION

Introduction

Hypoxic-ischemic brain injury is the leading cause of morbidity and mortality in patients who achieve ROSC after OHCA and accounts for a significant portion of un-favorable outcomes after resuscitation from in-hospital cardiac arrest.12 Most deaths attributable to brain injury after cardiac arrest are due to withdrawal of life support based on a predicted unfavorable environmental outcome.Prognostication is critically important as surrogates com-monly make decisions relying on the perceived estimat-ed likelihood of recovery that is shared by the treatment team. Accurate neuroprognostication is important to avoid inappropriate withdrawal of life support in patients who may otherwise achieve meaningful recovery and to avoid ineffective treatment when poor outcome is inevi-table(Figure 2).3

Neuroprognostication frequently incorporates assess-ment of structural injury (eg, neuroimaging and bio-markers) or neurological clinical function (eg, neurophysiologic tests and clinical examination). The ideal timing for neuroprognostic tests avoids the effects of confound-ing (eg, from temperature, medications, and systemic organ dysfunction). Multiple tests are incorporated to estimate the likelihood for recovery to a favorable or unfavorable state. Most neuroprognostic studies utilize dichotomized outcome scales, with a favorable functional outcome defined by the ability to achieve independence (ie, Glasgow-Pittsburg Cerebral Performance Category scores of 1-2 or modified Rankin Scale scores of 0-3),although some studies have thresholds characterized by recovery of consciousness (ie, Cerebral Performance Category score of 1-3 or modified Rankin Scale score of 0-4). These studies do not capture granular details on the functional state of patients, nor do they consider their individual preferences or values, limiting their utility. Fur-ther guidance on best practices on the interpretation of outcomes with a patient-centered approach is included in “Part 3: Ethics”

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General Considerations for Neuroprognostication in Adult Patients After Cardiac Arrest

Recommendations for General Considerations for Neuroprognostication in Adult Patients After Cardiac Arrest

|COR|LOE|Recommendations| |---|---|---| |1|B-NR|1. In adult patients who remain comatose after cardiac arrest, we recommend that neuroprognostication involve a multimodal approach and not be based on any single finding.| |1|B-NR|2. In adult patients who remain comatose after cardiac arrest, we recommend that neuroprognostic impressions be delayed until adequate time has passed to ensure avoidance of confounding by medication effect or a transiently poor examination in the early postirvion period.| |1|C-EO|3. We recommend that teams caring for adult patients who remain comatose after cardiac arrest have early, regular, and transparent multidisciplinary discussions with surrogates about the anticipated time course for uncertainties around neuroprognostication.| |2a|B-NR|4. In adult patients who remain comatose after cardiac arrest, it is reasonable to consolidate the interpretation of multimodal prognostic assessments at a minimum of 72 h after normothermia and discontinuation of sedatives.|

Synopsis

Neuroprognostication relies on interpreting the results of tests and correlating those results with outcome. Given that a false positive test for unfavorable neurological outcome could lead to inappropriate withdrawal of life support from a pa-tient who otherwise would have recovered, specificity is the most important test characteristic when predicting unfavor-able outcome. In some instances, prognostication and with-drawal of life support may appropriately occur earlier because of nonneurologic disease, catastrophic brain herniation, pa-tient's goals and wishes, or clearly nonsurvivable situations.Many of the tests considered are subject to error because of the effects of medications, organ dysfunction, and tempera-ture. Importantly, many published neuroprognostic studies are impacted by self-fulfilling prophecy bias, given that prac-tices of neuroprognostication are inherently part of PCAC,and in turn, outcomes are modulated by such practices. Fur-thermore, research studies have methodological limitations,including small sample sizes, single-center design, lack of blinding, failure(or inability) to account for unmeasured fac-tors that impact the pace of recovery, and the use of outcome at hospital discharge rather than a time point associated with maximal recovery(typically 3-6 months after arrest).3 Addi-tionally, prognostic tests may yield discordant or inconclusive results, and in such instances, continued observation and se-rial assessment remains a treatment option.

Recommendation-Specific Supportive Text

1. Any single method of neuroprognostication has an intrinsic error rate and may be subject to

confounding, therefore, multiple modalities should be used to improve decision-making accuracy.4-9 The overall certainty in the evidence of neuroprog-nostication studies is low due to inherent biases that limit the internal validity of studies and limited generalizability that challenge their external validity.Neuroprognostication approaches employing mul-timodal testing aim at mitigating error rates; con-cordant results increase certainty when predicting outcomes.3,5,6,8,10-19

2.Early withdrawal of life support based on presumed poor neurological prognosis remains frequent,despite the risk for unreliable outcome prediction within 72 hours after ROSC.2021 Sedatives and neu-romuscular blockers may be metabolized more slowly in post-cardiac arrest patients, and injured brains may be more sensitive to the depressant effects of various medications. Residual sedation or paralysis can confound the accuracy of clinical examinations.22

3. Establishing clear and cohesive communica-tion with families is a key aspect of PCAC.Communication should be implemented early and maintained longitudinally, addressing major needs,including the uncertainty of neurological progno-sis.23,24 Difficulties in family-team communication dynamics may contribute to premature withdrawal of life support.25 Discordance in goals of care between clinicians and families/surrogates has been reported in more than 25% of critically ill patients.26 Regular multidisciplinary meetings may help improve communication.

4.Operationally, the timing for prognostic impressions is typically at least 5 days after ROSC for patients treated with hypothermic temperature control(approximately 72 hours after normothermia) and is conducted under conditions that minimize the confounding effects of sedating medications. Each neuroprognostic test has a specific time window in which it has optimal test performance. Prognostic impressions more comprise results of tests integrated into the multimodality assessment synthesized at least 72 hours after normothermia. ${}^{11,13,27-35}$

Use of the Clinical Examination in Neuroprognostication

Synopsis

Historically, neuroprognostic studies evaluated findings from clinical examination that correlated with unfavor-able neurological outcome. More recently, the focus of neuroprognostication after cardiac arrest has shifted to include prognostication for both favorable and unfa-vorable outcome. Given that a test may perform better in predicting unfavorable but not favorable outcome or vice versa, specific recommendations are made depend-ing on the finding and the outcome (ie, favorable versus

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 Figure 2. Recommended approach to multimodal neuroprognostication.

A multimodal approach to neuroprognostication is recommended, denoted by the multicolored arrow at the right of the figure. Neuroprognostic impressions are delayed until adequate time has passed to ensure avoidance of confounding by medications, temperature control, organ failure, or other sources. ADC indicates activated diffusion coefficient; CT,computed tomography; EEG, electroencephalogram; GWR, gray-white ratio; MRI,magnetic resonance imaging; Nfl,neurofilament light chain; NSE,neuron-specific enolase; ROSC, return of spontaneous circulation; and SSEP,somatosensory evoked potential.

unfavorable outcome) with which it has correlated. Se-rial clinical examinations in comatose survivors of cardiac arrest assess the level of consciousness, pupillary light

and corneal reflexes, and best motor response to nox-ious stimulation. The presence of myoclonus during the first week after cardiac arrest is also noted. Myoclonus

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describes repetitive jerk-like involuntary movements that can be generalized, focal, multifocal, synchronous,or asynchronous in their involvement of body parts and may or may not have an electroclinical correlate with dis-charges on EEG(refer to the Seizures, Myoclonus, and Other Epileptiform Activity section). Clinical examination findings that correlate with poor outcome are subject to confounding by temperature and medications.

Recent ILCOR systematic reviews included studies regardless of temperature control, and findings were cor-related with neurological outcome at time points ranging from hospital discharge to 12 months after arrest.10,36 A 2023 systematic review specifically evaluated the prog-nostive value of different test modalities for the prediction of favorable outcome.37

Clinical Examination for Neuroprognostication of Unfavorable Outcome in Adults After Cardiac Arrest

|Recommendations for Clinical Examination for Neuroprognostication of Unfavorable Outcome in Adults After Cardiac Arrest||| |---|---|---| |COR|LOE|Recommendations| |2b|B-NR|1. When performed with other prognostic tests, it may be reasonable to consider bilaterally absent pupillary light reflex at ≥27 h after cardiac arrest to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose.| |2b|B-NR|2. When performed with other prognostic tests, it may be reasonable to consider quantitative pupillometry at≥72 h after cardiac arrest to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose.| |2b|B-NR|3. When performed with other prognostic tests, it may be reasonable to consider bilaterally absent corneal reflexes at≥72 h after cardiac arrest to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose.| |2b|B-NR|4. The usefulness of undifferentiated myoclonus as a predictor of unfavorable neurological outcome in adult patients who remain comatose is uncertain, even when occurring within 72 h after cardiac arrest.| |2b|B-NR|5. The usefulness of best motor response in the upper extremities of absent or extensor response as a predictor of unfavorable neurological outcome in adult patients who remain comatose after cardiac arrest is uncertain.| |2b|B-NR|4. The usefulness of best motor response in the upper extremities of absent or extensor response as a predictor of unfavorable neurological outcome in adult patients who remain comatose after cardiac arrest is uncertain.|

Recommendation-Specific Supportive Text

1. Twenty-seven retrospective studies demonstrated that absent pupillary light reflex evaluated imme-diately after ROSC and up to 7 days after arrest predicted unfavorable neurological outcome with specificity ranging from 48% to 100%5-8,11,2728,38-57;these studies support the reliability of pupillary light reflex as a prognostic tool.458,59 Studies with earlier time points for assessments of pupillary light reflex had lower specificity43,46; the highest

$\text{specificity was seen at time points}\geq 72\text{ hours after}$$\text{arrest}^{5,6,8,11,40,42}\text{ and when combined with absent cor-}$neal reflexes.5,78,42 The false positive rates of bilaterally absent pupillary light reflex when assessed at least 72 hours after arrest in predicting unfavorable out-come were consistently low across studies. However,pupillary light reflex is vulnerable to the effect of med-ifications and ambient light, subjective interpretation of the examiner, rigor of technique for assessment, indi-vidual factors, and self-fulfilling prophecy bias.

