2025+AHA心肺复苏与心血管急救指南-第8部分:儿童高级生命支持
PREAMBLE
Every year, more than 7000 out-of-hospital cardiac ar-rests(OHCA) and approximately 20000 in-hospital car-diac arrests(IHCA) occur in infants and children across the United States.1-3 In the United States, approximately 80% of emergency medical services-treated OHCA occur in the home.4 In contrast, the majority of IHCA arrests in infants and children occur in the intensive care unit (ICU)environment with incidence rates ranging from 1.8%for general pediatric ICU admissions(2011-2013)5 to 3.1% in pediatric cardiac ICUs, although variability exists between centers.6 Understanding the full spectrum of neurologic outcomes during the weeks to months after cardiac arrest across the pediatric age spectrum is lim-ited by variability in reporting metrics and time to follow-up across studies. Survival to hospital discharge rates for OHCA range from 6% to 38%.478 Although data on fa-vorable neurologic outcomes among survivors of OHCA are limited, the most recent Cardiac Arrest Registry to Enhance Survival data demonstrate rates of 5.7% in
infants to 12.8% in older children.4 In contrast, survival to hospital discharge for IHCA ranges from 38% for pulseless cardiac arrest to 66% for nonpulseless cardiac arrest.6,9 Definitions of neurologic outcome vary across studies, and neurologic outcomes are defined by differ-ent measures(eg,Vineland Adaptive Behavioral Score or Pediatric Cerebral Performance Category[PCPC]) and different thresholds. While guideline recommendations are based on review of combined data, readers should pay attention to individual study measures when look-ing for detailed information. Grossly favorable neurologic outcomes in survivors of IHCA based on the PCPC scor-ing system are much higher than OHCA neurological outcome rates at approximately 64% to 89%.5,10
These guidelines contain recommendations for PALS,excluding newborn infants, and are based on the best available resuscitation science. The Chain of Survival requires coordinated efforts from medical profession-als in various disciplines, as well as from lay responders,emergency dispatchers, and first responders in the case of OHCA. Pediatric guidance and recommendations are provided in“Part 6: Pediatric Basic Life Support.”11 Rec-ommendations for resuscitation training are in“Part 12:Resuscitation Education Science."12 Recommendations about systems of care are in“Part 4: Systems of Care.”13 Recommendations for special circumstances are in“Part 10: Special Circumstances."14 Considerations around ethics are provided in“Part 3: Ethics.”15
INTRODUCTION
Scope of Guidelines
These guidelines are intended to be a resource for health care professionals to identify and treat infants and chil-dren in the prearrest, intra-arrest, and post-cardiac ar-rest states. These apply to infants and children in multiple settings: the community, prehospital, and hospital envi-ronments. Prearrest, intra-arrest, and post-cardiac arrest topics are reviewed, including cardiac arrest in special circumstances, such as infants and children with con-genital heart disease.
For the purposes of the PALS guidelines, pediatric patients are infants and children up to 18 years of age.In contrast, pediatric basic life support guidelines apply to infants and children without signs of puberty. Nei-ther pediatric advanced nor basic life support guidelines address the resuscitation of newborn infants, who are transitioning from a fluid-filled to an air-filled environ-ment. Resuscitation of the newborn infant is addressed in "Part 5: Neonatal Resuscitation."16 Although pediat-ric basic and advanced life support guidelines may be applied to newborn infants younger than 28 days of age based on pathophysiology and institutional practice,neo-natal guidelines should be followed at birth to address unique aspects of transitional physiology. ${}^{17}$
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# Organization of the Pediatric Writing Committee
The PALS Writing Group consisted of pediatric clini-cians from the American Heart Association (AHA) and the American Academy of Pediatrics (AAP) including in-tensivists, cardiac intensivists, cardiologists, emergency medicine physicians, and nurses. A call for candidates was distributed to the AHA Emergency Cardiovascular Care (ECC) Committee and AAP subject matter ex-perts, and volunteers with recognized expertise in pedi-atric resuscitation were nominated by the writing group co-chairs. Writing group members were selected by the AHA ECC Science Subcommittee and AAP Executive Committee and then approved by the AHA Manuscript Oversight Committee. The AHA and AAP have rigorous conflict of interest policies and procedures to minimize the risk of bias or improper influence during the de-velopment of the guidelines. Before their appointment,writing group members and peer reviewers disclosed all commercial relationships and other potential (includ-ing intellectual) conflicts. Writing group members whose research informed guideline recommendations were re-quired to declare those conflicts during discussions and abstain from voting on those specific recommendations.This process is described more fully in "Part 2: Evidence Evaluation and Guidelines Development"18 Comprehensive review of disclosure information for writing group members and peer reviewers is listed in Appendixes 1 and 2.
METHODOLOGY AND EVIDENCE REVIEW
These pediatric guidelines are based on the extensive evidence evaluation performed in conjunction with the In-ternational Liaison Committee on Resuscitation(ILCOR)and affiliated ILCOR member councils. Three different types of evidence reviews(systematic reviews, scoping reviews, and evidence updates) were used in the 2025 process. This process is described more fully in“Part 2:Evidence Evaluation and Guidelines Development."18
Class of Recommendation and Level of Evidence
The writing group reviewed all relevant and current AHA guidelines for CPR and ECC and all relevant ILCOR con-sensus on CPR and ECC science with treatment rec-ommendations from 2020, 2022, 2023, and 2024.19-22 Evidence and recommendations were reviewed to deter-mine if current guidelines should be reaffirmed, revised,or retired or if new recommendations were needed. The writing group then drafted, reviewed, and approved rec-ommendations, assigning a class of recommendation(COR;ie, strength) and level of evidence (LOE;ie,quality,certainty) to each. Criteria for each COR and LOE are described in Table 1.
Guideline Structure
The 2025 Guidelines are organized in discrete modules of information on specific topics or management is-sues. ${}^{23}$ Each modular knowledge chunk includes a table of recommendations using standard AHA nomenclature of COR and LOE. Recommendations are presented in or-der of COR: most potential benefit (Class 1), followed by lesser certainty of benefit (Class 2), and finally no benefit or potential for harm (Class 3). Following the COR, rec-ommendations are ordered by the certainty of supporting LOE: Level A (high-quality randomized controlled trials)to Level C-EO (expert opinion). This order does not re-flect the order in which care should be provided.
A brief synopsis is provided to put the recommenda-tions 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, illustrations are included.Hyperlinked references are provided to facilitate quick access and review.
Document Review and Approval
The writing group consists of AHA and AAP representa-tives who voted on and approved all guideline recom-mendations. The guideline was submitted for blinded peer review to 10 subject matter experts nominated by the AHA and AAP. Before their appointment, all peer reviewers were required to disclose relationships with industry and any other conflicts of interest, and all dis-closures were reviewed by AHA staff. The guideline was also reviewed and approved for publication by the AHA Science Advisory and Coordinating Committee, the AHA Executive Committee, and the AAP Board of Directors.Comprehensive disclosure information for peer review-ers is listed in Appendixes 1 and 2.
These recommendations supersede the last full set of AHA recommendations for PALS24 made in 2020 unless otherwise specified. For topics that did not undergo full evidence review by the 2025 writing group,recommendations, recommendation supportive text, and references from the 2020 pediatric basic and advanced life support guidelines24 were not updated and were car-ried over and remain as the current guidelines for 2025.These topics are noted within the synopsis of their respective sections.
REFERENCES
1. Atkins DL, Everson-Stewart S, Sears GK, Daya M, Osmond MH, Warden CR, Berg RA; Resuscitation Outcomes Consortium Investigators. Epide-miology and outcomes from out-of-hospital cardiac arrest in children: the Resuscitation Outcomes Consortium Epistry-Cardiac Arrest. Circulation.2009,119:1484-1491. doi: 10.1161/CIRCULATIONAHA.108.802678
2.Knudson JD,Neish SR,Cabrera AG,Lowry AW,Shamszad P,Morales DL,Graves DE,Williams EA,Rossano JW. Prevalence and outcomes of pediatric in-hospital cardiopulmonary resuscitation in the United States: an analysis
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Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care(Updated December 2024)*
CLASS(STRENGTH) OF RECOMMENDATION
Class 1(STRONG)
Benefit >>> Risk
Suggested phrases for writing recommendations:
• Is recommended
- Is indicated/useful/effective/beneficial
Should be performed/administered/other
•Comparative-Effectiveness Phrases\dagger:
- 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$
- 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
$\cdot$ 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\# 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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of the Kids' Inpatient Database. Crit Care Med 2012;40:2940-2944. doi: 10.1097/CC006/03b1823873e
3. Holmberg MJ, Ross CE, Fitzaurma GM, Chan PS, Duval-Anould J,Grosseussre AV, Yankama T, Donnino MW, Andersen LW Annual inci-dence of adult and pediatric in-hospital cardiac arrest in the United States.Circ Cardiovasc Qual Outcomes.2019;12:e005580.
4. Martin SS,Aday Almazroz,G. Anderson CAM, Arora A P, Avery C,Baker-Smith CM, Barone Gibs B, Beaton AZ, Boehme AM, AK et al; Ameri-Can Heart Association Council on Epidemiology and Prevention Staistics Committee and Stroke Statistics Subcommittee. 2024 Heart Disease and Stroke Statistics: A Report of US and Global Data From the American Heart Association. Circulation. 2024:149e347-e913.doi: 1011.161/CIR/00000000000012000
5. Berg RA,Nadkarni VM,Clark AE,Amerol F,Meert K,Harrison RE,Newth CJ,Sutton RM, Wessel DL, Berger JT et al; Eunce Kennyellur Shriver National Institute of Child Health and Human Development Collaborative Pediatric Critical Care Research Network. Incidence and Outcomes of Cardiopul-monary Resuscitation in PICUs. Certif Med Med 2016;44:798-808 doi:10.1091/CC/000000000000001484
6. Alten JA, Klugman D, Raymond TT, Cooper DS, Donohue JE, Zhang W,Pasquali SK, GAes MG. Epidemiology and Outcomes of Cardiac Invasive in Pediatric Acric. Pediatrics Care Med. 2017;18:935-943. doi: 10.1097/PCC/00000000000001273
7. Moderel SW, Silverstein FS, Holubkov R, Slomine BS, Christensen JR,Nadkarni VM, Meert KL, Clark AE, Browning, B Pemberton VL, et al.;THAPCA Trial Investigators. Therapeutic hypothemia after other au-thol'hospital cardiac arrest in children. N Engl J Med.2015;372:1898-1908. doi:10.1056/NEJMOa1411480
8. Cardiac ARestistry to Enhance Survival. CARE home page. Accessed February 28,2025.https://myares.net/
9.Holmberg MU, Wberg S, Ross CE, Kleinman, M.Roehler-Nielsen AK,Donnino MW, Anders LW. Trends in survival after in-hospital cardiac arrest in the United States. Circulation. 2019;140:1398-1408. doi: 10.1161/CIRCULATIONAHA.1190.14676
10. Del Castillo J, Lopez-Herce J, Canadas S, Matoros M, Rodriguez-Nunez A, Rodriguez-Calvo A, Carrillo A; Iberoamican Pediatric Cardiac Arrest Study Network RIEPECI Cardiac arrest and resuscitation in the pediatric intensive care unit: a prospective multicenter multinational study. Resuscita-tion.2014;85:1380-1386. doi:10.1016/j.resuscitation.2014.06.024
11oyner BL, Dewan M, Bavare de A, Caen A, DiMaria K, Donirof-ODman J,Fosse G, Haskell S, Mahgoub M, Meckler G, et al. Part 6-Diatric Sacl life Support:2025 American Heart Association and American Adaem-ency of Pediatrics Guidelines for DicardiomyResuscitation and Emergency Cardiovascular Care. Circulation. 2025;152:S442-S447 doi:10.1161/CIR.00000000000001370
12. Donoghue A, Auerbach M, Banerjee A, Blewer A, Cheng A, Kadlec K, Lin Y, Diederich E, Sawyer T, Stallings D, et al. Part 12: Resuscitation Educa-tion Science: 2025 American Heart Association Guidelines for Cardio- pulmonary Resuscitation and Emergency Cardiovascular Care. Circulation.2025;152:S719-S750.doi:10.1161/CIR.000000000000001374
13.deZufian C, Cabasá J, Buckley JR, Cash RE, Grove RP, Drennan IR,Mahgoub M, Mannarino CN, May T, Salcido DD, et al. Part 4: Systems of Care: 2025 American Heart Association Guidelines for Cardiou-monary Resuscitation and Emergency Cardiovascular Care. Circulation.2025;152:S353-S384. doi: 10.1016/C1/000000000000001378
14. Cao D,Arens AM,Show LSaster SR,Hoffman RS,Lagina AT,Lavones E.J,Patil KD, Sutherland, LD,Tjissen JA,et al Part 10; adult and pediatric special circumstances of resuscitation: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Cir-culation.2025;152:S578-S672. doi:10.1011/CIR.00000000000001378
15.Elimer J, Alkins DL, Daya MR, Del Rosi M, Fry JT, Henderson CM,Lewis-Newmy, M ADrigal NR, Mac Orano JP,et al Part 3: Ethics:2025 American Heart Association Guidelines for Cardiopul-1161/CIR.000000000000001371 S2025 American Heart Association Guidelines for Cardiopulmonary Resus-5325-10.1161/CIR.00000000000001371
16. Lee HC, Strand ML, Finan E, Illuzzi J, Kamath-Rayne BD, Kapadia V,Mahgoub M,Niemeyer S, Schxneynder S. Schıomizer GM, et al Part S 5: Neonatal Resuscitation: 2025 American Heart Association and American Academy of Pediatrics Guidelines for Cardioplunary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025;152:S385-S423. doi:10.1161/CIR.00000000000001367
17. Sawyer, McBride, ME Aadaria, P.Vale, LAakshminirushusa, AIi,Nall Marsh,Schmolmer,KadleKD,et al.Considerations on the Use of Neonatal and Pediatric Resuscitation Guidelines for Hospitalized Noo rates and Infants: on behalf of the American Heart Association Emergency
Cardiovascular Care Committee and the American Academy of Pediatrics. Pediatrics.2024;153e2023064681.doi:10.1542/peds.2023-064681
10. Panchal AR,Bartos JA,Webckoff MH,Drennan IR,Mahgoub M,Schexnayder SM, Rodriguez AJ,Sasson C, Wright JI, Brooks SC, et al. Part 2: Evi-dence Evaluation and Guidelines Development: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emer-gency Cardiovascular Care. Circulation 2025;152:S313-S322. doi: 10.1161/C.IR.00000000000000000000000000000000000000000000000
19.Wyckoff MH,Greif R,Moley PT,Ng KC,Olasveengen TM,Singletary EM,Soraj Cheng, A Drennan IR, Liley HG,et al. 2022 International Consen-sus on cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations: Summary From the Basic Life Support;Advanced Life Sitter Support; Pediatric Life Support; Neonatal Life Sup-port; Education, Implementation, and Teams; and First Aid Task Forces. Re-suscitation;2022;181:208-288. doi:10.1016/j.resuscitation.2022.10.005
20. Greif R, Bray JE, Djarr T, Drennan IR, Liley HG, Ng KC, Cheng A, Douma MJ, Scholefield BR, Smyth M, et al. 2024 International Consensus on Car-diopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations: Summary From the Basic Life Support;Dwanced Life Support; Pediatr Res. Nonal and Early Resuscitation: Summary From the Basic Life Support;Advanced Life Support; Pediatric Life Support; Neonatal Life Support; Edu-cation, Implementation, and Teams; and First Aid Task Forces. Circulation;2024;150e580-e687.doi: 10.1161/CIR.00000000000001288
21. Maconochie IK,Aickin R,Hazinski MF,Atkins DL,Bingham R,Couto TB,Gueruian AG,Nadkari VM,Ng KC,Nuthall GA,et al; Pediatric Life Sup-port Collaborators. Pediatric Life Support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Sci-ence with Treatment Recommendations. Resuscitation. 2020;156:A120-A155. doi: 10.1016/j.resuscitation.2020.09.013
22. Bergs KM,BRJE.Ng KC,Liley HG,Greif R,Carlson JN,Morley PT,Drennan IR,Smyth M,Scholefield B,et al.;Collaborators.2023 International Consen-sus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations: Summary From the Basic Life Support; Advanced Life Support; Pediatric Life Support; Neonatal Life Sup-port; Education,Implementation, and Teams; and First Aid Task Forces. Cir-culation.2023;18e87-18e87-280. doi:10.1161/CIR.00000000000001179
23. 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/1CIR/000000000000000000000000000000000000000000000000000000000000000000000
24. Topian JJ, Raymond TT, Atkins D, Chan M, Duff JP, Joyner BL Jr., Lasa JJ, Lavonas EJ, Levy A, Mahgoub M, et al; Pediatric Basic and Advanced Life Support Collaborators. Part 4: pediatric advanced life support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020;142:S469-S523.doi: 10.1161/CIR000000000000000000000000000000000000000
Major Concepts
The epidemiology, pathophysiology, and common etiolo-gies of pediatric cardiac arrest are distinct from adult and neonatal cardiac arrest. Cardiac arrest in infants and children does not usually result from a primary cardiac cause; rather, it is most frequently the result of progres-sive respiratory failure or shock. In these patients, a vari-able period of physiologic deterioration ultimately leads to cardiac arrest. Among children with congenital and acquired heart disease, cardiac arrest is more often re-lated to underlying cardiac disease although the etiology is rarely related to coronary insufficiency or ischemia as is commonly observed in the adult population.
Outcomes for pediatric IHCA improved dramatically between 2000 and 2009.1 Subsequent reports of tempo-ral changes in rates of survival to hospital discharge have been variable with marginal improvements.2 Data from the Get With the Guidelines-Resuscitation Registry, a large
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 Figure 1. Cardiac Arrest Chain of Survival.
multicenter, hospital-based cardiac arrest registry, show that survival to hospital discharge from pulseless pediat-ric cardiac arrest increased from 19% in 2000 and 44%in 2022.3 Survival increased on average 0.67% per year and then plateaued in 2010.2 New directions of research and therapy may be required to improve cardiac arrest survival. In addition, more cardiac arrest events now occur in an ICU setting, which suggests that patients at risk for cardiac arrest are being identified sooner and transferred to a higher level of care before cardiac arrest.2,4
Survival rates from OHCA remain less encouraging.In a recent analysis of the Cardiac Arrest Registry to Enhance Survival, a multicenter OHCA registry, annual survival to hospital discharge of pediatric OHCA through 2022 ranged from 6.6% for infants younger than 1 year of age up to 17.3% for children 13 to 18 years of age.3 Survival rates have increased since earlier data from the Resuscitation Outcomes Consortium Epidemiologi-cal Registry demonstrated survival rates from 3.3% for infants<1 year of age to 8.9% for children 13 to 18 years of age.5 In this registry, survival from OHCA was higher in regions with more arrests that were witnessed by emergency medical services and with higher lay responder CPR rates, stressing the importance of early recognition and treatment of these patients.6
As survival rates from pediatric cardiac arrest have increased, there has been a shift in focus to neurodevel-opmental, physical, and emotional outcomes of survivors.Studies demonstrate that a quarter of patients with favor-able outcomes have global cognitive impairment and that 85% of older children who were reported to have favor-able outcomes have selective neuropsychological defi-cits at 1-year follow-up. ${ }^{7}$
The Cardiac Arrest Chain of Survival
Historically, cardiac arrest care has largely focused on the management of the cardiac arrest itself, highlighting high-quality CPR, early defibrillation, and effective teamwork.However, there are aspects of prerest and post-cardiac arrest care that are critical to improve outcomes. As pedi-atric IHCA survival rates have plateaued, ${ }^{2}$ the prevention of cardiac arrest becomes even more important. IHCA prevention includes early recognition and treatment of
<EndOfPara>cardiac arrest, such as children undergoing high-risk pro-cedures(eg, infants undergoing cardiac surgery or cath-eterization procedures), children with high-risk diagnoses(eg, shock, pulmonary hypertension, or acute respiratory distress syndrome), and children with severely abnormal vital signs or other signs of deterioration. In the out-of-hospital environment, lay responder CPR training, sudden unexpected infant death prevention, safety initiatives(eg,bike helmet laws), and early access to emergency care are imperative. When OHCA occurs, early lay responder CPR is critical in improving outcomes.
Following resuscitation from cardiac arrest, management of the post-cardiac arrest syndrome(which may include brain dysfunction, myocardial dysfunction with low cardiac output, and ischemia/reperfusion injury) is important to avoid known contributors to secondary injury, such as hypo-tension. ${ }^{89}$ There is recognition of growing differential use of the terms return of spontaneous circulation(ROSC) versus return of circulation(ROC) in the literature. For the purposes of these guidelines, after CPR, when ROC is achieved by native cardiac function, we use ROSC; when it has been achieved by either mechanical support(eg, extracorporeal membrane oxygenation, ECMO) or native cardiac function,we use ROC.Accurate neuroprognostication is important to guide caregiver discussions and decision-making. ${ }^{10}$ Finally,given the high risk of neurodevelopmental impairment in cardiac arrest survivors, early referral for rehabilitation assessment and intervention is key.
A single Cardiac Arrest Chain of Survival (Figure 1)that supports the paradigm of prevention and early rec-ognition through recovery after cardiac arrest has now been standardized across infants, children, and adults(outside of neonatal care).
REFERENCES
1.$\text{Girotra S, Spertus JA, Li Y, Berg RA, Nadkarni VM, Chan PS; on behalf}$of the American Heart Association Get With the Guidelines-Resuscita-tion Investigators. Survival trends in pediatric in-hospital cardiac arrests: an analysis from Get With the Guidelines-Resuscitation. Circ Cardiovasc Qual Outcomes.2013;6:42-49. doi: 10.1161/CIRCOUTCOMES.112,967968
2. Holmberg MJ, Wiberg S, Ross CE, Kleinman M, Hoeyer-Nielsen AK,Donnino MW, Andersen LW. Trends in survival after pediatric in-hospital cardiac arrest in the United States. Circulation. 2019;140:1398-1408. doi:10.1161/CIRCULATIONAHA.119.04.1667
3. Martin SS, Aday AW, Almarozoo ZI, Anderson CAM, Arora P, Avery CL, Baker-Smith CM, Barone Gibbs B, Beaton AZ, Boehme AK, et al;
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Pediatric Advanced Life Support: 2025 AHA/AAP Guidelines for CPR and ECC
American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Co242 Heart Disease and Stroke Statistics: A Report of US and Global Data From the American Heart Association. Circulation. 2024;149a347-8973.dol:10.1161/CIR.000000000000001209
4. Berg RA, Sutton RM, Holubkov R, Nicholson CE, Dean JM, Harrison R,Heidemann S, Moer K, Nethw C, Moler F, et al; Eunice Kennedy Shriver National Institute of Child Health and Human Development Collaborative Pediatric Critical Care Research Network and for the American Heart As-sociation's Get With the Guidelines-Resuscitation(formerly, the National Registry of Cardiopulmonary Resuscitation) Investigators. Ratio of PICU versus cardipulmonary resuscitation events is increasing. Opti Care Med 2013;41:22992-2297.12:099.107/1.CYC/0.06b0.13e31828cf0.06
5. Atkins DL, Everson-Stewart S, Sears G, Daya M, Osmond MH, Warden CR, Berg RA; Resuscitation Outcomes Consortium Investigators. Epide-miology and outcomes from out-of-hospital cardiac arrest in children: the Resuscitation Outcomes Consortium Epistry-Cardiac Arrest. Circulation 2009;119:1484-1491.doi:1011.166/CIRCULATIONAHA.108.02678
6. Fink EL, Prince DK, Kaltman JR, Atkins DL, Austin M, Warden C, Hutchison,J Daya M, Goldberg S, Herren H, et al.; Resuscitation Outcomes Con-sortum. Unchanged pediatric out-of-hospital cardiac arrest in incidence and survival rates with regional variation in North America. Resuscitation.2016;107:121-128. doi:10.1016/j/resuscitation.2016;07:244
7. Slorine SBS, Silverstein FS, Christensen JS, Page K, Holubkov R, Dean JM,Moler FW. Neuropsychological outcomes of 11 year after pediatric cardiac arrest: secondary analysis of 2 randomized clinical trials. JAMA Neu-rot.2018;75:1502-1510. doi: 10.1001/jamanoeur.2018.2628
8. Topjian AA, de Caen A, Wainwright MS, Abella BS, Abend NS, Atkins Dle, Bembea MM, Fink EL, Guerguan RM, Haskell, SE et al. Pedi-atic post-cardiac arrest care: a scientific statement from the Ameri-can Heart Association. Circulation. 2019;140:e194-e233. doi: 10.1161/CR.0000000000000697
9. Laverriere EK, Polansky M, French B, Nadkarni VM, Berg RA, Topjian AA. Association of duration of hypotension with survival after pedi-atic cardiac arrest. Pediatr Crit Care Med. 2020;21:143-149. doi:10.1097/PCC.00000000000002119
10. Scholefeld BR, Tijssen J, Ganesan SL, Kool M, Couto TB, Topjian A, Atkins DL, Acworth J, McDevitt W, Laughlin S, et al. Prediction of good neurologi-cal outcome after return of circulation following paediatric cardiac arrest: a systematic review and meta-analysis. Resuscitation. 2024;207:110483.doi:10.1016/j.resuscitation.2024.110483
VENTILATION AND ADVANCED AIRWAY STRATEGIES DURING CPR
|Recommendations for Ventilation and Advanced Airway Strategies During CPR||| |---|---|---| |COR|LOE|Recommendations| |2a|C-LD|1. In infants and children with out-of-hospital cardiac arrest, it is reasonable to perform bag -mask ventilation rather than advanced airway interventions (tracheal intubation or supraglottic airway [SGA] placement).| |2b|C-LD|2. In infants and children with in-hospital cardiac arrest who do not have an advanced airway in place, it may be reasonable to perform bag -mask ventilation or advanced airway interventions (tracheal intubation or supraglottic airway [SGA] placement).| |2b|C-LD|3. When performing CPR in infants and children with an advanced airway in place, it may be reasonable to perform bag -mask ventilation rate range of 20-30 breaths/ min(1 breath every 2-3 s), accounting for age and clinical characteristics. Hyperventilation may compromise hemodynamics.|
Synopsis
Most pediatric IHCA and OHCA are precipitated by respi-ratory deterioration or shock. Thus, airway management
<EndOfPara>and effective ventilation are fundamental components of pediatric resuscitation. Although most patients can be successfully ventilated with bag-mask ventilation, this method requires interruptions in chest compressions and is associated with risk of aspiration and barotrauma. Ad-vanced airway interventions, such as tracheal intubation or SGA placement, may improve ventilation, reduce the risk of aspiration, and enable uninterrupted compres-sion delivery. However, airway placement may interrupt the delivery of compressions or result in a malpositioned device, with catastrophic consequences if unrecognized.Advanced airway placement requires specialized equip-ment and skilled health care professionals and may be difficult for professionals who do not routinely intubate children.
In children receiving CPR with an advanced airway in place, provision of adequate minute ventilation while avoiding hyperventilation and associated deleterious hemodynamic effects is critical. There are limited data regarding ventilation rates during pediatric CPR and determination of optimal ventilation rates deserves fur-ther study. Other components of intra-arrest ventilation,such as the appropriate peak end-expiratory pressure or tidal volume, have not been studied extensively.
Recommendation-Specific Supportive Text
1. A clinical trial showed that tracheal intubation and bag-mask ventilation achieve similar rates of sur-vival with good neurologic function in pediatric patients with OHCA.1 Three propensity-matched retrospective studies show similar rates of sur-vival to discharge and survival with good neuro-logic function when comparing advanced airway placement(tracheal intubation or SGA) with bag-mask ventilation in pediatric OHCA.2-4 A fourth propensity-matched study demonstrated lower 1-month survival and survival with favorable neu-rologic status with advanced airway placement(tracheal intubation or SGA) when compared to bag-mask ventilation.5 No differences have been observed in outcomes between SGA and tracheal intubation in pediatric OHCA.2,3,6
2. There are limited data to compare outcomes between bag-mask ventilation versus tracheal intu-bation in the management of IHCA, and there are no studies of pediatric SGA use during in-hospital CPR. A propensity-matched retrospective cohort study found that intubation during cardiac arrest was associated with decreased survival to hospi-tal discharge compared to no intubation.7 Though there may be specific circumstances or populations in which early advanced airway interventions are beneficial(eg, children for whom bag-mask ventila-tion is technically difficult, children with severe lung disease), data supporting alternative approaches to these situations are lacking.
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3.One small, multicenter observational study of intu-bated pediatric patients found that ventilation rates at (at least 30 breaths/min in children younger than 1 year of age, at least 25 breaths/min in older children) were associated with improved rates of ROSC and survival to discharge.8 A ventilation rate of 20 to 30 breaths per minute was selected to account for(1) higher physiologic respiratory rates in children,(2) the preponderance of respiratory etiologies in pediatric arrest,(3) association with improved survival, and(4) avoidance of higher ven-tilation rates that were associated with lower sys-tolic blood pressures during CPR.8
REFERENCES
1. Gausche M, Lewis RJ, Stratton SJ, Haynes BE, Gunter CS, Goodrich SM, Poore PD, McCollough MD, Henderson DP, Pratt FD, et al. Effect of out-of-hospital pediatric endotracheal intubation on survival and neuro-logical outcome: a controlled clinical trial. JAMA. 2000;283:783-790. doi: 10.1001/jama.283.6.783
2. Hansen ML, Lin A,Eriksson C, Daya M, McNally B, Fu R, Yanez D, Zive D, Newgard C; CARES surveillance group and the CARES surveillance group. A comparison of pediatric airway management techniques during out-of-hospital cardiac arrest using the CARES database. Resuscitation.2017;120:51-56.doi:10.1016/j.resuscitation.2017.08.015
3. Ohashi-Fukuda N, Fukuda T, Doi K, Morimura N. Effect of prehospital ad-duced airway management for pediatric out-of-hospital cardiac arrest. Re-suscitation.2017;114:66-72. doi:10.1016/j.resuscitation.2017.03.002
4. Okubo M, Komukai S, Izawa J, Gibo K, Kiyohara K, Matsuyama T,Kiguchi T, Iwami T, Callaway CW, Kitamura T. Prehospital advanced air-way management for paediatric patients with out-of-hospital cardiac ar-reast: A haofwide cohort study. Resuscitation. 2019;148:175-184. doi:10.1016/j.resuscitation.2019.09.007
5.Tham LP Fook-Chong S,Binte Ahmad NS,Ho AF,Tanaka H,Shin SD,Ko PC,Wong KD,Jirang Sao,R G.VR,et al.Pre-hospital airway management and survival outcomes after paediatric out-of-hospital cardiac arrests.Re-suscitation.2022:176-9:18. doi:10.1016/j.resuscitation.2022.04.018
6. Fukuda T, Sekiguchi H, Taira T, Hashizume N, Kitamura Y, Terada T,Ohashi-Fukuda N,Kukita l. Type of advanced airway and survival after pedi-tracit of-outf-hospital cardiac arrest. Resuscitation.2020:150:145-153. doi:10.1016/j.resuscitation.2020.02.005
7. Andersen LW,Raymond TT,Berg RA,Nadkami VM,Grosesstreuer AV,Kurth T, Donnino MW; on behalf of the American Heart Association's Get With The Guidelines-Resuscitation Investigators. Association between tracheal intubation during pediatric in hospital-cardiac arrest and survival. JAMA 2016.316:1786-1797. doi: 10.1001/jama.2016.14486
8. Sutton RM, Reeder RW, Landis WP, Meert KL, Yates AR, Morgan RW,Berger JT, Newch CJ, Carillo JA, Mcquillen PS, et al; Eunice Kennedy Shriver National Institute of Child Health and Human Development Col-laborative Pediatric Critical Care Research Network(CPCCRN). Ventilation rates and pediatric in-hospital cardiac arrest survival outcomes. Crit Care Med.2019;47:1627-1636. doi:10.1097/CCM.000000000003898
DRUG ADMINISTRATION DURING CARDIAC ARREST
Drug Administration Methods During Cardiac Arrest
|Recommendations for Drug Administration Methods During Cardiac Arrest||| |---|---|---| |COR|LOE|Recommendations| |1|C-LD|1. Rapid initiation of vascular access IV or IO is recommended for drug administration in infants and children with cardiac arrest.|
|Recommendations for Drug Administration Methods During Cardiac Arrestst(Continued)|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-EO|Health care professionals caring for infants and children with cardiac arrest should choose the initial type of vascular access route(IV or IO) based on availability, expertise, and timeliness.||
Synopsis
Administration of vasoactive and antiarrhythmic medica-tions is a key component of PALS during CPR. Medi-cations, such as epinephrine, have historically been administered via multiple routes, including endotracheal,intravenous(IV) and intraosseous(10). Due to limited transevalocal drug absorption and limited pulmonary blood flow during CPR, IV and IO administration of medi-cations are preferred over the endotracheal route.12 Se-lecting the timeliest route to deliver medication based on clinical needs and available resources is appropriate.
Recommendation-Specific Supportive Text
1. Timely provision of vasoactive and antiarrhythmic medications during cardiac arrest is dependent on rapid sediment of vascular access across all pediatric age ranges. IV or IO administration of epinephrine is preferred over endotracheal admin-istration when possible.1,2
2.IO access is a rapid, safe, and an effective ini-tial vascular access route for pediatric cardiac arrest's-3-5 A recent systematic review did not iden-tify any studies comparing IV versus IO for vascular access in pediatric cardiac arrest.6 Two retrospec-tive nontraumatic OHCA registry studies showed that younger, more severely ill patients with lower rates of survival were more likely to have received IO access while older patients with higher rates of survival were more likely to have received IV access.78 Health care professionals should con-sider resource availability, expertise, and timeliness(time to confirmed vascular access) when choos-ing vascular access routes for drug administration.
Drug Administration During Cardiac Arrest
|Recommendations for Drug Administration During Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |2a|C-LD|1. For infants and children in cardiac arrest with initial nonshockable rhythm, it is reasonable to administer the initial dose of epinephrine as early as possible.|| |2b|C-LD|2. For infants and children in cardiac arrest with initial shockable rhythm, it may be reasonable to administer epinephrine after 2 attempts at defibrillation or sooner, only when rapid defibrillation is not possible.|| |2b|any-ends setting, it may be reasonable to administer epinephrine every 3-5 min until ROSC is achieved.|||
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|Recommendations for Drug Administration During Cardiac Arrest (Continued)|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|C-LD|4. For infants and children with shock-refractory VF/VT, either amodiradone or lidocaine may be considered.|| |3:No Benefit|B-NR|5. Routine administration of sodium bicarbonate is not recommended for infants and children in cardiac arrest,except in special circumstances(eg,sodium channel blocker toxicity or hyperkalemia).|| |3:No Benefit|B-NR|6. Routine administration of calcium is not recommended for infants and children in cardiac arrest,except for special circumstances(eg, hypocalcemia, calcium channel blocker overdose, or hyperkalemia).||
Synopsis
Administration of medications is a key component of PALS. Vasoactive agents, such as epinephrine, are used to increase coronary perfusion, primarily through alpha-1 receptor agonism. The optimal timing of initial dosing may differ in shockable cardiac arrest given the need to prioritize defibrillation. Antiarrhythmic agents are used to treat cardiac arrest with ventricular fibrillation(VF) and pulseless ventricular tachycardia(pVT). The existing lit-erature does not support routine use of other adjunctive therapies such as sodium bicarbonate and calcium ex-cept in special circumstances.
Recommendation-Specific Supportive Text
1. A recent meta-analysis of retrospective observa-tional studies showed that shorter time to admin-istration of epinephrine during pediatric cardiac arrest with initial nonshockable rhythm was associ-ated with favorable outcomes. ${}^{9-14}$
2. The optimal timing of administration of epinephrine in relation to defibrillation in pediatric cardiac arrest with shockable rhythm is unknown9 and may differ from nonshockable arrest given the need to priori-tize defibrillation. Observational studies of pediat-ric OHCA have included patients with shockable rhythm, but none reported the relationship between initial epinephrine and timing of defibrillation.11,13,15,16 Two observational studies in adults with shockable IHCA showed that early epinephrine, defined as before first defibrillation or within 2 minutes after first defibrillation, respectively, was associated with worse outcomes.17,18 No studies have examined the effect of epinephrine for pediatric shockable arrest when early defibrillation is not possible.