2. Quantitative pupillary light reflex of 0% is an objec-tive finding that describes bilateral absence of pupillary light reflex as assessed by pupillometry.49 The automated quantification of pupillary reactivity with pupillometry yields measurements of ampli-tude and velocity of constriction and dilatation. Four retrospective studies evaluated quantitative pupil-lary light response(ie, the percentage of reaction to light), 49,60-62 and 9 evaluated NPi(reactivity index from comparison with normal responses)13,18,49,62-67 at time points ranging from immediately after ROSC65 to 72 hours after arrest. Quantitative responses of 4% to 5% had higher sensitivity in predicting unfavorable neurologic outcome within 72 hours after arrest while maintaining 100%specificity. The NPi≤2 threshold at 24 hours dem-onstrated 100% specificity for unfavorable neuro-logical outcome in most studies.13,18,49,66,67 NPi is nonspecific and may be affected by medications;thus, an absolute NPi cutoff that predicts unfavor-able outcome remains unknown.4,13,18,49,59,62-67

3.Eighteen studies evaluated the bilateral absence of corneal reflexes at time points ranging from immediately after ROSC to 7 days after arrest with specificity ranging from 25% to 100%5,78,27-29,35,40,42-45,48,50,53,54,68,69; these studies support the reliability of corneal reflex as a prognostic tool.Studies with higher specificity evaluated corneal reflexes at time points≥72 hours after arrest or in combination with bilaterally absent pupillary light reflexes.5,78,42 Corneal reflexes are subject to con-founding by medications and rigor of technique of the examiner, and few studies specifically evalu-ated the potential of residual medication effect or described the type of stimuli used for testing.

4. Marked heterogeneity in study definition of myoclo-nus after cardiac arrest challenge the interpretation of this finding as a neuroprognostic tool.70 Eleven obser-vational studies evaluated the presence of myoclo-nus(not otherwise specified) within 96 hours after arrest with specificities for unfavorable neurological outcome ranging from 77.8% to 100%,11,13,27,29-35,68 yielding false positive rates up to 22.2%(and upper bound of 95% CI of 60%).4 Six studies evaluated status myoclonus within 72 hours from ROSC with specificities for unfavorable outcome ranging from

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94% to 100%.67,33,53,71,72 There were methodological limitations in all studies, including a lack of standard definitions, lack of blinding, incomplete data on EEG correlates, and the inability to differentiate between myoclonus subtypes. This imprecision may result in erroneous estimates of unfavorable outcome if undifferentiated myoclonus is used as a prognostic marker. Given these limitations in the interpretation of literature and the need for characterization of electroclinical subtypes of myoclonus after cardiac arrest, an expert consensus suggested avoiding using the term status myoclonus.73

5. Historically, the best motor examination in the upper extremities has been used as a prognos-tic tool, with extensor or absent motor responses being correlated with unfavorable outcome.Previous literature was limited by methodologi-cal concerns, including confounding for effects of hypothermic temperature control and medications,as well as self-fulfilling prophecy bias. The litera-ture was so imprecise with higher-than-acceptable false positive rates(up to 75.1%)4,758,59 that the finding of absent or extensor response as best motor response was considered potentially harm-ful when used alone for predicting a unfavorable neurological outcome.74 Conversely, multimodal neuroprognostic studies using the Glasgow Coma Motor subscore as an entry point have demon-strated sensitivity ranging from 23% to 71% while maintaining high specificity.5-9

Clinical Examination for Neuroprognostication for Favorable Outcome

|Recommendations for Clinical Examination for Neuroprognostication for Favorable Outcome|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|B-NR|1. The usefulness of quantitative pupillometry to support the prognosis of favorable neurological outcome in adult patients who remain comatose at cardiac arrest is not well established.|| |2b|B-NR|2. It may be reasonable to consider withdrawal motor response or better to support the prognosis of favorable neurological outcome in adult patients who remain comatose at cardiac arrest.|| |3:No Benefit|B-NR|3. The finding of preserved pupillary light reflexes is not useful to support the prognosis of favorable neurological outcome in adult patients who remain comatose at cardiac arrest.|| |3:No Benefit|B-NR|4. The finding of preserved coronal reflexes is not useful to support the prognosis of favorable neurological outcome in adult patients who remain comatose at cardiac arrest.||

Recommendation-Specific Supportive Text

1. Two retrospective studies evaluated the predic-tive performance of present pupillary light reflex

to support a prognosis for favorable neurological outcome, when evaluated alone12 or in combination with present corneal reflexes,16 from admission16 to up to 3 days following normothermia and dis-continuation of sedatives.12 Sensitivity when test-ing after mitigation of confounders reached 97.3%;however, specificities only surpassed 80% when both corneal and pupillary reflexes were present early after ROSC.12

2. Four observational studies evaluated the prediction performance of best motor responses(Glasgow Coma Motor subscores) from admission to 96 hours after arrest to support a prognosis of favor-able neurological outcome.7,12,16,75 Sensitivity ranged from 11.6% to 79.26% with specificity ranging from 71.7% to 97.7%; higher specificities were seen with higher motor scores(withdrawal or local-izing responses, Glasgow Coma Motor subscores of 4 or 5, respectively).37 This recommendation is supported by a 2022 ILCOR systematic review.36

3. Two retrospective studies evaluated the prediction performance of pupillometry when assessed at admission to up to 72 hours after arrest to support a prognosis for favorable neurological outcome.12,13 In a post hoc analysis of the largest(n=456) neu-roprognostic study evaluating the usefulness of pupillometry in cardiac arrest, the mean lowest NPi measured within 3 days after arrest in patients with a favorable outcome was 4.1.13 The ideal thresh-olds and timing of testing for pupillometry derived metrics that predict favorable outcome is unknown.

4. Two retrospective studies evaluated the prediction performance of the presence of corneal reflexes to support a prognosis for favorable neurological outcome, when evaluated alone12 or in combination with present pupillary light reflexes,16 from admis-sion16 to up to 3 days following normothermia and discontinuation of sedatives.12 Sensitivity when testing after mitigation of confounders reached 93.6%; however, specificities only surpassed 80%when both corneal and pupillary reflexes were present<72 hours after ROSC.12

Serum Biomarkers for Neuroprognostication of Favorable and Unfavorable Outcome in Adults After Cardiac Arrest

|Recommendations for Serum Biomarkers for Neuroprognostication of Favorable and Unfavorable Outcome in Adults After Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|B-NR|1. When performed in combination with other prognostic tests, it may be reasonable to consider high serum values of NSE or NFL within 72 h after cardiac arrest to support the prognosis of unfavorable neurological outcome in adult patients who remain||

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|Recommendations for Serum Biomarkers for Neuroprognostication of Favorable and Unfavorable Outcome in Adults After Cardiac Arrest (Continued)|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|B-NR|2. When evaluated with other prognostic tests, it may be reasonable to consider normal levels of NSE within 72 h after cardiac arrest to support the prognosis of favorable neurological outcome in adult patients who remain comatose after ROSC.|| |2b|B-NR|3. The usefulness of other serum biomarkers for neuroprognostication in adult patients who remain comatose after ROSC is uncertain.||

Synopsis

Serum biomarkers are blood-based tests that measure the concentration of proteins normally found in the central nervous system. These proteins are absorbed into blood in the setting of neurological injury, and their serum levels reflect the degree of brain injury. Limitations to their prog-nostic utility include variability in testing methods on the basis of site and laboratory, between-laboratory incon-sistency in levels, susceptibility to additional uncertainty due to hemolysis, and potential extracerebral sources of the proteins. The 2020 and 2022 ILCOR systematic re-views evaluated studies that obtained serum biomarkers within the first 7 days after arrest and correlated serum biomarker concentrations with favorable and unfavorable neurological outcomes.4,37 Other testing of serum bio-markers, including testing levels over serial time points after arrest, was not evaluated. The 2 most studied bio-markers were NSE and S100 calcium-binding protein B(S100B). Additional evidence for NfL in predicting fa-vorable neurological outcomes and levels of other blood biomarkers for predicting favorable neurological out-comes has accumulated since these reviews. Prospec-tive validation of different biomarkers and thresholds for both favorable and unfavorable neurological outcome in cohorts more broadly representative of resuscitated car-diac arrest patients is of high clinical importance.