3.The optimal interval between doses of epineph-rine for pediatric cardiac arrest is unknown.9 Observational studies for conventional CPR have shown mixed results. One study demonstrated that average intervals>5 minutes between doses were associated with increased survival compared to 1 to 5 minute intervals.19 A second study showed that average epinephrine intervals of 3 to<5 minutes
were associated with increased survival. ${}^{20}$ Two addi-tional studies found that intervals of<3 minutes between epinephrine doses were associated with better outcomes. ${}^{21,22}$ For pediatric patients under-going extracorporeal cardiopulmonary resuscita-tion(ECPR), one observational study showed that after the first 10 minutes of CPR, survivors received fewer epinephrine doses during each subsequent 10-minute interval compared to nonsurvivors.There was no difference in survival between epinephrine dosing intervals of≤5 minutes and>5 minutes dur-ing minutes 10 to 30 of CPR on adjusted analysis. ${}^{23}$
4.In an observational study of pediatric IHCA with VF/pVT,administration of lidocaine was associated with higher rates of ROSC and 24-hour survival although neither lidocaine nor amiodarone signifi-cantly affected the odds of survival to hospital dis-charge.24 A subsequent propensity-matched study of pediatric IHCA with initial VF/pVT demonstrated no difference in outcomes between patients who received lidocaine compared to amiodarone.25
5. A meta-analysis of sodium bicarbonate adminis-tration during pediatric IHCA demonstrated lower rates of survival to hospital discharge in patients who received bicarbonate.26-33 A subsequent pro-pensity score-weighted cohort study found that sodium bicarbonate was associated with a lower rate of hospital survival, but no difference in rates of ROSC were observed.34 However, these studies do not account for the fact that patients with longer durations of resuscitation, which are associated with lower survival rates, have greater exposure to medi-cations like sodium bicarbonate. This phenomenon,known as resuscitation time bias, may falsely impli-cate the medication with poor survival if timing of drug administration is not accounted for in the analysis.35 There are special circumstances in which bicarbon-ate is used, such as sodium channel blocker toxic-ity(eg, tricyclic antidepressants and cocaine) ${}^{36}$ and hyperkalemia. While a comprehensive list of special circumstances in which sodium bicarbonate may be beneficial has not been determined, it is important to note that sodium bicarbonate is routinely used in some of these circumstances(eg, hyperkalemia)which may significantly limit the emergence of new evidence due to lack of equipoise.37
6. A recent meta-analysis examining the administra-tion of calcium during pediatric IHCA demonstrated decreased survival to hospital discharge with cal-cium administration.32,38-40 Two subsequent studies in pediatric IHCA and arrests managed in the emer-gency department showed similar associations.41,42 However, as noted for sodium bicarbonate, none of the studies accounted for resuscitation time bias and calcium may be falsely implicated in the decreased survival rates in patients who undergo prolonged
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resuscitation.35 There are special circumstances in which calcium administration is used, such as hypo-calcemia, calcium channel blocker overdose, and hyperkalemia. It is important to note that calcium is routinely used in some of these circumstances(eg,hyperkalemia) which may significantly limit the emer-gence of new evidence due to lack of equipoise.37
Weight-Based Dosing of Resuscitation Medications
|Recommendations for Weight-Based Dosing of Resuscitation Medications|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-EO|1. For resuscitation medication dosing, it is recommended to use the infant or child's body weight to calculate resuscitation drug doses while not exceeding the recommended dose for adults.|| |2b|B-NR|2. It may be reasonable to use both habitus or anthropomorphic measurements to improve the accuracy of length-based estimated weight in infants or children, when possible.|| |2b|C-LD|3. If the infant or child's weight is unknown, a body length for estimating weight and other cognitive aids to calculate resuscitation drug dosing and administration may be considered.||
Synopsis
Medication dosing for children is based on weight, which is often difficult to obtain in an emergency setting. There are numerous approaches to estimating weight when an actual weight cannot be obtained.43
This topic was last reviewed in the 2020 AHA Guide-lines for CPR and ECC. These recommendations have not been re-reviewed and updated for this edition of the Guidelines.44
Recommendation-Specific Supportive Text
1. There are many theoretical concerns about the use of actual body weight(especially in overweight or obese patients).45-47 However, there are no data about the safety and efficacy of adjusting medi-cation dosing in obese patients. Such adjustments could result in inaccurate dosing of medications.48,49
2.Several studies suggest that inclusion of body habitus or anthropometric measurements further refines and improves weight estimations using length-based measures.43 However, there are considerable variations in these methods, and the training required to employ these measures may not be practical in every context.
3.Cognitive aids such as the Broselow, PAWPER XL,and Mercy tapes can assist in the accurate approx-imation of body weight(described as being within 10% to 20% of measured total body weight).Several studies demonstrated high variability of weight estimates, with a tendency toward under-estimation of total body weight yet closely approxi-mating ideal body weight.47,50,51
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6. Granfeld A, Avis SR, Lind PC, Holmberg MJ, Kleinman M, Maconochie I, Hsu CH, Fernanda de Almeida M, Wang TL, Neumar RW, et al. In-travousn vs. intraosseous administration of drugs during cardiac ar-rest: A systematic review. Resuscitation. 2020;149:150-157. doi:10.1016/j.resuscitation.2020.02.025
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11. Lin YR, Li YR, Huang CC, Lee TH, Chen TY, Yang MC, Chou CC, Chang CF, Huang HW, Hsu HY, et al. Early Epinephrine Improves the Stabiliza-tion of Initial Post-resuscitation Hemodynamics in Children with Non-shockable Out-of-Hospital Cardiac Arrest. Front Pediatr. 2019;7:220. doi:10.3389/fedp.2019.00220
12. Lin YR, Wu MH, Chen TY, Syue YJ, Yang MC, Lee TH, Lin CM, Chou CC, Chang CF, Li CJ. Time to epinephrine treatment is associated with the risk of mortality in children who achieve sustained ROSC after traumatic out-of-hospital cardiac arrest. Crit Care. 2019;23:101. doi: 10.1186/s13054-019-2391-z
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19. Hoyme DB, Patel SS, Samon RA, Raymond TT, Nakamii VM, Gaia MG,Atkins DL; American Heart Association Get With the Guidelines-Resuscita-tonig Investigators. Epinephrine dosing interval and survival outcomes dur-ing pediatric in-sospital cardiac arrest. Resuscitation: 2017;17:118-23. doi:1016.1017/resuscitation.2017.0523
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40. Dhillon GS, Kleinman ME, Staffa, Staffa SJ, Telee SA, Thiagarajan RR; American Heart Association's Get With The Guidelines- A Report from the Guidelines- Resuscitation (GWTG-R) In-vestigators. Calcium Administration During cardiopulmonary Resuscitation for In-Hospital Cardiac arrest in Children With Heart Disease Is Associated With Worse Suval-A Report from the American Heart Association's Get With The Guidelines-Resuscitation (GWTG-R) Registry. Pediatr Crit Care Med. 2022;23:860-871. doi: 10.1097/PCC.0000000000003040
41. Cashen K, Sutton RM, Reeder RW, Ahmed T, Bell MJ, Berg RA, Burns C, Carcilo JA, Carpenter TC, Michael Dean J, et al; Eunice Kennedy Shriver National Institute of Child Health and Human Development Col-laborative Pediatric Critical Care Research Network (CPCCRN) and National Heart Lung and Blood Institute ICU-RESUScitation Project In-vestigators. Calcium use during paediatric in-hospital cardiac arrest is associated with worse outcomes. Resuscitation. 2023;185:109673. doi:10.1016/j.resuscitation.2022.109673
42.Dillon DG, Wang RC, Shetty P, Douchee Y, Rodriguez RM, Montoy JCC.Efficacy of emergency department calcium administration in cardiac arrest:A 9-year retrospective: Evaluation. Resuscitation. 2023;191:109933. doi:10.1016/j/resuscitation.2023.109933.
43. Young KD, Korotzer Nor C. Weight Estimation Methods in Children: A Systematic Review. Ann Emerg Med. 2016;68:441-451.e10. doi: 10.1016/j.jannemerged.2016.02.043
44. Topjian AA, Raymond TT, Atkins D, Chan M, Duff JP, Joyner BL Jr, Lasa JJ,Lavons EJ, Levy A, Mahgoub M, et al; Pediatric Basic and Advanced Life Support Collaborators. Part 4: Pediatric Basic and Advanced Life Support:2020 American Heart Association Guidelines for Cardiopulmonary
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Resuscitation and Emergency Cardiovascular Care. Circulation.2020;142:S469-S523. doi: 10.1161/CR.0000000000000901
45. Wells M, Goldstein LN, Bentley L. It is time to abandon age-based emergency weight estimation in children A failed validation of 20 dfr-ferent age-based formulas. Resuscitation. 2017;116:73-83. doi:10.1016/j.resuscitation.2017.05.018
46. Tanner D,Negaard A,Huang R.,Evans R.,Nennes H.A. Prospective Evaluax-tion of the Accuracy of Weight Estimation Using the Broselow Tape in Over-weight and Obese Pediatric Patients in the Emergency Department. Pediatr Emerg Care.2017;33:675-678. doi: 10.1097/PEC.0000000000000849
47. Waseem M, Chen J, Leber M, Giambrone AE, Gerber LM. A Reex-amination of the Accuracy of the Browsel Tape as an Instrument for Weight Estimation. Pediatr Emerg Care. 2019;35:112-116. doi: 10.1097/PEC.00000000000000982
48. van Rongen A. Brill MJE, Vaughs JD, Valtino PAJ, van Dongen EPA,van RamshorBS,RTB etart, van den Anker JN, Knibbe CAJ. Higher Midazol-am Clearance in Obesity EdoAsents Compared with Morbidity obese Adults.Clin Pharmacokinet.2018:57:601-611. doi:10.1007/s40262-017-0579-4
49. Vughs JD, Ziesenzit 2016 Undergoing Bariatric A, Bachmann R, Skopp G, Weiss J, Mikus G, van den Anker JN. Use of Fentanyl in Adolescents with Clinically Severe Obesity Undergoing Bariatric Surgery: A Pilot Study.Paediatr Drugs.2017;19:251-257. doi: 10.1007/s40272-017-0216-6
50. Wells M, Goldstein LN. Benley L. The accuracy of paedial weight esti-mation during simulated emergencies: The effects of patient position, pa-tient cooperation, and human errors. Afr J Emerg Med. 2018;8:43-50. doi:10.1016/j.afjem.2017.12:003
51. Shrestha, K Subedi P. Pandey O, Shakya L, Chetrieth K, House DR. Estimating the weight of children in Nepal by Broselow, PAWPER XL and Meli-acymer method. Fluid J. Emerg Med 2018;9:2678-281: doi:10.5847/wjem.19.20-8642.2018.04.007
ENERGY DOSES FOR DEFIBRILLATION IN CARDIAC ARREST
|Recommendations for Energy Doses for Defibrillation in Cardiac Arrest||| |---|---|---| |COR|LOE|Recommendations| |2a|C-LD|1. In infants and children experiencing cardiac arrest with VF/pVT, it is reasonable to use an initial dose of 2-4 J/kg of monophasic or biphasic energy for defibrillation; for ease of teaching, it is reasonable to use an initial dose of 2 J/kg.| |2b|C-LD|2. In infants and children experiencing cardiac arrest with refractory VF/pVT, it may be reasonable to attempt subsequent defibrillation doses of 4 J/kg of monophasic or biphasic energy, and higher levels may be considered, though not to exceed 10 J/kg or the adult maximum dose.| |2b|C-LD|3. In infants and children experiencing cardiac arrest with refractory VF/pVT, a single defibrillation dose of monophasic or biphasic energy may be considered over sequential (stacked) shocks, followed by resumption of chest compressions.|
Synopsis
The proportion of cardiac arrests with initial VF/pVT steadily increases throughout childhood into adolescence yet remains lower than adults.1,2 In infants and children,cardiac arrests due to an initial rhythm of VF/pVT have better outcomes than cardiac arrests due to initial non-shockable rhythms.3 In addition, development of VF/pVT after the initiation of CPR for an initial nonshockable rhythm(subsequent VF/pVT) is associated with worse outcomes compared to patients in whom VF/pVT is the initial pulseless rhythm.' Timely defibrillation is the defini-tive treatment for VF/pVT; and the shorter the duration of
$VF/ pVT$ before defibrillation, the more likely the shock will result in a perfusing rhythm.3 Biphasic defibrillators require lower energy to terminate VF/pVT and have fewer side effects than monophasic defibrillators.4,5 Stacked shocks(the delivery of a rapid series of sequential defibrillations for VF/pVT via one set of pads) are associated with higher rates of VF/pVT termination in some adult studies; how-ever, this has not been well studied in pediatrics.6-9
Recommendation-Specific Supportive Text
1. A systematic review10 found insufficient data to determine a relationship between optimal initial energy dose and outcomes. An IHCA case series11 concluded that 2 J/kg was effective in terminating the majority of VF, but neither subsequent rhythm nor outcome was reported. An observational study of IHCA2 showed a higher initial energy dose of≥3 to 5 J/kg was less effective than 1 to 3 J/kg in achiev-ing ROSC. One observational IHCA study13 did not identify a specific initial energy dose associated with successful VF/pVT termination, while another obser-vational IHCA study14 found that 2 J/kg was an inef-fective initial dose compared to higher dose ranges of 2.5 to 3 J/kg, especially for secondary VF. A registry study of pediatric IHCA with initial VF/pVT evaluated children who received energy doses<1.7 J/kg, 1.7 to 2.5 J/kg or>2.5 J/kg. They found that children≤12 years of age who received initial energy doses of 1.7 to 2.5 J/kg. Furthermore, all children≤18 years of age who received initial energy doses of>2.5 J/kg for initial VF had lower survival rates compared to those who received J/kg for initial VF had lower survival rates compared to those who received J/kg for initial VF had lower survival rates compared to those who received 1.7 to 2.5 J/kg.15
2. Two IHCA studies ${}^{13,14}$ suggest that defibrillation doses>2 J/kg may be needed for subsequent shocks to terminate VF. Human and animal studies demonstrate higher defibrillation doses up to 10 J/kg can be provided without significant harm to the myocardium.14,16-21 Maximum energy doses as recommended for adults(see "Part 9: Advanced Life Support" recommendations on defibrillation22)may vary depending on monophasic versus bipha-sic defibrillators as well as specific manufacturer recommendations. ${}^{23}$
3. There are limited data for the use of sequential (stacked) shocks, where a series of rapid sequen-tial defibrillations is provided without resumption of compressions between shocks, for pediatric VF/pVT.6,24-26 An IHCA study evaluating transtho-racic impedance during defibrillation of children $\geq 8$ years of age suggests that stacked shocks do not improve defibrillation success. ${}^{6}$ Notably, stacked shocks lead to longer periods where chest com-pressions are not being performed.
Figure 2 shows the Pediatric Cardiac Arrest Algorithm.
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 Figure 2. Pediatric Cardiac Arrest Algorithm.
REFERENCES
1.Samson RA, Nadkarni VM, Meaney PA, Carey SM, Berg MD, Berg RA;American Heart Association National Registry of CPR Investigators. Outcomes of in-hospital ventricular fibrillation in children. N Engl J Med.2006;354:2328-2339. doi:10.1056/NEJMoa052917
2.Walsh CK,Krongrad E.Terminal cardiac electrical activity in pediatric patients.Am J Cardiol.1983:51:557-561.doi:10.1016/s0002-9149(83)80096-4
3.Nadkarni VM,Larkin GL,Peberdy MA,Carey SM,Kaye W,Mancini ME,Nichol G, Lane-Truitt T, Potts J,Ornato JP,et al; National Registry of Cardio-
pulmonary Resuscitation Investigators. First documented rhythm and clinical outcome from in-hospital cardiac arrest among children and adults. JAMA 2006;295:50-57. doi:10.1001/jama.295.1.50
4. Bardy GH, Marchlinski FE, Sharma AD, Worley SJ, Luceri RM, Yee R, Halperin BD, Fellows CL, Ahern TS, Chilson DA, et al. Multicenter comparison of truncated biphasic shocks and standard damped sine wave monophasic shocks for transthoracic ventricular defibrillation.Transthoracic investigators. Circulation. 1996;94:2507-2514. doi:10.1161/01/cir.94.102507
5.Clark CB, Zhang Y, Davies LR, Karlsson G, Kerber RE. Pediatric transthoracic defibrillation: biphasic versus monophasic waveforms
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Pediatric Advanced Life Support: 2025 AHA/AAP Guidelines for CPR and ECC
in an experimental model. Resuscitation. 2001;51:159-163. doi: 10.1016/s03005-9572(01)00398-7
6. Niles DE, Nishisaki A, Sutton RM, Brunner S, Stavland M, Mahadeviah S, Meanay PE, Mahasee MR, Berg RA, Nakdami VM. Analysis of transtho ric impedance during real cardiac arrest defibration attempts in older children and adolescents: are stacked-chocks appropriate? Resuscitation.2010:811:1540-1540:13. doi:1016/10.0167/resuscitation.2010.07/011.
7. Davis D, Aguilar SA, Sell R, Minokadeh A, Husra R. A focused investiga-tion of expedited, stack of three shocks versus chest compressions first followed by single shocks for monitored ventricular fibrillation/ventricular tachycardia cardiopulmonary arrest in an hospital setting. J Hosp Med 2016;11:264-268. doi: 10.1002/jhm.2499.
8. Kim S, Jung W, Roh Yim, KhI Yang, Hwang SO, Cha KC. Comparison of Resus-citation Outcomes Between 2-3 or-Stacked Defibrillation Strategies with Minimally Interrupted Chest Compression and the Single Defibrillation Strati-egy: A Sine cardiac Arrest Model. J Am Heart Assoc. 2021;10:e021250. doi: 10.1161/JAHA.121.021250
9. Dunning J, Babbri F, Kohl Pen, Levine A, Lockowand T, Mackay J, Pavie AJ,Strang T,Versteegh M, Nasher SA; EACTS Clinical Guidelines Commit-tee. Guideline for resuscitation in cardiac arrest after cardiac surgery. Eur J Cardiothorac Surg.2009;36:3-28. doi:10.1016/j.jects:2009.01.033
10. Mercier E, Laroche E, Beck B, Le Sage N, Cameron P, AMordn, Berthelot S, Sitra- B, Usgieel-Perfelet PH, Ebration-dermal energy dose during pediatric cardiac arrest: Systematic review of human and animal model studies. Re-suscitation.2019;139:241-252. doi:10.1016/j.resuscitation.2019.04.028
11. Gutgesel HP, Tacker WA. Geddes LA Davis S, Lie JT, McNamara DG, En-ergy dose for ventricular defibration of children. Pediatrics. 1976;58:898-901.
12. Meaney PAadkin, Nkampdani VM, Elsakin BD, Berg, Samson RA, Hazinski MF, Berg RA; American Heart Association National Registry of Cardiopulmo-nary Resucitation investigators. Effect of defibration energy dose during in-hospital cardiac arrest. Pediatrics.2011;127:e16-e23. doi:10.1542/peds.2010-1617
13. Rodriguez-Nunean A, Lopez-Herce J, del Castillo J, Bonlman J; Interman American Paediatric Cardiac Arrest Study Network RIBPECI. Shockable rhythms and defibrillation during in-hospital pediatric cardiac arrest. Resus-citafion 2014;85:387-391. doi 10.1016/j.resuscitation 2013.11:15.01
14. Tibballs J, Carter B, Kiryal NJ, Ragg P, Clifford M. External and internal biphasic direct current shocks for pediatric ventricular fibrillation and pulseless ventricular tachycardia. Pediatr Care Med. 2011;12:14-20. doi: 10.1097/PCC.0Ob13e3181dbp4cf
15.Hoyme DB,Zhou Y,Rogta S,Haskel SE, Samson RA, Meaney P,Bey M.,Nadkami VM, KRAg, BHazino MF,et al.2021/08-0338:In addition with cardiac cardiac arrest using 2 Joules/kilogram as first defibration dose for initial pulseless ventricular arrhythmia. Resuscita-tion.2020;153:88-96. doi:10.1016/j.resuscitation.2020.05.048
16. Berg MD, Samson RA, Meyer RJ, Clark LL, Valenzuela TD, Berg RA. Pe-diatric defibration doses often fail to terminate prolonged out-of-hospital ventricular fibrillation in children. Resuscitation. 2005;67:63-67. doi:10.1016/j.resuscitation.2005.04.018
17. Rossano JW, K onney MA, Kerea TD, Atkins DL Energy does for treatment of out-of-hospital pediatric ventricular fibrillation. Resuscitation.2006/80-89.10.1016/j.resuscitation.2005.01.003
18. Babbs CF, Tacker WA, Van Vleet JF, Bourland JD, Geddes LA. Thera-phetic indices for transchefitted oscillator: effects, dynamic, damag-ing, and lethal electrical doses. Am Heart J 1980;99:734-738. Do 10.1016/0002-8703(80)90623-7
19.Walcott GP, Melnick SB, Killingsworth CR, Iker RE. Comparison of low-energy versus high-energy biphasic defrillation shocks following pro-longed ventricular fibrillation. Prehosp Emerg Care. 2010;14:62-70. doi:10.3109/1090312090349838
20. Berg, RA, Chapman FW, Berg MD, Hilwig RW, Banville I, Walker RG, Nova RC, Sherrill D, Kern KB. Attenuated adult biphasic shocks compared with weight-based monophasic shocks in a swine model of prolonged pediatric ventricular fibrillation. Resuscitation. 2004;61:189-197. doi:10.1016/j.resuscitation.2003.12.021
21. Rossano JW, Jones W.Eerakis S, Millin MG, Nemeth I, Cassan P. Shook J, Kennedy S, Markenson D, Bradley RN. The Use of Automated Exter-nal Defibrillators in infants: A Report From the American Red Cross Sci-entific Advisory Council. Pediatr Care Energ. 2015;31:526-530. doi:10.1097/PEC.0000000000000490
22. Wigginton JG, Agarwal S, Bartos JA, Coute RA, Drennan IR, Haamid A,Kueden PJ, Link MS, Planarch AL, Pertler MM, et al. Part 9: advanced life support:2025 American Heart Association guidelines for cardiopu-
<EndOfPara>monary resuscitation and emergency cardiovascular care. Circulation.2025;152:S358-S577. doi:10.1161/CIR.00000000000001376
23.Panchal AR, Bartos JA, Cabanas JG, Donnino MW, Drennan IR, Hirsch KG,Kudenchuk PJ, Kurz MC, Lavonas EJ, Morley PT, et al; Adult Basic and Advanced Life Support V 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
24. de Caen AR,Kleinman ME,Chameides L,Atkinsd L,Berg RA,Berg MD,Bhanji F, Biarend D, Bingham R, Coovadia AH, et al; Paediatric Basic and Advanced Life Support Chapter Collaborators. Part 10: Paediatric basic and advanced life support: 2010 International Consensus on Cardiopul-monary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation. 2010;81:e213-e259. doi:10.1016/j.resuscitation.2010.08.028
25.Kleinman ME, Chameider L, Schexnayder SM, Samson RA, Hazinski MF,Atkins DL, Berg MD, de Caen AR, Fink EL, Freid EB,et al. Part 14: pediatric advanced life support; 2010 American Heart Association Guidelines for Car-dipulmonary Resuscitation and Emergency Cardiovascular Care. Circulation.2010;122:S876-S908.doi: 10.1161/CIRCULATIONAHA.110.971101
26. Maconchioie IK, Aickin R, Hazinski MF, Atkins DL, Bingham R, Couten TB,Guerguerian AM, Nadkarmi VM, Ng KC, Nuthall GA, et al; Pediatric Life Sup-port Collaborators. Pediatric Life Support: 2020 International Consensus on Cardiopulchi Cardiovascular Resuscitation and Emergency Cardiovascular Care Sci-ence With Treatment Resuscitation. Resuscitation. 2020;156:A120-A155. doi:10.1016/j.resuscitation.2020.09.013
MEASURING CPR PHYSIOLOGY AND QUALITY
|Recommendations for Measuring CPR Physiology and Quality||| |---|---|---| |COR|LOE|Recommendations| |2a|8.BN|1. For infants and children with continuous invasive arterial blood pressure monitoring in place during CPR, it is reasonable for health care professionals to use diastolic blood pressure to assess the child's response to resuscitation efforts.| |2b|B-NR|2. For infants and children with invasive airways in place during CPR,ETCO, monitoring may be considered to monitor CPR quality.| |2b|B-NR|3. For infants and children with continuous invasive arterial blood pressure monitoring in place for arterial blood pressure monitoring in place chronic S78, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC,|
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Synopsis
Initiating and maintaining high-quality CPR are asso-ciated with improved rates of ROSC, survival to hos-pital discharge, and favorable neurologic outcome, yet measured CPR quality is often suboptimal. ${}^{1-3}$ Noninva-sive and invasive monitoring techniques may be used to assess CPR quality and the patient's physiologic response to resuscitation. Invasive arterial blood pres-sure monitoring during CPR reveals compression and medication-generated pressures.45 ETCO, reflects both the cardiac output produced and ventilation efficacy and may provide feedback on the quality of CPR.6 A sudden rise in ETCO2 may be an early sign of ROSC.7 CPR feedback devices(ie, audio, and audiovisual de-vices) may improve compression rate, depth, and recoil within a system of training and quality assurance for high-quality CPR. Point-of-care ultrasound during CPR,specifically echocardiography, has been considered for the identification of reversible causes of arrest. Tech-nologies that are under evaluation to assess resuscita-tion quality include noninvasive measures of cerebral oxygenation, such as near-infrared spectroscopy, which measures regional oxygen saturation and does not re-quire pulsatile flow.
Recommendation-Specific Supportive Text
1 and 3. A multicenter observational study of children with IHCA demonstrated superior outcomes with higher diastolic blood pressure(≥25 mm Hg in infants<1 year of age and≥30 mm Hg in older children≥1 year of age) during the first 10 minutes of CPR.4 In a prospective multi-center validation study in 413 children, these thresholds were associated with higher rela-tive risk of ROSC(adjusted relative risk 1.49;1.13-1.97) and survival to hospital discharge(adjusted relative risk 1.32; 1.01-1.74).89 A secondary analysis of the same trial observed that patients who had an increase of≥5 mm Hg in diastolic blood pressure in response to the first dose of epinephrine had higher rates of ROSC.5 Clinical data regarding the efficacy or appropriate means of prospectively target-ing diastolic blood pressure during CPR are lacking.
2. Higher ETCO2 values during CPR are associ-ated with ROSC.10,11 A previous multicenter study of 43 children with IHCA did not iden-tify an association between mean ETCO2 and survival outcomes.12 However, a recent pro-spective multicenter study in 234 children evaluated average ETCO2 during the first 10 minutes of in-hospital CPR.13 On multivariable analysis, ETCO2≥20 mm Hg was associated
with higher odds of ROSC and survival to dis-charge and higher intra-arrest blood pressures,but not CPR quality metrics. A single-center study found that higher median event ETCO was associated with markers of high-quality CPR-chest compression rate less than 140 compressions per minute(P<0.0001) and chest compression fractions of 90% to 100%(P<0.0001). ${}^{11}$
4.One small single-center study of cerebral near-infrared spectroscopy(n=23) monitored dur-ing pediatric cardiac arrest demonstrated that higher median regional cerebral oxygen satura-tion during the overall CPR event and in the last 5 minutes of CPR was associated with higher rates of ROSC, but not survival to discharge.14 A multicenter study of 92 pediatric patients at 3 sites demonstrated an association between a higher median event regional cerebral oxygen saturation and ROSC, survival to hospital dis-charge, and survival with favorable neurologic outcome.15
5. A simulation trial of pediatric health care pro-fessionals demonstrated a significant improve-ment in chest compression depth and rate compliance when they received visual feed-back (compared to no feedback), although overall compression quality remained poor.16 One small observational study of 8 children with IHCA did not find an association between CPR with or without audiovisual feedback and survival to discharge, although feedback decreased excessive compression rates. ${ }^{17}$
6.Several case series have evaluated the use of bedside echocardiography during pediatric cardiac arrest to identify revers-ible causes of cardiac arrest and potentially direct management. However, data are very limited and the utility of echocardiography to direct care during pediatric CPR is unknown.Potential risks of echocardiography during CPR include prolonged interruptions in chest compressions.18-20
7. A single-center study found that 42% of infants and children with a median event ETCO2<20 mm Hg achieved ROSC.11 A prospective, multicenter study of ETCO2 dur-ing the first 10 minutes of CPR found that 47.5% of infants and children with ETCO2<20 mm Hg and 47.6% of those with ETCO,10 mm Hg survived to hospital discharge.13 Given these variable associations between low ETCO2 values during CPR and survival outcomes, there is potential harm in making termination of resuscitation decisions based on ETCO2 alone.13,21
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4. Berg RA, Sutton RM, Reeder RW, Berger JW, Tench AZ, Carlo JA,McQuillen PS, Meert LK, Yates AR, Harrison RE, et al.; Eunice Kennedy Striver National Institute of Child Health and Human Development Col-laborative Pediatric Care Research Network (CPCRN) PICCR(Pediatric Intensive Care Quality of Cardio-Pulmonary Resuscitation) Investigators. Association between diastolic blood pressure during pe-diatric in-hospital cardiopulmonary resuscitation and survival. Circulation,2018;137:1784-1795. doi:10.1161/CIRCULATIONAHA.117.032270
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6. Hamrick JL, Hamrick JT, Lee JK, Lee BH, Koehler RC, Shaffner DH. Ef-ficacy of chest compressions directed by end-dial CO, feedback in a pediatric resuscitation model of basic life support. J Am Heart Assoc 2014;3:e00450. doi: 10.1161/JAHA-113.000450
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8. Berg RA, Morgan RW, Reeder RW, Ahmed Bell, Tishon, Bship R, Bochkoris M, Burns C, Carillo JA, Carpenter TC, et al. Diastolic Blood Pressure Threshold During Pediatric Cardiopulmonary Resuscitation and Survival Outcomes: A Multicenter Validation Study. Crit Care Med.2023;51:91-102.doi:10.1097/CCM00000000005715
9. Sutton R M, Wolf HaE, Reeder R Whern, Ared T, Bishop R, Bochkoris M,Burns C, Diddle JW, Federman F, Fernandez R, et al; ICU-RESUS and Eunice Kennedy Shiver National Institute of Child Health. Effect of Physiologic Point-of-Carei Cardioplumary Resuscitation Training on Survival With Favorable Neurologic Outcome in Cardiac Arresti in Pediac III CAs: A Randomized Clinical Trial. JAMA 2022:327:934-945. doi:10.1001/jama.2022.1738
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11. Sercher LH, EA shaffner, DH O'Brien, CEffers JM, Jones SI, Newton H, Dual-Arnold J. Association of end-tidal carbon di-oxide levels during cardiopulmonary resuscitation with survival in a large paediatric cohort. Resuscitation. 2022;170:316-323. doi:10.1016/j.resuscitation.2021.10.029
12.Berg RA, Reeder RW, Reer ML K, Yates AR, Berger JT N,Carlo, CJcorlo JA, McQuillen PS, Harrison RE, Moler FW, et al; Eunice Kennedy Shriver National Institute of Child Health and Human Development Collabora-Tive Pediatric Critical Care Research Network (CPCCRN) Pediatric In-tensive Care Quality of Cardio-Pulmonary Resuscitation (PICcQCPR)investigators. End-tidal carbon dioxide during pediatric in-hospital car-diopulmonary resuscitation. Resuscitation. 2018;133:173-179. doi:10.1016/j.resuscitation.2018.08.013
13.Morgan RWER,Reeder RW,Bender Copper,KiFFs,ShH Gram,Keert KL,Mourani PM,Rurray R,Nadkari VM,et al;ICU-RESUS and Eurice Kennely Shriver National Institute of Child Health and Human Development Collaborative Pediatric Critical Care Research Network(CPCCRN) Investigator Groups. Associations Between End-Tidal Carbon Dioxide During Pediatric Cardiopulmonary Resuscitation, Cardiopulmonary
Resuscitation Quality, and Survival. Circulation. 2024;149:367-378. doi: 10.1161/CIRCULATIONAHA.123.066659
14. Francoeur C, Landis WP, Winters M, Naim MY, Donoghue A, Dominick CL,Hui JW, MacDonald JM, Lang SS, Yuan I, et al. Near-infrared spectros-copy during cardiopulmonary resuscitation for pediatric cardiac arrest: A prospective, observational study. Resuscitation. 2022;174:35-41. doi: 10.1016/j.resuscitation.2022.03.014
15. Raymond TT, Esangbedo ID, Rajarepyar P, Je S, Zhang X, Griffis HM,Wakeham MK, Petersen TL, Kirschen MP, Topjian AA, et al; pediatric Re-suscitation Quality(pediRES-Q) Collaborative Investigators. Cerebral Ox-imetry During Pediatric In-Hospital Cardiac Arrest: A Multicenter Study of Survival and Neurologic Outcome. Crit Care Med. 2024;52:775-785. doi: 10.1097/CCM.00000000000000000000000000000000000000
16. Cheng A, Brown LL, Duff of JP, Davidson J, Overly F, Tofil NM, Peterson DT,White ML, Bhanji F, Bank et al; International Network for Simulation-Based Pediatric Innovation, Research, & Education (INSPIRE) CPR Investigators. Improving cardiopulmonary resuscitation with a CPR feedback device and refresher simulations (CPRC RARES Study): a randomized clinical trial. JAMA Pediatr. 2015;1697-1374. doi: 10.1001/jamapediatrics.2014.2616
17.Sutton R, Miles D, Fenchen B, Maltese MR, Leffelman J, Eilevstonn J, Wolfe H, Nishisaki A, Meaney PA, Berg RA, et al. First quantita-tive analysis of cardiopulmonary resuscitation quality during in-hospital cardiac arrests of young children. Resuscitation. 2014;85:70-74. doi:10.1016/j.resuscitation.2013.08.014
18.Steffen K, Thompson W R, Pustavitoau A, Su E. Return of viable cardiac function after sonographic cardiac standstill in pediatric cardiac arrest. Pedi-atr Emerg Care.2017;33:58-59. doi: 10.1097/PEC.0000000000001002
19. Leviter JI, Feick M, Riera, A, White LJ. A Protocol for Using Point-of-Care Ultrasound as an Adjunct in Pediatric Cardiac Arrest: Pediatric Ultrasound for Life-Supporting Efforts. Pediatr Emerg Care. 2024;40:835-838. doi: 10.1097/PEC:00000000000003239
20.Morgan RW,Stinson HR,Wolfe H,Lindell RB,Topjian AA,Nadkarni VM,Sutton R, Berg RA, Kilbugh TJ. Pediatric in-hospital cardiac arrest sec-ondary to acute pulmonary embolism. Crit Care Med.2018;46:e229-e234. doi: 10.1097/CCM.0000000000000000000000000000000000000000000000000
21. Yates AR, Naim MY, Reeder RW, Ahmed T, Banks RK, Bell MJ, Berg RA,Bishop R, Bochloris M, Burns C, et al. Early Cardiac Arrest Hemodynamic ics,End-Tidal C o2, and Outcome in Pediatric Extracorporeal Cardiopulmo-nary Resuscitation: Second Analysis of the ICU-RESUScitation Project Dataset(2016-2021). Pediatr Crit Care Med. 2024;25:312-322. doi:10.1097/PCC.0000000000000003423
EXTRACORPOREAL CARDIOPULMONARY RESUSCITATION
|Recommendation for the Use of Extracorporeal Cardiopulmonary Resuscitation|| |---|---| |COR|LOE| |2b|C-LD|
Synopsis
ECPR is the rapid deployment of venoarterial ECMO for refractory cardiac arrest. This has been defined as the initiation of ECMO flow during active CPR or with-in 20 minutes of ROSC.1 The deployment of ECRPR by resourced and highly trained health care teams is as-sociated with improved survival outcomes compared to conventional CPR in specific IHCA patient populations with reversible causes.23 Pediatric patients with underly-ing cardiac disease continue to represent a population of patients with improved survival to hospital discharge and good neurologic outcomes following deployment of
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ECPR compared to conventional CPR for prolonged car-diac arrest.4,5 Emerging evidence suggests that risk pro-files for survival differ between cardiac subpopulations(ie, surgical cardiac versus medical cardiac populations).3 Pediatric ECR use is increasing beyond the pediatric cardiac population(eg, respiratory illness), with limited evidence suggesting benefit.2,6-8
See“Part 4: Systems of Care” for further discussion of ECR systems of care. 9
Recommendation-Specific Supportive Text
1.Two single-center, retrospective case series of ECPR in patients with preexisting cardiac disease showed rates of survival to hospital discharge of 43.8% to 48%, and survivors, 68% to 75%survived with a favorable neurologic outcome. ${}^{10,11}$ Similar findings were reported in 5 additional sin-gle/multicenter studies among patients across illness classifications, with the majority in the car-diac illness category.12-16 A retrospective multi-center study of cardiac ICU patients from a quality improvement registry showed higher survival to discharge of ECPR recipients with cardiac surgi-cal disease compared to cardiac medical disease,3 while analysis of 2 registries showed noncardiac diagnoses were associated with an increased risk of death following ECPR.17 A retrospective analysis from an inpatient pediatric database showed no dif-ference in mortality between patients who received conventional CPR and patients who received ECPR, the majority of whom were cardiac surgery patients. ${}^{18}$ Another retrospective analysis using a national registry showed higher rates of survival with ECPR in cardiac surgical patients who had a cardiac arrest.5 For noncardiac populations experi-encing IHCA, a retrospective study from a national database found no difference in survival to hospital discharge between ECPR and conventional CPR.8 additional data evaluating the use of ECPR in non-cardiac cardiac patients or those who experience OHCA is insufficient to make a recommendation at this time.
REFERENCES
1.Conrad SA, Broman LM, Taccone FS, Lorusso R, Malfertheiner MV,Pappalardo F, Diardo M, Belliato M, Grazioli L,Barbaro RP.The extrac-poreal life support organization Maastrich treatry for nomenclature in extra-corporal life support A position paper of the extracorporeal life support organization. Am J Respir Crit Care Med.2018;198:447-451.
2.Farhat A, Ling RR, Jenks CL, Poon WH, Yang IX, Li X, Liu Y,Darnell-Bowens C, Ramanathan K, Thiagarajan RR, et al. Outcomes of pediatric extracorporeal cardiopulmonary resuscitation: a system-atic review and meta-analysis. Crit Care Med. 2021;49:682-692. doi:10.1097/CC00000000004882
3.Brunetti MA, Gaynor JW, Rettzlo LB, Lehrich JL, Banerjee M, Amula V,Ballyd, Klugman D, Koch J, Lasa J, et al. Characteristics, risk factors & outcomes of extracorporeal membrane oxygenation use in pediatric cardiac intensive care units: a report from the PCA4 Registry. Pediatr Crit Care Med.2018;19:544.