Recommendation-Specific Supportive Text

1. For prediction of unfavorable outcome, 17 obser-vational studies evaluated NSE collected within 72 hours after cardiac arrest,4,13,187,276-86 and threshold levels for unfavorable outcome ranged from 17 to 106 μg/L with specificity for poor outcome of 44% to 100%. The evidence is limited because of a lack of blinding, laboratory inconsistencies,a broad range of thresholds needed to achieve 100% specificity, and imprecision. Data from only 2 observational studies assessing NfL for unfavor-able outcome prediction were included in the 2020 ILCOR systematic review.87,88 In the interim, 9 addi-tional observational studies evaluated NfL within 72 hours after arrest for predicting unfavorable out-come.81,82,89-95 Multiple studies directly compared

NfL to NSE for prognostication of unfavorable outcome and found both improved sensitivity with NfL while maintaining high specificity. Many of the included studies are secondary analyses of RCTs.Strengths of these studies include multiple sites,blinding of clinical staff, and standardized, blinded outcome assessment, but the trial populations may not reflect the overall post-cardiac arrest popula-tion. SIMOA(Quanterix) was the most used assay.Values may differ among commercially available assays.96 Studies reported multiple thresholds and collected samples at different times. In the postar-rest period, the optimal threshold and timing for both NSE and NfL levels are unknown, but very high levels may inform multimodal prognostication.

2. For predicting favorable outcome, the 2022 sys-tematic review identified normal levels of NSE(<17μg/L) between 24 and 72 hours as a predic-tor of favorable neurological outcome.37 Specificity was>80% in the included studies. The biomarkers S100B,NfL, ubiquitin carboxyl-terminal hydrolase-L1 (UCH-L1), glial fibrillary acidic protein (GFAP),and tau were also included. NfL and GFAP had the highest specificity for favorable outcome but had relatively fewer studies compared with NSE. Interval searches identified 5 studies of NSE,8,16,76,97,98 1 of NfL,90 and 1 of both GFAP and tau99 for predict-ing favorable neurological outcome. Specificity for favorable neurological outcome was>80% for each biomarker. Different threshold values and sample timing were reported between studies.While the evidence for favorable outcome predic-tion with biomarkers is less established than for prediction of unfavorable outcome, sustained low levels of biomarkers, in particular, NSE, may be an encouraging finding. Specificity may be lower when predicting favorable neurological outcome due to competing risks of nonneurological organ dysfunction or failure.

3. In addition to 2 prospective and 2 retrospective stud-ies identified in the 2020 ILCOR systematic review,43 observational studies evaluated S100B levels within the first 72 hours after arrest.84,85,93 The maxi-mal level that correlated with unfavorable outcome ranged broadly depending on the study and the tim-ing when it was measured after arrest. Interval stud-ies do not clarify the optimal timing or threshold value to inform prognostication. Only 1 study of GFAP100 and tau101 were identified. Seven observational studies investigated other biomarkers, including UCH-L1, GFAP, and serum and cerebrospinal fluid tau.89,993,95,102-104 In studies that included multiple biomarkers, performance was not consistently bet-ter than NSE. Given the low number of studies, the certainty of evidence was low and these biomarkers could not be recommended for clinical practice.

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Use of Electrophysiological Tests for Neuroprognostication

Synopsis

Electroencephalography is widely used in clinical practice to evaluate cortical brain activity and diag-nose seizures. Its use as a neuroprognostic tool for predicting both unfavorable and favorable neurologi-cal outcome is promising, but the literature is limited by several factors, including lack of standardized ter-minology and definitions, relatively small sample sizes,lack of blinding, subjectivity in the interpretation, and lack of accounting for effects of medications. There is also inconsistency in definitions used to describe specific findings and patterns. The EEG patterns that were evaluated in the 2020 ILCOR systematic review for predicting unfavorable neurological outcome in-clude unreactive EEG, epileptiform discharges, sei-zures,status epilepticus,burst suppression,and“highly malignant" EEG.4 Unfortunately, studies define“highly malignant" EEG differently or imprecisely, limiting use of this finding. Use of standardized terminology from the ACNS avoids this heterogeneity and limits poten-tial for misclassification. Several EEG patterns were observed in a 2022 systematic review for predicting favorable neurological outcome.37 While studies had several operational definitions, most classifications assessed EEG continuity, voltage, and absence of epi-leptiform discharges.

Somatosensory-evoked potentials (SSEPs) evaluate the integrity of the dorsal column-lemniscal sensory pathway and are subject to less interference from medi-cations than other modalities. In the context of neuro-prognostication after cardiac arrest, SSEPs are obtained by stimulating the median nerve and evaluating for the presence of cortical N20 potentials, which are gener-ated in the primary somatosensory cortex and demon-strate integrity of the thalamocortical pathway involved in cortical arousal and consciousness. The reliability of this modality is limited by technical challenges, includ-ing operator skill, interrater agreement, and impairment of signal to noise ratio from muscle and environmental contamination. Recommended technical standards are available. 105

Electrophysiology for Neuroprognostication of Unfavorable Outcome in Adults After Cardiac Arrest

|Recommendations for Electrophysiology for Neuroprognostication of Unfavorable Outcome in Adults After Cardiac Arrest||| |---|---|---| |COR|LOE|Recommendations| |2b|B-NR|1. When evaluated with other prognostic tests, the prognostic value of seizures in adult patients who remain comatose after ROSC is uncertain.|

|Recommendations for Electrophysiology for Neuroprognostication of Unfavorable Outcome in Adults After Cardiac Arrest (Continued)|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|B-NR|2. When evaluated with other prognostic tests, it may be reasonable to consider status epileptic conditions continuing≥72 h after cardiac arrest to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose after ROSC.|| |2b|B-NR|3. When evaluated with other prognostic tests, it may be reasonable to consider burst suppression on EEG in the absence of sedating medications at ≥72 h after arrest to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose after ROSC.|| |2b|B-NR|4. When evaluated with other prognostic tests, the usefulness of rhythmic or periodic discharges to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose after ROSC.|| |2b|B-NR|5. When evaluated with other prognostic tests, it may be reasonable to consider bilaterally absent cortical N20 waves on SSEPs at ≥48 h after cardiac arrest to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose after ROSC.|| |3: No Benefit|B-NR|6. We recommend that the absence of EEG activity within 72 h after cardiac arrest not be used to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose after ROSC.||

Recommendation-Specific Supportive Text

1.No additional studies have been identified since the publication of the 2020 ILCOR systematic review.4 The 2020 systematic review included observa-tional studies focused on electrographic seizures,though some studies also included convulsive sei-zures and the definitions for seizures were non-standardized across studies. The specificity of unequivocal seizures meeting ACNS critical care EEG criteria was 100%; however, the sensitivity of this finding was poor(0.3%-26.8%), and other studies that were not included in the review found patients with postarrest seizures who had favor-able outcomes.31,106,107 Additional methodological concerns include selection bias for which patients underwent EEG monitoring and inconsistent defi-nitions of seizure. Further, critical care EEG termi-nology has been updated since the publication of these studies. ${}^{108}$ The term seizure encompasses a broad spectrum of pathologies that likely have different prognoses, ranging from a single brief electrographic seizure to refractory status epilep-ticus, and this imprecision justifies the more limited recommendation.

2. In the 2020 ILCOR systematic review, the speci-ficity of status epilepticus for unfavorable out-come ranged from 82.6% to 100%.4 No additional studies were identified that reported sensitivity or specificity of this finding. One retrospective study

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reported electrographic characteristics of patients with definitive or possible status epilepticus.109 Of the 64 subjects included, 5 survived 30 days after arrest and 1 had a favorable outcome. The most common cause of death in decedents was withdrawal of life-sustaining therapies, which occurred a median of 8 days(IQR, 7-11) after arrest. Interestingly, although status epilepticus is a severe form of seizure the specificity of status epilepticus for unfavorable outcome was less than reported in the studies examining the seizures overall(as above). Additional concerns within the studies include the inconsistent definition of status epilepticus, lack of blinding, and the use of status epilepticus to justify withdrawal of life-sustaining prophe-cies. The 72-hour timing is based on most studies reporting presence of status epilepticus within this period and case reports of good outcome when status epilepticus is successfully treated within this period.