4. Lasa JJ, Rogers RS, Localio R, Shults J, Raymond T, Gaies M, Thiagarajan R, Laussen PC, Kilbaugh T, Berg RA, et al. Extracorporeal Cardiopul-monary Resuscitation(E-CPR) During Pediatric In-Hospital Cardiopul-monary Arresti Is Associated With Improved Survival to Discharge: A Report from the American Heart Association's Get With The Guidelines Resuscitation(GWTG-R) Registry. Circulation. 2016;133:165-176. doi: 10.1161/CIRCULATIONAHA.115.016082
5. Kobayashi RL, Gauvreau K, Alexander PMA, Teele SA, Fynn-Thompson F,Lasa JJ, Bembea M, Thiagarajan RR; American Heart Association's (AHA)Get With The Guidelines-Resuscitation (GWTG-R) Investigators. Higher Survival With the Use of Extracorporeal Cardiopulmonary Resuscitation Compared with Conventional Cardiopulmonary Resuscitation in Children Following Cardiac Surg�ry: Results of an Analysis of the Get With The Guidelines-Resuscitation (GRTG-R). Crit Care Med. 2024;52:563-573. doi: 10.1097/CCM.00000000000006103
6. Holberg MJ, Granfeld A, Guerugian A-M, Sandroni C, Hsu CH,Gardner RM, Lind PC, Egertsen MA, Johannsen CM, Andersen LW.Extracorporeal cardiopulmonary resuscitation for cardiac arrest: an updated systematic review. Resuscitation. 2023;182:109665. doi: 10.1016/j.resuscitation.2022.12.003
7. Beni CE, Rice-Townsend SE, Esangbedo ID, Jancelewicz T, Vogel AM,Newton C, Boomer L, Rothstein DH. Outcome of Extracorporeal Cardiopul-ary Resuscitation in Pediatric Patients Without Congenital Cardiac Dis-ease: Extracorporeal Life Support Organization Registry Study. Pediatr Crit Care Med.2023;24:927-936. doi: 10.1097/PCC.000000000003322
8.Loacem H, Mimebach AS, Reeder R, Alvey JS, Race JA, Su L, Lasa JJ, Slovis JC,Raymond TT,Coleman R,et al;American Heart Association's (AHA) Get With The Guidelines-Resuscitation (GWTG-R) Investigators. Outcomes of Extracorporeal Cardiopulmonary Resuscitation for In-Hospital Cardiac Ar-rest Among Children With Noncardiac Illness Categories. Crit Care Med.2024;52:551-562. doi: 10.1097/CCM.00000000000006153
9.Dezfulian C, Cabanas JG, Buckley JR, Cash RE, CrowE R, RPrenn AR,Mahgoub M, Mannarino CN, May T, Salcido DD, et al. Part 4: Systems of Care: 2025 American Heart Association Guidelines for Cardiopul-monary Resuscitation and Emergency Cardiovascular Care. Circulation.2025;152:S353-S384. doi: 10.1161/CIR.00000000000001378
10. Anton-Martin P, Moreira A, Kang P, Green ML. Outcomes of paediat-ric cardiac patients after 30 minutes of cardiopulmonary resuscitation prior to extracorpore support. Cardiol Young. 2020;30:607-616. doi:10.1017/S047951120000591
11.Beshish AG,Baginski MR,Johnson TJ,Deatrick BK,Barbaro RP,Owens GE.Functional status change among children with extracorporeal membrane oxygenation to support cardiopulmonary resuscitation in a pediatric cardiac ICU: A single institution report. Pediatr Crit Crit Care Med.2018;19:665-671.doi:10.1097/PCC.00000000000000000000000000
12. de la Lana RA, Marsney RL, Gibbons K, Anderson B, Haisz E, Johnson K,Black A, Venugopal PS, Mattke AC. Merging two hospitals: The effects on pediatric extracorporeal cardiopulmonary resuscitation outcomes. J Pediatr Intensive Care.2020;10:2022-209. doi: 10.1055/s-0040-1715853
13.De Mul A, Nguyen D-A, Doell C, Perez M-H, Cannizzaro V, Karam O. Prog-nostic evaluation of mortality after pediatric resuscitation assisted by ex-tracorporeal life support. J Pediatr Intensive Care. 2019;08:057-063. doi:10.1055/s-0038-1667012
14. Melvan JN, Davis J, Hearard M, Trivedi JR, Wolf M, Kanter KR, Deshpande SR,Aloufi B. Factors associated with survival following extracorporeal cardio-pulmonary resuscitation in children. World J Pediatcon Congenital Heart Surg.2020;11:265-274. doi:10.1177/2150135120902102
15.Shakoor A, Pedroso FE, Jacobs, Se, Okochi S, Zenilman A, Cheung EW,Middlesworth W.Extracorporeal cardiopulmonary resuscitation(ECPR) in in-fants and children: a single-center retrospective study. World J Pediatr Con-gental Heart Surg 2019;10:582-589. doi:10.1177/2150135119862598
16. Torres-Andres F, Fink EL, Bell MJ, Sharma MS, Yablonsky EJ,Sanchez-de-Toledo J. Survival and long term functional outcomes for chil-dren with cardiac arrest treated with extracorporeal cardiopulmonary resus-citation. Pediatr Crit Care Med.2018;19:451.
17. Bembea MM, Ng DK, Rikzalla N, Rycus P, Lasa JJ, Dalton H, Topjian AA,Thiagarajan RR, Nadkami VM, Hunt EA; American Heart Association's Get With The Guidelines-Resuscitation Investigators. Outcomes After Extra-corporal Cardiopulmonary Resuscitation of Pediatric In-Hospital Cardiac Arrest: A Report From the Get With the Guidelines-Resuscitation and the Extracorporeal Life Support Organization Repistries. Crit Care Med.2019;47:e278-e285.doi: 10.1097/CCM.0000000000003622
18. Hamah Z, Ohman HF, Almasri M, Al-Subu A, Lutfi R. Survival outcomes of in-hospital cardiac arrest in pediatric patients in the USA. Eur J Pediatr.2021;19:50215-3520. doi:10.1007/s00431-021-0408-3
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POST-CARDIAC ARREST CARE CARE
Post-Cardiac Arrest Targeted Temperature Management
|Recommendations for Post-Cardiac Arrest Targeted Temperature Management|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|A|1. For infants and children who remain comatose following cardiac arrest, continuous central temperature monitoring is recommended.|| |1|B-NR|2. For infants and children who remain comatose following cardiac arrest, avoiding central temperatures>37.5℃ is recommended.|| |2a|B-R|3. For infants and children between 24 h and 18 y of age who remain comatose after IHCA or OHCA, it is reasonable to use a 5-d course of targeted temperature management (TTM), either 32°C-34 °C followed by TTM of 36°C-37.5°C, or only TTM of 36°C-37.5°C.||
Synopsis
Hypoxic ischemic brain injury is a leading cause of morbidity and mortality following pediatric cardiac ar-rest. Hypoxic ischemic brain injury leads to free radical production, cellular apoptosis and necrosis.1 Primary and secondary brain injury can result in cerebral isch-emia or hyperemia, encephalopathy, seizures, and cere-bral edema. Fever is common post-cardiac arrest and is associated with worse neurologic outcomes. Fever is also associated with increased central nervous system metabolic demands which may exacerbate primary brain injury after arrest.2,3 Targeted temperature management(TTM) refers to actively maintaining a patient's tempera-ture within a closely prescribed temperature range while continuously monitoring central temperature. All forms of TTM actively prevent fever. Maintaining TTM between 32°C and 34°C attempts to treat systemic ischemic re-perfusion injury.4,5 A systematic review of pooled animal studies comparing TTM between 32°C and 36°C to control groups showed a strong effect of TTM on favor-able neurologic outcome and reduced mortality.6
Recommendation-Specific Supportive Text
1. Accurate measurement of temperature is most reli-ably obtained at a core site(eg, rectal, esophageal,or bladder). Continuous temperature monitoring assesses temperature swings in patients at high risk for temperature instability. Continuous core temperature monitoring was used for the 5 days of TTM in Therapeutic Hypothermia After Pediatric Cardiac Arrest(THAPCA) trials. ${}^{78}$
2. Hyperthermia in the post-cardiac arrest period is common3 and is associated with decreased survival from both IHCA and OHCA. Avoiding hyperther-mia offers a potential means to improve neurologic outcome.9-11 Effective prevention of fever has been
$\text{shown with active cooling with servo-regulated}$devices compared to air-cooled devices or passive cooling techniques ${}^{12}$ and with adoption of lower target temperature. ${}^{13}$
3.The THAPCA randomized clinical trials of TTM(32°C-34°C for 48 hours followed by 3 days of TTM 36°C-37.5°C versus TTM 36°C-37.5°C for a total of 5 days) after IHCA or OHCA in chil-dren with coma following ROSC found no differ-ence in 1-year survival with a favorable neurologic outcome.78 Secondary analyses of the THAPCA trials showed no difference between temperature groups in any of the following subgroups: ECMO or ECPR, hypotension post-ROSC, open chest resus-citation, combined cohort of IHCA and OHCA, and acute kidney injury.14-19 A Bayesian reanalysis of the THAPCA-OH trial found a high probability that hypothermia provides a modest benefit in neurobe-havioral outcome and survival at 1 year.20 A recent retrospective observational study found that chil-dren who received TTM 33°C per clinician deci-sion had higher health-related quality of life scores versus those who received TTM 36°C evaluated at 3 years after the cardiac arrest.21
Post-Cardiac Arrest Blood Pressure Management
|Recommendations for Post-Cardiac Arrest Blood Pressure Management|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|1. After cardiac arrest in infants and children, it is recommended to maintain systolic and mean arterial blood pressure greater than the 10th percentile for age.||| |1|B-NR|2. After cardiac arrest in infants and children, it is recommended to maintain systolic and mean arterial blood pressure greater than the 10th percentile for age.|| |1|C-EO|2. After cardiac arrest in infants and children, it is continuous arterial pressure monitoring is recommended to identify and treat hypotension when appropriate resources are available.||
Synopsis
Hypotension(<fifth percentile for age and sex) is com-mon following ROC from cardiac arrest, occurring in 25% to 50% of infants and children.15,22 In addition to the primary causes of cardiac arrest, hypotension can be related to myocardial dysfunction and systemic re-perfusion, which is associated with inflammation and vasoplegia.Hypotension can exacerbate brain ischemia and myocardial ischemic injury, systemic hypoperfusion and resultant tissue hypoxia. Myocardial dysfunction,which is often present regardless of arrest etiology,typically occurs within hours of arrest and resolves in 48 to 72 hours.23 Both the presence and severity of postarrest hypotension are associated with lower rates of survival to discharge.15,22,24 whereas normal or high blood pressures are associated with survival to dis-charge.14,25 When post-cardiac arrest hypotension is
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present, there is paucity of data regarding the asso-ciation between interventions to treat hypotension and outcomes.
Recommendation-Specific Supportive Text
1 and 2. Blood pressure is often labile in the post-car-diac arrest period and recognition of hypoten-sion is important. Continuous blood pressure monitoring allows for rapid identification of hypotension and can facilitate immediate treat-ment. Two observational studies associated systolic blood pressure below the fifth per-centile for age in the first 12 hours following cardiac arrest with decreased rates of survival to discharge.15,22 The severity and duration of systolic hypotension within the first 72 hours post-cardiac arrest care in the pediatric ICU(PICU) are associated with decreased survival to discharge,24 whereas the combined absence of both post-cardiac arrest systolic hypoten-sion and fever was associated with increased odds of survival to discharge.13 A secondary analysis of the ICU-Resuscitation trial of pedi-atric IHCA found higher rates of survival to hospital discharge as well as survival to hos-pital discharge with favorable neurologic out-come when blood pressure targets were above a threshold of systolic blood pressure>10th percentile for age and diastolic blood pres-sure>50th percentile for age during the first 6 hours post-cardiac arrest.26 A multicenter study of IHCA and OHCA found that mean arterial blood pressure between the fifth and 74th percentiles for age was associated with favorable neurologic outcome.27 An additional study showed that mean arterial blood pres-sure<10th percentile for age in the first 24 hours after cardiac arrest, quantified as bur-den of hypotension(duration and magnitude),was associated with unfavorable neurologic outcomes.28
Post-Cardiac Arrest Oxygenation and Ventilation Management
|Recommendations for Post-Cardiac Arrest Oxygenation and Ventilation Management|Recommendations|Recommendations|| |---|---|---|---| |COR|LOE|Recommendations|| |2b|C-LD|1. After cardiac arrest in infants and children, it may be reasonable to target nomoxemia that is appropriate to the specific patient's underlying condition.|| |2b|C-LD|2. After cardiac arrest in infants and children, it may be reasonable to wean oxygen to target an oxyhemoglobin saturation between 94% and 99%.||
|Recommendations for Post-Cardiac Arrest Oxygenation and Ventilation Management (Continued)|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|C-LD|3. After cardiac arrest in infants and children, it may be reasonable to target a Paco2, that is appropriate to the specific patient's underlying condition and limit exposure to hypercapnia or hypocapnia.||
Synopsis
Post-cardiac arrest care is a critical component of the Chain of Survival. Monitoring of gas exchange with oxygen and ventilation titration is a key component of post-cardiac arrest care with the goal of preventing secondary end-organ injury. Although current recom-mendations are to administer 100% oxygen during cardiac arrest to maximize oxygenation during CPR as well as to minimize hypoxic-ischemic injury, ${}^{29}$ tar-get ranges for post-ROC oxygenation are less certain.Animal studies ${}^{30,31}$ have shown associations with hy-peroxia and reactive oxygen species, inflammation and brain injury, yet observational studies in infants and children post-ROC(whether spontaneous or achieved by mechanical means) have demonstrated mixed as-sociations for hyperoxemia with survival and neurologic outcomes. ${}^{32-36}$ While most studies demonstrated ad-verse outcomes with hypoxemia, 1 recent observation-al study did not find an association with hypoxemia in the post-cardiac arrest period. ${}^{37}$ Associations of either duration or severity of hypoxemia or hyperoxemia with adverse outcomes in the post-cardiac arrest setting are unknown.
Extremes of arterial carbon dioxide levels lead to cerebral vasoconstriction when low(hypocnapia) and vasodilation when high(hypercapnia).38 Carbon dioxide level fluctuations and their impact on cerebral blood flow in the pediatric post-cardiac arrest population remains poorly understood, although emerging evidence sug-gests mild hypercapnia may be associated with survival and favorable neurologic outcome.35,37
Recommendation-Specific Supportive Text
1 and 2. Because an arterial oxyhemoglobin saturation of 100% may correspond to a $PaO_{2}$ between approximately 80 mm Hg and 500 mm Hg, it is reasonable to target an oxyhemoglobin satu-ration between 94% and 99%. Of note, pulse oximeters may overestimate oxygen satura-tion levels in patients with darker skin, which can lead to lower oxygen levels(hypoxemia)going undetected.39,40 Six small observational studies of pediatric IHCA and OHCA did not show an association between hyperoxemia and outcome.32,36,37,41-43 One larger observational study of pediatric IHCA and OHCA, as well as study of pediatric IHCA and OHCA, as well as
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a secondary analysis of the ICU-Resuscitation trial, found associations between hyperox-emia after ROC and either decreased survival to PICU discharge34 or decreased survival to hospital discharge with favorable neurologic outcome.35
3.Four observational studies found an associa-tion between hypercapnia and increased mor-tality and worse neurologic outcomes.33,35,37,41 Hypercapnia and hypocapnia impact cerebral blood flow. Targeting normocapnia(Paco2-35-45 mm Hg) or the patients' baseline arte-rial partial pressure of carbon dioxide when chronically hypercapnic may prevent these perturbations.
Post-Cardiac Arrest Electroencephalography Monitoring and Seizure Treatment
|Recommendations for Post-Cardiac Arrest Electroencephalography Monitoring and Seizure Treatment|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-LD|1. When resources are available, continuous electroencephalography and exceptional research (EEG) monitoring is recommended for the detection of seizures after cardiac arrest in infants and children with persistent encephalopathy.|1. When resources are available, continuous electroencephalography (EEG) monitoring is recommended for the detection of seizures after cardiac arrest in infants and children with persistent encephalopathy.| |1|C-LD|2. It is recommended to treat clinical seizures after cardiac arrest in infants and children.|3. It is recommended to treat nonconvulsive status epilepticus after cardiac arrest in infants and children.| |2a|C-EO|3. It is reasonable to treat nonconvulsive status epilepticus after cardiac arrest in infants and children.|4.3. It is reasonable to treat nonconvulsive status epilepticus after cardiac arrest in infants and children.|
Synopsis
Post-cardiac arrest brain injury remains a leading cause of morbidity and mortality in children because the brain has limited tolerance of ischemia, hyperemia, or edema.Post-cardiac arrest seizures occur in 5% to 30% of patients and can be nonconvulsive, which can only be detected on electroencephalography.44,45 Post-cardiac arrest status epilepticus is associated with worse out-comes, including death and neurologic injury in survivors.There are no pediatric studies assessing the efficacy of antiseizure medications for either prophylaxis or treat-ment of seizures and their association with outcomes such as survival to hospital discharge or survival with fa-vorable neurologic outcome.
Recommendation-Specific Supportive Text
1. Nonconvulsive seizures and nonconvulsive sta-tus epilepticus are common after pediatric cardiac arrest and are associated with worse out-comes.44-47 The American Clinical Neurophysiology Society recommends continuous EEG monitoring for encephalopathic patients after pediatric cardiac arrest.48 Nonconvulsive seizures and nonconvulsive status epilepticus cannot be detected without EEG monitoring.48
2 and 3. There is insufficient evidence to determine whether treatment of convulsive or noncon-vulsive seizures improves neurologic or func-tional outcomes after pediatric cardiac arrest.Both convulsive and nonconvulsive status epi-lepticus are associated with worse outcomes,but no study has evaluated treatment with antiseizure medications compared to no treat-ment.44,45 A study comparing treatment to no treatment of rhythmic and periodic discharges following adult cardiac arrest found no differ-ence in survival or neurologic outcomes.49 The Neurocritical Care Society recommends treat-ing status epilepticus with the goal of stopping convulsive and electrographic seizure activity.50
Figure 3 shows the checklist for post-cardiac arrest care.
REFERENCES
1.Perkins GD,Neumar R,Hsu CH,Hirsch KG,Aneman A,Becker LB,Couper K,Callaway CW,Hoedemaekers CWE, Lim SL,et al; on behalf of the In-ternational Liaison Committee on Resuscitation. Improving outcomes after post-cardiac arrest brain injury: a scientific statement from the International Liaison Committee on Resuscitation. Circulation. 2024;150:e158-e180.doi:10.1161/CIR.0000000000000001219
2.Bembea MM, Nadkarni VM, Diener-West M, Venugopal V, Carey SM, Berg RA, Hunt EA; American Heart Association National Registry of Cardio-pulmonary Resuscitation o Investigators. Temperature patterns in the early postresuscitation period after pediatric inhospital cardiac arrest. Pediat-Care Med.2010;11:723-730. doi: 10.1097/PCC.0b013e3181dde659
3. Hickey RW, Kochanek PM, Ferimer H, Graham SH, Safar P. Hypothermia and hyperthemia in children after resuscitation from cardiac arrest. Pediat-rics.2000;106:118-122. doi:10.1542/peds.106.1.118
4. Topjian AA, de Caen A, Wainwright MS, Abella BS, Abend NS, Atkins DL, Bembea MM, Fink EL, Guerguerian AM, Haskell SE, et al. Pedi-atri post-cardiac arrest care: a scientific statement from the Ameri-can Heart Association. Circulation. 2019;140:e194-e233. doi:10.1161/CIR.00000000000000697
5.Neumar RW,Nolan JP,Adrie C,Aibiki M,Berg RA,Bottiger BW,Callaway C,Clark RS,Geocadin RG,Jauch EC,et al.Post-cardiac arrest syndrome,epidemiology,pathophysiology, treatment, and prognostication. A consen-sus statement from the International Liaison Committee on Resuscitation(American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foun-dation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, the Resuscitation Council of Southern Africa); the Ameri-can Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anstige; the Council on Car-diopulmonary,Perioperative, and Critical Care; the Council on Clinical Car-diology; and the Stroke Council. Circulation. 2008;118:2452-2483. doi:10.1161/CIRCULATIONAHA.108.190652
6.Arrich J, Herkner H, Mullner D, Behringer W. Targeted tempera-ture management after cardiac arrest. A systematic review and meta-analysis of animals studies. Resuscitation. 2021;162:47-55. doi:10.1016/j.resuscitation.2021.02.002
7. Moler FW, Silverstein FS, Holubkov R, Slomine BS, Christensen JR,Nadkari VM, Meert KL, Browning B, Pemberton VL, Page K,et al;THAPCA Trial Investigators. Therapeutic Hypothermia after In-Hospital Cardiac Arrest in Children. N Engl J Med. 2017;376:318-329. doi:10.1056/NEJmoA1610493
8. Moler FW, Silverstein FS, Holubkov R, Slomine BS, Christensen JR,Nadkarni VM, Meert KL, Clark AE, Browning B, Pemberton VL, et al;THAPCA Trial Investigators. Therapeutic hypothermia after out-of-hospital cardiac arrest in children. N Engl J Med. 2015;372:1898-1908. doi:10.1056/NEJmoa1411480
9. Langhelle A, Tylovd SS, Lexow K, Happes SA, Sunde K, Steen PA. In-hospital factors associated with improved outcome after out-of-hospital
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|Components of Post-Cardiac Arrest Care|Check| |---|---| |Ensure normoxia and normocapnia|| |Monitor Spo2 and target 94%-99%(or child's normal/appropriate oxygen saturation).|□| |Measure and target Paco2 appropriate to the patient's underlying condition and limit exposure to severe hypercapnia or hypocapnia.|□| |Optimize cardiac function and end-organ perfusion.|| |Monitor with cardiac telemetry.|□| |Monitor arterial blood pressure.|□| |Review hemodynamic goals daily.|□| |Monitor serum lactate and urine output to help guide therapies.|□| |Use parenteral fluid bolus with or without inotropes or vasopressors to maintain a systolic blood pressure and mean arterial blood pressure greater than the 10th percentile for age.|□| |Consider echocardiography to assess for myocardial dysfunction.|□| |Maintain electrolytes within normal ranges to avoid possible life-threatening arrhythmias.|□| |Apply targeted temperature management(TTM).|| |Continuously monitor core temperature.|□| |Prevent and treat fever immediately after cardiac arrest and after rewarming.|□| |If patient is comatose, apply TTM(32°C-34°C) followed by (36°C-37.5°C) or only TTM(36°C-37.5°C) for up to 5 days.|□| |Prevent shivering.|□| |Remember that rewarming is a high-risk time for hypotension, electrolyte abnormalities, hypoglycemia, and seizures.|□| |Provide neuromonitoring.|| |If patient is not at neurologic baseline and resources are available, monitor with continuous electroencephalography.|□| |Treat seizures.|□| |Measure glucose.|| |Measure blood glucose and avoid hypoglycemia.|□| |Prevent agitation and pain.|| |Treat with sedatives, anxiolytics, and analgesics to a sedation score target.|□| |Consider prognosis.|□| |Always consider multiple modalities(clinical and other) over any single predictive factor.|□| |Delay prognostication until at least 72 hours after cardiac arrest.|□| |Remember that prognostics assessments may be modified by TTM.|□|
Figure 3. Post-Cardiac Arrest Care Checklist.
cardiac arrest. A comparison between four regions in Norway. Resuscitation.2003;56:247-263. doi: 10.1016/s0300-9572(02)00409-4
10. Takasu A, Saitoh D, Kaneko N, Sakamoto T, Okada Y. Hyperthermia: is it an ominus sign after cardiac arrest? Resuscitation. 2001;49:273-277. doi:10.1016/s0300-9572(00)00360-9
11. Zeiner A, Holzer M, Sterz F, Schorkhuber W, Eisenburger P, Havel C, Kliegel A, Laggner AN. Hyperthermia after cardiac arrest is associated with an un-favorable neurologic outcome. Arch Intern Med.2001;161:2007-2012. doi:10.1001/archinte. 161.16.2007
12. Kadden M, Zhang A, Shoykhet M. Association of temperature management strategy with fever in critically ill children after out-of-hospital cardiac arrest.Front Pediatr:2024;12:1355385. doi: 10.3389/fped.2024.1355385
13. Fowler JC, Morgan RW, O'Halloran A, Gardner MM, Appel S, Wolfe H,Kienzie MF, Raymond TT, Scholefield BR, Guerguerian AM, et al.The impact of pediatric post-cardiac arrest care on survival: A multicenter review from the AHA get with the Guidelines®-resuscitation post-cardiac arrest care registry. Resuscitation. 2024;2021:110301. doi:10.1016/j.resuscitation.2024.110301
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14. Topjian AA, Telford R, Holubkov R, Nadkarni VM, Berg RA, Dean JM, Moler FW; Therapeutic Hypothermia after Pediatric Cardiac Arrest (THAPCA)Trial Investigators. Therapeutic Hypothermia after Pediatric Cardiac Arrest (TRHAPCA)with discharge survival following targeted temperature management for pediatric in-hospital cardiac arrest. Resuscitation.2019;141:24-34. doi:10.1016/j.resuscitation.2019;05.032
15. Topjian AA, Telford R, Holubkov R, Nadkarni VM, Berg RA, Dean JM, Moler FW; Therapeutic Hypothermia After Pediatric Cardiac Arrest (THAPCA)Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigators. Therapeutic Hypothermia After Pediatric Cardiac Arrest (TIAL Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (TIAL Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (TIAL Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (TIAL Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (Trial Investigations. Therapeutic Hypothermia After Pediatric Cardiac Arrest (TIAL Investigations. Ther�) 1331-69.88:10.1016/j.resuscitation.2018.07:362
16. Schoelberg DR, Silverstein FS, Telford R, Holubkov R, Slomel R, Slomine BS,Meert KL,Christensen JR, Nadkarni VM, Dean JM, Moler W. Ther-apeutic hyperemia after pediatric cardiac arrest: Pooled ran-domized controlled trials. Resuscitation. 2018;133:101-107. doi:10.1016/j.resuscitation.2018.09.011
17. Meert KL, Guerquian AM,Barbaro R, Somine BS,Christensen JR, Berger J, Topjan A,Bembea M,Tabtabb S, Fink EL, et al; Therapeutic Hypothermia After Pediatric Cardiac Arrest (THAPCA) Trial Investigators. Extracorporeal Cardiopulmonary Resuscitation: One-Year Survival and Neurobehavioral Outcome Among Infants and Children With In-Hospital Cardiac Arrest. Crit Care Med 2019;47:393-402. doi: 10.1097/CM0000000000000354.
18. Meert KL, Delius R, Slomine BS, Christensen JR, Page K, Holubkov R,Dean JM, Moler FW; Therapeutic Hypothermia after Pediatric Cardiac Ar-rest Trial Investigators. One-Year Survival and Neurologic Outcomes after Pediatric Open-Chest Cardiopulmonary Resuscitation. Ann Thorac Surg.2019;107:1441-1446. doi:10.1016/athocratus,2018;11.028
199 Mart II, Setle WWI, Stelton JA, Atten JA, Scensaki D, Fitzgerald JC, Topian J,Aholubkov R, Page K, Slomine BS, Christensen JR, et al. acute kidney injury after out of hospital pediatric cardiac arrest. Resuscitation. 2018:131:63-68. doi:10.1016/j.resuscitation.2018.07.362
20 Harhao MO, Blette BS, Granholm A, Moler FW, Zampieri F, Goligher EC,Gardner MM, Topian AA, Yéthya N. A Bayesian Interpretation of a Pediatric Cardiac Arrest Trial (THAPCA-OH). NE,EM Vid. Evid.2023;EVDoa2200196. doi: 10.1056/EVIDo2200196
21.Magee A, Deschamps D, R!Ozdoppo,C. Pan KK, Bult W. Dagan M, Forest A. Namachivayam S. Temperature Management and Health-Related Qual-ity of Life in Children 3 Years After Cardiac Arrest. Piotid Care Med.2023;23:13-11. doi:10.1097/CC.00000000000002821
22. Topjian AA, French B, Sutton RM, Conlon T, Nadkarni M, Vomer F,Dean DJ. BMC Berg, Early postsuscitation hypotension is associated with increased mortality following pediatric cardiac arrest. Crit Care Med.2014;42:1518-1523. doi: 10.1097/CCM.00000000000000216
2023.Laurent, Li Moch, Chiche J, JDym, LJM, Spauding C, Bourgeois E, Cario A,Rozenberg A,Carli P, Weber S,et al.Reversible myocardial dysfunction in survivors of out-of-hospital cardiac arrest.J Am Coll Cardiol 2002;40:2110-2116. doi:10.1016/s0735-1097(02)02594-9
24. Laverrie EK, Polansky M, French B, Nadkarni VM, Berg RA, Topjian AA. Association of duration of hypotension with survival after pedi-atic cardiac arrest. Pediatr Care Med. 2020;21:143-149. doi: 10.1097/PCC.00000000000002119
25. Lin YR, Li U, CIu, TK. Chang YI, Li SC, Liu T, Haisa MH, CHU CC,Chang CF. Post-resuscitative clinical features in the first hour after achiev-ing sustained ROSC predict the duration of survival in children with non-trumatic out-of-hospital cardiac arrest. Resuscitation.2010;81:410-417.doi:10.1016/j.resuscitation.2010.101.006
26. Gardner MM, HeirDA, Reeder RW, Ahmed T, Bell MJ, Berg RA,Bishop R, Bochkor M, Burns C, Carcilo JA, et al. Identification of post-cardiac arrest blood pressure thresholds associated with outcomes in children: an ICU-Resuscitation study. Crit Care 2023:2738: doi:10.1186/s13054-023-04662-9
27. Ushpol A, Je S, Niles D, Majumdar T, Kirschen M, Del Castillo J, Buysse C,Topjian A, Nadkami V, Gangbanar S, PediE-Rious Observations. Associa-tion of blood pressure with neurologic outcome at hospital discharge after pediatric cardiac arrest resuscitation. Resuscitation:2024;194:110066. doi:10.1016/j.resuscitation.2023.110066
28. Liu R, Majumdar T, Gardner MM, Burnett R, Graham K, Beaulieu F, Sutton RM, Nadkami VM, Berg RA, Morgan RW, et al. Association of Postar-ht reypostation Burden With Unfavorable Neurologic Outcome Af-ter Pediatric Cardiac Arrest. Crit Care Med. 2024;52:1402-1413. doi:10.1097/CCM00000000000006339
29. Topjian AA, Raymond TT, Atkins D, Chan M, Duff JP, Joyner BL Jr., Lasa JJ,Lasonva EJ, LeV A, Mahgoub M, et al; Pediatric Basic and Advanced Life Support-Cosput Collaborators. Part 4: Pediatric Basic and Advanced Life Support:2020 American Heart Association Guidelines for Cardiopulmonary Resus-citation and Emergency Cardiovascular Care. Circulation. 2020;142:S469-S523. doi:10.1161/CIR/00000000000000901
30.Zwemer CF, Whitesain SE, D'Alecy LG. Cardiopulmonary-cerebral resus-citation with 100% oxygen exacerbates neurological dysfunction follow-ing nine minutes of northern thermic cardiac arrest in dogs. Resuscitation.1994;27:159-170. doi: 10.1016/0300-9572(94)90009-4
31. Liu Y, Rosenthal RE, Haywood Y, Miljovic-Lolic M, Vanderhoek JY,Fiskum G. Normoatic ventilation after cardiac arrest reduces oxidation of brain lip-ids and improves neurological outcome. Stroke.1998;29:1679-1686. doi: 10.1161/01str.298.8:1679
32. van Zellem L, de Jonge R, van Rosmalen J, Reiss I, Tibboel D, Buysse C.High cumulative oxygen levels are associated with improved survival of chil-dren treated with mild therapeutic hypothermia after cardiac arrest. Resus-citation.2015;90:150-157. doi: 10.1016/j.resuscitation.2014.12.013
33.Del Castillo J, Lopez-Herce J, Matamoros M, Canadas S, Rodriguez-Calvo A, Cechetti C, Rodriguez-Ronz-Nunez A, Alvarez A; Iberoamanic Pediatric Cardiac Arrest Study Network RIBEPCl. Hyperoxia, hypoxia and hypocra percapnia as outcome factors after cardiac arrest in children. Resuscitation.2012:83:1456-1461: doi:10.1016/j.resuscitation.2012.07.019
34. Ferguson LP, Durward A, Tibby SM. Relationship between arte-rial partial oxygen pressure after resuscitation from cardiac ar-rest and mortality in children. Circulation. 2012;126:335-342. doi:10.1016/CIRCULATIONHA,111.085100
35.Frazier AH,Topjian AA,Rededer RW,Morgan RW,FinkEL,Franzon D,Graham K,Harding ML,Mourian PM,Nadkarni VM,et al.Association of Pediatric Post-cardiac Arrest Ventilation and Oxygenation with Survival Outcomes. Ann Am Thorac Soc.2024:21895-906. doi:10.1513/AnnalsATS.202311-9480OC
36.Barreto JA, Weiss NS, Nielsen KR, Farris R, Roberts JS. Hyperaxia after pe-diatric cardiac arrest: Association with survival and neurological outcomes.Resuscitation:2022;1718:4-14. doi:10.1016/j.resuscitation.2021.12.003
37.Albrecht M, de Jonge RJC, Del Castillo J, Christoff A, De Hoog M, Je S,Nadkarni VM,Niles D E, Tegg O, Wellnitz K, et al; pediRES-Q Collab-erative investigators. Association of cumulative oxygen and carbon dioxide levels with neurologic outcome after pediatric cardiac arrest resuscita-tion: A multicenter cohort study. Resusc plus. 2024;20:100804. doi:10.1016/j.respuol.2024.100804
38. MengL, GelbAW.Regulation of cerebral autoregulation by carbon dioxide.An-esthesiology.2015;122:196-205. doi:10.1097/ALN.00000000000000506
39. Ruppel H, Maneken S, Faerber JA, Lane-Fall MB, Foglia EE, O'Byrne ML, Bonafide CPE. Evaluating the Accuracy of Pulse Oximetry in Chil-dren According to Race. JAMA Pediatr. 2023;177:540-543. doi: 10.101/jiampediatras.2023.0071
40. Henry NR, Hanson AC, Schulte PJ, Warner NS, Manento MN, Weister TJ,Warner MA. Disparities in Hypoxemia Detection by Pulse Oximetry Across Self-Identified Racial Groups and Associations With Clinical Outcomes. Crit Care Med.2022:2040-211.doi:10.1097/CCM.00000000000005394
1. López-Herce, J. Delastio J, Matamoros M, Canadas, S. Rodriguez-Calvo-Egac, C. Cecettich, R. Rodriguez-Nunez A, Carrillo A; leroamerican Pediatric Cardiac Arcest Study Network RIBEPCI. Post return of spontaneous cir-culation factors associated with mortality in pediatric in-hospital cardiac ar:rest: a prospective multicenter multinational observational study. Crit Care 2014:18:607 doi:10.1186/s13054-014-0607-9
42. Bennett KS, Clark AE, Meert KL, Topjian AA, Schleien CL, Shaffner DH,Dean JM, Moler FW; Pediatric Emergency Care Medicine Applied Re-search Network. Early oxygenation and ventilation measurements after pediatric cardiac arrest:ack of association with outcome. Crit Care Med.2013:41:1534-1542.doi:10.1097/CCM.0b013e318287f54c
43.Holton C, Lee BR, Escorah B, Benton B,{Tenton B, Bauer P. Admission PaO2 and mortality among PICU patients and select diagnostic subgroups. Pediatr Crit Care Med 2023/24:e362-3871. doi:10.1097/PCC.000000000003247
44.Mazzio EL, Topjian AA, Reeder RW, Sutton RM, Morgan RW, Berg RA,Ndakkari VM, Wolfe H., Graham K, Naim MY, et al; ICU-RESUS Eu-tice \& Kennedy Shiver National Institute of Child Health. Association of EEG characteristics with outcomes following pediatric ICU cardiac ar-rest: A secondary analysis of the ICU-RESuscitation trial. Resuscitation.2024:2011:10271. doi:10.1016/j.resuscitation.2024.110271
45.Bach AM,Kirschen MP,Fhung FW,Abend NS,Ampah S,Mondal A,Huh JW,Chen S-Lian Y, Graham K, et al. Association of EEG Background With Diffusion-Weighted Magnetic Energy Neuroaging and Short-Term Outcomes After Pediatric Cardiac Arrest. Neurology. 2024;102:e209134.doi:10.12117/000000000000000000000000000000
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46. El-Seify M, Shata MO, Salahelid S, Bawady S, Rezk AR. Evaluation of Serum Biomarkers and Electronecephalogram to Determine Survival Out-comes in Pediatric Post-Cardiac-Arrest Patients. Children(Basel, Switzer-land).2023;10:180. doi: 10.3390/children 10020180
47. Lin JJ, Hsu MH, Hsia SH, Lin YJ, Wang HS, Kuo HC, Chiang MC, Chan OW, Lee EP, Lin KL; the iCNS Group. Epileptiform discharge and electro-graphic seizures during the hypothermia phase as predictors of rewarming seizures in children after resuscitation. J Clin Med.2020;9:2151-2111.doi.10.3390/jcm9072151
48. Herman ST, Abend NS, Bleck TP, Chapman KE, Drislane FW, Emerson RG, Gerard EE,Hahn CD, Husain AM, Kaplan PW, et al; Critical Care Continuous EEG Task Force of the American Clinical Neurophysiology Society. Consensus statement on continuous EEG in critically ill adults and children, part I: indications. J Clin Neurophysiol. 2015;32:87-95. doi: 10.1097/WNP0000000000000166
49. Ruijter BJ,Keijzer HM,Tjepkema-Cloostmans,MC Blans,JeBishuizen A,Tromc SC, Scholten E, Horn J, van Rootselaar AF, Admiral MM, et al;TELSTAR Investigators. Treating Rhythmic and Periodic EG Patterns in Comatose Survivors of Cardiac Arrest. N Engl J Med. 2022;386:724-734.
50.Brophy GM,Bell R,Classen J,Aldredge B,Block TP,Glauser T,Laroche SM, Rivello JJ Jr, Shutter L, Sperling MR, et al; Neurocritical Care Society Status Epilepticus Guideling Writing Committee. Guidelines for the evalua-tion and management of status epilepticus. Neurocrit Care. 2012;17:3-23. doi: 10.1007/s12028-012-9695-z
NEUROLOGICAL PROGNOSTICATION FOLLOWING CARDIAC ARREST
Introduction
Hypoxic ischemic brain injury is the leading cause of death and disability after cardiac arrest. Early and reliable neurological prognostication after resuscitation from pe-diatric cardiac arrest is essential to guide treatment, en-able accurate counseling, and provide family support. In addition, accurate neurological prognostication is critical to avoid inappropriate withdrawal of life-sustaining thera-py in patients who may have a meaningful recovery while also avoiding potentially inappropriate life-sustaining treatments. For further discussion of ethical consider-ations regarding prognostication and uncertainty, refer to“Part 3: Ethics.”
The definitions of favorable and unfavorable neuro-logical outcome are complex and dynamic throughout the recovery period after cardiac arrest. Recovery pro-gresses along a temporal continuum such that a child assessed as having a favorable or unfavorable outcome at hospital discharge may be assessed differently sev-eral months to years after discharge. Gross scoring sys-tems such as the PCPC are limited in the granularity of assessment and not standardized across ages, such that the same PCPC of a 6-month-old and 10-year-old may not be comparable. Thus, when classifying patients into favorable versus unfavorable outcome categories and combining timepoints of assessment, it is important to understand that these dichotomous outcomes may not give a complete picture of the individual patient's com-plex reality. However incomplete the portrait of outcomes,health care professionals must still provide guidance to families, thereby necessitating criteria to classify patient outcomes.
These 2025 recommendations are based on 2 ILCOR systematic reviews of potential prognostic modalities for neurological outcome; one for prediction of good(favorable) neurological outcome and one for prediction of poor(unfavorable) neurological outcome.3,4 These reviews used the same data but analyzed them differently based on the outcome being assessed(good or poor). Definitions of good neurological outcome are not standardized and vary across studies, most often defined as a PCPC of 1 or 2; 1, 2, or 3; no change from baseline; or a Vineland Adaptive Behavioral Score of>70.5,6
Good neurological outcome was assessed as a threshold false positive rate(FPR) of less than 30%(ie, predicting a good neurological outcome but having a poor neurological outcome).3.7 For poor neurological outcome, they used an FPR of<1%(ie, predicting a poor neurological outcome but having a good neuro-logical outcome).4 Sensitivity(eg, probability of a good neurological outcome in a patient who has a positive finding) was assessed for all studies but was not the primary assessment of predictive accuracy. An FPR of<1% was selected for predictors of poor neurological outcome to minimize the risk of making recommenda-tions for limitation of care in patients who would have a good neurological outcome. Adult studies have used FPR thresholds to predict poor neurological outcome between<0% and 5%,8,9 Standard thresholds to pre-dict outcome from pediatric cardiac arrest have not been established.
The systematic review for predicting good (favorable)neurological outcome-assessed associations of posi-tive test findings (eg, bilateral reactive pupils) with good neurological outcome, whereas the systematic review for poor neurological outcome-assessed associations of negative findings (eg, bilateral unreactive pupils) with poor neurological outcome. It cannot be presumed that positive findings for favorable outcome (ie, presence of reactive pupils with good neurological outcome) will have the same predictive value as negative findings for unfa-vorable neurological outcome (ie, absence of reactive pupils with poor neurological outcome). For the purposes of this guideline, we have chosen the terms favorable (good) and unfavorable (poor).
Neurological Prognostication Following Cardiac Arrest
|Recommendation for Multimodal Prognostication Following Cardiac Arrest|| |---|---| |COR|LOE| |1|1. It is recommended that health care professionals consider multiple modalities when predicting neurological outcomes (favorable or unfavorable) after resuscitation from cardiac arrest in infants and children.|
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Synopsis
Health care professionals use various assessments to guide neurological prognostication in the post-cardiac arrest period including neurological examination, bio-markers,EEG, and neurological imaging modalities(eg,brain computed tomography and magnetic resonance imaging). Studies reporting the predictive accuracy of individual assessments must be interpreted in the context of timing following ROC, outcome assessed(ie, survival versus survival with a good functional out-come), and unmeasured confounders(eg, sedation).Some modalities can predict favorable neurological outcome, unfavorable neurological outcome, or both.Each must be considered in conjunction with other modalities.
Recommendation-Specific Supportive Text
1. Numerous studies demonstrate associations between clinical examination findings, biomarkers,electrophysiology patterns, and neurological imag-ing findings with outcomes following pediatric car-diac arrest.10-22 However, these studies are limited by their retrospective designs, lack of blinding, and unadjusted and unmeasured confounding. In addi-tion, there are no established predictive accuracy thresholds(eg, sensitivity, specificity, Area Under the Receiver Operating Curve) for individual or com-bined criteria. Thus, multiple modalities are needed for neurological prognostication.
|Recommendations for Prognostication Using Clinical Examination Following Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|C-LD|1. The usefulness of cough or gag reflexes or response to pain to support a favorable or unfavorable neurological prognosis at any timepoint after cardiac arrest in infants and children is not well established.|| |2b|C-LD|2. The usefulness of motor response to any stimulus to support a favorable or unfavorable neurological prognosis at any timepoint after cardiac arrest in infants and children is not well established.|| |2b|C-LD|3. The usefulness of total Glasgow Coma Scale (GCS) score or GCS motor score to support a favorable neurological prognosis at any timepoint after cardiac arrest in infants and children is not well established.|| |2b|C-LD|4. When interpreted in the context of other prognostic criteria, it may be reasonable to use the presence of bilateral pupillary light reflexes in the first 12 h after cardiac arrest in infants and children to support a favorable neurological prognosis.|| |2b|C-LD|5. When interpreted in the context of other prognostic criteria, it may be reasonable to use the absence of bilateral pupillary light reflexes between 48 and 72 h after cardiac arrest in infants and children to support an unfavorable neurological prognosis.||
|Recommendations for Prognostication Using Clinical Examination Following Cardiac Arrest(Continued)|||| |---|---|---|---| |COR|LOE|Recommendations|| |3:No Benefit|B-NR|6. The absence of pupillary light reflex in the first 24 h after cardiac arrest in infants and children to support an unfavorable neurological prognosis is not recommended.|| |3:No Benefit|B-NR|7. The GCS score in the first 24 h after cardiac arrest in infants and children to support an unfavorable neurological prognosis is not recommended.||
Synopsis
Neurologic assessments routinely include brainstem re-flexes such as pupillary response, cough and gag, and motor response to stimuli. The neurologic examination evolves in the days after cardiac arrest, and a given find-ing(eg, pupillary reactivity) at an early timepoint may not have the same accuracy for prediction of outcome at a later timepoint. Furthermore, the predictive accuracy of an exam finding(eg, pupillary reflexes) at one timepoint for favorable neurological outcome may not have the opposite predictive accuracy when the exam finding is absent(eg, absence of pupillary reflexes for unfavorable neurological outcome). Exam findings in these studies are often obtained through retrospective chart review,thus patient condition and potential confounders may not be reported which may impact the accuracy of the as-sessment. Clinical examination may also be confounded by sedation administration. Therefore, caution must be used when interpreting these data and health care pro-fessionals must avoid the use of isolated exam findings to predict neurological outcome.
Recommendation-Specific Supportive Text
1. Three studies assessed the associations between cough or gag reflexes or evoked pain response and neurological outcome. The presence of cough and gag reflex at 24 hours predicted favorable neuro-logical outcome with a low sensitivity of 40% for both and an FPR of 35% and 32% respectively.2223 The absence of cough and gag predicted an unfavorable neurological outcome with an FPR of 60% and a sensitivity of 65% to 69%.23 The sensitivity for evoked pain response for favorable neurological outcome was 100%, but the FPR was as high as 67%.22,24 The absence of an evoked pain response at 6 and 12 hours to predict unfavorable neurological outcome in 1 study had an FPR of 0%(0%-15%) with a sensi-tivity of 33%.22 The FPR for these assessments did not meet predefined thresholds to predict favorable or unfavorable neurological outcome.
2. In a small study of 29 patients, any motor response at 48 and 72 hours after ROC had a sensitivity 80% to 100% and low FPR(23%-27%) for favor-able neurological outcome.25 In that same study,the absence of any motor response to predict
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unfavorable neurological outcome at<1 hour, 48 hours, and 72 hours after ROC had a sensitivity 61% to 73%. The FPR for unfavorable neurologi-cal outcome was 62% at less than 1 hour, 20%at 48 hours and 0% at 72 hours. These data are limited to 1 small single-center study and require further evaluation.25
3. Three studies including 296 patients assessed the association of mental status measured by the total GCS score >4, 7 or 8, or GCS motor score >4 within 24 hours of ROC with neurological outcome at ICU or hospital discharge or 6-month follow-up. They had low sensitivity(<50%), and low FPR(<14%) for favorable neurological outcome, 26-28 but only 1 study assessed each timepoint and threshold and thus data were limited.
4. Three studies evaluating the presence of bilateral pupillary reflexes within 12 hours of ROC dem-onstrated a sensitivity(ie, probability of patients with a favorable neurological outcome having bilateral pupillary response) of at least 82% for favorable neurological outcome(PCPC 1-2 or 1-3) and FPRs(ie, bilaterally reactive pupils with an unfavorable neurological outcome) of 16% to 31%,22,25,27 At timepoints>24 hours from ROC,while sensitivity of bilateral pupillary reactivity was 75% to 100%, a high FPR of 68% was observed thus demonstrating its lack of reliability for pre-diction.23-25,28-30 Therefore, findings of bilateral pupillary reactivity>24 hours post-cardiac arrest are less reliable and pupillary response alone is inadequate for neurological prognostication at any timepoint.
5. Three studies evaluated the absence of pupil-lary reflexes to predict unfavorable neurologi-cal outcome at 48 and 72 hours after ROC with an FPR<$1\%$ but with wide confidence intervals(95% CI, $0\%$ -40\%) and low sensitivity of 12\% to 46\%.24,25,31 These FPRs met the prespecified FPR threshold and are moderately reliable, but should only be used in conjunction with other predictors.
6.Six of 7 studies that assessed the absence of bilateral pupillary reflexes to predict unfavorable neurological outcome between <1 hour and 24 hours after ROC had an FPR >10% up to 60%with sensitivities of 33% to 93%.23,25,27-30 These studies show that the absence of pupillary reflex within 24 hours after ROC are not accurate to pre-dict outcome.
7. Three studies including 296 patients assessed the association of mental status measured by the total GCS or GCS motor score within 24 hours of ROC with neurological outcome at ICU or hos-pital discharge or 6 month follow-up.26-28 A GCS motor score of <4 at 1 hour after ROC to predict unfavorable neurological outcome had high FPRs
<EndOfPara>of 83% and 50%, respectively, with high sensitivi-ties of 93% to 94%.27 A total GCS score of<4 at resuscitation or within 1 hour of ROC predicted unfavorable neurological outcome with a high FPR of 70% and a high sensitivity of 86%.26 A total GCS score<7 to predict unfavorable neu-rological outcome had a high FPR of 69% and high sensitivity of 92%.28 These data demonstrate that these GCS data are not accurate to predict outcome.
|Recommendations for Prognostication Using Biomarkers Following Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|B-NR|1. When interpreted in the context of other prognostic criteria, it may be reasonable to use a plasma lactate value <2 mmol/L up to 12 h after cardiac arrest in infants and children to support a favorable neurological prognosis.|| |2b|C-LD|2. The usefulness of neuronal biomarkers (eg, S100B, neuron-specific enolase) to support a favorable or unfavorable neurological prognosis at any timepoint after cardiac arrest in infants and children is not well established.|| |3: No Benefit|B-NR|3. The use of blood lactate after cardiac arrest in infants and children to support an unfavorable neurological prognosis is not recommended.|| |3: No Benefit|B-NR|4. The use of blood pH after cardiac arrest in infants and children to support a favorable or unfavorable neurological prognosis is not recommended.||
Synopsis
Serum biomarkers are blood-based tests that measure levels of proteins that are found in the central nervous system or measure inflammation or systemic ischemic reperfusion. Central nervous system proteins are re-leased across the blood brain barrier when the brain is injured: Neuron-specific enolase is released from injured neurons, glial fibrillary acidic protein from injured glia,neurofilament light from injured axons, and S100B from injured astrocytes. Hypoxic ischemic brain injury and re-perfusion injury may cause injury to these cells different-ly, and release of these proteins may occur and peak at different times after injury. Studies of these neuronal bio-markers are limited by different assessment platforms,different baseline values across platforms and extracere-bral sources for some proteins.
Commonly measured blood-based markers of inflammation or systemic ischemic reperfusion are pH and lactate levels. Lactate levels may reflect the sever-ity of systemic hypoxia and ischemia before, during, or after cardiac arrest, pH is impacted by both systemic acidosis, of which lactate acidosis may be a major con-tributor, as well as respiratory acidosis, which may be due to inadequate ventilation. These systemic markers change over time after arrest. pH can be modified by titration of the ventilator to correct respiratory acido-sis as well as administration of sodium bicarbonate to
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treat metabolic acidosis. Lactate clearance refers to the decrease in lactate over time after cardiac arrest;earlier clearance is associated with decreased mortal-ity in adults. ${}^{32}$
Recommendation-Specific Supportive Text
1. Serum lactate<2 mmol/L within 12 hours of ROC had low sensitivity of 16% to 28% for favorable neurological outcome, but a very low FPR rang-ing from 4% to 7%.33-35 Lactate thresholds of<2 mmol/L at 24 and 48 hours and<5 mmol/L at 1 and 24 hours had high FPRs of 17% to 68% and were moderately sensitive(61%-89%).33,36 Thus only timepoints before 12 hours should be consid-ered to predict outcomes in conjunction with other findings.
2.Neuronal biomarkers S100B, neuron-specific enolase, myelin basic protein, neurofilament light,ubiquitin C-terminal hydrolase-L1, glial fibril-lary acidic protein, and tau have been assessed at timepoints ranging from<1 hour through 96 hours after ROC.20,29,37,38 Various thresholds were assessed for biomarkers to predict favorable neu-rolological outcome at different timepoints result-ing in very wide ranges of FPR(0% to 96%)and sensitivities(5% to 100%). Three studies of various thresholds for S100B had an FPR of 0%with sensitivities of 29% to 38% for unfavorable neurological outcome and for neuron-specific enolase had FPR of 0% with sensitivities of 19%to 26%.20,29,37 While these FPRs for favorable out-come were low, there were no consistent thresh-olds evaluated for these markers. Further study is needed to validate specific biomarker thresholds and discrete timepoints.
3. Lactate was assessed in 6 studies. ${}^{20,34,35,39-41}$ Two studies had an FPR of $<1\%$ for unfavorable neu-rological outcome, 1 with a sensitivity of 11% with a threshold greater than 28.8 mmol/L 1 hour after ROC and 1 with a lactate clearance less than 2 mmol/L by 48 hours post-ROC.20,39 All other stud-ies had FPR ranging from 11% to 83% for unfa-vorable neurological outcome.33-35,41
4. pH level was assessed in 4 studies. ${}^{20,34,35,39}$ A pH threshold of $>7.0$ at 1 hour and 6 to 12 hours post-cardiac arrest had high sensitivities of 71%to 96%, but high FPRs ranging from 45% to 97%for favorable neurological outcome. A pH threshold of $>7.3$ at 1 hour and 24 hours post-cardiac arrest had sensitivities of 49% and 89% respectively but FPRs of 38% and 81% respectively for favorable neurological outcome. ${}^{40}$ For unfavorable neurologi-cal outcome, 3 studies had FPRs $<5\%$ , but sen-sitivities of $3\%$ to $14\%.20,34,45 pH$ is not accurate enough to predict favorable or unfavorable neuro-logical outcome.
|Recommendations for Prognostication Using Electrophysiology Following Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |2a|B-NR|1. When interpreted in the context of other prognostic criteria, it is reasonable to use EEG up to 72 h after cardiac arrest in infants and children to support a favorable or unfavorable neurological prognosis.|| |2b|B-NR|2. When interpreted in the context of other prognostic criteria, it may be reasonable to use the presence of continuous or normal EEG background in the first 72 h after cardiac arrest in infants and children to support a favorable prognosis.|| |2b|C-LD|3. When interpreted in the context of other prognostic criteria, it may be reasonable to use the presence of sleep spindles or stage ll sleep architecture on EEG between 12 and 24 h after cardiac arrest in infants and children to support a favorable neurological prognosis.|| |2b|C-LD|4. When interpreted in the context of other prognostic criteria, it may be reasonable to use the presence of EEG reactivity between 6 and 24 h after cardiac arrest in infants and children to support a support a favorable neurological prognosis.|| |2b|C-LD|5. When interpreted in the context of other prognostic criteria, it may be reasonable to use the presence of status epilepticus, or the presence of burst suppression, burst attenuation or generalized periodic epileptiform discharges between 24 and 72 h after cardiac arrest in infants and children to support an unfavorable neurological prognosis.|| |2b|C-LD|6. The usefulness of the presence of attenuated isoelectric or flat EEG, or presence of myoclonic status epilepticus at any timepoint after cardiac arrest in infants and children to support an unfavorable neurological prognosis is not well established.|| |3: No Benefit|B-NR|7. The presence of clinical or electrographic seizures, absence of sleep spindles and stage ll sleep architecture, absence of continuous or normal EEG background, absence of EEG reactivity, and absence of EEG variability at any timepoint after cardiac arrest in infants and children is not recommended to support an unfavorable neurological prognosis.|| |3: No Benefit|B-NR|8. The absence of burst suppression, burst attenuation, generalized periodic epileptiform discharges, attenuated, isoelectric, or flat EEG at any timepoint after cardiac arrest in infants and children to support a favorable neurological prognosis.|| |3: No Benefit|B-NR|9. The absence of clinical or electrographic seizures, absence of status epilepticus, or absence of myoclonic seizures in infants and children is not recommended|| |3: No Benefit|B-NR|myoclonic seizures in infants and children is not recommended to support a favorable neurological prognosis.||
Synopsis
EEG is broadly used to monitor for subclinical seizures and to assess background states after brain injury. Pa-tients who are encephalopathic after cardiac arrest may have subclinical seizures due to cortical injury which cannot be detected without EEG monitoring. Electro-encephalography for neurological prognostication has
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Pediatric Advanced Life Support: 2025 AHA/AAP Guidelines for CPR and ECC
promise as it directly assesses neurologic activity. How-ever, studies are limited because most are single center,utilize nonstandardized terminology, lack clinician blind-ing to EEG data when caring for patients, and do not describe the impact of medications on EEG background.These systematic reviews assessed multiple EEG fea-tures including the presence and absence of normal and abnormal EEG features with favorable and unfavorable neurological outcomes.5.7
Recommendation-Specific Supportive Text
1. EEG monitoring up to 72 hours after ROC identifies EEG background features and diagnoses electro-graphic seizures. In patients who are encephalo-pathic,clinical exams can be unreliable and seizures can be subclinical. Electroencephalography is the only way to identify subclinical seizures.21,22,30,42-46
2. Ten studies with more than 560 patients evaluated the association of either continuous or routine(brief) EEG at either<1 hour; 6 to 12 hours; 24,48,72 hours; or 4 to 6 days with favorable neuro-logical outcome at PICU or hospital discharge or 6 months following cardiac arrest. Among the studies evaluating EEG performed at 6 to 12 and 24 hours post-ROC,6 of 7 studies had FPRs less than 29%for favorable neurological outcome with sensitivi-ties that ranged from 7% to 100%,23,30,42,44,45,47,48 Studies at 48 and 72 hours reported FPRs ranging from 0% to 50% for favorable neurological out-come, although 50% of the studied timepoints had FPRs less than 30%,21,24,29,47
3. The presence of sleep architecture at 6 to 12 hours or sleep spindles at 24 hours had an FPR of 16% and 8% for favorable neurological outcome,with sensitivities of 57% and 80%, respectively.Sleep spindles or sleep II architecture should not be used as the sole assessment to prognosticate at any timepoint.23,30
4.At 6 to 12 and 24 hours post-ROC, the presence of reactivity had an FPR of less than 27% with a sensitivity of 53% to 63% for favorable neurologi-cal outcome.42,44 At 48 hours, 1 study had an FPR of 50%.44 Thus EEG reactivity, based on these data,is accurate only at 6 to 24 hours, not 48 hours for favorable neurological outcome.
5. The presence of status epileptic predicted unfa-vorable neurological outcomes with a low FPR of 0% at 24 to 72 hours after ROC in 3 studies,21,24,48 but an FPR of 4% to 5% at 4 to 6 hours and 6 to 12 hours, all with low sensitivity.42,45 Thus, the presence of status epileptic at 24 to 72 hours moderately predictive for unfavorable neurologi-cal outcome. The presence of burst suppression,burst attenuation or generalized periodic epilepti-form discharges within 24 hours of ROC had an FPR that ranged from 0% to 19% and sensitivity
of 9% to 30% for unfavorable neurological out-come.23,44,45,49 From 48 to 72 hours after ROC,3 studies had FPRs<1%(95% CI, upper limit range 16%-54%) with sensitivities of 0% to 67% for unfavorable neurological outcome.21,22,24 The pre-diction of unfavorable neurological outcome was moderately reliable from 24 to 72 hours.
6. Two studies of 61 patients, of which 8 had myo-clonic status epilepticus, had an FPR of 0%(95%CI, 0%-34%) and sensitivity of 17% to 21% at PICU/hospital discharge.22,44 The presence of attenuated, isoelectric, or flat EEG before 24 hours in 5 studies had FPRs ranging from 6% to 95%,23,42,45,47,49 except for 2 studies that had and FPR of 0% with upper limit confidence intervals of 4% to 31%,30,50 In 6 studies from 48 hours to 7 days,2 had FPRs<1% with 95% CI up to 34% to 52%22,44; while other studies had FPRs that ranged from 3% to 71%.21,29,47,51 There are conflicted data and further study is needed.
7. Of 10 studies, the presence of seizures between 4 to 6 hours and 24 hours post-ROC had an FPR of 0% to 20%, of which only 1 had an FPR of<1%with wide confidence intervals44,45,50 and a sensitiv-ity of 2% to 38% for predicting unfavorable neu-rological outcome.27,30,34,42,44,45,48-50 At 48 hours and onward only 2 studies reported an FPR for pre-dicting unfavorable outcome of<1%41,44; others had FPRs up to 58%. The presence of seizures is accurate to predict unfavorable neurologic out-come at any of these timepoints. The absence of a normal/continuous EEG background patterns(defined as normal, continuous, and reactive; con-tinuous and unreactive; and nearly continuous) by ACNS definitions52 had variability and high FPRs ranging from 0% to 90%21-24,29,30,42,44,45,47-50, only 2 studies had an FPR<1%.48,51 The absence of a normal/continuous EEG background pattern is not accurate to predict unfavorable neurologi-cal outcome. The absence of EEG reactivity had an FPR of 0% to 93% and sensitivity of 36% to 100%21,42,44; absence of sleep II architecture had an FPR of 0% to 43% and sensitivity of 84% to 92%23,30,42; and absence of variability on EEG42,44 had an FPR of 0% to 80% and sensitivity of 21%to 82% for unfavorable neurological outcome pre-diction. These were unreliable tests for unfavorable outcome prediction.
8.Absence of attenuated, isoelectric or flat EEG to predict favorable neurological outcome was assessed in 10 studies.21-23,29,30,42,44,45,47,51 The FPR was greater than 40% in most studies and the sensitivity was high in most studies at all timepoints (71%-100%).23,30,42,44,45,47,51 While the absence of burst suppression, burst attenuation, or generalized periodic epileptiform discharges had
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Pediatric Advanced Life Support: 2025 AHA/AAP Guidelines for CPR and ECC
a sensitivity for favorable neurological outcome of>81% at all timepoints, the FPR was>67% at all timepoints.21-23,42,44,45 These EEG features should not be used to predict favorable neurological outcome.
9.The absence of seizures had FPRs of 58% to 100% and sensitivities that ranged from 50% to 100% for favorable neurological outcome at PICU or hospital discharge, or 6 or 12 months post-cardiac arrest.21,22,27,30,34,35,42,44,45,51 Absence of sta-tus epilepticus at 6 to 12 or 72 hours had a high sensitivity(>96%) for favorable neurological out-come, but very high FPRs(75% to 91%).21,24,42,45 The absence of myoclonus in the 48 hours post-cardiac arrest was 100% sensitive for favorable neurological outcome but had high FPRs(79% to 83%).22,44 Thus these EEG features should not be used to predict favorable neurological outcome at any timepoint.
|COR|LOE|Recommendations| |---|---|---| |2b|B-NR|1. When interpreted in the context of other prognostic criteria, it may be reasonable to use normal brain magnetic resonance imaging (MRI) between 72 h and 2 wk after cardiac arrest in infants and children to support a favorable neurological prognosis.| |2b|C-LD|2. When interpreted in the context of other prognostic criteria, it may be reasonable to use an abnormal brain MRI showing high ischemic burden at 72 h or later after cardiac arrest in infants and children to support an unfavorable neurological prognosis.| |2b|C-LD|3. When interpreted in the context of other prognostic criteria, it may be reasonable to use a CT with loss of gray-white matter differentiation within 24 h after cardiac arrest in infants and children to support an unfavorable neurological prognosis.| |3: No Benefit|C-LD|4. A normal brain CT scan within the first 48 h after cardiac arrest in infants and children is not recommended to support a favorable neurological prognosis.|
Synopsis
Early neuroimaging after cardiac arrest is useful to de-tect structural brain injury and potential etiologies of car-diac arrest that may be amenable to intervention such as evacuation of intracranial hemorrhage. MRI can assess the severity of cytotoxic injury through diffusion weighted imaging. Ischemic injury on diffusion weighted imaging peaks at days 3 to 7 after cardiac arrest and may have the appearance of normalizing, or“pseudonormalization,”2 weeks after injury. Both computed tomography(CT)and MRI findings evolve over the days after cardiac arrest-rest and must be interpreted in the context of other find-ings and based on time from injury. Studies assessing neuroimaging for the prediction of neurological outcome
require careful interpretation as they are limited by ret-rospective designs where health care professionals have likely used imaging results to guide treatment decisions.
Recommendation-Specific Supportive Text
1. In 3 studies, absence of diffusion restriction or absence of any abnormality on MRI had a sensi-tivity of 42% to 88% with FPRs of 0% to 2% for favorable neurological outcome.24,51,53 Apparent diffusion coefficient thresholds of>600x10-6 mm2/s in>93% and>650x10-6 mm2/s in>89%of brain volume, at a median of 4 days after ROC,predicted favorable neurological outcome with a sensitivity of 100% and low FPR of 20%.54 While the absence of specific regional abnormalities on MRIs were highly sensitive for favorable neurologi-cal outcome, they had very high FPRs.31,55
2. In 3 studies, the presence of high burden of isch-emia defined as apparent diffusion coefficient threshold<650x10-6 mm2/s in≥10% of brain vol-ume at a median of 4 days after ROC, predicted unfavorable neurological outcome with a sensitivity of 49% to 52% and an FPR of 0% to 6%(95%CI,1%-21%)49,54,56 but only 1 had an FPR<1%with a sensitivity of 80%.54 The presence of diffu-sion restriction based in any brain region based on nonstandardized definitions at a median of 4 days and up to 14 days had high FPR(12%-58%) for unfavorable neurological outcome.24,56 The studies found that the abnormalities in diffusion weighted imaging, T1-, and T2-weighted imaging in indi-vidual regions of the brain, at 4 to 6 days post-ROC, predicted unfavorable outcome with FPR of 0% to 10% but wide confidence intervals up to 50%.24,31,55
3.One study of 78 children had an FPR 0%(CI 0%-12%) and sensitivity of 65% for the loss of gray-white matter differentiation on CT within 24 hours of arrest to predict unfavorable neurologi-cal outcome(PCPCC>3) at hospital discharge.16 Clinicians were not blinded to the CT results in any study.
4. In 2 studies, the absence of grey-white matter differentiation on CT within 24 hours from ROC had a sensitivity of 64% to 100% with an FPR between 35% and 75% for favorable neurological outcomes at hospital discharge.16,57 Absence of a reversal sign and cistern or sulcal effacement had high FPRs that ranged from 14% to 80% sensi-tivities despite sensitivities that ranged from 93%to 100%.16,57 Normal CT early after cardiac arrest is not accurate to predict favorable neurologic outcome.
Figure 4 provides a timeline summary of recommen-dations for prognosticating good or bad neurologic outcomes.
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Consider using as part of multimodal testing for favorable outcome
|Day 1|Day 1|Day 2|Day 2|Day 3|Day 4|Day 5-2 weeks| |---|---|---|---|---|---|---| |0-12h|13-24 h|25-48 h|49-72 h|73-96 h|42-72 h|Day 5-2 weeks| |Presence of bilateral pupillary light reflex 0-12 hours|||||Normal MRI≥72 hours|| |Plasma lactate <2 mmol/L within 12 hours||||||| |Presence of EEG reactivity 6-24 hours||||||| |Presence of continuous or normal EEG background 1-72 hours||||||| |Presence of sleep spindles or stage II sleep on EEG 12-24 hours|||||||
Consider using as part of multimodal testing for unfavorable outcome

Recommendation against the use of
Insufficient evidence for a recommendation for or against the use of
 Neuronal biomarkers:S108N, neuron specific enolase,neurofilament light chain
 Any single test in isolation
Blood pH for any outcome Lactate values to support unfavorable outcome
 EEG:attenuated,isoelectric,or flat EEG,or myoclonic status epilepticus to support unfavorable neurological outcome
 Clinical exam: GCS or absent pupillary reactivity to light within 24 hours of ROC to support an unfavorable outcome
 Normal head CT within the first 48 hours after ROC to support favorable outcome
Clinical exam: cough,ag, or any motor response for any outcome Total GCS or GCS motor score for favorable outcome
 EEG: presence of clinical or electrographic seizures,absence of sleep spindles or sleep III architecture,absence of continuous or normal EEG background,absence of EEG reactivity, and absence of EEG variability to support unfavorable neurologic prognosis
EEG:absence of burst suppression; burst attenuation;generalized periodic epileptiform discharges;attenuated, isoelectric, or flat EEG; absence of clinical or electrographic seizures; absence of status epilepticus or myoclonic seizures to support favorable neurologic prognosis
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36. Meert KL, Delus R, Slomine BS, Christensen JR, Page K, Holubkov R,Dean JM, Moler FW; Therapeutic Hypotheria after Pediatric Cardiac Ar-rest Trial Investigators. One-Year Survival and Neurologic Outcomes After Pediatric Open-Chest Cardiopulmonary Resuscitation. Ann Thorac Surg.2019;107:1441-1446. doi:10.1016/jathocrasur.2018.11.028
37. Bangsho J, Liebetra B, Wiberg, S.jeldsted J, Kjaergaard J, Hassager C,Wischer M. The Value of the Biomarkers Neuron-Specific Enolase and S100 Calcium-Binding Protein for Prediction of Mortality in Children Re-susclated After Cardiac Restat. Pediatr Cardiol. 2022;43:1659-1665. doi:10.1007/s0024-022-02899-9
38.Fink EL, Kochanek PM, Panigrahy A, Beers SR, Berger RP, Bayir H,Fineda J, Newch E, Topian AA, Press CA, et al: Personalizing Out-comes After Child Cardiac Arrest (POCCYA) Investigators. Association of Blood-Based Brain Injury Biomarker Concentrations with Outcomes af-ter Piodatic Cardiac Astrop. JAMA Netw Open 2022;230518.1001.1097/iamanetworkopen.2022.30518
39.De La liana RA,Le Marsney R, Gibbons K, Anderson B, Haisz E, Johnson K,Black A, Venugopal P, Mattke AC. Merging two hospitals: The effects on pediatric extracorporeal cardiopulmonary resuscitation outcomes. J Pediatr Intensive Care 2021;10:2020-209.
40. Lopez-Herce J, del Castillo Matis M., Camadas S. Rodriguez-Calvo A,Cechetti C, Rodriguez-Nunez A, Carrillo A; Iberoamerican Pediatric Cardiac Asture Study Network RIBEPiC. Post return of spontaneous cir-culation factors associated with mortality in pediatric in-hospital cardiac ar-reast: a prospective multicenter multilingual observational study. Crit Care 2014;18:607 doi:10.1186/s13054-014-0007-9
41. Meert KL, Guerguerian AM,Barbaro R, Slomine BS,Christensen JR, Berger J,Topian A Bemmea B, Tabbut S, Frink E, et al.; Therapeutic Hypotheremia After Pediatric Cardiac Arrest (THAPCA) Trial Investigators. Extracoreporal cardiopulmonary Resuscitation: One-Year Survival and Neurobehavioral Outcome among infants and Children with In-Hospital Cardiac Arrest. Crt Care Med.2019;47:393-402. doi: 10.1097/CCM.00000000000003545
42. Topjian AA, Sanchez SM, Shults J, Berg RA, Dlugos DJ, Abend NS. Ear-ly Electroencephalic Background Features Predict Outcomes in Children Resuscitated from Cardiac Arrest. Pediatr Calc. Predict Care Med.2016;17:547-557. doi:10.1097/PCC.00000000000000740
48. Bourgoin B, Parrault V, Jornem L, Leclair Visonneau L, Toultog F,Anthoine E, Loron G, Chenouard A. The prognostic value of early amplitude-integrated electroencephalography monitoring after pe-diatric cardiac arrest. Pediatr Care Med. 2020;21:248-255. doi:10.1097/pcc.000000000000002171
44. Ostendorf AP Hartman ME, Fissr SS. Early electroencephalo-graphic findings correlate with neurologic outcome in children fol-lowing cardiac arrest. Pediatr Crit Care Med. 2016;17:667-676. doi:10.1097/PCC.0000000000000791
45. Fung FW, Topjian AA, Xiao R, Abend NS. Early EEG Features for Out-come Prediction After Cardiac Arrest in Children. J. Clin Neurophysiol 2019;36:349-357. doi: 10.1097/WNP00000000000591
46. Lee S, Zhao X, Davis KA, Topjian AA, Litt B, Abend NS. Quantitative EEG pre-dicts outcomes in children after cardiac arrest. Neurology.2019:92e2392-e2338. doi:10.1212/WNL/1000000000007504
47. Kessler SK, Topjian AA, Gutierrez-Colina AM, chorden, DNnelly, Ndendri,Ndakkami VM, Berg RA, Duplos DJ, Clancy RR, Aend BN. Short-term outcome prediction by electroencephalographic features in children treated with therapeutic hypothermia after cardiac arrest. NeurocRT.2011;14:37-43. doi:10.1007/s10280-010-9450-2
48. Smith AE, Ganninger AP, Mian AY, Friesh, Guerrino RM, Guilliams K. Magnetic resonance imaging adds prognostic value to EEG af-ter pediatric cardiac arrest. Resuscitation. 2022;173:91-100. doi:10.1016/j.resuscitation.2022.02.017
49.Bach AM,Kirschen MP,Fung FWABk End NS,Apham S,Mondal A,Hui JW,Chen SL,Yuan I, Graham K,et al. Association of EEG Background With Diffusion-Weighted Magnetic Resonance Neuroimaging and Short-Term Outcomes After Pediatric Cardiac Arrest Neurology. 2024;102:e209134.doi:10.1212/WNL0000000000209134
50.Mazio EL, Topjian AA, Reeder RW, Sutton RM, Morgan RW, Berg RA,Narkdami WM, Wolfe HA, Graham K, Kim M, Ayre, et al; ICU-RESUS Eu-nice Kennedy Shriver National Institute of Child Health. Association of EEG characteristics with outcomes following pediatric ICU AC cardiac ar-rest: A secondary analysis of the ICU-RESUSCitation trial. Resuscitation 2024;2011:10271. doi:10.1016/j.resuscitation.2024.110271
51. Kirsch MP,Licht DJ,Faerber J, Mondal A,Graham K,Winters M,Balu R,Diaz-Arastria R, Berg RA, Topjian A, et al. Association of MRI brain in-jury with outcome after pediatric out-of-hospital cardiac arrest. Neurology.2021;96:e719:e731. doi: 10.1212/WNL.000000000011217
52. Hirsch LJ, Fong MWK, Leitinger M, LaRoche SM, Beniczky S, Abend NS, Lee JW, Wusthoff CJ, Hahn 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
53. Smith AE, Friess SH. Neurological Prognostication in Chil-dren After Cardiac Arrest. Pediatr Neurol. 2020;108:13-22. doi: 10.1016/j/pediatneurol.2020.03.010
54. Yacoubom, M. Birchansky B, Mlyn Mash, Berg M, Knight L, Hirsch KG, Su F;Revive Initiative at Stanford Children's Health. The prognostic value of quan-titative diffusion-weighted MRI after pediatric cardiopulmonary arrest. Re-suscitation.2019;135:108-109. doi:10.1016/j.resuscitation.2018.11.003
55. Fink EL, Wisnowski J, Clark R, Berger RP, Fabio A, Furtado A, Narayan S,Angus DC, Watson RS, Wang C, et al. Brain MR imaging and spectroscopy for outcome prognostication after pediatric cardiac arrest. Resuscitation.2020;157:185-194. doi: 10.1016/j.resuscitation.2020.06.033
65. Kirschen M. Berman J.Liu H, Ouyang M, Mondal A, Griffis H, Levov C, Winters M, Lang SS, Huh J, et al. Association between quantitative diffusion-weighted magnetic resonance neuroimaging and outcome af-ter pediatric cardiac arrest. Neurology. 2022;99:e2615-e2626. doi:10.1212/WNL0000000000201189
57. Yang D, Ha SG, RyoE, Choi JY, Kim HJ. Multimodal assessment us-ing early brain CT and blood pH improve prediction of neurologic out-comes after pediatric cardiac arrest. Resuscitation. 2019;1016/j.resuscitation.2019.01.033
POST-CARDIAC ARREST RECOVERY AND SURVIVORSHIP
Recommendations for Post-Cardiac Arrest Recovery and Survivorship
|COR|LOE|Recommendations| |---|---|---| |1|1|1. It is recommended that infants and children who survive cardiac arrest be evaluated for rehabilitation services.| |2a|C-LD|2. It is reasonable that infants and children who survive cardiac arrest be evaluated for physical, cognitive, and emotional needs to guide follow-up care within the first year following cardiac arrest.|
Synopsis
Survivors of both in-hospital and out-of-hospital cardiac arrest are at significant risk for both short-term and long-term physical, neurological, neurological, cognitive,emotional, and so-cial morbidities.1-3 Children who survive a cardiac arrest with a grossly favorable outcome on the PCPC scale may have more subtle and sustained neuropsychological impairment.4 The full impact of brain injury on children's development may not be fully appreciated until months to years after the cardiac arrest and discharge outcome does not necessarily predict long-term outcome, as some survivors with unfavorable outcome at discharge worsen over time.Recovery and Survivorship is the sixth ring in the Chain of Survival and acknowledges that survivors of cardiac ar-rest may require ongoing integrated medical, rehabilita-tive, caregiver, and community support in the months to years after their cardiac arrest(see Figure 5).6 The overall societal burden of pediatric OHCA was assessed from
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 Figure 5. Roadmap to recovery.