3. The term highly malignant EEG was inconsis-tently applied in studies included in the 2020 ILCOR systematic review.4 Twelve studies evalu-ated burst suppression or suppression on EEG monitoring.6,8,9,40,69,72,8,110-114 Across these studies,highly malignant EEG was classified as burst sup-pression or suppression according to the ACNS critical care EEG terminology.108,115 Specificity ranged from 90.7% to 100%, and sensitivity was 15% to 51%. The potential for self-fulfilling proph-ecies, interrater disagreement, and lack of control for medication effects limited the ability to make a stronger recommendation, despite the overall high specificity.112 Further, in a preplanned analysis of the TTM2 trial, specificity of burst suppression or suppression for unfavorable outcome was lower(93%) compared to studies with specific central-ized or expert EEG review.114 Additional studies identifying subtypes of burst suppression, such as synchronous or identical bursts, are needed.116 Burst suppression can be caused by medications,so it is particularly important that clinicians have knowledge about the potential effects of medica-tion on this prognostic tool.

4. The 2020 ILCOR systematic review considered discharges as either rhythmic/periodic or nonrrhyth-mic/periodic.4 Sensitivity and specificity of rhyth-\$mic/periodic patterns for unfavorable outcome ranged from 0.5% to 50.8% and 77.7% to 100%,respectively, with wide confidence intervals. As the time from the cardiac arrest to test increased,the specificity of rhythmic/periodic discharges for unfavorable outcome improved. Nonrrhythmic/periodic patterns had a similar range of sensitiv-ity(0.5%-38.5%) and specificity(84.6%-100%).

One observational study reported outcomes in patients with stimulus-induced rhythmic or periodic patterns recorded>36 hours after arrest.117 Of the 142 included patients, 20(14%) had stimulus-induced rhythmic or periodic patterns recorded on EEG monitoring. The rate of unfavorable outcome was not different between patients with(n=13,65%) or without stimulus induced rhythmic or peri-odic patterns(n=88,72%)(P=0.596). The litera-ture of both rhythmic/periodic and nonrhythmic/periodic discharges are limited by lack of account-ing for effects of medications and variable timing of EEG monitoring. Low specificity currently limits the use of these findings to support an unfavorable prognosis.

5. Bilateral absence of N20 peaks following median nerve stimulation is the most stud-ied and well-accepted neuroprognostic pre-dictor for SSEP testing. Twenty observational studies5-8,11-13,27,35,38,39,41-43,47,49,50,55,57,69,72,118-130 evaluated bilateral absent N20 peaks assessed up to 6 days after arrest with specificity ranging from 50% to 100%. Six studies had specificity below 100%,11,27,47,50,118,123 and additional method-ological limitations included lack of blinding and potential for self-fulfilling prophecy bias. Newer studies evaluated the unilateral absence of N20 combined with amplitude thresholds, which may increase sensitivity for detection of unfavorable outcome.6,57,131,132 While studies evaluated SSEPs obtained at any time starting immediately after ROSC, there is a high likelihood of potential con-founding factors early after cardiac arrest, leading to the recommendation that SSEPs should only be obtained>48 hours after arrest.

6. A preplanned analysis of the TTM2 trial data reported the prognostic value of unreactive EEG between 24 hours to 14 days.114 Specificity for unfavorable neurological outcome was 60% with a sensitivity of 79%. The study relied on local EEG reviewers to assess reactivity rather than a cen-tralized expert review. Specificity was lower than in studies included in the 2020 ILCOR review, which ranged from 41.7% to 100% but was below 90%in most studies.4 One study assessed EEG reactiv-ity during hypothermia and normothermia intending to assess agreement for reactivity between raters and sensitivity for unfavorable outcome for reactiv-ity to different stimulations.35 Percent agreement ranged from 58% to 70%, and sensitivity ranged from 52% to 86% depending on stimulation type and whether assessment occurred during hypo-thermia or normothermia. Thus, the overall cer-tainty of the evidence was rated as very low. There is interest in automated reactivity assessment and stimulation paradigms.

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Electrophysiology for Neuroprognostication of Favorable Outcome in Adults After Cardiac Arrest

|Recommendations for Electrophysiology for Neuroprognostication of Favorable Outcome in Adults After Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|B-NR|1. When evaluated with other prognostic tests, it may be reasonable to consider a continuous EEG background without discharges within 72 h after cardiac arrest to support the prognosis of favorable neurological outcome in adult patients who remain comatose after ROSC.|| |2b|B-NR|2. The usefulness of the amplitude of the N20 wave on SSEP following medium nerve stimulation to support the prognosis of favorable neurological outcome in adult patients who remain comatose after ROSC is not well established.||

Recommendation-Specific Supportive Text

1. The 2022 systematic review for prediction of favorable outcome found a continuous EEG background with-out discharges within 72 hours after cardiac arrest to predict a favorable neurological outcome.37 Specificity ranged from 51% to 100%, with most studies report-ing a specificity >80%. Specificity was higher in ear-lier(12 and 24 hours) compared to later time points(48 and 72 hours). One additional observational study evaluated continuous normal voltage background without discharges on EEG 24 hours after cardiac arrest.16 Sensitivity and specificity for favorable neu-rological outcome at 6 months after arrest were 64%and 89%, respectively. When compared to unfavor-able outcome, the specificity for predicting favorable outcome is overall less given the competing risk of nonneurological mortality and morbidity.

2. Quantitative characteristics of the N20 signal are of interest as prognostic indicators, and there are sev-eral methods for calculating the amplitude of the N20 wave. The threshold of>4μV when measured as the peak-to-trough difference between the peak of the N20 wave and the trough of the subsequent P25 wave has achieved specificity above 90% with sensi-tivity above 40% in most studies using this finding to predict favorable neurological outcome. ${}^{16,36,3772}$ One study found that patients sedated with midazolam had lower amplitudes(measured as N20/P25 peak-to-peak amplitude) when compared to propofol. ${}^{14}$The ideal amplitude thresholds, measurement meth-ods, and timing of N20 wave amplitude testing for SSEP that predict favorable outcome is unknown.

Use of Neuroimaging for Neuroprognostication Synopsis

Neuroimaging may be helpful to detect and quantify struc-tural brain injury after cardiac arrest. The most common

modalities are CT and magnetic resonance imaging(MRI).The use of quantitative analysis modalities assessing the burden of hypoxic-ischemic brain injury in clinical practice is limited by the availability of quantitative methods outside research settings, while qualitative imaging results are of-ten subjective and have lower sensitivity. ${}^{133,134}$ On CT, cy-totoxic brain edema can be quantified as the gray-white ratio (GWR), defined as the ratio between the density(measured as Hounsfield units) of gray matter and white matter. Normal brain has a GWR of approximately 1.3. In the setting of cerebral edema,GWR declines, either due to decreased density of gray matter (representing cytotoxic edema) or decreased attenuation of white matter. On MRI cytotoxic brain edema can be measured as restricted dif-fusion on diffusion-weighted imaging (DWI) and can be quantified by the apparent diffusion coefficient (ADC). The ADC is a sensitive measure of injury, with normal values ranging between 650 and $1000 \times 10^{-6} ~mm^{2} / s$ and val-ues decreasing with injury. Brain injury findings from CT and MRI evolve over the first several days after arrest, so the timing of the imaging study of interest is particularly important as it relates to prognosis.

Neuroimaging for Neuroprognostication of Unfavorable Outcome in Adults After Cardiac Arrest

|Recommendations for Neuroimaging for Neuroprognostication of Unfavorable Outcome in Adults After Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|B-NR|1. When performed with other prognostic tests, it may be reasonable to consider reduced GWR on brain CT after cardiac arrest to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose after ROSC.|| |2b|B-NR|2. When performed with other prognostic tests, it may be reasonable to consider extensive areas of reduced diffusion on brain MRI at 2 to 7 d after cardiac arrest to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose after ROSC.|| |2b|B-NR|3. When performed with other prognostic tests, it may be reasonable to consider extensive areas of reduced ADC on brain MRI at 2 to 7 d after cardiac arrest to support the prognosis of after cardiac arrest to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose after ROSC.|| |2b|B-NR|3. When performed with other prognostic tests, it may be reasonable to consider extensive areas of reduced ADC on brain MRI at 2 to 7 d after cardiac arrest to support the prognosis of after cardiac arrest to support the prognosis of unfavorable neurological outcome in adult patients who remain comatose after ROSC.||

Recommendation-Specific Supportive Text

1. Forty-one observational studies ${}^{6,1755,56,68,121,125,133-166}$ evaluated GWR-the most commonly studied method for quantification of hypoxic-ischemic brain injury on brain CT. ${}^{167}$ Whole-brain GWR(GWR average) and GWR in specific regions were evaluated with high specificity in predicting unfa-vorable neurological outcome; lower prediction performance was seen when using thalamus as a region of interest and with higher cutoffs for GWR.