2016 to 2020, in terms of disability-adjusted life years as a common public health metric to estimate burden of disease, placing nontraumatic OHCA as 1 of the top 10 leading causes of annual disability-adjusted life years.
Recommendation-Specific Supportive Text
1. Two randomized controlled trials of TTM for coma-tose children after IHCA or OHCA, with a primary outcome of favorable neurobehavioral function defined by the Vineland Adaptive Behavioral Score at 1 year post-cardiac arrest, showed that new morbidity in survivors is common.89 Many children who survived to 1 year with a favorable neurobe-havioral outcome on Vineland Adaptive Behavior Scales-II had global cognitive impairment or selec-tive neuropsychological deficits.10
2.Recent statements from the AHA highlight the importance of follow-up after discharge.1,11 Several case series of pediatric cardiac arrest outcomes
at greater than 1 year post-cardiac arrest demon-strate ongoing cognitive, physical, and neuropsy-chological impairments.2-5 Longitudinal follow-up studies up to 5 years after cardiac arrest identified cognitive and behavioral deficits in pediatric survi-vors who had absent or minimal neurologic change from prearest baseline at hospital discharge.5,10 Compared to healthy controls, survivors of cardiac arrest have specific cognitive deficits correlated with structural brain abnormalities demonstrated on MRI.12 Patients discharged with functional impairments often face years of impaired function and significant health care needs. The impact of ongoing childhood development on recovery fol-lowing pediatric cardiac arrest is unknown.
REFERENCES
1. Topjian AA, Scholefield BR, Pinto NP, Fink EL, Buysse CMP, Haywood K,$$\text{ MaconochieI,Nadkarni VM,de Caen A,Escalante-Kanashiro R,et al.P-COS-}$$CA(Pediatric Core Outcome Set for Cardiac Arrest) in Children: An Advisory
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Statement From the International Liaison Committee on Resuscitation. Re-suscitation.2021;162:351-364. doi:10.1016/j.resuscitation.2021.01.023
2. van Zellem L, Buysse C, Madderm M. Legerest JS, Aarsen F, Tibboel D,Utens EM. Long-term neuropsychological outcomes in children and adoles-cents after cardiac arrest. Intensive Care Med. 2015;41:1057-1066. doi:10.1007/s00134-015-3789-y
3. van Zellem L, Etens M, Maddormer M, Legerste JS, Aarsen F, Tibboel D,Byusse C. Cardiac arrest in infants, children, and adolescents: long-term emotional and behavioral functioning. Eur J Pediatr. 2016;175:977-986.doi:10.1007/s0041-016-2728-4
4. Hunfeld M, Ketharanathan N, Catsman C, Straver DCG, Dremmen MHG.Bramer W, Wildschut E, Tibboel D, Buysse C. A Systematic Review of Neurromonitoring Modalities in Children Beyond Neonatal Period af-ter Cardiac Arrest. Pediatr Crit Care Med. 2020;21:e927-e933. doi: 10.1097/PCC.00000000000002415
58. Hickson MR Winters, M Thomas MH, Gardner MM, Kirschen MP,Nadkarni V, Berg R, Slomine BS, Pinto NP, Topjian A. Long-term func-tion, quality of life and healthcare utilization among survivors of pediat-ric out-of-hospital cardiac arrest. Resuscitation. 2023;187:109768. doi: 10.1016/j.resuscitation.2023.109768
6. Sawyer KM, Camp-Rogers TR, Kotini-Shah P, Delos R, Moss Gip,MR,Moitra VK, Haywood KL, Dougherty CM, Lubitz SA, Rabinstein AA, et al;American Heart Association Emergency Cardiovascular Care Committee;Council Cardiovascular and Stroke Nursing; Council on Genomic and Precision Medicine; Council on Quality of Care and Outcomes Research;and Stroke Council. Sudden Cardiac Arrest Sturvship: A Scientific State-ment From the American Heart Association. Circulation.2020;141:e654-e685. doi: 10.1161/CIR.00000000000000747
7. Coute RA, Nathanson H, DeMasi S, Mader T, KuZ MC; CARES sur-veillance Group. Disability-Adjusted Life Years Due to Pediatric Out-of-Hospital Cardiac Arrest in the United States: A CARES Survallance Group Study. Circuit Cardiovasc Dual Ocones. 2023;16:e009786. doi: 10.1161/CRCOUTCOMES.122.009786
8. Moler FW,Silverstein FS, Holubkov R, Slomine BS, Christensen JR,Avem KL:Wedien RS,Pombertson VL,Page K,et al;THAPCA Trial Inves-tigators. Therapeutic Hypothermia after In-Hospital Cardiac Arrest in Chil-dren NGJ Med.2017;376:318-329. doi 10.1056/NElMoi,610493
9. Moler FW, Silverstein FS, Holubkov R, Slomine BS, Christensen JR,Nadkarni VM, Meert KL, Clark AE, Browning B, Pemberton VL, et al;THAPCA Trial Investigators. Therapeutic hypothermia after out-of-hospital cardiac arrest in children. N Engl J Med. 2015;372:1898-1908. doi:10.1056/NEJmoA1411480
10. Slomine BS, Silverstein FS, Christensen JR, Page K, Holubkov R, Dean JM,Moler FW. Neuropsychological outcomes of children 1 year after pediatric cardiac arrest: secondary analysis of 2 randomized clinical trials. JAMA Neu-rol.2018;75:1502-1510. doi:10.1001/jamaneur.2018.2628
11. Geocadin RG,Callaway CW,Fink El, Golan E,Greer DM,Ko NU, Lang E, Licht DJ, Marino BS, McNair ND, et al; American Heart Association Emergency Cardiovascular Care Committee. Standards for Studies of Neurological Prognostication in Comatose Survivors of Cardiac Arrest:A S actifici Statement From the American Heart Association. Circulation.2019;140:e517-e542. doi:10.1161/CIR.00000000000000702
12.Geva S,Hoskote A,Saini M,Clark CA,Banks T,Chong WK,Baldweg T,de Haan M, Vragha-Khade F. Cognitive outcome and its neural correlates after cardiorespiratory arrest in childhood. Dev Sci 2024;27:e13501. doi:10.1111/desc.13501
FAMILY PRESENCE DURING RESUSCITATION
|Recommendations for Family Presence During Resuscitation||| |---|---|---| |COR|LOE|Recommendations| |1|B-NR|1. Family members should be provided the option of being present during the resuscitation of their infant or child.| |1|B-NR|2. When family members are present during resuscitation of their infant or child, it is recommended for a designated team member to provide comfort, answer questions, and support the family.|
|Recommendations for Family Presence During Resuscitation (Continued)|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-LD|3. If the presence of family members is considered detrimental to the resuscitation of the infant or child, family members should be respectfully asked to leave.||
Synopsis
The practice of allowing family presence during resuscita-tion has become more common over the last 25 years.1 Parents to provide emotional support, share information with the care team,2 and observe resuscitation measures. Parental presence may offer a sense of involvement, re-duce helplessness, and provide closure.3 Presence at their child's death can lead to lower rates of anxiety and de-pression as well as improved grieving behaviors such as social withdrawal and changes in activity levels.4,5
Health care professionals' perspectives on family presence differ significantly, but acceptance generally rises with prior experience and among senior profession-als.3 Parental presence can be encouraged by providing parents with adequate support and consistent updates throughout the resuscitation process, benefiting both the family and the health care team. While health care profes-sionals often worry about the potential negative psycho-logical effects on families, evidence suggests benefit for families to be present during resuscitation of their child.
Recommendation-Specific Supportive Text
1. A systematic review of qualitative survey-based studies reported that 85% of parents surveyed expressed a desire to be present during their child's resuscitation.6 Additionally, parents of 272 children who underwent resuscitation perceived benefits from their presence, such as reduced anxiety and improved understanding and process-ing of the event.6 The presence of family members can enhance parental satisfaction with the care provided, provide families with a greater sense of control,7 and improve self-reported adjustment to the loss of their child.38 Additionally, parent surveys indicated a strong desire to be present to under-stand what was happening, ensure that all possible measures were being taken, and maintain physi-cal contact with their child.39,10 Not all parents who have witnessed their child's resuscitation would choose to do so again.11 While concerns have been raised regarding family presence during resus-citation including potential trauma for the family,interference with procedures, effects on techni-cal performance, and challenges for teaching and clinical decision-making, these concerns have not been substantiated by current evidence.7,12-14
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2. The presence of a facilitator to support families is beneficial and helps reduce stress.15-19 One study reported that 72% of health care professionals support the use of a dedicated staff member for this role during resuscitation.20 A systematic review emphasized the significance of family facilitators in providing emotional support and reducing parental anxiety during resuscitation.21 Team members serv-ing as communication liaisons have been reported to update families in real-time, explain medical ter-minology, and ensure effective two-way communi-cation. Both parents and health care professionals emphasized the importance of training personnel to support family presence.22,23 A qualitative study highlighted essential competencies for facilitators,such as the ability to provide active listening, fostering partnership, and facilitate communication between the family and resuscitation team leader.20 In addi-tion, 2 systematic reviews showed that parents often seek spiritual and cultural comfort during pediatric resuscitations.19,21 Including spiritual health care professionals/chapins can help align clinical care with families' needs, enhance the emotional safety of resuscitations, and support long-term healing.24 While having a dedicated team member to support families during resuscitations can help in the processing of traumatic events,this may not always be feasible, and the absence of such a team member does not preclude family presence during resuscitation.
3.Most surveys suggest that family presence dur-ing resuscitation is not disruptive, although some health care professionals report increased stress.25 Health care professionals with extensive experi-ence in family presence recognize that occasional negative experiences may occur.26 Concerns have been raised by both health care professionals and family members that parental presence during resuscitation may be distracting and could impact the resuscitation. Health care professionals, in par-ticular, often worry about the risk of litigation and the potential negative psychological effects on fam-ilies.37 One randomized trial found that witnessed resuscitation increased health care professionals'anxiety yet reduced anxiety in family members.27 In randomized controlled simulation studies, fam-ily presence did not affect hands-on time or CPR quality, but led to increased frustration, perceived temporal demands, and mental demands on health care professionals.28,29
REFERENCES
1. Tiscar-Gonzalez V, Gea-Sánchez M, Blanco-Blanco J, Pastells-Peiró R,De Rios-Briz M, Moreno-Casbas MT. Witness resucitation of adult and paediatric hospital patients: An umbrella review of the evidence. Int J Nurs Stud.2021;113:103740. doi:10.1016/j.jinurstu.2020.103740
2. Bradford KK, Kost S, Selbst SM, Renwick AE, Pratt A. Family mem-ber presence for procedures: the resident's perspective. Ambul Pediatr.2005;5:294-297. doi: 10.1367/A04-024R1.1
3. Dainty KN, Akits DL, Breckwoldt J, Maconochie l, Schexnayder SM, Skrifus MB, Tijssen J, Wyllie J, Furuta M, Aickin R, et al; Inter-national Liaison Committee on Resuscitation's (ILCOR) Pediatric.Family presence during resuscitation in paediatric and neonatal car-diac arrest: A systematic review. Resuscitation. 2021;162:20-34. doi:10.1016/j.resuscitation.2021.01.017
4. Robinson SM, Mackenzie-Ross S, Campbell Hewson GL, Egleston CV,Prevost AT.Psychological effect of witnessed resuscitation on bereaved rela-tives. Lancet 1998;352:614-617.doi:10.1016/s0140-6736(97)12179-1
5. Carlsson N, A_restedt K, Alvariza A, Axelsson L, Bremer A. Factors As-sociated With Symptoms of Prolonged Grief and Psychological Dis-tress Among Bereaved Family Members of Persons Who Died From Sudden Cardiac Arrest. J Cardiovasc Nurs. 2023;38:454-461. doi: 10.1097/JCN.0000000000000937
6. Cochrane N, Donnelly P. Should parents be present during paediatric re-suscitation? A systematic review. Br J Child Health. 2022;3:222-228. doi: 10.12968/chhe.2022.3.5.222
7. Timmis V. Should family members be present at resuscitation? Arch Dis Child.2020;105:506-508. doi:10.1136/archischild-2019-318314
8. Tinsley C, Hill JB, Shah J, Zimmerman G, Wilson M, Freier K, Abd-Allah S. Experience of families during cardiopulmonary resuscitation in a pediatric intensive care unit. Pediatrics. 2008;122:e799-e804. doi:10.1542/peds.2007-3650
9. Maxton F.J. Parental presence during resuscitation in the PICU:the parents' experience. Sharing and surviving the resuscitation: a phenomenological study. J Clin Nurs.2008;17:3168-3176. doi:10.1111/j.1365-2702.2008.02525.x
10.Stewart SA. Parents' Experience During a Child's Resuscitation: Getting Through It.J.PediatrNurs.2019;47:58-67. doi:10.1016/j.pedn.2019.04.019
11. Curley MA, Meyer EC, Coppettuolo LA, McGannan EA, Trainor BP, Rachwal CM, Hickey PA. Parent presence during invasive procedures and resus-citation: evaluating a clinical practice change. Am J Respir Crit Care Med.2012;186:1133-1139.doi: 10.1164/rccm.201205-09150C
12.McClenathan BM, Tornington KG, Uyehara CF. Family member pres-ence during cardiopulmonary resuscitation: a survey of US and inter-national critical care professionals. Chest. 2002;122:2204-2211. doi:10.1378/chest.1226.2204
13. Vavarouta A, Xanthos T, Papadimitriou L, Kouskouni E, lacovidou N. Fam-ly presence during resuscitation and invasive procedures: physicians' and nurses' attitudes working in pediatric departments in Greece. Resuscitation.2011;82:713-716. doi: 10.1016/j.resuscitation.2011.02.011
14. Pasek TA, Licata J. Parent Advocacy Group for Events of Resuscitation. Crit Care.Nurse.2016;36:58-64. doi:10.4037/ccn2016759
15.Jarvis AS. Parental presence during resuscitation: attitudes of staff on a paediatric intensive care unit. Intensive Crit Care Nurs.1998;14:3-7. doi: 10.1016/s0964-33997(98)80029-3
16. Zavotsky KE,McCoy J,Bell G,Haussman K,Joiner J,Marcoux KK,Magarelli K,Mahoney K,Maldonado L,Mastro KA,et al.Resuscitation team percep-tions of family presence during CPR. Adv Emerg Nurs J.2014;36:325-334.doi:10.1097/TME.0000000000027
17. Grimes C. The effects of family-witnessed resuscitation on health profes-sionals. Br J.Nurs.2020;29:892-896. doi: 10.12968/bjon.2020.29.15.892
18.Mark K. Family presence during paediatric resuscitation and invasive pro-cedures: the parental experience: an integrative review. Scand J Caring Sci.2021;35:20-36. doi:10.1111/scs.12829
19. Ghavi A, Hassankhani H, Powers K, Arshadi-Bostanabad M,Namdar-Areskanhtab H,Heidarazadeh M. Parental support needs during pe-diatric resuscitation: A systematic review. Int Emerg Nurs.2022;63:101173 doi:10.1016/j.jienj.2022.101173
20. Powers K, Duncan JM, Renee Twibell K. Family support person role during resuscitation: a qualitative exploration. J Clin Nurs.2023;32:409-421. doi:10.1111/joc.16248
21. Ghavi A, Hassankhani H, Powers K. Resuscitation Team Members' Percep-tions of Supporting Parents During Cardiopulmonary Resuscitation of Chil-dren: A Systematic Review. Dimens Crit Care Nurs. 2023;42:263-276. doi:10.1097/DCC.00000000000000000000000000
22. Brunt J, Alnababah T, The experiences of parents witnessing their child's resuscitation in hospital. Br J Nurs. 2023;32:136-142. doi:10.12968/jonj.2023.32.136
23. Howlett O, Gleeson J, Jackson L, Rowe E, Truscott M, Maggs JA. Family support role in hospital rapid response teams: a scoping review. JBI Evid Shan2022;2020:2001-2024.doi:10.11124/JBIES-2021-0189
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24. Tennyson CD, Oliver JP, Jooste KR. A Descriptive Study of Chap-lains' Code Blue Responses. Am J Crit Care. 2021;30:419-425. doi:10.4037/ajcc2021854
25. Kuzin JK, Yborra JG, Taylor MD, Chang AC, Altman CA, Whitney GM, Mott AR. Family-member presence during interventions in the intensive care unit: perceptions of pediatric cardiac intensive care providers. Pediatrics.2007;120:e895-e901.d. doi:10.1542/peds.2006-2943
26. Fulbrook P, Latour JM, Albarran JW. Paediatric critical care nurses' at-titudes and experiences of parental presence during pulmonaryproven-suscitation: a European survey, Int J Nurs Stud.2007;44:1238-1249.doi:10.1016/j.jjnrustu.2006.05.006
27. Celik C, Celik G, Buyukamc F. The witness of the patient's relatives increas-es the anxiety of the physician, but decreases the anxiety of the relatives of the patient. Hong Kong J Emerg Med.2019;28:1024907919860632.
28. Willmes, Sellmann T, Semner T, Nschan T, Wetzchewald D, Schwager H,Russo SG, Marsch S. Impact of family presence during cardiopulmonary resuscitation on team performance and perceived task load: a prospec-tive randomised simulator-based trial. BMJ Open. 2022;12:e056798. doi: 10.1136/bmjopen-2021-056798
29.Sellment T, Ondorf A, Wetwewcheld D, Schwager H, Thal SC, Marsch S.The Impact of Withdrawal vs. Agitated Relatives during Resuscitation on Team Workload: A Single-Center Randomised Simulation-Based Study. J Clin Med. 2022;11:3163. doi: 10.3390/jcm11113163
EVALUATION OF SUDDEN UNEXPLAINED CARDIAC ARREST
|Recommendations for the Evaluation of Sudden Unexplained Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|B-NR|1. A complete unrestricted autopsy of infants and children with sudden unexplained death is recommended, preferably performed by a pathologist with training and experience in cardiovascular pathology with preservation of biological material for further genetic analysis to determine the presence of inherited cardiac disease.|| |1|B-NR|2. When conventional autopsy does not identify a cause of death or diagnosis in infants and children with sudden unexplained death, a postmortem genetic evaluation is recommended, when resources allow, especially if clinical evidence suggests the diagnosis of an inherited cardiac disease.|| |1|B-NR|3. When autopsy does not identify a cause of death or is not performed in infants and children with sudden unexplained death, it is recommended that first-degree family members be referred to a health care professional or center with expertise in inherited cardiac disease and cardiac genetic counseling.|| |1|C-EO|4. For infants and children who survive sudden unexplained cardiac arrest, obtain a complete past medical and family history(including a history of syncopal episodes, seizures, unexplained accidents or drowning or sudden unexpected death before 50 y of age), review previous electrocardiograms, and refer to a cardiologist with expertise in inherited cardiac disease.||
Synopsis
Inherited cardiac diseases(ie, cardiomyopathies, chan-nelopathies), and coronary artery anomalies are common causes of sudden unexplained cardiac arrest in infants
and children. In patients who do not survive, autopsy plays an essential role to correctly identify the etiology of the cardiac arrest. Up to one third of young patients who do not survive,sudden unexplained cardiac arrest have no abnormalities found on gross and microscopic autotopsies. ${}^{1-4}$ Postmortem genetic evaluation ("molecu-lar autopsy") is increasingly used as an important tool to evaluate potential causes of sudden unexplained death and identify inheritable cardiac diseases. ${}^{5}$ In addition to providing an explanation, genetic diagnosis can enable necessary screening and preventive measures for rela-tives and survivors.
Recommendation-Specific Supportive Text
1.Previous reviews and consensus guidelines state the importance of an autopsy following sudden unexplained cardiac death to aid in determining the cause of death and to identify possible inher-ited cardiac conditions.6-9 An autopsy can identify several causes of death in infants and children with sudden unexplained cardiac death, includ-ing cardiomyopathy(ie, hypertrophic, dilated, or arrhythmogenic) and anomalous coronary arter-ies. When no cause of death is identified on gross examination, microscopic evaluation and pres-ervation of biological tissue is paramount to be able to perform a molecular autopsy if resources allow.
2.Previous systematic reviews and consensus guide-lines emphasize the use of postmortem genetic testing for inherited cardiac causes of sudden death(ie, cardiomyopathies, channelopathies).A review reported up to 50% of sudden cardiac death cases in infants and children had a poten-tial genetic disease identified.7 In multiple studies,genetic mutations causing channelopathies were identified in 2% to 10% of infants with sudden infant death syndrome.10-16 Among children with sudden unexplained death and a normal autopsy,9 cohort studies report identification of genetic mutations associated with channelopathy or cardiomyopathy.14,17-24
3. In multiple studies, 13% to 53% of first- and second-degree relatives of patients with unex-plained cardiac arrest are remetted by diagnosed with inher-ited cardiac disease after screening using medical and family history, clinical exam, and laboratory evaluation.7,17-20,25-32 A small case series suggested that genetic screening of family members should be directed by clinical history. ${}^{17}$
4. A retrospective study of 155 adult survivors of nonischemic sudden cardiac arrest reported 49% of survivors were diagnosed with an inher-ited cardiac condition.27 Several cohort studies report the utility of obtaining a complete past
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medical and family history, including multigen-erational pedigree, after sudden unexplained cardiac arrest as well as review of prior electro-cardiograms. Three small cohort studies and 1 population-based study reported relevant clinical symptoms or medical combotiorities before car-diac arrest, such as seizure, scope, pallita-tions, chest pain, left arm pain, and shortness of breath, among patients who had a sudden unex-plained cardiac arrest.18,19,21,22
REFERENCES
1. Doolan A, Langlois N, Semarian C. Causes of sudden cardiac death in young Australians. Med J Aust. 2004;180:110-12. doi:10.50694/j.1326-53772.2004.tb05830.x
2.Eckart RE, Scoville SL, Campbell SL, Shry EA, Stajudhar KC, Potter RN,Pearlase LA, Virman R. Sudden death in young adults: a 25-year review of autopsies in military recruits. Ann Intern Med 2004;141:829-834. doi:10.7326/0003-4819-141-11-200412070-00005
0G. MeI Stell, Olmos M, Neshitz L, Gerein R, Campbell S, McLellan B; OPALS Study Group. Etiology of pediatric out-of-hospital cardiac ar-rest by coroner's diagnosis. Resuscitation. 2006;68:335-342. doi:10.1016/j.resuscitation.2005.06:026
4. Puranik R, Chow CK, Dufoula JA, Kilborn MJ, McGuire MA. Sud-den death in the young. Heart Rhythm. 2005;2:1277-1282. doi:10.1016/j.hrformul.2005.09.008
5. Torkamani A, Museed ED, Spencer EG, Rueda M, Wagner GN, Lucas JR,Topol EJ. Molecular Autarosis for Sudden Unexpected Death: JAMA 2016;316:1492-1494. doi: 10.1001/jama.2016.11445
6.Kelly KL,Lin PT,Basso C,Bois M,Buja LM,Cohle SD,d'Amati G,Duncanson E,Fallon J,Tifchir,Faud et al. Sudden cardiac death in the young: A consen-sus statement on recommended practices for cardiac examination by pa-thologists from the Society for Cardiovascular Pathology. Cardiovascular Pathology 2023;63:107497. doi:10.1016/j.carpatho.2022.107497
7. Lynge TH, Albert CM, Basso C, Garcia R, Krahn AD, Semsarian C, Sheppard MN, Behr-Etir,Hansen J. Autopy of all young sudden death cases is important to increase survival in family members left behind. Europace 2024;26:euea128. doi: 10.1093/europae/euae 128
8.Baley A, Shepard M, Scoville S, Apanwise and Autopy: Sudden Death With Likely Cardiac Pathology. London: Royal College of Pathologists.2022. Accessed February 28, 2025.
9.Canci V, Forzeese, Sapienza D, Cinci- A, leni A, Germana A, Guerrero MC, Omero F, Speranza D, Craco A, et al. Arrhythmogenic Right Ventricular Cardiomyopathy Post-Mortern Assessment: A Systematic Review. Int J Mol Sci.2024;25:2467. doi: 10.3390/jms25052467
10. Cronk LB, Ye B, Kaku T, Tester D7, Matto M, Makiels JC, Ackerman MJ. Novel mechanism for sudden infant death syndrome: persistent late sodium current secondary to mutations in caveelin-3. Heart Rhythm. 2007;4:161-166. doi: 10.1016/j.rthm.2006.11.030
11.Milat K.,Güner,K. Devier P., Chaline H., Huang H., Malier D,Rodriguez-Lafrasse C., Rousson R. Contribution of long-OT syndrome genetic variants in sudden infant death syndrome. Pediatr Cardiol.2009;30:502-509. doi:10.1007/s0024-06-009-9417-2
12.Otagiri T, Kijima K,Oaswara M,Ishii K,Makita N,Matoba R,Umetsu K,Hayasaki K.Cardiol ion channel gene mutations in sudden infant death syndrome.Pediatr Res.2008;64:482-487. doi:10.1023/PDR.0b013e3181481eca
13. Plant LD, Bowers PN, Liu Q, Morgan Z, Thang State, MWen, K Wittles,RAO Goldstein SA, A common cardiac sodium channel variant associated with sudden infant death in African Americans SNC5A S11093.Y. Clin In-vest 2006;116:430-435. doi:10.1172/JCI25618
14.Tester DJ, Dura, Martcuran E, Reiken S, Wonska A, Marks AR, Ackerman MJ.A mechanism for sudden infant death syndrome(SIDS): stress-induced leak ys via radionec receptors. Heart Rhythm 2007;4:733-739. doi:10.1016/jhrithm.200702.026
15. Ackerman M, Jiu S, Blurner WQ, Tester D, Valdric CR, Makiki Jc,Tobin JA. Postmortem molecular analysis of SCN5A defects in sudden infant death syndrome. JAMA 2001;286:2264-2269. doi:10.1001/jama.286.18.2264
16. Armestad M, Crotti L, Rognum TO, Insolia R, Pedrazzini M, Ferrandi C,Vege A, Wang DW, Rhodees TE, George AL Jr, et al. Prevalence of long-QT syndrome gene variants in sudden infant death syndrome. Circulation. 2007;115:361-367 doi:10.1161/CIRCULATIONAHA.106.658021
17. Anastasakis A, Papatheodorou E, Ritsatos K, Protonotarios N, Rentoumi V, Gatzoulis K, Antoniades L, Agapitos E, Koutsaftis P, Spiliopoulou C, et al.Sudden unexplained death in the young: epidemiology, aetiology and value of the clinically guided screening. Europace. 2018;20:472-480. doi:10.1093/europe/oeuw362
18. Hellenthal N, Gaertner-Rommel A, Klauke B, Paluszkiewicz L, Stuhr M,Kerner T, Farr M, Puscheel K, Milting H. Molecular autopsy of sudden un-explained deaths reveals genetic predispositions for cardiac diseases among young forensic cases. Eurospace. 2017;19:1881-1890. doi: 10.1093/europace/euw247
19. Hendrix A. Borets CJ, V. Jink A, Doevendans PA, Wilde AA, van Langen IM, van der Magt JJ, Bots ML, Mosterd A. Diogenetic screening of first-degree relatives after sudden cardiac death in the young: a population-based approach.Europe.2011;13:716-722. doi:10.1093/europace/euq460
20.Jimenez-Jamez J, Alcalde Martinez V, Jimenez Fernandez M,Bermudez Jimenez F, Rodriguez Vazquez Del Rey MDM, Perin F,Oyonare Jramine ZM, Lopez Fernandez S, de la Torre I, Garcia Orta R, et al.Clinical and Genetic Diagonosis of Nonischemic Sudden Cardiac Death Rev Esp Cardiol(Engl Ed).2017;70:808-816. doi:10.1016/j.rec.2017.04.024
21. Lahrouchi N, Raju H, Louder EM, Papatheodorou E, Ware J, Papadakis M,Tadros R, Cole D, Skinner JR, Crawford J, et al. Utility of Post-Mortem Genetic Testing in Cases of Sudden Arrhythmic Death Syndrome. J Am Coll Cardiol.2017;69:2134-2145. doi:10.1016/j.jacc.2017.02.046
22. Scheiper S., Ramos-Luis,E. Blanco-Verea A, Niess C, Beckmann BM,Schmidt U, Kettner M., Geisen C, Verhoff MA, Brion M., et al. Sudden un-expected death in the young-value of massive parallel sequencing in postmortem genetic analyses. Forensic Sci Int 2018;293:70-76. doi: 10.1016/j.forscinti.2018.09.034
23. Albert CM, Nam EG, Rimm EB, Jin HW, Hajjar RJ, Hunter DJ, MacRae CA, Ellin PT. Cardiac sodium channel gene variants and sud-den cardiac death in women. Circulation. 2008;117:16-23. doi: 10.1161/CIRCULATIONAHA.107:736330
24.Chugh SS,Sensashova O, Watts A, Tran PT, Zhou Z, Gong Q, Titus JL,Hayfick SJ. Postmortem molecular screening in unexplained sudden death.J Am Coll Cardiol.2004;43,1625:1629.doi:10.1016/j.jacc.2003.11.052
25.Brunet-Garcia L,Ja,F.,Field E,Norrish G,Tollit J,Shoshan J,French N,Addis A,Dady K,Cervi E,et al.Prevalence of Inherited Cardiac Conditions in Pedi-atic First-Degree Relatives of Patients with idiopathic Ventricular Fibrillation.Pediatr Cardiol.2022;43:114-1121. doi:10.1007/s00246-022-02831-1
26.Dalgaard CV, Hansen B, Jacobsen EM, Kjerrumgaard A, Teltf-Hansen A, Teltf-Hansen J, Weeke PE, Winkel BG, Christensen AH, Bundgaard H. Sudden unex-plained death versus nonautopsied possible sudden cardiac death: Find-ings in relatives. J Cardiovasc Electrophysiol. 2022;33:254-261. doi:10.1111/jce.15333
27.Jacobsen EM, Hansen BL, Kjerrumgaard A, Teltf-Hansen J, Hassager C,Kjergaard J, Christersen AH, Bundgaard H, Winkel BG. Diagnostic yield and long-term outcome of nonischemic sudden cardiac arrest survivors and their relatives: Results from a tertiary referral center. Heart Rhythm 2020:17:1679:1686. doi: 10.1016/j.jhrthm.2020.06.030
28. Kjerguaraard A, Jacobsen EM, Hansen BL, Teltf-Hansen J, Winkel BG,Christensen H, Bundhagard H. Diagnostic findings and follow-up outcomes in relatives to young non-autopsied sudden death victims. Int J Cardiol.2020;2018:61-66. doi:10.1016/j.jicard.2020.06.012
29.Behr E, Wood D, RAft M, Syris P, Sheppard MN, Casey A, Davies MJ, McKenna W; Sudden Arrhythmic Death Syndrome Steering Group. Cardiological assessment of first-degree relatives in sud-den arrhythmic death syndrome. Lancet. 2003;362:1457-1459. doi:10.1016/s010-6736(03)14692-2
30.Behr ER, Dalgeorgou C, Christiansen M, Syrisr P, Hughes S,Tome Esteban MT, Rowland E, Jeffery S, McKenna WJ. Sudden arrhythmic death syndrome: familial evaluation identifies inheritable heart dis-ease in the majority of families. Eur Heart J. 2008;29:1670-1680. doi:10.1093/seurheart/ehr219
31. Hofman N, Tan HL, Clur SA, Alders M, van Langen IM, Wilde AA. Contribu-tion of inherted heart disease to sudden cardiac death in childhood. Pediat-nics.2007;10:120:e967-e973. doi: 10.1542/peds.2006-3751
32.Tan HL,Hofman N, van Langen IM, van der Wal AC, Wilde AA. Sudden unexplained death: heritability and diagnostic yield of cardiological and ge-netic examination in surviving relatives. Circulation.2005;112:207-213. doi:10.1001/J/cIRCULATIONAHA.104.522581
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MANAGEMENT OF SHOCK
Fluid Resuscitation and Management of Septic Shock
|Recommendations for Fluid Resuscitation and Management of Septic Shock||| |---|---|---| |COR|LOE|Recommendations| |1|C-LD|1. Health care professionals should reassess infants and children after every third bolus to assess for fluid responsiveness and signs of volume overload.| |2a|B-R|2. Either isotonic crystalloids or colloids can be effective as the initial fluid choice for resuscitation in infants and children.| |2a|B-NR|3. Either balanced or unbalanced solutions can be effective as the fluid choice for resuscitation in infants and children.| |2a|C-LD|4. In infants and children with septic shock, it is reasonable to administer fluid in 10-mL/kg or 20- mL/kg aliquots with frequent reassessment.| |2a|C-LD|5. In infants and children with fluid-refractory septic shock, it is reasonable to enter using bienephrine or norepinephrine as an initial vasoactive infusion.| |2a|C-EO|6. For infants and children with cardiac arrest and sepsis, it is reasonable to apply the standard PALS algorithm compared with any unique approach for sepsis-associated cardiac arrest.| |2b|B-NR|7. For infants and children with septic shock unresponsive to fluids and requiring vasoactive support, it may be reasonable to consider stress- dose corticosteroids.| |2b|C-LD|8. In infants and children with fluid-refractory septic shock, if epinephrine or norepinephrine are unavailable, dopamine may be considered.|
Synopsis
Shock is the failure of oxygen delivery to meet tissue metabolic demands and can be life threatening. The most common type of pediatric shock is hypovolemic, in-cluding hemorrhagic shock, with distributive, cardiogenic,and obstructive shock occurring less frequently. Multiple types of shock can occur simultaneously, and early pre-sentations can be subtle; health care professionals must be vigilant.
Shock progresses over a continuum of severity, from a compensated to a decompensated(hypotensive) state.Compensatory mechanisms include tachycardia and increased systemic vascular resistance to maintain car-diac output and end-organ perfusion. As compensatory mechanisms fail, hypotension and signs of inadequate end-organ perfusion develop, such as depressed mental status, decreased urine output, acidosis, and weak cen-tral pulses.
Sepsis is a life-threatening response to infection,where the body's immune system overreacts, leading to widespread inflammation and organ dysfunction. Sep-tic shock is characterized as sepsis with cardiovascular—lar dysfunction including hypotension. Early recognition and prompt treatment(eg, antibiotics, fluids) are critical
for improving outcomes in infants and children. Mortal-ity from pediatric septic has declined, concurrent with implementation of guidelines emphasizing early antibiotic and fluid administration.1 Controversies in septic shock management include volume and type of fluid adminis-tration, vasopressor timing and choice, and use of cor-ticosteroids. Previous AHA guidelines2 had considered large studies of patients with malaria, sickle cell anemia,and dengue shock syndrome; however, generalization of results from these studies is problematic.
This topic was last reviewed in the 2020 AHA Guide-lines for CPR and ECC. These recommendations have not been updated for this edition of the Guidelines, with the exception of No. 6, which was reviewed and updated. ${ }^{3}$
Recommendation-Specific Supportive Text
1. Although fluids remain the mainstay initial therapy for infants and children in shock, especially in hypovolemic and septic shock, fluid overload can lead to increased morbidity.4 In 2 randomized trials of patients with septic shock, those who received higher fluid volumes5 or faster fluid resuscitation6 were more likely to develop clinically significant fluid overload characterized by increased rates of mechanical ventilation and worsening oxygenation.
2. In a systematic review, 12 relevant studies were identified, though 11 assessed colloid or crystalloid fluid resuscitation in patients with malaria, dengue shock syndrome, or“febrile illness” in sub-Saharan Africa.7 There was no clear benefit to crystalloid or colloid solutions as first-line fluid therapy in any of the identified studies.
3.One randomized controlled trial compared the use of balanced (lactated Ringer's solution) to unbal-anced (0.9% saline) crystalloid solutions as the ini-tial resuscitation fluid and showed no difference in relevant clinical outcomes. ${ }^{8}$ A matched retrospec-tive cohort study of pediatric patients with septic shock showed no difference in outcomes, ${ }^{9}$ though a propensity-matched database study showed an association with increased 72-hour mortality and vasoactive infusion days with unbalanced crystal-loid fluid resuscitation. ${ }^{10}$
4. In a small, randomized controlled study, there were no significant differences in outcomes with the use of 20 mL/kg as the initial fluid bolus volume in septic shock, compared to 10 mL/kg; however, the study was limited by a small sample size. ${}^{5}$
5. Two pediatric randomized controlled trials compar-ing escalating doses of dopamine or epinephrine demonstrated improvement in timing of resolution of septic shock11 and 28-day mortality12 with the use of epinephrine over dopamine. Both studies were conducted in resource-limited settings, and the doses of inotropes used may not have been directly comparable, limiting conclusions from the
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studies. Medications that increase systemic vascu-lar resistance, such as norepinephrine, may also be a reasonable initial vasopressor therapy in septic shock patients.1,13-15 International sepsis guidelines recommend the choice of medications to be guided by patient physiology and clinician preferences.
6.No studies support deviations from standard life-support algorithms to improve outcomes in patients with sepsis-associated cardiac arrest. Sepsis-associated cardiac arrest is associated with worse outcomes than other causes of cardiac arrest.16
7. A meta-analysis ${ }^{17}$ showed no change in survival with corticosteroid use in pediatric septic shock, though a subsequent randomized controlled trial suggested a shorter time to reversal of shock with steroid use. ${ }^{18}$ Two observational studies ${ }^{19,20}$ suggested there may be specific subpopulations, based on genomics, that would either benefit or experience harm from ste-roid administration, though these subpopulations are difficult to identify clinically. Patients at risk for adrenal insufficiency(eg, those on chronic steroids,patients with purpura fulminans) are more likely to benefit from steroid therapy. ${ }^{14}$
8. In situations when epinephrine or norepinephrine are not available, dopamine is a reasonable alter-native initial vasoactive infusion in patients with fluid-refractory septic shock.11,12 Patients with vasodilatory shock may require a higher dose of dopamine.13
Management of Cardiogenic Shock
|Recommendations for Management of Cardiogenic Shock|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-EO|1. For infants and children with cardiogenic shock,early expert consultation is recommended.|| |2b|C-EO|2. For infants and children with cardiogenic shock,it may be reasonable to use epinephrine, dopamine, dobutamine, or nilrinone as an inotropic infusion.||
Synopsis
Cardiogenic shock occurs when the heart is unable to pump blood efficiently, resulting in decreased cardiac output and inadequate oxygen delivery to tissues. While it is relatively rare in children compared to other forms of shock, it is associated with high rates of mortality.21 Causes of cardiogenic shock include congenital heart disease, myocarditis, cardiomyopathies, and arrhythmias.Clinical manifestations vary by severity and underlying cause. Initial compensatory mechanisms include tachy-cardia, tachypnea, and increased systemic vascular re-sistance. As compensatory mechanisms fail, hypotension and signs of inadequate end-organ perfusion develop,such as depressed mental status, decreased urine out-put, lactic acidosis, and weak central pulses. Initial treat-ment is focused on improving oxygen delivery, minimizing
<EndOfPara>oxygen consumption, and restoring cardiac function through administration of vasoactive medications. It is important to note that cardiogenic shock can occur with other forms of shock simultaneously. In its early stages,it can be difficult to diagnose, so a high index of sus-picion is warranted. This topic was last reviewed in the 2020 AHA Guidelines for CPR and ECC. These recom-mendations have not been updated for this edition of the Guidelines. 3
Recommendation-Specific Supportive Text
1 and 2. Cardiogenic shock in infants and children is uncommon and associated with high mortal-ity rates. No studies were identified comparing outcomes between vasoactive medications.For patients with hypotension, vasoactive medica-tions such as epinephrine may be more appro-priate as an initial inotropic therapy. Because of the rarity and complexity of these presen-tations, expert consultation is recommended when managing infants and children in cardio-genic shock.
Management of Traumatic Hemorrhagic Shock
|Recommendation for Management of Traumatic Hemorrhagic Shock|||| |---|---|---|---| |COR|LOE|Recommendation|$$\begin{array}{l}\\ 2a\\ \\ \end{array}$$| |2a|C-EO|1. Among infants and children with hypotensive hemorrhagic shock following trauma, it is reasonable to administer blood products, when available, instead of crystalloid for ongoing volume resuscitation.||
Synopsis
Resuscitation guidance for children with hemorrhagic shock is evolving, as crystalloid-then-blood paradigms are being challenged by resuscitation protocols using blood products early in resuscitation. However, the ideal resuscitation strategy for a given type of injury is often unknown.
This topic was last reviewed in the 2020 AHA Guide-lines for CPR and ECC.These recommendations have not been updated for this edition of the Guidelines. ${}^{3}$
Recommendation-Specific Supportive Text
1.There are no prospective pediatric data comparing the administration of early blood products versus early crystalloid for traumatic hemorrhagic shock. A scoping review identified 6 retrospective studies that compared patient outcomes with the total volume of crystalloid resuscitation received in the first 24 to 48 hours among children with hemorrhagic shock.22-27 Four studies reported no differences in survival to 24 hours, survival at 30 days with good neuro-logical outcome, or survival to discharge.22,24-26,28 Large-volume resuscitation was associated with increased hospital/ICU length of stay in 5 of the
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6 studies. ${ }^{23-28}$ One study reported lower survival to hospital discharge among children who received more than 60 mL/kg crystalloid compared to lower volume groups. ${ }^{27}$ Despite limited pediatric data,guidelines for adults from the Eastern Association for the Surgery of Trauma, ${ }^{29}$ the American College of Surgeons, and the National Institute for Health and Care Excellence ${ }^{30}$ suggest the early use of balanced ratios of packed red blood cells, fresh frozen plasma, and platelets for trauma-related hemorrhagic shock. ${ }^{29}$ The American College of Surgeons and the National Institute for Health and Care Excellence ${ }^{30}$ suggest the early use of bal-anced ratios of packed red blood cells, fresh frozen plasma, and platelets for trauma-related hemorrhagic shock. ${ }^{29}$ The American College of Surgeons and the National Institute for Health and Care Excellence ${ }^{30}$ suggest the early use of bal-anced ratios of packed red blood cells, fresh frozen plasma, and platelets for trauma-related hemorrhagic shock. ${ }^{29}$ The American College of Because Excellence ${ }^{30}$ suggest the early use of bal-anced ratios of packed red blood cells, fresh frozen plasma, and platelets for trauma-related hemorrhagic shock.
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1. Inwald DP, Center R, Woolfall K, Mouncey P, Zenzi S, O'Hara C, Carter A,Jones N, Lyttle MD, Nadel S, et al; PERUKI(Paediatric Emergency Re-search in the UK and Ireland) and PICS SG(Pediatric Intensive Care Sci-ety Study Group). Restricted fluid bolus volume in early septic shock: results of the Fluids in Shock pilot trial. Disci L.2019;104:426-431.doi:10.1163/charchidild-2018-314924
6. Sankar J, Ismail J, Sankar MJ, Suresh CP, Meena RS. Fluid bolus over 15-20 versus 5-10 minutes each in the first hour of resuscitation in children with septic shock: a randomized controlled trial. Pediatr Crit Care Med 2017;18:e435-e445.doi:10.1097/PCC.000000000000001269 Med
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8.Balamuth F, Kittick M, McBride P, Woodford AL, Vestal N, Casper TC,Metheyner M, Smith K, Akin NJ, Baren JM, et al. Prasigmatic pediatricial trial of balanced versus normal saline fluid in sepsis: the preMPT BOLLUS ratio-601 sized controlled trial pilot feasibility study. Acad Emerg Med.2019;26:1346-1356. doi:10.111/1ae.cem.18135
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12.Ramassamy Kn, Singh S, Jayashree M, Bansal A, Nallasamy K. Double-Blind Randomized Clinical Trial Comparing Dopamine and Epinephrine in Pediatric Fluid-Refractory Hypotensive Septic Shock. Pediatr Crit Crit Care Med.2016;17:1097/e5021-52. doi:10.1097/PCC.000000000000954
13. Davis AL, Carcilo JA, Aneja RK, Deymann AJ, Lin JC, Nguyen TC, Okhuysen-Cawley RS, Revelas MS, Rozenfeld RA, Skippen PW, et al. Ameri-can College of Critical Care Medicine Clinical Practice Parameters for He-modynamic Support of Pediatric and Neonatal Septic Shock. Crit Care Med.2017;45:1061-1093.doi: 10.1097/CCM.0000000000002425
14. Deep A, Goonasekera CD, Wang Y, Brierley J. Evolution of haemodynamics and outcome of fluid-refractory epticse shock in children. Intensive Care Med.2013;39:1602-1609, doi: 10.1007/s00134-013-3003-z
15. Lampin ME, Rousseaux J, Botte A, Sadik A, Cremer R, Leclerc F. Nor-adrenaline use for septic shock in children: doses, routes of adminis-tration and complications. Acta Paediatr. 2012;101:e426-e430. doi: 10.1111/j.1651-222720.121202725.x
16. Del Castillo J, Lopez-Herce J, Canadas S, Matamoros M, Rodriguez-Nunez A, Rodriguez-Calvo A, Carrillo A; Iberoamericer Pediatric Cardiac Arrest Study Network RIBEPC. Cardiac arrest and resuscitation in the pediatric intensive care unit: a prospective multicenter multistural study. Resuscita-tion.2014;85:1380-1386. doi:10.1016/j.resuscitation.2014.06.024
17. Menon K, McNally D, Choung K, Sampson M. A systematic review and meta-analysis on the effect of steroids in pediatric shock. Pediatr Crit Care Med.2013;14:474-480. doi: 10.1097/PCC.0b013e31828a8125
18. El-Nawawy A, Khater D, Omar h, Wali Y. Evaluation of Early Corticoste-roid Therapy in Management of Pediatric Septic Shock in Pediatric In-tensive Care Patients: A Randomized Clinical Study. Pediatr Infect Dis J.2017;38:155-159. doi: 10.1097/INF0000000000001380
19.Wong HR,Atkinson SJ,Cvijanovich NZ,ASnAL; Allen GL,Thomas NJ,Bigham MT,Beugham ST,Weiss L,FLitzgeral JC,Checchia PA,et al. Combining Prog-nostic and Predictive Enrichment Strategies to Identify Children With Septic Shock Response to Corticosteroids. Crit Care Med.2016;44:e1000-1003. doi:10.1097/CCM.00000000000001833
20.Wong HR,Cvjanovich NZ, Anas N, Allen GL, Thomas NJ, Bealth AM, TitzS, Fitzgerald JC, Checchia PA, Meyer K, et al. Endotype Transi-tions During the Acute Phase of Pediatric Septic Shock Reflect Changing Risk and Treatment Response. Crit Care Med. 2018;46:e242-8249. doi:10.1097/CCM.0000000000000002932
21. Puri K, Jenter JC, Spinner JA, Hope KD, Adachi I, Tume SCun-tunglna HP, Choudhry S, Cabrera AG, Price JF. Clinical Presentation, Classifica-tion, and Outcomes of Cardiogenic Shock in Children. J Am Coll Cardiol.2024:895:698-08. doi:10.1016/j.ijacc.2023.11.019
22. Hussmann B,Lefering R,Kaurth MD,Ruchholtz S,Moldzio P,Lendemans S,Trauma Register DGU. Influence of prehospital volume replacement on outcome in polytraumized children. Crit Care. 2012;16:R201. doi: 10.1186/cc11809
23.Edwards M.J., Lustick MB, Clark ME, Creamer KM, Tuggle D. The effects of balanced blood component resuscitation and crystalloid administra-tion in pediatric trauma patients requiring transfusion in Afghanistan and lraq 2002 to 2012. J Traumma Acute Care Surg. 2015;78:330-335. doi:10.1097/2480000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000
24. Coons BE, Tam S., Tsubian J, Stylianos S, Duron V. High volume crystal-loid resuscitation adversely affects pediatric trauma patients. J Pediatr Surg.2018;53:522-2208. doi:10.1016/j.jpedsurg.2018.07.009
25.Zhu H,Chen B,Guo C.Aggressive crystalloid adversely affects outcomes in a pediatric trauma population. Eur J Trauma Emerg Surg. 2021;47:85-92.doi:10.1007/s00086-019-01134-0
26.Eukibl A, Zujd S, Ehrhardt JD Jr, McKenney M, Boneva D. Aggressive Crys-tallid Resuscitation Outcomes in Low-Severity Pediatric Trauma. J Surg Res.2020:247:350-355 doi:10.1016/j.jsss.2019.10.009
27. Acker SN.Ruott J, Patrick DA, DeWitt P, Bensard DD. Injured children are resistant to adverse effects of early high volume crystalloid resuscitation.J Pediatr Surg.2014;49:1852-1855. doi:10.1016/j.jpedsurg.2014.09.034
28.Zhu H. Chen B, Guo C. Aggressive crystaloid adversely affects outcomes in a pediatric trauma population. Eur J Trauma Emerg Surg. 2019;47:85-92.doi:10.1007/00086-019-01134-0
29. Cannon JW, Khan MA, Raja AS, Cohen MJ, Como JJ, Cotton BA, Dubose J, Fox, Exe, Inaba K, Rodriguez CJ, et al. Damage control resuscitation in pa-tients with severe traumatic hemorrhage: A practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg.2017;82:605-617. doi:10.1097/TA.00000000000001333
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30. Kanani AN, Hartshorn S. NICE clinical guideline NG39: Major trauma:assessment and initial management. Arch Dis Child Educ Pract Ed.4017;102:20-23. doi: 10.1136/archildisch-2016-310869
INTUBATION
Use of Cuffed Endotracheal Tubes for Intubation
|Recommendations for the Use of Cuffed Endotracheal Tubes for Intubation|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-EO|1. When a cuffed endotracheal tube(ETT) is used in infants and children, attention should be paid to ETT size, position, and cuff inflation pressure (usually<20-25 cm $H_{2}O)$).|| |2a|B-NR|2. It is reasonable to choose cuffed ETTs over uncuffed ETTs for intubating infants and children.||
Synopsis
Cuffed and uncuffed ETTs have been studied in the perioperative period and up to 48 hours postintuba-tion. These studies have shown that cuffed ETTs are safe in infants and children and are not associated with significant differences in postextubation airway compli-cations.1-6 The primary advantage of cuffed ETTs over uncuffed tubes is a reduction in the need for ETT chang-es, which reduces high-risk reintubations and interrupt-tions in chest compressions during CPR that may occur during reintubation. Additional potential benefits include improved capography accuracy and a lower risk of atel-ectasis.2,5-13 Although several studies have identified that cuffed tubes may decrease airway trauma by decreasing tube exchanges, attention must be directed to selecting the correct tube size3 and cuff inflation pressure.14 ETT cuff pressures are dynamic during transport at altitude,15 and with increasing airway edema or pressure, make it necessary to monitor the cuff pressure to avoid damage to the airway mucosa.
Recommendation-Specific Supportive Text
1. A retrospective study of 155 neonates and children under 12 years of age undergoing cardiac surgery with cardiopulmonary bypass and intubated for at least 4 hours postoperatively found larger ETT size as the only significant factor associated with air-way complications.3 A retrospective study of 2953 children found that applying 25 cm H2O of cuff pressure with a slight leak around the ETT resulted in no cases of clinically significant subglotic ste-nosis and the incidence of reintubation for stridor was less than 1%.1
2. Three systematic reviews, 5 randomized controlled trials, and 3 retrospective reviews support the safety of cuffed ETTs in infants and children.2-5,7-13 While these studies were almost entirely performed in the perioperative patient population, 2 studies
included patients who remained intubated for 4 hours3 or over 12 hours postoperatively.5 An addi-tional retrospective review evaluating the use of perioperative cuffed ETTs in 1162 infants weigh-ing 2 to 5 kg demonstrated no increase in post-operative airway complications.6 The use of cuffed ETTs is associated with lower reintubation rates,more successful ventilation, and improved accu-racy of capnography without increasing the risk of complications.25-9,11-13,16-18 Cuffed ETTs may also decrease the risk of aspiration and atelectasis.5,19,20
The Use of Cricoid Pressure During Intubation
|Recommendations for the Use of Cricoid Pressure During Intubation|||| |---|---|---|---| |COR|LOE|Recommendations|| |3:No Benefit|C-LD|1. Routine use of cricoid pressure to reduce the risk of regurgitation is not recommended during bag- mass ventilation of infants and children.|| |3:No Benefit|C-LD|2. Routine use of cricoid pressure is not recommended during tracheal intubation of infants and children.|| |3: Harm|C-LD|3. If cricoid pressure is used, discontinue if it interferes with ventilation or the speed or ease of tracheal intubation in infants and children.||
Synopsis
Cricoid pressure during bag-mask ventilation and dur-ing intubation has historically been utilized to minimize the risk of regurgitation of gastric contents into the air-way while potentially aiding in visualization of laryngeal structures.21,22 However, uniform application of cricoid pressure may impede bag-mask ventilation or obscure visualization of the airway during laryngoscopy.23-25 Cricoid pressure should be distinguished from ex-ternal laryngeal manipulation where pressure is ap-plied to the larger thyroid cartilage to facilitate airway visualization.26
Recommendation-Specific Supportive Text
1. A retrospective study from a large international pediatric ICUU intubation registry showed that cricoid pressure during bag-mask ventilation before tracheal intubation was not associated with lower rates of regurgitation. ${}^{26}$
2 and 3. A bronchoscopic study of 30 children revealed distortion of the airway with the application of cricoid pressure at forces below those rec-ommended by usual intubation guidelines.27 Acknowledging anatomic differences in the airway from infancy through adulthood, rel-evant adult data was considered, given limited pediatric data for the use of cricoid pressure in pediatric patients. A systematic review of cricoid pressure during rapid sequence intuba-tion in adult emergency department patients found insufficient evidence to conclude if
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cricoid pressure affected the rate of first pass intubation success or the incidence of compli-cations such as aspiration. ${}^{25}$ In a study of 60 adult patients undergoing elective anesthesia,cricoid pressure interfered with bag-mask ven-tilation in over 50% of patients. ${}^{24}$
Atropine Use for Emergency Intubation
|Recommendations for Atropine Use for Emergency Intubation|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|C-LD|1. It may be reasonable to use atropine as a premedication to prevent bradycardia in infants and children during emergency intubation.|| |2b|C-LD|2. When atropine is used as a premedication for emergency intubation of infants and children, a dose of 0.02 mg/kg with no minimum dose may be considered.||
Synopsis
Pediatric emergency intubation is a lifesaving, high-risk procedure that can be complicated by hypoxemia, bra-dycardia, hypotension, and cardiac arrest. Peri-intubation bradycardia may occur in response to (1) the underly-ing disease process that led to respiratory failure, (2) hypoxemia, (3) medications given for rapid sequence intubation, (4) the transition from negative to posi-tive pressure ventilation, and (5) vagus nerve stimula-tion during laryngoscopy and endotracheal intubation,particularly in infants.28.29 Previous guidelines have dis-couraged the routine administration of atropine before intubation but state that atropine pretreatment may be reasonable to prevent vagally mediated bradycardia in select populations.30 Observational studies demonstrate an association between atropine pretreatment and de-creased bradycardia, higher heart rates without ventricu-lar arrhythmias, and increased ICU survival.31.32 However,there is little evidence to support the use of atropine as a pretreatment for the prevention of peri-intubation cardio-pulmonary compromise or cardiac arrest.
Recommendation-Specific Supportive Text
1. Two prospective, observational studies conducted between 2007 and 2009 in patients<8 years of age intubated in the PICU or by critical care trans-port teams showed associations between atropine pretreatment and(1) decreased ICU mortality after propensity score adjustment and(2) signifi-cant acceleration in heart rate without provoking arrhythmias and a decrease in bradycardia.31,32 Conversely, 4 retrospective, observational studies did not demonstrate an association between atro-pine use and occurrence of bradycardia during the peri-intubation period.33-36
2.Historically, a minimum dose of atropine(0.1 mg)was recommended to prevent paradoxical bra-dycardia based on a 1971 study of 79 patients undergoing elective surgery, of which 5 participants
were between 6 weeks and 3 years of age. These infants and children had a small and statistically insignificant decrease in heart rate after receiving doses of atropine ranging from 0.0018 to 0.0036 mg/kg,approximately 10% to 20% of the recom-mended dose for atropine pretreatment for intu-bation.37 In 2015, in a prospective, observational study of 60 infants less than 15 kg undergoing elective surgery all of whom received<0.1 mg of atropine before intubation, no patient experienced paradoxical bradycardia or arrhythmias.38
Monitoring Exhaled CO ${}_{2}$ in Patients With Advanced Airways
|Recommendations for Monitoring Exhaled CO2 in Patients With Advanced Airways|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-LD|1. In all settings, for infants and children with a perfusing rhythm,exhaled CO2 detection (colorimetric detector or capnography) should be used for confirmation of ETT placement.|| |2a|C-LD|2. In infants and children with a perfusing rhythm and ETT in place, it is beneficial to monitor exhaled CO2(colorimetric detector or capnography) during out-of-hospital and intra-hospital transport.||
Synopsis
Confirmation of ETT placement in patients with a per-fusing rhythm is not reliably achieved by auscultation of breath sounds, mist in the tube, or chest rise. Either colorimetric exhaled CO2 detection or capnography is a more reliable method to assess initial ETT placement. In patients with decreased pulmonary blood flow from low cardiac output or cardiac arrest, exhaled CO2 may not be reliable.
Recommendation-Specific Supportive Text
1. Although there are no randomized controlled tri-als linking use of exhaled $CO_{2}$ detection with clini-cal outcomes, the Fourth National Audit Project of the Royal College of Anesthetists and the Difficult Airway Society concluded that the failure to use capography contributed to adverse events, includ-ing death and persistent neurological injury, in a study of adults and children in the ICU and emer-gency department settings. ${}^{39}$ One small, random-ized study showed that capnography was faster than clinical assessment in premature newborns intubated in the delivery room. ${}^{40}$ There has been no difference in patient outcomes in pediatric studies comparing qualitative(colorimetric) and quantita-tive(capnography or numeric display) exhaled $CO_{2}$detectors in the delivery room, ICU, or emergency department. ${}^{41-43}$
2. Adult literature suggests monitoring and correctly interpreting capnography in intubated patients may prevent adverse events.39,44,45 This has
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been demonstrated in pediatric simulation stud-ies, in which capnography improved health care professional recognition and response to ETT dislogement.46,47
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2. KamaladeVI,Rishu SK,Rudgingwa P.,Mohapatra DP,Badhe AS,Senthilathan M. Comparison of performed microcumbly and preformed uncuffed endotracheal tubes in pediatric cleft palate survey-A ran-domized controlled trial Paediatr Anaesth. 2024;34:340-346. doi:10.1111/pan.14837
3. Naidos S, Kuelis B, Gopalan P. Upper array obstruction and sepsis fol-lowing endotracheal intubation in paediatric cardiac surgical patients in South Africa. Southem Ar J Anaese Thalgn 2022;28:172-177. doi:10.36303/sajaa.2022.28:5.2808
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6. Williams ZC, Kim S, Naguab A, Shafy ZS, Tobias JD. Use of cuffed troundechal tube in infants less than 5 kilograms: a retrospective cohort study.J Pediatr Surg.2022;57:375-381. doi:10.1016/j.1jedsurg.2021.02.064
7. Chambers R, Ramagolam A, Sommerfeld D, Zhang G, Ledowski T, Thum Lethbrak M, Hegarty M, von Ungern-Sternberg B. Cuffed vs. uncuffed tracheal tubes in children: a randomised controlled trial comparing leak, tidal volume and complications. Anaesheast 2018:7316-168.
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9.De Orange FA, Andrade RG, Lemos R, ASpes G, Fiquees R, Almoune JN, Kovatsis PG. Cuffed versus uncudent orcheal tube in substances. A meta-chemal. A. Pierine and Pierine Syst. Rev.2017;11:CD011954. doi:10.1002/14651858:cd011954.pub2
10.de 10.0 de Melsen L, Van Mewolfluxer K, de Graaff JC. The incidence of postoperative respiratory complications: A retrospective analysis of cuffed vs unclrfected tubeal tubes in children 0-7 years of age. DPaediatr anaethys-2018;28:210-217 doi:10.1111/pan.13340
11.Dorseay DP,Bowman SM,Klein MB,Archer D,Sharar SR. Perioperative use of cuffed endotracheal tubes is advantageous in young pediatric burn pa-tients. B016;30S:866-860.120.10.1016/j.burns.2009.11.011
12.Schweiger C,Marostica PC,Smith,Manica D,Carvalho PA,Kuhl G.Inci-dence of post-inubation subglotic stenosis in children: prospective study.J Laryangol. Otol.2013;127:399-403.
13. Shi F, Xiao Y, Xiong W, Zhou Q, Huang X. Cuffed versus unclued endo-trachetal tubes in children: a meta-analysis. A Janesthe 2016;30-30.1: doi:10.1007/s00540-015-2062-4
14.Tobias JD. Pediatric airway anatomy may not be what we thought: implica-tions for clinical practice and the use of crafted endotracheal tubes. Pediatr Anaesth. 2015;25:9-19. doi:10.1111/pan.12528
15.Orsorbom J, Graham J, Moss M, Melguzo M, Nick T. Stroud M. Pediatric en-dotracheal tube buffer cns pressures during aeromedical transport. Pediatr Emerg Care.2016;32:20-22. doi:10.1097/PEC.00000000000000000065
16.James I. Cuffed tubes in children. Paediatra ASnest 2001;11:259-263.doi:10.1046/j.1460-9529.2001.00675x
17. Khine HH, Cordry DH, Ketrick RG, Martin TM, McCloskey JJ,Rose JB,Thorera M, Scagnoev M. Comparison of cuffed and un-cuffed endotracheal tubes in young children during general an-esthesis. Anesesthesiology. 1997;86:827-31; discussion 27A.2018.109.10000542-199703000-00015
18.Weiss M,Dulenkopf A, Fischer J, Keller C, Gerber A; European Paediatric Endotracheal Induction Study Group. Prospective randomized controlled multi-centre trial of cuffed endotracheal tubes in small children.Br J Anaesth.2009;103:867-873. doi:10.1093/bja/aep290
19. Browning D, Graves S, Thompson DS. Incidence of Aspiration with Endotra-cheal Tubes in. Surv Anesthesiol. 1984;28:31.
20.Gopalareddy V, He Z, Saturand S, Bolling L, Shah M, Penfil S, McCloskey JJ, Mehta DI, Assessment of the prevalence of microaspiration by gastric pepsin in the airway of ventilated children. Acta Paediatric(Oslo, Norway:1992) 2008;97:55-60. doi:10.1111/j.1651-22272007.00578.x
20.Moyinah RJ, Brock-Utne JG, Archer JH, Feld LH, Kreitzman TR. The effect of cricoid pressure on preventing gastric insuffla-tion in infants and children. Anesthesiology. 1993;78:652-656. doi: 10.1097/000005842-199304000-00007
22.Salem M,Wong A,Mani M,Sellick B.Efficacy of cricoid pressure in prevent-ing gastric inflation during bag-mask ventilation in pediatric patients.J Am Soc Anesthesiol.1974;40:96-98.
23. Hartsilver E, Vanner R. Ariver obstruction with cricoid pressure. Anaesthe-sia 2000055:208-211.
24.Joshi S, Prakash S, Mullick P, Usha G, Pawar M. Clinical Evaluation of the Cricoid Pressure Effect on Bag Mask Ventilation, ProSeal Laryn-geal Mask Airway Placement and Ventilation. Turk J Anaesthesiol Reanim.2018;46:381-387. doi:10.5152/TJAR.2018.37539
25.Tessaro O, Elakhouri H, Lelos N, Sarrami P, McCarthy S. Review ar-ticle: Effectiveness and risks of cricoid pressure during rapid sequence induction for endotracheal intubation in the emergency department:A systematic review. Emerg Med Australas. 2022;34:484-491. doi: 10.1111/1472-6723.13993
26. Kojima T,Harwayne-Gaidensky I,Shenoi AN,Owen EB,Napolitano N,Rehder K1,Adu-Darko MA,Nne TT, Spear D,Meyer K,et al; National Emergency Airway Registry for Children(NEAR4KIDS) and Pediatric Acung Lung Injury and Sepsis Investigators (PALISI). Cricoid Pressure During Induction for Tra cheal Intubation in Critically III Children: A Report From National Emergency Airway Registry for Children. Pediatr Crit Care Med.2018;19:528-537. doi:10.1097/PCC000000000000000000000000000000000000000000000
● 17. Walker RAV, RAY Irett K. Effect of cricoid force on airway calibre in children: a bronchoscopic assessment. Br J Anaesth.2010;104:71-74. doi:10.1093/paa/baep337
28.Engstrom K, Brown CS, Mattson AE, Lyons N, Rech MA. Pharmacotherapy optimization for rapid sequence intubation in the emergency department.Am J Emerg Med 202370:19-29. doi: 10.1016/j.ajem.2023.05.004
29.Miller KA, Nagler J. Advances in Emergent Airway Management in Pediatrics. Emerg Med Clin North Am. 2019;37:473-491. doi:10.1016/j.emc2019.03.006
30.Topian AA,Raymond TT,Atkins D,Chan M,Duff JP,Joyner BL Jr.,Lasa JJ,Lavonas EJ,Ley,A. Mahgoub M,et al; Pediatric Basic and Advanced Life Support Collaborators. Part 4: Pediatric Basic and Advanced Life Support:2020 American Heart Association Guidelines for Cardiopulmonary Resus-citation and Emergency Cardiovascular Care. Circulation. 2020;142:S469-S523. doi:10.1161/CIR/0000000000000901
31.Jones P,Dauger S,Denjoy I, Pinto da Costa N, Alberti C, Boulkedid R, Peters ML.The effect of atropine on rhythm and conduction disturbances during 322 critical care intubations. Pediatr Crit Care Med.2013;14:e289-e297.doi:10.1097/PCC013e31828a8624
2013.Jones P.,Peters MJ.,Pinto da Costa N.,Kurth T, Alberti C.,Kessous K.,Lode N,Nauger S. Aropine for critical care intubation in a cohort of 264 chil-dren and reduced mortality unrelated to effects by bradycardia. PLoS One.2013;8:574877. doi:10.10371/journal.pone.0057478
33. Carvalho VEL, Couto TB, Moura BMH, Schvartsman C, Reis AG. Atropine does not prevent hypoxemia and bradycardia in tracheal intubation in the pediatric emergency department: observational study. Rev Paul Pediatr.2023;42:e2022220. doi: 10.1590/1984-0462/2024/42/2022220
34.Fastle RK, Roback MG. Pediatric rapid sequence intubation: incidence of reflex bradic bradycard and effects of pretreatment with atropine. Pediatr Emerg Care.2004;20:651-655. doi: 10.1097/01.pec.00000142947:35394.81
<BeginOfPara>Sycantie 0197,ELsson AC,Mercormick T, Kaucher KA. Incidence of Brady-cardia and the Use of Atropine in Pediatric Rapid Sequence Intubation in the Emergency Department. Pediatr Emerg Care.2022;38:e540-e543. doi:10.1097/PEC.0000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000
36. Bisesi SA,Stauber SD, Hustchinson DJ, Acquisto NM. Current Practices and Safety of Medication Use During Pediatric Rapid Sequence Intubation. J Pe-diatar Pharmacol Ther.2024;29:66-75. doi: 10.5863/1551-6776-29.1.66
37. Dauchot P, Gravenstein JS. Effects of atropine on the electrocardiogram in different age groups. Clin Pharmacol Ther. 1971;12:274-280. doi: 10.1002/cpt 1971122ptart 1274
38.Eisa, L Passi Y.,Lerman J.,Raczka M.,Heard C. Do small doses of atro-pine(<1.01 mg) cause bradycardia in young children? Arch Dis Child.2015;1001684-6888: doi:10.1136/archischild-2014-307868
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39. Cook TM, Woodall N, Harper J, Bender J; Fourth National Audit Project. Major complications of airway management in the UK: results of the Fourth National Audit Project of the Royal College of Anaestheists and the Dif-fuct airway Society. Part 2: intensive care and emergency departments. Br J Anaesth.2011;106:632-642.doi:10.1093/bja/aer059
40. Hosono S, Inami I, Fujita H, Minato T, Aahashi S, Mugishima H. A role of end-tid:OCAM(20) monitoring for assessment of tracheal intubations in very low birth birth infants during neonatal reexsitation at birth. J Perinat Med.2009;37:79-84. doi:10.1515/JPM.2009.017
41. Hawkes GA, Finn D, Kenoski, L. Livingstone V, O'Toole JM, Boylan GB,O'Halloran KD, Ryan AC, Dempsey EM. A Randomized Controlled Trial of End-Tidal Carbon Doxide Deletion of Preterm infants in the Delivery Room. J Pediatr.2017;182:74-78.e2.d. 10:1016/j.jpeds.2016.11.006
42. Hunt KA, Yamada Y, Murthy V, Srihari Bhat P, Campbell M, Fox GF, Milner AD, Greenough A. Detection of enhanced carbon dioxide following intuba-tion during resuscitation at delivery. Arch Dis Child Fetal Neonatal Ed 2019;104F187-F191. doi: 10.1136/archidild-2017-313982
43. Langhan ML,Emerson BL Nett,S Pinto M,Haranney-Gidansky I,Rehder KJ,Krawiec C, Meyer K,Giuliano JSr, Owen EJ, Ben't and; for Pediatric Acute Lung Injury and Sepsis Investigators (PALI) and National Emergency Airway Registry for Children(NEAR4KIDS) Investigators. End-Tidal Carbon Dioxide Use for Tracheal Intubation: Analysis From the National Emergency Airway Registry for Children(NEAR4KIDS) Registry. Pediatr Care Med 2018;19:98-105. doi:10.1097/PCC.0000000000001372
44. Cook TM. Strategies for the prevention of airway complications-a narrative review. Anasesthesia 2018;79:83-11. doi: 10.1111/anaa.14123
45. Fanar B, Manzon C, Barbot O, Desmettre, Cellapier G. Recommendations for the intra-hospital transport of critically ill patients. Crit Care.2010;14:R87.doi:10.1186/cc9018
46. Langhan ML, Auerbach M, Smith AN, Chen L. Improving detection by pediatric residents of endotrachae table dislodgement with capnogra-phy: a randomized controlled trial. J Pediatr. 2012;160:1009-1014. doi:1016/j.jpds.2011.12.012
47. Langhan ML,Ching K,Norupth V,Aletag M,Kadia P,Sancuotti K,Ken L.A randomized controlled trial of capography in the correction of simulated endotracheal tube dislogement. Acad Emerg Med.2011;18:590-596. doi:10.1111/j.1553-2721201.2011.01090.x
MANAGEMENT OF BRADYCARDIA
|Recommendations for the Management of Bradycardia With Cardiopulmonary Compromise|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-LD|1. In infants and children with bradycardia and cardiopulmonary compromise due to increased vagal tone or atrioventricular conduction block not due to factors such as hypoxia, atropine is recommended.|| |2|C-EO|2. In infants and children with heart rate<60 beats/ min and cardiopulmonary compromise despite effective ventilation with oxygen, start CPR.|| |1|C-EO|3. In infants and children with bradycardia and cardiopulmonary compromise that persists after correction of other factors(eg, hypoxia), give epinephrine IV/IO.|| |2b|C-EO|4. Emergency transcutaneous pacing may be considered for infants and children with bradycardia and cardiopulmonary compromise due to complete heart block or sinus node dysfunction unresponsive to CPR.||
Synopsis
Bradycardia associated with cardiopulmonary compro-mise, even with a palpable pulse, may be a harbinger of impending pulseless cardiac arrest. As such, bradycar-dia with a heart rate of less than 60 beats per minute
<EndOfPara>in infants and children should prompt an evaluation for cardiopulmonary compromise, including acutely altered mental status, hypotension or other signs of shock. Cor-rectable factors that contribute to bradycardia include hypoxia,hypotension, hypoglycemia, hypothermia, acido-sis, and toxic ingredients.
Recommendation-Specific Supportive Text
1. Atropine increases heart rate in both children and adults.1-4 As atropine is a vagolytic agent, use is limited to bradycardia with cardiopulmonary com-promise due to increased vagal tone or atrioven-tricular conduction block, but not due to other factors such as hypoxia.
2. Retrospective studies have shown that children who received CPR for bradycardia with cardiopul-mary compromise have better outcomes than children who receive CPR for pulseless cardiac arrest-5-8 No studies compared outcomes between children with bradycardia and cardiopulmonary compromise who did or did not receive CPR,though 1 study reported 8 patients who received drug therapy without CPR, and all survived to hos-pital discharge.9
3. A retrospective, time-dependent propensity-score matched study of pediatric patients with bradycar-dia and cardiopulmonary compromise found that patients who received epinephrine had worse out-comes than patients who did not receive epinephine. ${}^{10}$ A subsequent retrospective study did not show differences in outcomes for patients who did or did not receive "early" epinephrine within the first 2 minutes of CPR for bradycardia and cardiopul-nary compromise." Due to limitations of these studies, further research on the impact of epineph-rine on patients with bradycardia and cardiopulmo-nary compromise is required.
4.There are limited data about transcutaneous pac-ing for refractory bradycardia in children with or without congenital/acquired heart disease.12-14 In patients with complete heart block or sinus node dysfunction when have not responded to oxygen-ation, ventilation, medications, or CPR, emergency transcutaneous pacing may be considered.
Figure 6 shows the algorithm for pediatric bradycardia with a pulse.
REFERENCES
1. Brady WJ, Swart G, DeBehnke DJ, Ma OJ, Aufderheide TP. The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrio-ventricular block: prehospital and emergency department considerations.Resuscitation.1999;41:47-55.doi:10.1016/s0300-9572(99)00032-5
2. Fullerton DA, St Cyr JA, Clarke DR, Campbell DN, Toews WH, See WM.Bezold-Jarisch reflex in postoperative pediatric cardiac surgical patients. Ann Thorac Surg.1991;52:534-536.doi:10.1016/0003-4975(91)90919-h
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 Figure 6. Pediatric Bradycardia With a Pulse Algorithm.