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Thirty-four of the studies evaluated CT obtained within 24 hours after arrest,6,175,55,56,68,121,133-139,141-143,145,147-153,155,156,158-161,163-166 and 6 studies included brain CTs obtained up to 10 days after arrest.125,140,146,154,157,162 In retrospective studies, the predictive performance improved when images were obtained at 24 to 72 hours134,151,155 and up to 10 days from ROSC.156,162 There were meth-odological limitations, including selection bias, risk of multiple comparisons, and heterogeneity of measurement techniques, such as anatomic sites,equipment, and calculation methods. Thus, spe-cific methods for calculation of and thresholds for GWR and ideal timing for CT acquisition that pre-dict unfavorable prognosis with highest specificity remain unknown. Fewer studies have evaluated CT metrics as predictors of death by neurological criteria148,150;external validation and reproducibility of methods are lacking.

2.Ten observational studies16,55,69,11,168-173 investi-gated DWI changes on MRI qualitatively within 2 to 7 days after arrest for unfavorable outcome predic-tion. The studies evaluated MRI qualitatively. And definitions of relevant findings differed between studies, such as use of “high signal intensity” and“positive findings.” In some studies, only specific brain regions were examined, with or without using a standardized scoring system. Moreover, stud-ies are limited by subjective thresholds and lack of blinding. The specificity ranged from 55.7% to 100%. In the context of multimodal prognostica-tion, an extensive burdened of reduced DWI on MRI may be correlated with unfavorable prognosis, but a broader recommendation could not be supported.The imprecise definition and short-term outcome in some studies led to significant uncertainty about how to use qualitative DWI MRI to predict unfavor-able prognosis.

3.Ten observational studies investigated quantitative ADC on MRI within 2 to 7 days after arrest for unfa-vorable prognosis prediction. 176,158,164,170,171,174-177 The studies used custom-made computational tools to quantitatively determine the whole brain or region of interest volume below a specific ADC threshold for poor outcome prediction. The ADC thresholds used, ADC calculation methods used,and regions included for analyses varied among studies, with cutoffs for unfavorable outcome with 100% specificity using 650 x 10-6 mm/s or 450 x 10-6 mm/s varying from 20.5% to 42.2%and 1.3% to 5.2%, respectively. There is no stan-dardization of quantitative measurements of ADC in cardiac arrest, and such analyses require expertise in advanced computational methods; hence, there are concerns about feasibility and reliability. In the context of multimodal prognostication, an extensive

burden of decreased ADC on MRI may be corre-lated with unfavorable prognosis. A specific ADC threshold for global or regional brain injury that pre-dicts unfavorable prognosis is not known.

Neuroimaging for Neuroprognostication of Favorable Outcome in Adults After Cardiac Arrest

|Recommendations for Neuroimaging for Neuroprognostication of Favorable Outcome in Adults After Cardiac Arrest||| |---|---|---| |COR|LOE|Recommendations| |2b|B-NR|1. The usefulness of GWR on brain CT after cardiac arrest to support the prognosis of favorable neurological outcome in adult patients who remain metatose after ROSC is not well established.| |2b|B-NR|2. When performed with other prognostic tests, it may be reasonable to consider the absence of restricted diffusion on brain MRI at 2 to 7 d after cardiac arrest to support the prognosis of favorable neurological outcome in adult patients who remain metatose after ROSC. who remain comatose after ROSC.|

Recommendation-Specific Supportive Text

1. Three observational studies evaluated the role of GWR on brain CTs performed within 6 hours up to 36 hours after arrest to identify patients with favorable outcomes.56,142,158 In the largest cohort,patients who regained consciousness before hos-pital discharge had a median GWR 1.38. The ideal thresholds and methods of calculation for GWR and timing for CT acquisition that predict favorable prognosis are unknown.36,37

2.Six studies investigated the absence of qualitative DWI abnormalities within 2 to 7 days from arrest as a predictor of favorable outcome.16,45,168-171 These studies had a sensitivity for favorable outcome pre-diction of 51% to 100%, but there was heterogene-ity of DWI assessment methods and which regions were evaluated. In the context of multimodal prog-nostication, the absence of injury using DWI on MRI may be correlated with a favorable prognosis,but imprecise definitions and criteria for brain MRI assessment led to uncertainty about how to use DWI MRI to predict favorable prognosis.

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154. Kenda M, Scheel M, Kemming A, Aalberts N, Guettler C, Streitberger KJ, Storm C, Ploner CJ, Leithner C. Automated Assessment of Brain CT After Cardiac Arrest-An Observational Derivation/Vali-dation Cohort Study. Critic Care Med.2021;49:e1212-e1222. doi:10.1097/CCM.000000000000000000198

155. Kirsch K,Heymel S,Ginher A,Vahl K,Schmidt T,Michalski D,Fritzenwanger M,Schulez PC, Pfeier R,Prognostication of neurologic outcome using gray-white-matter-ratio in comatose patients after cardiac arrest. BMC Neurol.2021;21:456. doi:10.11836/s12883-021-02480-6

156. Ong HN, Chen WU, Chuang PY, Lee BC, Huang CH, Huang CC, Chang WT, TsA. Prossignity: Value of Gray-White-Matter Ratios in Comatose Survivors After In-Hospital Cardiac Arrest. J Acute Med.2020;10:9-19. doi:10.6705/j.jacme.202003.10(1),0002

157. Hrdicka J, Smalcova J, Bircakova B, Lambert L, Belohlavek J, Burgetova A. Both decreased and increased grey-to-white matter attenuation ratio in the putamen and caudate on early head computed tomography differentiate patients with favorable and unfavorable outcomes after prolonged cardiac arrest-secondary analysis of the Prague OHCA study. Quant Imaging Med Surg.2023;13:6205-6214. doi:10.21037/qims-23-430

158. Huang Sien, T YT, Lee HY, Ong HN, Huang CH, Chen WT, Chen WJ,Chang WT,Tsai M. Sombination of Cerebral Computed Tomography and Simplified Cardiac Arrestel, Hospital Prognosis(sCAHP) Score for Predict-ing Neuroallic Recovery in Cardiac Arrestur Survivors. Rev Cardiovasc Med.2023;24:25. doi:10.31083/3.jrcm2401025

159. Adriaensns KO, Jewellu SJ, LMD, Lemkes JS, Spoomans EM, Meuwissen M, Blans MJ, van der Harst P, Eikemans BJW, Bleeker GB, Beishuizen A, et al. Routine reporting of grey-white matter differentiation in early brain computed tomography in comatose patients after cardiac arrest:A substudy of the COACT trial. Resuscitation. 2022;175:13-18. doi:10.1016/j.resuscitation.2022.03.028

160. Lee BK,Callaway CW,Coppler PJ,Rittenberger JC; Pittsburgh Post-Cardiac Amrest Service. The prognostic performance of brain ventricular character-istic differ according to sex, age, and time after cardiac arrest in comatose out-of-hospital cardiac arrest survivors. Resuscitation.2020;154:69-76. doi:10.1016/j.resuscitation.2020.05.031

161. Beekman R, Maciel CB, Ormethset CH, Zhou SE, Galluzzo D, Miyares LC,Torres-Lopez VM, Payavshav S, Mak,A Greer DM,etal.Early head CT in post-cardiac arrest patients: A helpful tool or contributor to self-fulfilling prophecy?Resuscitation.2021;165:68-76. doi: 10.1016/j.resuscitation.2021.06.004

162.Wang GN,Zhang ZM,Chen W,Xu XQ,Zhang JS.Timing of brain comput-ed tomography for predicting neurological prognosis in comatose cardiac arrest survivors: a retrospective observational study. World J Emerg Med.2022;13:349-354.doi:10.5847/wjem.J.1920-8642.2022.080

163.Yeh HF, Ong HN, Lee BC, Huang CH, Huang CC, Chang WT, Chen WU, Tsai MS. The Use of Gray-White-Matter Ratios May Help Predict Survival and Neurological Outcomes in Patients Resuscitation From Out-of-Hospital Cardiac Arrest. J ute Acute Med. 2020;10:77-89. doi:10.1016/j.acsme.202003_10(2).0004

164. Yoon JA, Kang C, Park JS, You Y, Min JH, In YN, Jeong W, Ahn HJ, Lee IH,Jeong HS,et al. Quantitative analysis of early apparent diffusion coefficient values from MRIs for predicting neurological prognosis in survivors of out-of-hospital cardiac arrest: an observational study. Crit Care.2023;27:407.doi:10.1186/s13054-023-04696-z

16. Pereira S, Lee DH, Park JS, Kang C, Lee BK, Yoo IS, Lee IH, Kim M, Lee JG(Yre- to-White Matter Ratio Values in Early Head Computed Tomography(CT) as a Predictor of Neurologic Outcomes in Survivors of Out-of-Hospital Cardiac Arrestes on 2015.88747/jem. Jemmered.2024.03.037