3.Smith I,Monk TG,White PF. Comparison of transesophageal arial pacing with anticholinergic drugs for the treatment of intraoperative bradycardia. Anesth Analg.1994;78:245-252. doi:10.1213/00000539-199402000-00009
4.Zimmerman G,Steward DJ. Bradycardia delays the onset of action of intra-venous atrip in infants. Aesthenology.1986;65:320-322.
5. Khera R, Tang Y, Girotra S, Nadkarni VM, Link MS, Raymond TT,Guerguerian AM, Berg RA, Chan PS; on behalf of the American Heart
Association's Get With the Guidelines-Resuscitation Investigators.Pulselessness after initiation of cardiopulmonary resuscitation for bra-dycardia in hospitalized children. Circulation. 2019;140:370-378. doi:10.1161/CIRCULATIONAHA.118.039048
6. Morgan RW, Reeder RW, Meert KL, Telford R, Yates AR, Berger JT, Graham K,Landis WP,Kilbaugh TJ,Newth CJ,et al; Eunice Kennedy Shriver Nation al Institute of Child Health and Human Development/Collaborative Pediatric
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Critical Care Research Network(CPCCRN) Pediatric Intensive Care Quality of Cardio-Pulmonary Resuscitation(PICqCPR) Investigators. Survival and Hemodynamics During Pediatric Cardiopulmonary Resuscitation for Brady-cardia and Poor Perfusion Versus Pulseless Cardiac. Arest. Crit Care Med.2020;48:881-889. doi:10.1097/CCM.0000000000004308
7. Donoghue A, Berg RA, Hazinski MF, Praestgaard AH, Roberts K, Nadkarni VT, American Heart Association National Registry OF CPR Investiga-tors. Cardiopulmonary resuscitation for brachydary via poor perfusion versus pulseless cardiac arrest. Pediatrics. 2009;124:1541-1548. doi:10.1542/peds.2009-0727
8. Holmberg MJ, Wiberg S, Ross CE, Kleinman M, Hoeyer-Nielsen AK,Donnino MW, Andersen LW. Trends in survival after pediatric in-spatial cardiac arrest in the United States. Circulation. 2019;140:1398-1408. doi: 10.1161/CIRCULATIONAHA.119.041667
9. Atabek ME, Aydin K, Ekul I. Different clinical features of ami-traz poisoning in children. Hum Exp Toxicol. 2002;21:13-16. doi:10.1191/0960327102ht2070a
10. Holmberg MJ, Ross CE, Yankama T, Roberts JS, Andersen LW; American Heart Association's Get With The Guidelines®-Resuscitation Investiga-tors. Epinephrine in children receiving cardiopulmonary resuscitation for bradycardia with poor perfusion. Resuscitation. 2020;149:180-190: doi: 10.1016/j.resuscitation.2019.12.032
11. O'Halloran AJ,Reeder RW,Berg RA,Ahmed T,Bell MJ,Bishop R,Bochkoris M, Burns C, Carcillo JA, Carpenter TC, et al. Early bolus epinephrine ad-ministration during pediatric cardiopulmonary resuscitation for bradycardia with poor perfusion: an ICU-resuscitation study, Cott Care.2024;28:242.doi:10.1186/s13045-024-05018-
12. Pirasath S, Arulnithy K. Yellow oader poisoning in eastern province: an analysis of admission and outcome. Indian J Med Sci.2013;67:1783-183.doi: 10.4103/0019-5359.125879
13. Bolouchi M, Silver ES, Liberman L. Advanced Heart Block in Chil-dren with Lyme Disease. Pediatr Cardiol. 40;2019:513-517.10:1007/s00246-018-2003-8
14. Nazim TM, Vazquez J,Honig LS,Nizdum JM,Anti-N-methyl-D-aspartate recep-itor conephalitis: an emerging cause of centrally mediated sinus node dys-function.Europace.2012;14:1188-1194.doi:10.1093/europace/eus014
TACHYARRHYTHMIAS
Treatment of Supraventricular Tachycardia With a Pulse
|Recommendations for Treatment of Supraventricular Tachycardia With a Pulse||| |---|---|---| |COR|LOE|Recommendations| |1|C-LD|1. In infants and children with SVT without cardiopulmonary compromise, it is useful to attempt vagal stimulation first.| |1|C-LD|2. If IV/IO access is readily available, adenosine is recommended for the treatment of SVT in infants and children.| |1|C-EO|3. For infants and children without cardiopulmonary compromise whose SVT is unresponsive to vagal maneuvers and IV adenosine, expert consultation is recommended.| |2a|C-LD|4. In infants and children with SVT and cardiopulmonary compromise, it is reasonable to perform electrical synchronized cardioversion starting with a dose of 0.5 to 1 J/kg. If unsuccessful, increase the dose to 2 J/kg.| |2b|C-LD|5. For infants and children with SVT and cardiopulmonary compromise unresponsive to vagal maneuvers, adenosine, and electrical synchronized cardioversion and for whom expert consultation is not available, it may be reasonable to consider either IV procainamide, amiodarone, or sotalol.|
Synopsis
Regular, narrow-complex tachyarrhythmias(QRS dura-tion 0.09 second or less) are most commonly caused by re-entrant circuits, although other mechanisms such as ectopic atrial tachycardia or junctional tachycardia may occur. Regular, wide-complex tachyarrhythmias(WCT;ORS>0.09 second) can have multiple mechanisms, in-cluding SVT with aberrant conduction, antidromic SVT, or VT. SVT with aberrant conduction is the most common cause of WCT in infants and children.1
The hemodynamic impact of SVT in the pediatric patient can be variable, with signs of cardiopulmonary compromise such as altered mental status, signs of shock, or hypotension occurring in a minority of patients.In infants and children without cardiopulmonary compro-mise, re-entrant SVT can often be terminated with vagal maneuvers.2-5 Adenosine remains the preferred medica-tion initially unresponsive to vagal maneuvers.3,6-14 For patients with hemodynamically stable SVT that recurs after initial successful treatment, expert consultation is important to diagnose etiology and customize treatment.The use of other IV antiarrhythmics including procain-amide, amiodarone, and sotalol have been studied with varying levels of success.15-20 When cardioversion is pro-vided, the administration of sedation before synchronized cardioversion can minimize the pain associated with the shock. However, extreme caution is warranted in the selection and dosage of sedatives in a patient with car-diopulmonary compromise.
Recommendation-Specific Supportive Text
1. Vagal maneuvers are noninvasive, have few adverse effects, and effectively terminate SVT in many cases; exact success rates for each type of maneuver(ie, ice water to face, postural modifica-tion) are unknown.3 Although improved success rates have been reported with a postural modifica-tion to the standard Valsalva maneuver in adults,2 published pediatric experience with this technique is very limited. Upside-down positioning may be an additional form of a vagal maneuver that is effec-tive in children.4
2. IV adenosine remains generally effective for ter-minating re-entrant SVT within the first 2 doses. In retrospective observational studies on the manage-ment of tachyarrhythmias, none directly compared adenosine to other drugs.6,7,9-14 A Cochrane review that included mostly adult studies and 1 pediatric study showed that either adenosine or calcium channel blockers can be used for quick termination of SVT.8 Given the fast onset of action, short half-life, and favorable side effect profile, adenosine is preferred for infants and children.21
3. For infants and children with SVT without cardio-pulmonary compromise that is refractory to vagal
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maneuvers or adenosine, expert consultation can guide the choice of alternative second-line agents.The risk for proarrhythmic and life-threatening hemodynamic collapse increases with the admin-istration of multiple antiarrhythmic agents. Multiple medications have been used as second-line agents for the management of adenosine-refractory SVT,including IV verapamil,β-blockers, amiodarone,procainamide, and sotalol.3,6,7,10,11,15,16,18-20,22,23 Few comparative studies exist.
4.Direct current transcutaneous synchronized car-dioversion remains the treatment of choice for infants and children with SVT and cardiopulmo-nary compromise(characterized by altered mental status, signs of shock, or hypotension).However,these cases are uncommon, and there are few studies that report outcomes from cardioversion of SVT.713,24 The administration of sedation before synchronized cardioversion can minimize the pain associated with the shock. However, extreme caution is warranted in the selection and dosage of sedatives in a patient with cardiopulmonary compromise.
5. Procainamide and amiodarone are moderately effective treatments for adenosine-resistant SVT.16 Procanainide may be slightly more efficacious;adverse effects are frequent with both therapies.IV sotalol was approved for the treatment of SVT in 2009. Since its approval, several single-center and 1 multicenter registry have shown that IV sotalol is effective in acute conversion of SVT, with a 60% to 100% termination rate of SVT and atrial tachyar-rhythmias. ${}^{15,17,18-20}$ In these studies, IV sotalol was administered under the guidance of pediatric elec-trophysiologists in acute care settings and no sig-nificant adverse events were reported.
Treatment of Wide-Complex Tachycardia With a Pulse
|Recommendations for Treatment of Wide-Complex Tachycardia With a Pulse|||| |---|---|---|---| |COR|LOE|Recommendations|| |1|C-LD|1. In infants and children with wide-complex tachycardia without cardiopulmonary compromise, expert consultation is recommended prior to administration of antiarrhythmic agents.|| |2a|C-EO|2. In infants and children with wide-complex tachycardia with regular and monomorphic QRS without cardiopulmonary compromise, adenosine administration can be useful in conjunction with expert consultation.|| |2a|C-EO|3. In infants and children with wide-complex tachycardia and cardiopulmonary compromise, it is reasonable to perform electrical synchronized cardioversion starting with a dose of 0.5-1 J/kg. If unsuccessful, increase the dose to 2 J/kg.||
Synopsis
The occurrence of WCT(QRS duration >0.9 second)with a pulse is rare in children and may originate from either the ventricles or the atria.25 SVT with aberrant con-duction is the most common cause of WCT in infants and children; however, other etiologies can include antidromic SVT or VT.1 For patients with WCT and no cardiopulmo-nary compromise, expert consultation is important to diagnose etiology and customize treatment. The admin-istration of sedation before synchronized cardioversion can minimize the pain associated with the shock. How-ever, extreme caution is warranted in the selection and dosage of sedatives in a patient with cardiopulmonary compromise.
Recommendation-Specific Supportive Text
1.Both pediatric and adult studies have identi-fied potential populations at risk of proarrhyth-mic complications from antiarrhythmic therapies,including patients with underlying cardiomyopa-thies, long-QT syndrome, Brugada syndrome, and Wolff-Parkinson-White syndrome.26-30 Given this potential risk, expert consultation can help provide a tailored antiarrhythmic choice to minimize the chances of arrhythmia.
2. Given that the most common cause of WCT in infants and children is SVT with aberrancy,1 the use of adenosine can be either therapeutic or diagnos-tic. If the cause of the WCT is SVT with aberrancy,administration of adenosine is likely to terminate the arrhythmia. If the cause of the WCT is VT,the administration of adenosine can be diagnos-tic if it demonstrates ventriculo-atrial dissociation.Adenosine should only be administered in WCT if the tachycardia is monomorphic and regular. If WCT is irregular, it can represent pre-excited atrial fibrillation, and the administration of adenosine can lead to VF. When possible, the administration of adenosine should be done with a running rhythm strip or multilead electrocardiogram to help with interpretation of the adenosine response. ${}^{1,31}$
3. Cardiopulmonary compromise is a key factor in determining the use of electrical therapy over pri-mary pharmacologic management in children with WCT and a pulse. In patients with cardiopulmonary compromise, electrical direct current synchronized cardioversion should be provided urgently, regard-less of suspected atrial or ventricular origin. There is insufficient evidence describing the incidence of WCT without cardiopulmonary compromise,and there is no support for or against the use of specific antiarrhythmic drugs in the management of children with wide-complex tachycardia with a pulse.
Figure 7 shows the algorithm for pediatric tachyarrhyth-mia with a pulse.
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 Figure 7. Pediatric Tachyarrhythmia With a Pulse Algorithm.
REFERENCES
1. Escudero CA, Tan RBAM, Beach CM, Dalal AS, LaPage MJ, Hill AC. Approach to Wide Complex Tachycardia in Paediatric Patients. CJC Pediatr Congenit Heart Dis.2022;1:60-73. doi:10.1016/j.jcpc2022.02.003
2. Appelboam A, Reuben A, Mann C, Gagg J, Ewings P, Barton A, Lobban T,Dayer M, Vickery J, Benger J; REVERT trial collaborators. Postural modifi-cation to the standard Valsana voaneare for emergency treatment of su-proventricular tachycardias(REVERT): a randomised controlled trial. Lancet 2015;386:1747-1753. doi:10.1016/S0140-6736(15)61485-4
3.Campbell M, Buitrago SR. BET 2:Ice water immersion, other vagal manoeu-vres or adenosine for SVT in children. Emerg Med J.2017;34:58-60. doi:10.1136/emerned-2016-206487.2
4. Bronzetti G, Brighenti M, Mariucci E, Fabi M, Lanari M, Bonvicini M, Gargiulo G, Pension A. Upside-down position for the out of hospital management of children with supraventricular tachycardia. Int J Cardiol. 2018;252:106-109. doi: 10.1016/j.jcijard.2017.10.120
5. Uysal F, O A, Genc A, Cil E. Evaluation of Clinical Features and Prognosis in Children with Supraventricular Tachycardia. J Curr Pediatr:2023;21:202-208.
6. Losek, Endom E, Dietrich A, Stewart G, Zempsky W, Smith K. Adenosine and pediatric supraventricular tachycardia in the emergency department:
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multicenter study and review. Ann Emerg Med. 1999;33:185-191. doi:10.1016/s016-09644(09)979032-6
7. Clausen H, Theophilos T, Jackno K, Babl FE. Paediatric arrhythmias in the emergency department. Emerg Med J. 2012/29:732-737: doi:10.1136/emerned-2011-200242
8. Alabed S, Sabouni A, Providencia R, Atallah E, Qintar M, Chico TJ. Ade-nosine versus intravenous calcium channel antagonists for supraventricile at larachcy. Cochrane Database Syst Rev. 2017;10:CD005154. doi:10.1002/14651858.CD005154.pub4
10. Balagargul Gallo, M ordan Garcia I, Bolagri Bosch, J. Camba Lasasa FJ, Prada Hermogenes F, Palomaque Rico A. [Supraventricular tachycar-dia in infants and children]. An Pediatr(Abarc). 2007;67:1338:138. doi:10.1016/s1695-0433(07)70753-8
10. Chu PY,Hill KD, Clark RH, Smith PB, Hornik CP. Treatment of supravening tricularchacta in infants: Analysis of a large multicenter database. Early Hum Dev.2015;91:3455-350. doi:10.1016/j.earhumdev.2015.04.001
11. Diaz-Parra S, Sanchez-Yanez P, Zabala-Arguelles L, Picoaz-Angelin B,Conjoe-Munoz L, Cuenca-Peiro V, Duran-Holda I, Garcia-Soler P. Use of adenosine in the treatment of supraventricular tachycardia in a pediat:ric emergency department. Pediatr Emerg Care. 2014;30:388-393. doi:10.1097/PEC.00000000000000014
12. Hashim HT, S J., Hashim AT, Mohamed OA, Abdeljali MS, Varney J. The drugs used in the treatment of supraventricular tachycardia in pediatrics: a systematic review and meta-analysis. Cor Vasa 2023;65:477-484.
13. Lewis J, Arora G, Tudorascu DL, Hickey RW, Saladino RA, Manole MD. Acute Management of Refractory and Unstable Pediatric Su-praventricular Tachycardia. J Pediatr. 2017;181:177-182.e2. doi: 10.1016/j.jpeds.2016.10.051
14. Quresu Al, Hymer South, Sheikh AM, Sadig M. Optimal dose of adenosine effective for supraventricular tachycardia in children. J Coll Physicians Surg Pak 2012;22:648-651. doi:10.2012/JCPSP648651
15. Borquez AA,Aljohani A, Williams MR, Perry JC. Intravenous Sotatal in the Young: Safe and Effective Treatment With Standardized Protocols. JACC Clin Electrophysiol 2020;64:425-432. doi: 10.1016/j.jacept.2019.11.019
16. Chang PM, Silka MJ, Morisomato DY, Bar-Cohen Y, Imamodoriar versus pro-cainamide for the acute treatment of recurrent supraventricular tachycardia in pediatric patients. Circ 477333333331.10:1410.8611.161/CIRCEP.109.901629
17. Li X,Zhang Y,Liu H,Jiang H,Ge H,Zhang Y.Efficacy of intravenous so-tail for treatment of increasant tachyardium in children. Am J Cardio-sonal 2017;119:1366-1370. doi: 10.1016/j.amjcard.2017.01.034
18.Malloy-Waiton L, Von Bereng N, Halbaj S, Fischbach PS, Gamreiter JM,Asaki SY,Moak JP,Ohao L,Chang PA,Nyngu Nguyen,ALH,et al.VI Sotalol Use in Pediatric and Congenital Heart Patients: A Multicenter Registry Study.J Am Heart Assoc.2022;11:e024375; doi:10.1161/JAHA-12102.04375
19. Valdes SO, Howard TS, Pham TDN, Lemming KI, Rochelson E, Backes ER,Lam WW, Patel R, Miyake CY, Kim JJ. When adenosine is not enough. Heart Rhythm.2022;19:1015-1016. doi:10.1016/j.thrmm.2022.00202
20. Valdes SO, Miyake CY, Niu MC, de la Uz CM, Asaki SY, Landstrom AP,Schneider AE, Rusin CG, Patel R, Lam W E, et al) Early experience with intravenous solotal in children with and without congenital heart disease Heart Rhythm.2018;15:1862-1869. doi:10.1016/j.hrthm.2018.070.010
21.Greco R. Musto B, Arieno V, Alborino A, Garofalo S, Marsico F. Treat-ment of peroxysmal supraventricular tachycardia in infancy with digital,adenosine-5-triphosphate, and verapari: a comparative study. Circulation.1982:664-681-508. doi:10.1016/1.0167/1.corr.663.504
22. Lapge MJ, Bradley DJ, DickM 22k and Veraplim in infants: anexaggered fear?Pediatr Cardiol. 2013;34:1532-1534.10.1007/s00246-013-0739-8
23. Lim SH,Ananthanar Vera, Te WS, Chen YH. Slow infusion of calcium chan-nel blockers compared with intravenous adenosine in the emergency treat-ment of supraventricular tachyocardia. Resuscitation 2009;805:528-528. doi:10.1016/j.resuscitation.2009.01.017
24. Sacchetti A, Moyer V, Baricella R, Cameron M, Joakme ME. Primary car-dac arrhythmias in children. Pediatr Emerg Care 1999;195:95-98. doi:10.1097/00006565-199904000004
25. Brady WJ, Mattu A, Tabas J, Ferguson JD. The differential diagnosis of wide ORS complex tachyardia. Am J Emerg Med. 2017;35:1525-1529. doi:10.1016/j.ajem.2017.07056
26.Ramusimovic S, Laer S, Meibboh B, Lagler FB, Paul T. Pharmacokinetics of intravenous aramoditive inon children. Arch Dis Child.2013;98:989-993. doi:10.1136/archischd-2013-304483
27.Sarganas G, Garbe E, Kimpel A Heing R, Bronder E, Haverkamp W. Epidemiology of symptomatic drug-induced long QT syndrome and Torsade de Pointes in Germany. Eurospace. 2014;16:101-108. doi:10.1093/eurospace/eu214
28. Coughriet AL, Behr Ehr, Layton D, Marshall V, Camm AJ, Shakir SAW. Drugs and Drs. Me-threatening ventricular arrhythmia risk: re-sults from the DARE study cohort. BMJ Open. 2017;7:e016627. doi: 10.1136/jmemben-2017-016627
29.Chen S, Motonaga KS, Hollander SA, Almond CS, Rosenthal DN, Kaufman BD, May LJ, Avarasala K, Dao DT, Dubin AM, et al. Electrocardiographic re-polarization abnormalities and increased risk of life-threatening arrhythmias in children with dilated cardiomyopathy. Heart Rhythm.2016;13:1289-1296.doi:10.1016/j.hrthm.2016.02.014
30. Ortiz M, Martin A, Aribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J.; PROCAMIO Study Investigators. Randomized comparison of intrave-nous procramide vs. intravenous amiodarone for the acute treatment of tolerated wide RPS tachycardia: the PROCAMIO study. Eur Heart J.2017;38:1329-1335.doi: 10.1093/eurheart/ehw230
31. Maril KA, Woltram F, Desouza IS, Nishijima DK, Kay D, Setnik GS, Stair TO,Ellin Parto. Anenosine de wide-complex tachycardia: efficacy and safety. Crit Care Med.2009;37:2512-2518. doi:10.1097/CCM.0b013e3181a93661
TREATMENT OF MYOCARDITIS AND CARDIOMYOPATHY
|Recommendations for Treatment of Myocarditis and Cardiomyopathy||| |---|---|---| |COR|LOE|Recommendations| |1|B.-NR|1. Given the high risk of cardiac arrest in infants or children with myocarditis who demonstrate arrhythmias, heart block, ST-segment changes, or low cardiac output, early consideration of transfer to an ICU for monitoring and therapy is recommended.| |2a|B-NR|2. For infants and children with myocarditis or cardiomyopathy with refractory low cardiac output, ECMO/mechanical cardiac support(MCS) can be beneficial to provide end-organ support and to prevent cardiac arrest.| |2a|B-NR|3. In infants and children with myocarditis or cardiomyopathy experiencing cardiac arrest, early deployment of ECPR is reasonable.| |2a|C-LD|4. For infants and children with myocarditis or cardiomyopathy experiencing cardiac arrest, early deployment of ECPR is reasonable.|
Synopsis
Acute decompensated heart failure can result in end-organ compromise and rapid progression to cardiac arrest'1 Fulminant myocarditis and cardiomyopathy are common causes of acute decompensated heart failure in children. ${}^{1-6}$ Outcomes can be optimized by early diag-nosis and prompt intervention, including ICU monitoring and therapy. Heart block, ventricular arrhythmias, require-ment for invasive mechanical ventilation, or signs of or-gan failure in the patient with fulminant myocarditis are considered a prearest state. ${}^{2-5,7,8}$
Early consideration of transfer to a center capable of providing mechanical circulatory support(MCS) in the form of a ventricular assist device is important3,4,9-11 Centers with more experience in the management of these patients may have better outcomes.3 Early ECMO cannulation of patients requiring invasive ventilation may be associated with survival.39 The use of ECMO and MCS have improved outcomes of patients with acute
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myocarditis, with a high possibility of partial or complete recovery of myocardial function.3-6,9,11-15
Recommendation-Specific Supportive Text
1. Multiple retrospective studies have evaluated pre-dictors of worse outcome in patients with acute decompensated heart failure with most studies in patients with fulminant myocarditis. There is an increased incidence of cardiac arrest and need for ECMO/MCS in this high-risk population.1-3,5,78,10,11 Incidence of cardiac arrest in fulminant myocarditis ranges from 25% to 75%.3,5,7,8,10 signs of organ fail-ure, a requirement for invasive mechanical ventila-tion, and even modest decreases in left ventricular fraction are associated with the need for ECMO/MCS.3-5,8,9,11 In 1 registry study, ventricular arryth-mias that required treatment were strongly associ-ated with mortality (OR,8.47; 95% CI,7.16-10.04;P<0.001).3
2.The prognosis for patients with fulminant myocar-dits who receive ECMO or MCS can be good and is generally better than for patients who require ECMO due to other causes, especially those with congenital heart disease.1,12 In 4 observational studies, transplant-free survival to hospital dis-charge in myocarditis patients without congenital heart disease requiring ECMO or MCS ranged from 72% to 80%.4,59,10
3.In a cohort of 847 myocarditis patients, 60/847(7.1%) had a cardiac arrest with 43/60(72%) of these patients receiving ECPR. Among ECPR patients,31/43(72.1%) survived to hospital discharge com-pared to 11/17(64.7%) of non-ECPR cardiac arrest patients.4 In 1 study, 95% of children with myocarditis who were placed on ECMO(n=15) or MCS(n=1)after cardiac arrest were alive 6 months later com-pared to 85% in nonycarditis patients.14
4. In a retrospective study, shorter time to ECMO can-nulation after intubation was associated with sur-vival in patients with fulminant myocarditis(3 h in survivors, 6 h in nonsurvivors).9 A registry analysis from Japan noted improved outcomes if pediatric patients with myocarditis were managed in higher-volume centers.3
REFERENCES
1. Lasa JJ,Gaies M,Bush L,Zhang W,Banerjee M,Alten JA,Butts RJ,Cabrera AG,Chechcia PA,Elhoff J,et al.Epidemiology and Outcomes of Acute De-compensated Heart Failure in Children. Circ Heart Fail.2020;e006101.doi:10.1161/CIRCHEARTFAILURE.1196.001061
2. Miyake CY,Teele SA,Chen L,Motonaga KS,Dubin AM,Balasubramanian S, Balise RR, Rosenthal DN, Alexander ME, Waish EP, et al. In-hospital arrhythmia development and outcomes in pediatric pa-tients with acute myocarditis. Am J Cardiol. 2014;113:535-540. doi:10.1016/j.jamcard.2013.10.021
3. Ohki S, Hosokawa K, Tomioka S, Matsuoka M, Fushimi K, Matsuda S,Shime N. Pediatric Fuminant Myocarditis in Japan: A Retrospective
Nationwide Database Shudy of Hospital Volume, Management Prac-tices, and Mortality. Pediatr Crit Care Med. 2021;22:e391-e401. doi:10.1097/PCC.00000000000002692.
4. Peng DM, Kwiatkowski DM, Lasa JJ, Zhang W, Banerjee M, Mikesell K,Joong A, Dykes JC, Tume SC, Niebler R, et al. Contemporary Care and Outcomes of Critically-ill Children with Clinically Diagnosed Myocarditis. J Card Fail.2024;30:350-358. doi:10.1016/j.cardfail.2023.04.010
5.Sun M, Zong Q, Ye LF, Fan Y, Yang L, Lin R. Prognostic factors in chil-dren with acute fulminant myocarditis receiving venoarterial extracorpo real membrane oxygenation. World J Pediatr Surg. 2022;5:000271. doi: 10.1136/wjps-2021-000271
6. Teele SA, Allan CK, Lausen PC, Newburger JW, Gauvreau K, Thiagarajan RR. Management and outcomes in pediatric patients presenting with acute fulminant myocarditis. J Pediatr. 2011;158:638-643.e1. doi:10.1016/j.jpgs.2010.10.015
7. Casadonte Jr, Mazwi ML, Gambetta KE, Palac HL, McBride ME, Eltayeb OM, Monge MC, Backer CL, Costello JM. Risk Factors for Cardiac Arrest or Mechanical Circulatory Support in Children with Fulminant Myocarditis. Pediatr Cardiol. 2017;38:128-134. doi: 10.1007/s00246-016-1493-5
8. Othman HF, Byrnes J, Elsammy E, Hamzah M. Impact of ventricular ar-rhythmias on outcomes in children with myocarditis. Eur J Pediatr.2020;179:1779-1786.doi:10.1007/s00431-020-03687-4
9.Gutierrez ME, Anders M.; Guffey D, Denfield SW, Deshpande SR,Rajagopal SK, Thiagarajan RR, Alexander PMA, Lasa JJ. Extroroac real Membrane Oxygen annulation Timing in the Pediatric Myo-carditis Population: An Exploratory Analysis From the Extracorporeal Life Support Organization Registry. Crit Care Explor. 2023;5:e0826. doi:10.1097/CCE.000000000000826
10. Kobayashi RL, Przybylski R, Gauvreau K, Esteso P, Nathan M, Thiagarajan RR, Fynn-Thompson F, Blume ED, Teele SA. Contemporary Outcomes of Pediatric Patients with Acute Fulminant Myocarditis supported with Extra corporeal membrane Oxygenation.J Heart Lung Transplant.2022;41:S505-S506. doi: 10.1016/j.heaun.2021.1282
11. Wu HP, Lin MJ, Yang WC, Wu KH, Chen CY. Predictors of Extracoro-real Membrane Oxygenation for Children with Acute Myocarditis.
12. Conrad SJ,Bridges BC,Kalray R, Pletsch JB, Smith AH. Extracorporeal diopulmonary Resuscitation Among Patients with Structurally Normal Hearts.ASIAO.J.2017;63:781-786. doi:10.1097/MAT.0000000000000568
13. Rajagopal SK, Almond CS, Laussen PC, Rycus PT, Wypij D, Thiagarajan RR.Extracorporeal membrane oxygenation for the support of infants, children and young adults with acute myocarditis: a review of the Extracorporeal Life Support Organization registry. Crit Care Med.2010;38:382-387. doi:10.1097/CCM.0b013e3181bc8293
14.Schubert S, Opgen-Rhein B, Boehne M, Weigelt A, Wagner R, Muller G,Rentzsch A, Zu Knyphausen E,Fischer M, Papakostas K, et al. Severe heart failure and the need for mechanical circulatory support and heart transplan-tation in pediatric patients with myocarditis: Results from the prospective multicenter registry "MYKKE". Pediatr Transplant. 2019;23:e13548. doi: 10.1111/petr.13548
15.Wilmot I,Morales DL, Pricre JF, Rossano JW, Kim JJ, Decker JA, McGarry MC,Denfield SW,Dreyer WJ,Towbin JA,et al.Effectiveness of mechanical circulatory support in children with acute fulminant and persistent mycardi-tis.J Card Fair.2011;17:487-494. doi:10.1016/j.cardfail.2011.02.008
RESUSCITATION OF PATIENTS WITH SINGLE VENTRICLE CONGENITAL HEART DISEASE
|Recommendations for the Resuscitation of Patients With Single Ventricle Congenital Heart Disease||| |---|---|---| |COR|LOE|Recommendations| |1|C-EO|1. For infants and children with aortopulmonary shunt-dependent congenital heart disease with known or suspected shunt obstruction, early consideration for transfer to a center with advanced cardiac therapy capabilities (ie, cardiac catheterization, cardiac surgery,ECMO) is recommended if these services are not available.|
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|Recommendations for the Resuscitation of Patients With Single Ventricle Congenital Heart Disease (Continued)||| |---|---|---| |COR|LOE|Recommendations| |2a|C-LD|2. In infants and children with single ventricle congenital heart disease following initial palliative procedures(eg, Stage I Norwood, Hybrid procedure, Blalock-Thomas-Taussig shunt), timely ECMO deployment can be useful to treat low cardiac output syndrome.| |2a|C-EO|3. For infants and children with aortopulmonary shunt-dependent congenital heart disease with known or suspected shunt obstruction, it is reasonable to administer oxygen, vasoactive agents, and heparin while preparing for catheter-based or surgical intervention.| |2b|C-LD|4. In infants and children with single ventricle congenital heart disease following initial palliative procedures(eg, Stage I Norwood, Hybrid procedure, Blalock-Thomas-Taussig shunt) experiencing cardiac arrest, timely ECPR deployment may be a useful rescue strategy to achieve ROC.| |2b|C-LD|5. In infants and children with single ventricle congenital heart disease following Stage II (bidirectional Glenn, fiem-Fontan) or Stage III (Fontan) palliation, timely ECMO deployment may be considered to treat low cardiac output syndrome.|
Synopsis
The complexity and variability in pediatric congenital heart disease (CHD) pose unique challenges during resuscitation. Children with single-ventricle CHD typi-cally undergo 3 staged palliative operations. The first procedure, typically performed during the neonatal period, creates unobstructed systemic blood flow, an atrial communication to allow for atrial level mixing, and regulated pulmonary blood flow to prevent pulmonary overcirculation and to decrease the volume load on the systemic ventricle1,2(Figure 8). During the second stage,a superior cavopulmonary anastomosis (ie, bidirectional Glenn/hemi-Fontan operation) is created to aid in the
 Figure 8. Stage I palliation for single ventricle with a Norwood repair and either a Blalock-Thomas-Taussig shunt from the right subclavian artery to the right pulmonary artery or a Sano shunt from the right ventricle to pulmonary artery.
 Figure 9. Stage II palliation for single ventricle with a bidirectional Glenn shunt connecting the superior vena cava to the right pulmonary artery.
redistribution of systemic venous return directly to the pulmonary circulation(Figure 9). The Fontan procedure is the final palliation where inferior vena cava blood flow is baffled directly to the pulmonary circulation,thereby making the single(systemic) ventricle preload dependent on passive flow across the pulmonary vascu-lar bed(Figure 10).
Neonates and infants with single-ventricle physiol-ogy have an increased risk of cardiac arrest because of increased myocardial work from ventricular volume loading, imbalances in relative systemic(Qs) and pulmo-nary(Qp) blood flow, and potential shunt occlusion.1-3 Depending on the stage of repair, resuscitation may require control of pulmonary and systemic vascular resis-tance, administration of supplemental oxygen, interven-tion for shunt obstruction, or the use of ECMO.
Recommendation-Specific Supportive Text
1. In aortpulmonary shunt-dependent CHD patients with suspected shunt obstruction, either cardiac catheterization or cardiothoracic surgery can be performed to restore patency of an obstructed shunt. Although observational single-center reports have not compared outcomes between procedural interventions (catheter-based or surgical) versus no procedural intervention for treatment of aor-topulmonary shunt obstruction, lack of pulmonary blood flow can lead to severe cardiopulmonary compromise and cardiac arrest.1-4 ECMO can be deployed to rescue the shunt-dependent patient with cardiopulmonary compromise related to shunt obstruction before performing interventions to restore shunt patency.1-5
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 Figure 10. Stage III Fontan single ventricle palliation with an extracardiac conduit connecting the inferior vena cava to the right pulmonary artery.
2. For children with single ventricle CHD after initial surgical palliation(eg, Blalock-Thomas-Taussig shunt, Stage I Norwood) needing postoperative ECMO for management of low cardiac output state, reported survival rates range from 31%to 53%.35,7-9 In 1 small observational study of patients undergoing staged palliation, survival rates were statistically unchanged in patients who received elective ECMO(n=15) compared to ECPR(n=10)(55% versus 36%, P=0.17).7 In another study, neonates with hypoplastic left heart syndrome status post-Stage I palliation supported with ECMO had a survival rate of 31%, compared to 51% survival for neonates placed on ECMO for cardiac indications as reported to Extracorporeal Life Support Organization registry database.5 Though reported survival rates for ECPR in this cohort(32%-57%) after initial surgical palliation are similar to survival rates for elective ECMO(31%-53%), clinical practice standards advocate for earlier recognition of the postoperative low cardiac output state and deployment of elective ECMO before cardiac arrest, as this may be asso-ciated with improved long-term functional out-comes.5,7,10,11 There are no studies which directly compare children with single ventricle CHD after initial surgical palliation experiencing impending hemodynamic collapse receiving postoperative elective ECMO to cohorts not receiving ECMO under similar hemodynamic conditions.
3.Medical treatment for acute aortopulmonary shunt obstruction obstruction in peri-arrest and cardiac arrest states can include administration of supplemental oxygen,vasoactive agents(eg, epinephrine, phenyleph-rine, norepinephrine) to maximize shunt perfusion
pressure, and anticoagulation with heparin(50-100 units/kg bolus) to mitigate clot propagation.1,3,6
4.In children with single ventricle CHD after initial surgical palliation(eg, Blalock-Thomas-Taussig shunt, Stage I Norwood) experiencing cardiac arrest, observational and registry studies identify rates of survival to hospital discharge ranging from 32% to 57%.3,5,79,11-16 One observational and 1 reg-istry study of neonates with hypoplastic left heart syndrome undergoing ECPR after Stage I palliation noted survival rates of 32% to 36%, similar to the survival rate of patients undergoing elective ECMO(30%).5,16 There are no studies of single ventricle populations after initial stage palliation receiving ECPR for cardiac arrest that provide compari-sons to conventional CPR. There are limited data on ECPR outcomes in children after Stage II and Stage III surgical palliation. Observational studies of ECMO support after Stage II palliation showed an overall survival rate of 41%, with subanalysis of ECPR in Stage II cohorts noting a survival rate of 44% to 45%17,18 and rates of neurological injury as high as 57% in Stage II ECPR survivors(Pediatric Overall Performance Category/PCPC score ≥3).18 One observational study of children receiving post-operative ECMO after Stage III surgical palliation identified a survival rate of 27% for the subgroup of Stage III cohorts receiving ECPR.19 Due to a lack of significant literature supporting ECPR use after Stage II and III surgical palliations,17-19 spe-cific recommendations for ECPR in these cohorts are not provided.
5.In a retrospective analysis of the Extracorporeal Life Support Organization database, among infants undergoing Stage II palliation receiving postop-erative ECMO support, survival rates for those undergoing effective ECMO were similar to those patients undergoing ECPR (41% versus 45%,respectively), with a higher rate of neurological injury for the cohort who received ECMO versus ECPR (23% versus 0%).17 An Extracorporeal Life Support Organization database study evaluat-ing children after Stage III palliation(Fontan) who received postoperative ECMO noted a survival rate of 35%.19 There are no studies which directly com-pare children with single ventricle CHD after Stage II or III surgical palliation experiencing impending hemodynamic collapse receiving postoperative elective ECMO to analogous cohorts not receiving ECMO under similar hemodynamic conditions.