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166.Esilledai CJ,Coppler RJ,Faro JW,Weinser ZM,Clondle JP,Elmer J,Callaway CW; Pittsburgh Post Cardiac Arrest Service. Duration and clinical fea-tures of cardiac arrest predict early credible severe cerebral ada. Resuscitation 2020;153:111-188. doi:10.1016/j.resuscitation:2020.05.049

167. Lopez Soto C, Dragoi L, Heyn C, Kramer A, Pinto R, Adhikari NKJ, Scales DC. Imaging for Neuroprognostication After Cardiac Arrest: Sys-tematic Review and Meta-analysis. Neurocrust Care 2020:206-216. doi: 10.1007/s20128-019-00842-08

168. Oh SH, Park KN, Choi SP, Oh JS, Kim HJ, Youn CS, Kim SH, Chang K,Kim SH. Beyond dichotomy: patterns and amplitudes of SSEPs and neurological outcomes after cardiac arrest. Crit Care. 2019;23:224. doi: 10.1186/s13054-019-2510x

169.J Jang,OH,Sham,N,Yang Ke,HJ HSun,JQ.Chai H,Shun A,NhJ K, Park KN, Kim BS.Prognostic value of phase information of 2D T2*-weighted gradient echo brain imaging in cardiac arrest survivors: A preliminary study. Resuscitation 2019;140:142-149. doi:10.1016/j.resuscitation.2019.05:026.07

170. Park JS,In YN,You YH,Min JH,Ahn HJ,Youo IS,Kim SW,Lee JW,Ryu S,Jeong WL,et al.Ultra-early neurologic outcome prediction of out-of-hospital cardiac arrest survivors using combined diffusion-weighted imaging find-ings and quantitative analysis of apparent diffusion coefficient. Resuscita-tion.2020:148:39-48. doi:10.1016/j.resuscitation.2019.12.021

171. Vanden Berghe S,Cappelle S,De Keyzer F,Peeters R,Couriers K,Depotter A. Van Cauler S, Ameelot K, Dens J, Lemens R, et al. Qualitative and quantitative analysis of diffusion-weighted brain MR imaging in comatose survivors after cardiac arrest. Neuroradiology. 2020;62:1361-1369. doi: 10.1007/s00234-020-02460-6

172.ten M, Moser A, Wagner F, Haenggi M. Performance of the MRI lesion pattern score in predicting neurological outcome after out of hospital car-diac arrest: a retrospective cohort analysis. Crit. Care 2024:28:215. doi: 10.1186/s13054-024-05007-w

173. An C, You Y, Park JS, Min J, Hjeong W, Ahn HJ, Kang C, Yoo I, Cho Y, Ryu S, et al. The cut-off value of a qualitative brain diffusion-weighted image(DWI) scoring system to predict poor neurologic outcome in out-of-hospital cardiac arrest(OHCA) patients after target temperature management. Re-suscitation.2015;157:202-210. doi:10.1016/j.resuscitation.2020.08.130

174. Hirsch KG, Fischbein N, Mlynash M, Kemp S, Bammer R, Eyngorn I, Tong J, Mosecy M, Venkatsubramanian C, Caucfield AF, et al. Prognostic val-ue of diffusion-weighted MRI for post-cardiac arrest coma. Neurology.2020;94:e1684-e1692. doi: 10.1212/WNL.00000000000009289

175. Moon HK,Jang J,Kark PN,Kim SH,Lee BK,Oh SH,Jeung KW,Choi SP,Cho IS,Youn CS. Quantitative analysis of relative volume of low apparent dif-fusion coefficient value can predict neurologic outcome after cardiac arrest. Resuscitation.2018;126:36-42. doi:10.1016/j.resuscitation.2018.02.020

176. Yoon JA, Kang C, Park JS, You Y, Min JH, In YN, Jeong W,Ahn HJ, Jeong HS, Kim YH,et al. Quantitative analysis of apparent diffusion coefficients to predict neurological prognosis in cardiac arrest survivors: an observational derivation and internal-external validation study. Crit Care.2024;28:138. doi:10.1186/s13054-024-04909-z

177. Calabrese E, Gandhi S, Shih J, Otero M, Randazzo D, Hemphill C, Huie R,Talott JF, Amorim E, Parieto-Occital Injury on Diffusion MRI Correlates with Poor Neurologic Outcome following Cardiac Arrest. AJNR Am J Neuro-radiol.2023;44:254-260. doi: 10.3174/ajnr.A7779

ORGAN DONATION AFTER CARDIAC ARREST IN ADULTS

|Recommendations for Organ Donation After Cardiac Arrest in Adults||| |---|---|---| |COR|LOE|Recommendations| |1|B-NR|1. Organ donation should be considered in all adult patients resuscitated from cardiac arrest who meet neurological criteria for death (ie, brain death).| |2|B-NR|2. Organ donation should be considered in all adult patients resuscitated from cardiac arrest before planned withdrawal of life-sustaining therapies.| |1|C-EO|3. Decisions about organ donation should follow local legal and regulatory requirements.| |1|C-EO|4. Organ donation is an important outcome that should be considered in the development and evaluation of systems of care.|

|Recommendations for Organ Donation After Cardiac Arrest in Adults (Continued)|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|C-LD|5. It may be reasonable to consider utilization of organs from adult patients resuscitated with ECPR who remain supported on ECMO and who meet neurological criteria for death (ie, brain death) or for whom withdrawal of life-sustaining therapies is planned.||

Synopsis

Organ transplantation in wait times in the United States are increasing as patients in need of transplant outpace available organs.1 The thousands die annually waiting for transplantation.1 Patients with cardiac arrest make up an important pool of potential donors because cardiac arrest is common and a substantial proportion of those who cannot recover are still able to donate.2-7 However,organ donation is rarely reported as an outcome in car-diac arrest clinical trials or as a metric in large registry data.

Deceased organ donation may occur after death is determined by neurological criteria(donation after brain death) or circulatory criteria(donation after circu-latory death [DCD]). After sudden cardiac arrest, DCD can be pursued in patients with ROSC after planned withdrawal of life-staining therapies and the transi-tion to comfort- oriented care, called controlled DCD,or in patients who fail to achieve ROSC after unsuc-cessful resuscitation, called uncontrolled DCD. Uncon-trolled DCD has unique logistic, ethical, and legal requirements-factors that hinder its widespread appli-cation in many settings.

The role of extracorporeal membrane support in organ donors is complex and evolving. Patients with car-diac arrest may receive extracorporeal membrane sup-port either through ECPR or through having it placed in the postarrest period. Those patients who remain on extracorporeal membrane support and die by brain death or have a planned withdrawal of life-sustaining therapies represent a unique population of potential organ donors.

Recommendation-Specific Supportive Text

1,2. Numerous observational studies demonstrate that allograft function and recipient outcomes are simi-lar when transplanted organs are recovered from patients with cardiac arrest compared with other deceased donors8-14; this holds true for donation after brain death and controlled DCD.

3.Laws and regulations governing the determination of death and organ donation vary not only between countries15,16 but also by state despite efforts to standardize death determined by neurological cri-teria worldwide.15

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4. A 2023 ILCOR CoSTR scientific statement focuses on the importance of increasing organ availability after cardiac arrest.7 It recognizes organ donation as an important outcome of car-diac arrest and emphasizes the importance of research and clinical protocols incorporating this principle. Organ donation after cardiac arrest are directly benefits recipient patients.

5. A 2024 meta-analysis $^{17}$ based mostly on retro-spective observational studies, case reports, and one retrospective analysis of a prospective trial $^{18}$ demonstrated that organs donated from patients who were already on extracorporeal membrane support were viable for transplantation. In a subset of patients receiving ECP, graft survival was high,reaching 89% . The most common organ donated was kidney, followed by liver and heart. The included studies indicate that patients who received ECPR are a potential source of donor organs and that organs donated from patients who received ECPR can have good graft survival.

REFERENCES

1. US Department of Health and Human Services. Organ Procurement and Transplant Network. Accessed January 8,2025. https://optn.trans-plantastrhs.gov/.

2.Elmer J,Molyneaux BJ,Shutterky K,Stuart SA,Callaway CW,Darby JM,Weisberger AR. Organization after resuscitation from cardiac arrest,Re-suscitation.2019;145:63-69. doi: 10.1016/j.resuscitation.2019.10.0013

3.Pilcher D, Gladakis L, Arcia B, Bailey M, Cook D, Cass Y, Opdam H. Esti-mating the Number of Organ Donors in Australian Hospitals-implications for Monitoring Organ Donation Practices. Transplantation. 2015;99:2203-2209. doi: 10.1097/TP0000000000000716

Cheutham OV, Thomas MJ, Hadfield J, O'Higgins F, Mitchell C, Rooney KD. Rates of organ donation in a UK tertiary cardiac arrest centre fol-lowing out-of-hospital cardiac arrest. Resuscitation. 2016;101:41-43. doi: 10.1016/j.resuscitation.2016.01.003

5.Sandroni C,D'Arrigo S,Callaway CW,Cariou A, Dragancea I,Taccone FS,Artononi M. The rate of brain death and organ donation in patients resusciti-tated from cardiac arrest: a systematic review and meta-analysis. Intensive Care Med.2016;42:1661-1671. doi:10.1007/s00134-016-4549-3

6. Elmer J, Weegerber AR, Wallace DJ, Alice DJ, Homei, Stuart, South Park, C. Pudilay, www. Havierk an Callaway CW. Between-hospital variability in organ donation after resuscita-tion from out-of-hospital cardiac arrest. Resuscitation. 2021;167:372-379.10.1016/j.resuscitation.2021.0738

7. Morrison LJ, Sandroni C, Grunau B, Parr M, Macnell F, Perkins GD, Abiki M,Censulo E, Lin S, Neumar RW et al; International Liaison Committee on Re-suscitation: Organ Fundation After/of Hospital Cardiac Arrest: A Scientific Statement From the International Liaison Committee on Resuscitation: Re-suscitation: 2031;190:108964. doi: 10.1016/j.resuscitation.2023.109864.

8.West S, Soar J, Callaway CW. The viability of transplant organs from do-nors who underwent cardiopulmonary resuscitation: A systematic review.Resubuscitation:2016.108:27-33. doi:10.1016/j.resuscitation.2017.06:229

9.Echertíder F, Kitterer D, Dippon J, Paul G, Schwenger V, Latus J. Impact of cardiopulmonary resuscitation on outcome of kidney transplantations from braideband used as gross 65 years. Clin Transplant. 2021;35:e14452. doi:10.1111/ctr.14452

10. Hinzmann J, Grzella S, Lengenfeld T, Pilloketit N, Hummels M, Vahinger HM, Westhoff TH, Viebahn R, Shenker P. Impact of donor cardiopul-monary resuscitation on the outcome of simultaneous pancreas-kidney transplantation-a retrospective study. Transyl Int 2020;33:644-656: doi:10.1111/tri.13588

11. Hoyer DP, Paul A, Saner F, Gallinat A, Mathé Z, Treckmann JW, Schulze M, Kaiser, GM Bayan, Mallom et al. Lett, et al. Safely expanding the donor pool: brain dead donors with history of temporary cardiac arrest. Liver Int 2015;35:1756-1766.1: doi:10.1111/vi.12766

12.Mehdiani A, Immohr MB, Sipahi NF, Boettger C, Dalyanoglu H, Scheiber D,Westenfeld R, Aubin H, Lichtenberg A, Boeken U, et al. Successful Heart Transplantation after Cardiopulmonary Resuscitation of Donors. Thorac Car-diovasc Surg.2021;69:504-510.doi:10.1055/s-0040-1713351

13. Messner F, Etra JW, Yu Y, Massie AB, Jackson KR, Brandacher G,Schneeberger S, Margireter C, Segev DL. Outcomes of simultaneous pan-creas and kidney transplantation based on donor resuscitation. Am J Trans-plant:2020;20:1720-1728. doi: 10.1111/ajt.15808

14. Mohite PN, Zych B, Sabatnikov A, Popov AF, Garcia-Saez D, Patil NP, Koch A, Zeriohu M, Rahmanian PB, Dhar D, et al. Effect of donor cardiac arrest and arrest duration on outcomes of lung transplantation. Clin Transplant.2016;30:421-428. doi: 10.1111/ctr.12704

15. Greer DM, Shemie SD, Lewis A, Torrance S, Varelas P, Goldenberg FD,Bernat JL, Souter M, Topoecuog LA, Alexandrov AW, et al. Determination of Brain Death/Death by Neurologic Criteria: The World Brain Death Project.JAMA 2020;324:1078-1097. doi: 10.1001/jama.2020.11586

16. Etheredge HR. Assessing Global Organ Donation Policies: Opt-In vs Opt-Out. Risk Manag Healthc Policy.2021;14:1985-1998. doi: 10.2147/RMHP.SZ072304

17. Raisci S, Treml B, Innerhofer N, Eckhardt C, Radovanovic Spurnic A,Breitkopf R. Organ Donation from Patients Receiving Extracorporeal Mem-brane Oxygenation: A Systematic Review. J. Cardiothorac Vasc Anesth.2024:38:1531-1538.doi: 10.1053/j.jvca.2024.03.020

18. Smalcova J, Havranek S, Pokorna E, Franek o, Huptych M, Kavalkova P, Pudil J, Rob D, Dusile M, Belohlavek J. Extracorporeal cardiopulmo-nary resuscitation-based approach to refractory out-of-hospital car-diac arrest: A focus onto organ donation, a secondary analysis of a Prague OHCA randomized study. Resuscitation. 2023;193:109993. doi: 10.1016/j.resuscitation.2023.109993

RECOVERY AND SURVORSHIP AFTER CARDIAC ARREST

|Recommendations for Recovery and Survivorship After Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|B-R|1. It is recommended that cardiac arrest survivors and their caregivers have structured assessment treatment/referral for emotional distress after medical stabilization and before hospital dis- charge.|| |2|B-R|1. It is recommended that cardiac arrest survivors have structured assessment treatment/referral for emotional distress after medical stabilization and before hospital dis- charge.|| |3|1|2. It is recommended that cardiac arrest survivors have multimodal rehabilitation assessment and treatment for cognitive,physical,neurological, and cardiopulmonary impairments before hospital dis- charge.|| |4|C-LD|1. It is recommended that cardiac arrest survivors have multidisciplinary dis- charge planning, to include medical and rehabiliti- atative treatment recommendations and return to activity/work expectations.|| |2|B-R|4. Interventions to address health care professional burnout may be beneficial.|| |2|B-LD|5. Debriefings and referral for follow-up for emotional support for lay rescuers, emergency medical services professionals, and hospital-based health care professionals after a cardiac arrest event may be beneficial.||

Synopsis

Survivors of cardiac arrest experience emotional, social,physical, neurological, and cognitive sequelae, which can manifest during or after hospitalization.1,2 Broadly defined,survivorship is the journey from stabilization through re-habilitation, recovery, and societal reintegration.1 Improv-ing cardiac arrest survivorship involves families, health

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care partners, and communities. Caregivers of cardiac arrest survivors also experience emotional and social challenges as they navigate survivorship issues. ${ }^{1,2}$

Optimizing survivorship for survivors and their caregiv-ers involves in-hospital screening, treatment, referral, and postdischarge surveillance of postarrest sequelae.1 Sur-vivorship plans given at discharge can provide direction by including a summary of the inpatient course, individu-alized medical and rehabilitative treatment recommen-dations, and postdischarge recovery expectations.1 All those impacted by cardiac arrest can be powerful advocates for informing community responses to car-diac arrest, tailored interventions, and relevant patient-/family-centered outcomes.1

Finally,lay rescuers, emergency medical services pro-fessionals, and hospital-based health care professionals who care for cardiac arrest patients often experience distress.34 Debriefness after witnessing cardiac arrest events, identifying the natural stressors associated with caring for such patients, and offering well-being inter-ventions or referrals for follow-up mental health ser-vices may provide opportunities to mitigate distress and burnout.

Recommendation-Specific Supportive Text

1. Approximately one fourth of cardiac arrest survi-vors and their caregivers experience emotional distress(including anxiety, depression, and post-traumatic stress).1,5-8 Fatigue is also common and may be related to distress and physical and cogni-tive symptoms.2,9-11 Often, these symptoms begin to manifest during hospitalization and can linger from months to years.79,10

One RCT compared a psychosocial intervention between 2 groups; both groups included survivor-caregiver pairs, but in one group, only the survi-vors received the psychosocial intervention and in the other group, both the survivors and caregivers received the psychosocial intervention.12,13 There were improvements in emotional distress for the survivors in both groups; however, those in the survivor-caregiver intervention group had the great-est benefit. Caregivers in the survivor-caregiver intervention group had more improvements in caregiver burden compared with the caregivers in the survivor-only intervention group.12,13 Two other RCTs in survivors showed improvements in emotional distress in those receiving psychosocial care coordination and referral.

2.Cognitive impairments,particularly in memory,atten-tion, and executive function, are common in cardiac arrest survivors.17-19 Physical, neurological, and car-diopulmonary impairments are also prevalent.10,20-23

One RCT found improved quality of life in survivors enrolled in an early, cognitive-focused screening,self-management, and referral program compared to treatment as usual.24 Three other preliminary tri-als demonstrated feasibility of a residential physi-cal rehabilitation intervention, cardiac rehabilitation,and a telephone-based occupational therapy inter-vention in cardiac arrest survivors, with preliminary benefits in physical, cardiopulmonary, and quality of life outcomes.25-27 The evaluation prior to dis-charge is important to facilitate care coordination and referral.

3. Community reintegration and return to work or other daily activities may be slow and depend on availability of social support and degree of postar rest sequelae.27-31 Survivors and caregivers need direction on managing their postarrest challenges(eg, guidance on possibility of experiencing psy-chological, cognitive, physical, neurological, and cardiopulmonary symptoms and which profession-als to seek out should they arise) and returning to daily activities.1,2

4. Burnout among health care professionals is com-mon,32 is not unique to those who provide care for patients with cardiac arrest, and is often character-ized by emotional exhaustion, depersonalization/cynicism, and reduced sense of personal accom-plishment.33 Burnout negatively impacts health care professionals' productivity(eg, absenteeism,turnover) and patient care(eg, reduced patient satisfaction and increased clinician errors).34,35

Seven RCTs targeting burnout in health care professionals all led to some improvement in at least one dimension of burnout or mental health outcome. Intervention mechanisms varied consid-erably,including yoga,mindfulness,gratitude jour-naling, various other positive psychology exercises,and individualized professional coaching. Benefits included improved well-being, work engagement,quality of life, perceived stress, and depressive and anxiety symptoms.36-42

Although these results are promising, variability in intervention methods and outcome measures,considerable attrition, and high risk of bias inher-ent in behavioral trials limit the degree to which any single well-being intervention method can be recommended.

5. Rescuers and hospital-based health care profes-sionals may experience emotional distress caring for a cardiac arrest patient.3,4,43,44 Team debriefings may allow for quality improvement as well as rec-ognition of the natural stressors associated with caring for a cardiac arrest patient. In one qualita-tive study of lay rescuers and one nonrandomized study of emergency department professionals,participants reported benefitting emotionally from

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debriefings45,46; however, a scoping review found that nurses may prefer to not discuss distress dur-ing debriefings and rather to pursue support later.43

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2.Douma VL M Myhre, C Ali S, Graham TAD, Ruther K, Brindley PG, Dainty KN, Smith KE, Montgomery CL, Dentet L, et al. What are the Care Needs of Families Experiencing Sudden Cardiac Arrest? A Servor and Family-Performance Systematic Review, Qualitative Meta-Synthesis, and Clinical Practice Recommendations. J. Emerg Nurs. 2023;49:912-950. doi:10.1016/j.jenj.2023.07001

Spencer S. Arnold JPan, Osborn M, Georgiou A. The presence of psy-chological trauma symptoms in resuscitation providers and an explo-ration of debriefing practices. Resuscitation: 2019;142:175-181. doi:10.1016/j.resuscitation.2019.06.280

4. Mathiesen WT, Bjershol CA, Braut GS, Soreide E. Reactions and coping strategies in lay rescers who have provided CPR to out-of-hospital car-diac arrest victims: a qualitative study. BMJ Open. 2016;6:e010671. doi:10.1136/bmjpen-2015-061057

Ya. Yuey CTL, SeH, Lim WS, Wang RK, Huan MK, Pek PP, Tan BY, Ong ME,HNg,QX,Ho AFW.Prevalence of anxiety, depression, and post-traumatic stress disorder after cardiac arrest: A systematic review and meta-analysis.Resuscitation 2022;170:82-91.doi:10.1016/j.resuscitation.2021.11.023

6.Chen X,Li D,He L,Yang W,Dai M,Lan L,Diao D,Zou L,Yao P,Cao Y.The prevalence of anxiety and depression in cardiac arrest survivors: A sys-tematic review and meta-analysis. Gen Hosp Psychiatry.2023:83:8-19. doi:10.1016/j.genoshpsych.2023.03.013

7. Precutius AM, Flickinger KL, Coppler RJ, Ratay C, Doshi AA, Perman SM,anceau AM,Elmer J. Protective positive psychology factors and emo-tional distress after cardiac arrest. Resuscitation. 2023:188910846.

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9.Blenown Nordstrom E, Vestberg S, Vald L, Mion, S. Segrimen M,Ulén S, Bro-Jeppesen J, Friberg H, Heimburg K, Grejs AM, et al. Neu-ropsychological outcome after cardiac arrest's results from a sub-study of the targeted hypothermia versus targeted normothery out-out-of-hospital cardiac arrest(TTM) trial. Crit Care. 2023;27:328. doi: 10.1186/31054-03-024617-0

10. Flickinger K, Larrasm, Iopke R, M93, Lorkor M, Holm M, Skidimore E,Callaway A, Cittenberger JC. One-year outcomes in individual domains of the cerebral performance category extended. Resuscit. Plus 2021:81:00184.

11.Joshi VL,Tang LH,Mikkelsen TEb,Nielsen ZJF,Znckernagel L,Borergard B,Agarwal S,Kjaer Ellr Ason,Yis H,Kraghak K M,et al.Hees time healpy,psychological, cognitive, and disability problems in people who experience an out-of-hospital cardiac arrest? Results from the DANCAS survey study, Re-suscitation.2023;182:109639. doi:10.1016/j.resuscitation.2022.11.005

12. Alud JP, Thompson EA, Dougherty CM. Social cognitive intervention fol-lowing an initial implantable cardioverder 格ilibrator: Better treatment re-sponse for secondary versus primary prevention. Pacing Clin Electrophysio 2020;43:974-982.doi:10.1111/pace.13929

13.Dougherty KL,Emson PE,Kudenhckur,El. Pair plus partner trial: A randomized controlled trial of 2 interventions to improve outcomes after an initial implantable cardioverelf-brillator. Heart Rhythm 2019;16:4535-459:10.1016/j.hrthm.2018.10.0011

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Disclosures

Appendix 1. Writing Group Disclosures

|Writing group member|Employment|Research grant|Other research support|Speakers bureau/nonoraria|Expert witness|Ownership interest|Consultant/ advisory board|Other| |---|---|---|---|---|---|---|---|---| |Karen G. Hirsch|Stanford University|NIH*|None|None|None|None|None|None| |Jon C. Rittenberger|Guthrie Medical Center|None|None|None|Cipriani& Wanner: Interner: Defense expertt|None|UpToDate*|None| |Edilberto Amorim|University of California, San Francisco, Weill Institute for Neurosciences|NINDSt; American Heart Associationt; Hellman Foundation; Zoll Foundation; CURE Epilepsyst; Regents of the University of Californiat; Department of Defenset; Cures Within Reacht; Department of Defenset;NIHt|None|None|None|None|None|None| |Patrick J. Coppler|University of Pittsburgh|NIH*|None|None|None|None|None|None| |Ian R. Drennan|University of Toronto Ornge Critical Care and Transport Medicine Sunnybrook Health Sciences (Canada)|ZOLLt|None|ZOLLt|None|None|None|None| |Andrea Elliott|Regents of the University of Minnesota|None|None|None|None|None|None|None| |Alexandra June Gordon|Stanford University|None|None|None|None|None|None|None| |Jacob C. Jentzer|Mayo Clinic|None|None|None|None|None|None|None| |Nicholas J. Johnson|University of Toronto Washington/Harborview Medical Center|NIHt; American Heart Associationt|None|None|None|None|Neuroptics, Inc*|None|

$\text{(Continued)}$

Hirsch et al

Post-Cardiac Arrest Care: 2025 AHA Guidelines for CPR and ECC

Appendix 1. Continued

|Writing group member|Employment|Research grant|Other research support|Speakers bureau/ honoraria|Expert fitness|Ownership interest|Consultant/ advisory board|Other| |---|---|---|---|---|---|---|---|---| |Ari Moskowitz|Montefiore Medical Center|NIH/NHLBlt; American Heart Associationt|None|None|Expert Winess*|None|Aquostive Therapeutics*|| |Bryn E. Mumma|University of California Davis|None|None|None|None|None|None|None| |Alexander M. Presciuti|Massachusetts General Hospital|National Center for Complementary and Integrative Healtht; Neurocritical Care Society*|None|None|None|None|Cardiac arrest survivor alliance*|None| |Amber J. Rodriguez|American Heart Association National Center|None|None|None|None|None|None|None| |Albert Yen|University of California|None|None|None|None|None|None|None|

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"mostest" if it is less than"significant" under the preceding definition.*Modest.

*Modest.

tSignificant.

包

Appendix 2. Reviewer Disclosures

|Reviewer|Employment|Research grant|Other research support|Speakers bureau/ honoraria|Expert witness|Ownership interest|Consultant/ advisory board|Other| |---|---|---|---|---|---|---|---|---| |Justin N. Carlson|Allegheny Health Network|None|None|None|None|None|None|None| |Romergryko G. Geocadin|Johns Hopkins University School of Medicine|NIH (Preclinical and clinical research on cardiac arrest brain injury)t|None|None|Medicological Consulting|None|None|None| |Teresa L. May|MaineHealth|NINDS(PRECICEAP co-l)*|None|None|None|None|None|None| |Mary Ann Peberdy|Virginia Commonwealth University|American Heart Association (drone delivery of AEDs)*|None|None|None|None|None|None| |Janice Zimmerman|The Methodist Hospital|None|None|None|None|None|None|None| |$$\text{ Zimmerman}$$|Physician Organization|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.