REFERENCES
1. Marino BS, Tibby SM, Hoffman GM. Resuscitation of the patient with the functionally univentricular heart. Curr Pediatr Rev. 2013;9:148-157. doi:10.2174/1573396311309020008
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2. Feinstein JA, Benson DW, Dubin AM, Cohen MS, Maxey DM, Mahle WT,Pahl E,Villane J, Baffard AB, Peng LF,et al. Hypoelasticity left heart syndrome:current considerations and expectations. J Am Coll Cardiol. 2012;59:S1-42.dol:1016/j.jacc.2011.09:02:02
3. Marino BS, Tabbutt S, MacLaren G, Hazinsky MF, Adatia I, Atkins DL,Checchia,PA,DeCena A,Fink L,EHoffman GM,et al; American Heart As-sociation Congential Cardiac Defects Committee of the Council on Car-diovascular Disease in the Young; Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Cardiovascular Surgery and Anesthesia; and Emergence Cardiovascular Care Committee. Cardio-pulmonary Resuscitation in Infants and Children With Cardiac Disease:A Scientific Statement From the American Heart Association. Circulation 2018;137:e91-e782.doi:10.10161/CIR0000000000000524
4.Bonnet M, Petit J, Lambert V, Brenot P, Riou J, Angel CY,Belli E, Baruteau AE. Catheter-based interventions for modified Blakot-Taussig shont ob-struction: a 20-year experience. Pediatr Cardiol. 2015;36:835-841. doi: 10.1007/s00246-014-1086-0
5. Shenwin ED, Gaureau K, Scheurer MA, Rycus PT, Savlin JW,Almodarov MC, Fynn-Thompson F, Thiagarajan RR. Extracorporeal membrane oxygenation after stage 1 palliation for hypoplastic left heart syndrome. J Thorac Cardiovasc Surg.2012;144:1337-1343. doi:10.1016/j.jtcvs.2012.03.035
6. Giglia TM, AgassicMO TP, Weddell JS, Barst RJ, Bauman M, Erickson CC,Feftes TF, Foster E, Hinoki K, lchord RN, et al; American Heart Associa-tion Congential Heart Defects Committee of the Council on Cardiovascular disease in the Young, Council on Cardiovascular and Stroke Nursing, Council on Epidemiology and Prevention, and Stroke Council. Prevention and treatment of thrombosis in pediatric and congenital heart disease: a scientific statement from the American Heart Association. Circulation 2013;128:2622-2703. doi: 10.1161/01/cir.0000436140.77832.7a
7. Hoskote A, Bohn D, Gruwald E, Cedgell, D Cai S, Adata I, Van Arsell G. Extracoreal life support after staged palliation of a functional single ventricle: subsequent morbidity and survival. J Thorac Cardiovasc Surg.2006;11:1114-1121. doi:1010.1016/j.jvts.2005.11.035
8. Alsophu A, Wan A, Manlihot C, Al-Halees Z, Al-Ahmadi M, McCrindle BW, Alwadai A. Does single ventricle physiology affect survival of chil-dren requiring extracorporeal membrane oxygenation support following cardiac surgery? World J Pediatr Congent Heart Surg. 2014;5:7-15. doi: 10.1177/2015135113507292
9. Stephens EH, Shaoakor A, Jacobse S, Keochi S, Zeniman AL, Middleworth W, Kalfa D, Chai PJ, Chaves DV, Bacha E, et al. Characterization of Ex-tracorporeal Membrane Oxygenation Support for Single Vritcrene Pia-tients. World J Pediatr Conent Heart Surg. 2020;11:183-191. doi:10.1177/2150135119894294
10. Sperotto F, Saenginsin K, Danetyh A, Goday S, Geisseril D, Rivkin M,Amigoni A, Tiagarajan RR, Khein J. Modeling severe functional im-pairment or death following ECPR in pediatric cardiac patients: Plan-ning for an interventional trial. Resuscitation 2021:167:12-21. doi:10.1016/j.resuscitation.2021.07.041
11. Polimenakos AC, Wojtyla P, Smith R, Pizzo V, Nater M, El Ziein CF, Ibliwa MN. Post-cardiotary extracorporeal cardiopulmonary resuscitation in neonates with complex single ventricle: analysis of outcomes. Eur J Car-dioothac Sug.2011;40:1396-1405. doi:10.1016/j.jectiys.2011.01.087.discussion 1405
12. Alsoufi B, Awan Manliot C, Guechef A, Al-Halees Z, Al-Ahmadi M,McCordle BW Kalghian A. Results of rapid-response extracorporeal cardiopulmonary resuscitation in children with refractory cardiac arrest fol-lowing cardiac surgery. Eur J Cardiorthac Surg. 2014;45:268-275. Do 10.1093/ejctz319
13. Polimenakos AC, Rizzo V, El-Zein CF, Ibliwam N. Post-cardiomyal resuscitation in neonates with single ventricle after retraining cardiac arrest: attrition after hospital discharge and predictors of outcome. Pediatr Cardiol. 2017;38:314-323. doi:10.1007/s20246-016-1515-3
14. Wolf MJ,Kanter KR, Kirshbom PM, Kogon BE, Wagoner SF. Extracorporeal cardiopulmonary resuscitation for pediatric cardiac patients. Ann Thorac Surg.20129:847-9-9 discussion 87980
15. Chan T, Thiagarajan RR, Frank D, Bratton SL. Survival after extra-corporeal cardiopulmonary resuscitation in infants and children with heart disease. J Thorac Cardiovasc Surg. 2008;136:984-992. doi:10.1016/jjjtcs.2008.03.007
16.McMullan DM, Tiagarajan RR, Smith Kryus, Rycus PT, Brogan TV. Ex-tracorporeal cardiopulmonary resuscitation outcomes in term and
premature neonates. Pediatr Crit Care Med. 2014;15:e9-e16. doi: 10.10197/PCC.0b013e3182a553f3
17. Jolley, M.Thiagarajan RR, Barrett CS, Salvin JW, Cooper DS, Rycus PT, Telee SA. Extracoreal membrane oxygenation in patients undergoing superior cavopulmonary anastomosis. J Thorac Cardiovasc Surg. 2014;148:1512-1518. doi: 10.1016/j.jtctv.s.2014.04.028
18. Kane DA, Thiagarajan RR, RR, Wypij D, Scheurer MA, Fynn-Thompson F,Emani S, del Nido PJ, Betit P, Laussen PC. Rapid-response extracoro-real membrane oxygenation to support cardiopulmonary resuscitation in children with cardiac disease. Circulation. 2010;122:S241-S248. doi: 10.1161/CIRCULATIONAHA.109.928390
19. Rood KL, Telle SEA, Banetti CS, Salvador JW, Rycus PT, Fynn-Thompson F,Lausse PC, Thiagarjana RR. Extracorporeal membrane oxygenupat-port after the Fontan operation. J Thorac Cardiovasc Surg. 2011;142:504-510. doi: 10.1016/j.jtcvs.2010.11.050
MANAGEMENT OF PULMONARY
Management of Infants and Children at Risk for Pulmonary Hypertensive Crises
|Recommendations for the Management of Infants and Children at Risk for Pulmonary Hypertensive Crises|| |---|---| |COR|LOE|Recommendations| |COR|1. For infants and children who are at risk for pulmonary hypertensive crises, provide careful respiratory management and monitoring to avoid hypoxia and acidosis.| |1|C-EO| |1|2. For infants and children who are mechanically ventilated and at risk for pulmonary hypertensive crises, provide adequate analgesics, sedatives, and neuromuscular blocking agents.| |1|C-EO|
Synopsis
Pulmonary hypertensive crises are acute rapid increases in pulmonary artery pressure that can lead to systemic hypotension, myocardial ischemia, cardiac arrest, and death. Optimization of physiologic conditions and avoid-ance of potential triggers of pulmonary hypertensive crises can potentially avoid these events. Acidosis and hypoxemia are both potent pulmonary vasoconstric-tors. ${}^{1-4}$ Inadequate separation or uncontrolled pain can lead to increased sympathetic activity, which raises pulmonary vascular resistance and can exacerbate pulmonary hy-pertension. ${}^{1,5-7}$ Hypovolemia in children with pulmonary hypertension decreases preload and potentially com-promises cardiac output, worsening the condition and increasing hypoxia risk. Conversely, fluid overload causes venous congestion and impairs heart function in the setting of right ventricular dysfunction. ${}^{8}$ Anemia can be problematic in patients with pulmonary hypertension due to reduced oxygen-carrying capacity. ${}^{8}$
Recommendation-Specific Supportive Text
1. One review,1 consensus statement, and 1 scientific statement highlight the importance of identifying and treating environmental factors that contribute
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to pediatric pulmonary hypertensive crises, such as hypoxia and acidosis, especially in high-risk popu-lations with preexisting idiopathic pulmonary arte-rial hypertension or with congenital heart disease and pulmonary arterial hypertension. 79,10 Two phys-iologic reviews, 1 randomized clinical trial, and 2 retrospective observational studies demonstrated that hypercarbia, hypoxemia, acidosis, atelectasis,and ventilation-perfusion mismatch can lead to increases in pulmonary vascular resistance and,hence, elevation of pulmonary artery pressures in the immediate postoperative period.1-4,11
2. Two observational studies in select high-risk post-operative cardiac patients found an attenuation in the stress response in those patients receiv-ing fentanyl in the postoperative period.5.6 Three studies indicate that triggering factors, such as pain and anxiety, can precipitate pulmonary hypertension crises both during the perioperative period and outside of it, particularly in the pres-ence of acute lung injury, infection, or noncardiac interventions. Managing and preventing these aggravating factors with sedatives and analge-sics can help prevent recurrent,more severe,and prolonged pulmonary hypertension crises.7,10.12 Neuromuscular blockade can be used in addi-tion to sedation and analgesia in critically ill,mechanically ventilated children with pulmonary hypertension.7,12
3. Hypovolemia and hypervolemia can be deleterious to the cardiac function. Right ventricular decom-pensation may result from conditions leading to increases in cardiac demand or increases in ven-tricular afterload. Two consensus statements on the treatment of pediatric pulmonary hypertension emphasize the importance of managing triggering factors such as volume overload, dehydration, and anemia in critically ill children with acute pulmonary hypertension.8,10
Treatment of Infants and Children With Pulmonary Hypertensive Crises
|Recommendations for the Treatment of Infants and Children With Pulmonary Hypertensive Crises||| |---|---|---| |COR|LOE|Recommendations| |1|B-R|1. In infants and children with pulmonary hypertensive crises or acute right-sided heart failure secondary to increased pulmonary vascular resistance, inhaled nitric oxide or prostacyclin should be used as the initial pulmonary vasodilator therapy.| |2a|C-LD|2. For the initial treatment of infants and children with pulmonary hypertensive crises, oxygen administration and induction of alkalosis through hyperventilation or alkali administration can be useful while pulmonary vasodilators are administered.|
|Recommendations for the Treatment of Infants and Children With Pulmonary Hypertensive Crises(Continued)|||| |---|---|---|---| |COR|LOE|Recommendations|| |2b|C-LD|3. For infants and children with refractory pulmonary hypertension, including signs of low cardiac output or profound respiratory failure despite optimal medical therapy,ECMO may be considered.||
Synopsis
During a pulmonary hypertensive crisis, elevated pulmo-nary vascular resistance reduces pulmonary blood flow,impairing left-heart(or single ventricle) preload and ul-timately leading to a fall in cardiac output. Hypoxia and hypercarbia can significantly increase pulmonary vas-cular resistance and trigger pulmonary hypertension crises.1,8,10 Supplemental oxygen helps maintain oxygen levels and lowers pulmonary artery pressures, as does inducing alkalosis. Pulmonary vasodilators, including in-haled nitric oxide, inhaled prostacylin and IV prostacy-clin analogs have been used to treat acute pulmonary hypertensive crises while IV and oral phosphodiesterase type-5 inhibitors, oral endothelin receptor antagonists and oral soluble guanylate cyclase stimulators are used as long-term therapies to lower pulmonary vascular re-sistance and prevent pulmonary hypertensive crises.13-16 ECMO may stabilize infants with severe pulmonary hy-pertension, low cardiac output, or severe respiratory failure when other treatments fail,12 or during high-risk cardiac interventions.17 Children with pulmonary hyper-tension who require ECMO have higher mortality rates compared to those without pulmonary hypertension.18,19
Recommendation-Specific Supportive Text
1 and 2. Treatment with inhaled nitric oxide reduces the frequency of pulmonary hypertensive crises and shortens time to extubation.20 In patients with atrioventricular septal defect repair and severe postoperative pulmonary hypertension,haled nitric oxide administration is associated with reduced mortality. ${}^{15,21}$ Inhaled prostacyclinally transiently produces pulmonary vasodilation and improves oxygenation, but the alkalinity of the drug can irritate airways, and precise dosing can be complicated by drug loss in the nebu-lization circuit.1,22 Two physiologic reviews and 1 randomized clinical trial demonstrated that hypercarbia, hypoxemia, acidosis, atelectasis,and ventilation-perfusion mismatch can lead to increases in pulmonary vascular resistance and elevation of pulmonary artery pressures in the immediate postoperative period after cardiac surgery.2-4 One prospective study on the right ventricular response to hypercarbia following cardiac surgery showed that hypercarbia sig-nificantly increased pulmonary vascular resis-tance by 54% and mean pulmonary arterial pressure by 34%.23 In addition, a prospective
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study in infants after cardiopulmonary bypass demonstrated that increasing the arterial pH by the administration of sodium bicarbonate resulted in significant reduction of pulmonary vascular resistance with both a decrease in mean pulmonary arterial pressure and a con-comitant increase in cardiac index.24
3.Extracorporeal membrane oxygenation has been used in children with pulmonary vascular disease in refractory low cardiac output states and cardiac arrest.25,26 Although outcomes remain poor in certain populations,27 advances in technology of extracorporeal devices may allow for bridging to durable MCS or to trans-plantation.17,28 Although patients with pulmo-nary hypertension who require ECMO have a high mortality rate, provision of ECMO can be lifesaving.12,29,30
Pulmonary Hypertension-Specific Therapies and Interventions for the Treatment of Infants and Children in Cardiac Arrest
|Recommendation for Pulmonary Hypertension-Specific Therapies and Interventions for the Treatment of Infants and Children in Cardiac Arrest||| |---|---|---| |COR|LOE|Recommendation| |2b|C-EO|1. In infants and children with pulmonary hypertension experiencing cardiac arrest, it is unknown whether the addition of pulmonary hypertension-specific therapies improves CPR outcomes compared to standard CPR.|
Synopsis
Among children with in-hospital cardiac arrest, pulmonary hypertension is a common preexisting condition, and sev-eral observational studies have found an association be-tween pulmonary hypertension and lower cardiac arrest survival rates.19,31-34 Despite inhaled nitric oxide showing efficacy in preclinical large animal models of cardiac ar-rest associated with pulmonary hypertension, 35,36 stud-ies on optimal management for children with pulmonary hypertension-associated cardiac arrest are scarce, and the efficacy of specific intra-arrest therapies is unknown.
Recommendation-Specific Supportive Text
<BeginOfPara>1. No intra-restar therapies have been prospectively compared to standard resuscitation therapies for pulmonary hypertension-associated cardiac arrest.One observational study reported that 55% of chil-dren with pulmonary hypertension and in-hospital cardiac arrest were receiving inhaled nitric oxide at the time of arrest, but did not identify associations with survival.32 No studies have prospectively inves-tigated pulmonary vasodilator therapy during pedi-atric cardiac arrest.
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2.Morris K, Beghetti M, Petros A, Adatia I, Bohn D. Comparison of hyper-ventilation and inhaled nitric oxide for pulmonary hypertension after re-pair of congenital heart disease. Crit Care Med. 2000;28:2974-2978. doi: 10.1097/00003246-20008000-00048
3. Moudgil R, Michelakis ED, Archer SL. Hypoxic pulmonary va-soconstriction. J Appl Physiol(1985). 2005;98:390-403. doi: 10.1152/japplphysiol.00733.2004
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5.Anan KJ, Hansen DD, Hickey PR. Hormonal-metabolic stress responses in neonates undergoing cardiac surgery. Anesthesiology. 1990;73:661-670.doi:10.1097/00000542-199010000-00012
6. Hopkins RA, Bull C, Haworth SG, de Leval MR, Stark J. Pulmonary hypertensive crises following surgery for congenital heart defects in young children. Eur J Cardiothorac Surg. 1991;5:628-634. doi: 10.1016/1010-7940(91)90118-4
7. Marino BS, Tabbutt S, MacLaren G, Hazinski MF, Adata I, Atkins DL, Checchia PA, DeCaen A, Fink EL, Hoffman GM, et al; American Heart As-sociation Congenital Cardiac Defects Committee of the Council on Car-diovascular Disease in the Young; Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Cardiovascular Surgery and Anesthesia; and Emergency Cardiovascular Care Committee. Cardio-$$\text{ pulmonary Resuscitation in Infants and Children With Cardiac Disease:}$$A Scientific Statement From the American Heart Association. Circulation.2018;137:e961-e782.doi: 10.1161/CIR.000000000000524
8. Olsson KM, Halank M, Egenlauf B, Fistera D, Gall H, Kaehler C, Kortmann K, Kramm T, Lichtblau M, Marra AM, et al. Compensated right heart failure, intensive care and perioperative management in patients with pulmonary hypertension: Updated recommendations from the Cologne Consensus Conference 2018. Int J Cardiol. 2018;272S: 46-52. doi:10.1016/j.jicard.2018.08.081
9.Sullivan RT, Raj JU, Austin ED. Recent Advances in Pediatric Pulmo-nary Hypertension: Implications for Diagnosis and Treatment. Clin Ther.2023;45:901-912. doi:10.1016/j.clthena.2023.07.001
10.Hansmann G, Koestenberger M, Alastalo TP, Apitz C, Austin ED, Bonnet D,Budws W, DAlto M, Gatzoulis MA, Hasan BS, et al. 2019 updated con-sensus statement on the diagnosis and treatment of pediatric pulmonary hypertension: The European Pediatric Pulmonary Vascular Disease Network(EPPVDN), endorsed by AEPC, ESPR and ISHLT. J Heart Lung Transplant 2019;38:879-901. doi:10.1016/j.healun.2019.06.022
11. Ploegstra MJ, Arjaans S, Zijlstra WMH, Douwes JM, Vissia-Kazemier TR,RooftoothFT MTR, Hillegel SH, Berger RM. Clinical Worsening as Compos-ite Study End Point in Pediatric Pulmonary Arterial Hypertension. Chest 2015;148:655-666. doi:10.1378/chest.14-3066
12.Abman SH, Hansmann G, Archer SL, lyv DD, Adatia I, Chung WK, Hanna BD,Rosenzweig EB,Raj,JU,Cornfield D,et al; American Heart Association Council on Cardioplumary, Critical Care, Perioperative and Resuscitation;Council on Clinical Cardiology; Council on Cardiovascular Disease in the Young; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Surgery and Anesthesia; and the American Thoracic Soci-ely.Pediatric Pulmonary Hypertension: Guidelines From the American Heart Association and American Thoracic Society. Circulation. 2015;132:2037-2099. doi: 10.1011/CIRI,0000000000000329
13.Avilav-Alezra,A Del Cerro Marin MJ, Bautista-Hernandez V. Pulmonary vasodilators in the management of low cardiac output syndrome af-ter pediatric cardiac surgery. Curr Vasc Pharmacol. 2016;14:37-47. doi:10.2174/1570161113665151014124912
14.Sabri MR, Bigdelian H, Hosseinzadeh M, Ahmadi A, Ghaderian M, Shoja M. Comparison of the therapeutic effects and side effects of tadailful and sildenafil after surgery in young infants with pulmonary arterial hypertension due to systemic-to-pulmonary shunts. Cardiol Young.2017;27:1686-1693.doi:10.1017/S1047951117000981
15.Bizzarro M, Gross I, Barbosa FT. Inhaled nitric oxide for the postoperative management of pulmonary hypertension in infants and children with con-genital heart disease. Cochrane Database Syst Rev.2014;2014:CD005055.doi:10.1002/14651858CD005055.pub3
16.Unegwe,Cnoe,Coulson JD,Segal JB,Romer L. Pulmonary Hyperterson a Sion Therapy and a Systmatic Review of Efficacy and Safety of PDE-5 In-hibitors. Pediatrics.2017;139:e20161450. doi:10.1542/peds.2016-1450
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17. Rosenzig EB, Abman SH, Adatia I, Beghetti M, Bonnet D, Haworth S,lyDD, Berger RMF. Paediatric pulmonary arterial hypertension: updates on definition, classification, diagnostics and management. Eur Respir J.2019;53:181916 doi:10.1183/139930303196018-2018
18. Morel E, Rajagopal SK, Oishi P, Thiagarajan RR, Fineman JR, Steurer MA. Extracorporeal Membrane Oxygenation in Pediatric Pulmo-nary Hypertension. Pediatr Crit Care Med. 2020/2126-266. doi: 10.1097/PCC.000000000000002127
19. Nasr VG, Faraoni D, DiNardo JA, Thiagarajan RR. Adverse Out-comes in Neonates and Children with Pulmonary Artery, Hyper-tension Supported with ECMO. ASAIO J. 2016;62:728-731. doi:10.1097/MAT.000000000000419
20. Liou P, Stang Fe, Jampc A, Beich B, Lonnet B, Celeremaj DS. Inhaled nitric oxide and prevention of pulmonary hypertension after congenital heart surgery a randomised double-bind study. Lancet 2000;356:1464-1469: doi:10.1016/S0140-6760(00)02869-5
21. Journois D, Baufreton C, MauriT P, Pouhé P, Safran D. Effects of inhaled nitric oxide administration on early postoperative mortality in patients operated for correction of atrioventricular canal defects. Chest 2005;128:3537-3544. doi: 10.1378/chest.128.5537
22. Kelly Lk, Porta NF, Goodman DM, Carroll CL, Steinhoff RH. Inhaled prostacyclin for term infants with persistent pulmonary hypertension refractory to inhaled nitric oxide. J Pediatr: 2002;14:8382; doi:10.1067/mp.2002.129849
23. Vitanen A, Salmenpera M, Heinenon J. Right ventricular response to hy-percbaria after cardiac surgery. Anesthesiology: 1990;73:393-400; doi:10.1097/00000542-1990090000-00005
24. Chang AC, Zucker HA, Hickey PR, Wessel DL. Pulmonary vascu-lar resistance in infants after cardiac surgery: role of carbon di-oxide and hydrogen ion. Crit Care Med. 1995;23:568-574. doi:10.1097/00003246-199503000-00024
20505, Roson BST, Plaat SNR, Lofery B, OveH, Eloy RG, Bartlett RH, Kulik TJ. Outcome of pediatric patients treated with extracorporeal life support after cardiac surgery. Ann Thorac Surg. 2003;1435-41; discussion 1441; doi: 10.1016/s003-4975(03)00898-1
26. Dhillon R, Pearson GA, Firmin RK, Chan KC, Leanage R. Extracorporeal membrane oxygen and the treatment of critical pulmonary hyperten-sion in congenital heart disease. Eur J Cardiothorac Surg. 1995;95:553-556. doi: 10.1016/s1010-7940(05)80004-1
27 Puri, E Vstein, R. Dalthei SG, Gandhi SK, Sweet SC, Faro A, Huddeston CB. Extracorporeal membrane oxygenation in pediatric lung trans-plantation. J Thorac Cardiovasng S, Ford 2010:140:427-432: doi:10.1016/j.jtcvts.2010.04.012
28. Ricci M, Gaughan CB, Rossi M, Andreopoulos FM, Novello C, Salerno TA, Rosenkrz ER, Panos AL, Initial experience with the Tandem-Heart circulatory support system in children. ASA/O J. 2008;84:542-545. doi:10.1097/MAT.Ob013e31818312f1
29. Morrell NW, Aldred MA, Chung WK, Elliott EC, Nichols WC, Soubrier F, Trembath RC, Loyd JE. Genetics and genomics of pul-monary arterial hypertension. Eur Respir J. 2019;53:1801899. doi:1016.1183/19993018.00918-20
30. Frank DB, Crystal MA, Morales DL, Gerald K, Hanna BD, Mallory GB Jr,Rossano JW. Tends in pediatric pulmonary hypertension-related hospital-izations in the United States from 2000-2009. Pulm Circ 2015;5:339-348.doi:10.1086/681226
31. Morgan RW, Himebach SA, Griffis H, Quarshie WO, Yeung T,Kilbaugh TJ, Topjan AA, Traynor D., Nadkarni VM, Berg RA, et al. Pul-amon hypertension among children with in-hospital cardiac ar-rest: A multicenter study. Resuscitation. 2021;168:52-57. doi:10.1016/j.resuscitation.2021.09.009
32.Morgan RW Reeder RW Ahmed T, Beil M, Bell R, Bishop R, Bochkoris M,Burns C, Carcilo, AA Carpenter TC,et al Outcomes and characteristics of cardiac arrest in children with pulmonary hypertension: A secondary analy-sis of the ICU-RESUS clinical trial. Resuscitation. 2023:190897: doi:1016/j.resuscitation.2023.109897
33.Morgan RW,Topjian AA, Wang Y,Atkin NJ, Kilbaugh TJ,McGowan FX,Berg RA, Mercer-Rosa L, Sutton RM, Hibeau BS, A Plevence and Outcomes of Pediatric In-Hospital Cardiac Arrest Associated With Pul-monary Hypertension. Pediatr Crit Care Med.2020;21:305-313. doi:10.1097/PCC/0000000000002187
34.Morell E, Gaies M, Fineman JR, Charple J, Rao R, Sasaki J, Zhang W,Reichie G, Banerjee, Tabt S. Mortality from Pulmonary Hypertension in the Pediatric ACIC. UJ Am Resir Crit Care Med. 2021;404:454-461.doi:10.1164/rccm.202011-4183OC
35. Morgan RW, Sutton RM, Karlsson M, Lautz AJ, Mavroudis CD, Landis WP, Lin Y, Jeong S, Craig N, Nadkarni VM, et al. Pulmonary vasodilator therapy in shock-associated cardiac arrest. Am J Respir Crit Care Med.2018;197:905-912.doi:10.1164/rccm.201709-18180C
36. Derwall M, Ebeling A, Nolite KW, Weis J, Rossaint R, Ichinose F, Nix C, Fries M, Brucken A. Inhaled nricic oxide improves transpulmonary blood flow and clinical outcomes after prolonged cardiac arrest: a large animal study. Crit Care.2015;19:328.28. doi: 10.1186/s13054-015-1050-2
MANAGEMENT OF TRAUMATIC CARDIAC ARREST
|Recommendations for the Management of Traumatic Cardiac Arrest|||| |---|---|---|---| |COR|LOE|Recommendations|1. In infants and children with traumatic cardiac arrest, evaluation and treatment for potentially reversible causes such as hemorrhage, tension pneumothorax, and pericardial tamponade are recommended.| |2b|C-EO|Infants and children with traumatic cardiac arrest|2. In infants and children with traumatic cardiac arrest with traumatic chronic injury with a short transport time, it may be reasonable to perform resusitative thoracotomy.|
Synopsis
Unintentional injuries are the most common cause of death among children and adolescents.1 Although many organizations have established trauma care guidelines,2-4 the management of traumatic cardiac arrest is often in-consistent cardiac arrest are lost due to major blunt or pene-trating injury in children has a very high mortality rate.5-8 Suspect thoracic injury in all thoraco-abdominal trauma because tension prehumothorax, hemothorax, pulmonary contusion, or pericardial tamponade may impair hemody-namics, oxygenation, and ventilation.
This topic was last reviewed in the 2020 AHA Guide-lines for CPR and ECC.These recommendations have not been updated for this edition of the Guidelines.
Recommendation-Specific Supportive Text
1.Early correction of reversible causes by reducing delays in the delivery of trauma-specific interven-tions may increase survival following penetrating traumatic cardiac arrest.10,11 Guidelines for cardiac arrest due to trauma recommend opening the airway,relieving tension pneumothorax hemorrhage control,restoring circulating blood volume, and relieving ten-sion pneumothorax. Perform these measures simul-taneously with conventional resuscitation.
2. Systematic reviews,12-15 multicenter retrospec-tive studies,16-17 and single-center retrospective studies18 recommend emergent thoracotomy for pediatric patients who present pulseless after penetrating thoracopy injury. However, there is no evidence to support emergent thoracotomy for infants and children with blunt injury presenting in cardiac arrest.13,19
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Pediatric Advanced Life Support: 2025 AHA/AAP Guidelines for CPR and ECC
Table 2.Critical Knowledge Gaps Due to Insufficient Pediatric Data
|Topic|Knowledge gap| |---|---| |Guidelines development|What is the appropriate age and setting to transition from(1) neonatal resuscitation protocols to pediatric resuscitation protocols and(2) from pediatric resuscitation protocols to adult resuscitation protocols?| |Drug administration|What is the optimal method(ie, age, weight, or physiology) to estimate body weight for medication administration?| |Drug administration|What is the optimal method to transition from weight-based dosing to fixed-dose medication administration during cardiac arrest in adolescents or children with high BMI?| |Drug administration|With what frequency should subsequent doses of epinephrine be administered?| |Drug administration|Should epinephrine dosing strategies be individualized to patients based on hemodynamic response, blood pressure targets, or both?| |Drug administration|With what frequency should epinephrine be administered in infants and children during CPR who are undergoing ECMO cannulation?| |Drug administration|What are special circumstances in which sodium bicarbonate and calcium are beneficial to administer during pediatric cardiac arrest? are There circumstances where these medications are harmful?| |CPR techniques|Are alternative compression techniques (cough CPR, precordial thump,fist pacing, interposed abdominal compression CPR, mechanical CPR devices) equally or more effective than conventional CPR?| |CPR techniques|What are the optimal chest compression techniques for patients immediately postestomy?| |CPR techniques|Is double sequential defibrillation, vector change, or stacked shocks more effective to achieve ROSC than traditional single defibrillation? When are these strategies appropriate in defibrillation sequences when single shocks have failed?| |CPR techniques|What is the optimal timing and dosing of initial defibrillation for VF/vT or subsequent defibrillation for refractory VF/vT?| |Airway management, ventilation, oxygenation during cardiac arrest|Are there specific situations in which advanced airway placement is beneficial or harmful in OHCA?| |Airway management, ventilation, oxygenation during cardiac arrest|What is the appropriate timing of advanced airway placement in IHCA?| |Airway management, ventilation, oxygenation during cardiac arrest|What is the optimal Fio2 to administer during CPR?| |Airway management, ventilation, oxygenation during cardiac arrest|What is the optimal ventilation rate during CPR in patients with or without an advanced airway? Is it age dependent?| |Airway management, ventilation, oxygenation during cardiac arrest|What is the optimal PEEP, PIP, and tidal volume to administer during CPR?| |Airway management, ventilation, oxygenation during cardiac arrest|For mechanically ventilated infants and children with IHCA, does manual ventilation versus remaining on the ventilator impact the efficacy of ventilation or outcomes?| |Airway management, ventilation, oxygenation during cardiac arrest|Is there an ETCO2 value that health care professionals should target during CPR?| |Monitoring during cardiac arrest|What are the optimal blood pressure targets during CPR? Is it age dependent?| |Monitoring during cardiac arrest|Can transthoracic or transesophageal echocardiography diagnose reversible causes/contributors to cardiac arrest?| |Monitoring during cardiac arrest|Can transesophageal echocardiography during cardiac arrest guide and improve CPR quality?| |Monitoring during cardiac arrest|Can NIRS or other cerebral perfusion monitoring technologies improve CPR quality or outcomes when used during cardiac arrest?| |Monitoring during cardiac arrest|Should specific heart rate, blood pressure or other factors be used as the threshold for performing CPR in children with poor perfusion?| |Monitoring during cardiac arrest|Mechanical circulatory support(ECPR/VAD)| |What other patient/arrest factors should be considered in determining ECPR candidacy?|Mechanical circulatory support(ECPR/VAD)| |Should the optimal dosing frequency of vasoactive medications be modified for ECPR?|Mechanical circulatory support(ECPR/VAD)| |What approach to minimizing chest compression pauses during cannulation is optimal during ECPR?|Mechanical circulatory support(ECPR/VAD)| |What is the role of ECPR deployment in patients with single ventricle heart disease at each stage of palliation(Stage I, II, III)?|Mechanical circulatory support(ECPR/VAD)| |Should post-cardiac arrest care hemodynamic, oxygenation, ventilation targets be similar for ECPR patients when compared to conventional CPR patients?|Mechanical circulatory support(ECPR/VAD)| |What are optimal CPR practices for patients with intra- or extracorporeal ventricular assist devices (continuous flow or pulsatile) experiencing low-flow alarm, absent pulse, hypotension, with or without evidence of VAD malfunction?|Mechanical circulatory support(ECPR/VAD)| |Termination of resuscitation|What clinical tools can be used to help in the decision to terminate pediatric IHCA and OHCA resuscitation?| |Family presence|What is the long-term emotional and psychological impact on family members who witness resuscitation, including potential trauma, grief processing, or closure?| |Family presence|What is the impact on health care professionals' emotional well-being when families are present during resuscitation?| |Family presence|How do cultural, religious, or individual family beliefs influence the perception of FPDR and how should we tailor practices to respect these differences?|
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Table 2. Continued
|Topic|Knowledge gap| |---|---| |Post-cardiac arrest care, neuroprognostication|What are the blood pressure targets during post-cardiac arrest period and for what time period post-cardiac arrest should they serve as hemodynamic targets?| |Post-cardiac arrest care, neuroprognostication|Should seizure prophylaxis be administered post-cardiac arrest?| |Post-cardiac arrest care, neuroprognostication|Does the treatment of post-cardiac arrest convulsive and nonconvulsive seizure improve outcomes?| |Post-cardiac arrest care, neuroprognostication|What is the optimal temperature and duration of TTM for post-cardiac arrest care?| |Post-cardiac arrest care, neuroprognostication|Does TTM benefit subpopulations of cardiac arrest patients?| |Post-cardiac arrest care, neuroprognostication|What are the reliable methods and optimal timing for post-cardiac arrest prognostication?| |Post-cardiac arrest care, neuroprognostication|What are the modalities and timing of physical, cognitive, and psychological assessments that should be provided in the year following cardiac arrest?| |Post-cardiac arrest care, neuroprognostication|Which modalities and their respective timing should be used to predict good and poor neurological outcomes after cardiac arrest?| |Arrhythmia management|What are the most effective and safest medications for adenosine-refractory SVT?| |Specific disease etiologies presenting in cardiac arrest- myocardium or cardiomyathy|Are there specific modifications to the cardiac arrest algorithm that should be used when treating a patient with myocarditis/ cardiomyopathy and cardiac arrest?| |Specific disease etiologies presenting in cardiac arrest-pulmonary hypertension|What intra-arteral therapies are effective to treat pulmonary hypertension-associated cardiac arrest compared to standard resuscitation therapies?| |Specific disease etiologies presenting in cardiac arrest-pulmonary hypertension|What is the optimal approach to ventilation during the resuscitation of infants and children with pulmonary hypertension?|
BMI indicates body mass index; CPR, cardiopulmonary resuscitation; ECMO, extracorporeal membrane oxygenation; ECPR, extracorporeal cardiopulmonary resuscitation; ECOT, end-tidal carbon dioxide; Fio, fraction of inspired oxygen; FPDR, family presence during resuscitation; HIIHCA, in-hospital cardiac arrest; IO, intraosseous;IV, intravenous; NIRS, near-infrared spectroscopy; OHCA, out-of-hospital cardiac arrest; PEEP, positive end-expiratory pressure; PIP, peak inspiratory pressure; pVT,pulseless ventricular tachycardia; ROSC, return of spontaneous circulation; SVT, supraventricular tachycardia; TTM, targeted temperature management; VF, ventricular fibrillation; and VAD, ventricular assist device.
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2. Western Trauma Association. Western Trauma Association algorithms.2011.Updated.Accessed March 6,2020.https://www.westentreraum.org algorithms/algorithms.html
3. Eastern Association for the Surgery of Trauma.EAST practice management guidelines. Accessed February 3,2020.https://www.eastorg/education/practice-management-guidelines
4. Pediatric Trauma Society. Pediatric trauma society clinical practice guide-lines. Accessed February 3,2020. https://pediatrictrausopiesorti.edu/resources/clinical-resources/cgi
5.Calkins CM, Bensard DD, Partrick DA, Karrer FM, A critical analysis of outcome for children sustaining cardiac arrest after blunt trauma. J Pediatr Surg.2002;37:180-184. doi:10.1053/jpsu.2002.30251
6. Crewson K, Lockey D, Davies. Outcome from paediatric cardiac arrest associated with trauma. Resuscitation: 20075:75-29.44. doi: 10.1016/j.resuscitation.2007.02.018
7. Peron AD, SingRF, BransCAS, C:HHynT. Picturing survival inpediatric trauma patients receiving cardiopulmonary resuscitation in the prehospital setting.Prehosp Emerg Care.2001;5:6-9. doi:10.1080/9093120190904245
8. Lopez-Herce Dij C, Dominuez Sampedro P, Rodriguez Nunear A,Garcia Sanz C, Carrillo Alvarez A, Calvo Macias C, Bellon Cano JM; Grupo Espanol de Estudio de la Parada Cardiores diprerainspectoria en Ninos.[Cardiorespi-ratory arrest in children with trauma]. An Pediatr(Barc). 60065:439-447.doi:10.1157/13094250
9.Topian AA Raymond TT, Atkins D, Chand U, Joyner BL Jr, Lasa JJ,Lavones LJ, EYA, Mahgoub M, et al; Pediatric Basic and Advanced Life Support Collaborators. Part 4: Pediatric Basic and Advanced Life Support:2020 American Heart Association Guidelines for Cardipulmonary Resus-citation and Emergency Cardiovascular Care. Circulation. 2020;142:S469-S523. doi: 10.1161/CIR.0000000000000000000
10. Shibahashi K, Sugiyama K, Hamabe Y. Pediatric out-of-hospital traumatic cardiopulmonary arrest after traffic accidents and ter-
mination of resuscitation. Ann Emerg Med. 2020;75:57-65. doi:10.1016/j.annemerged.2019.05.036
11. Alquidah Z,Nehme Z,Williams B,Oteir A,Bernard S,Smith K.A descrip-tive analysis of the epidemiology and management of paediatric traumatic out-of-hospital cardiac arrest. Resuscitation. 2019;140:127-134. doi:10.1016/j.resuscitation.2019.05.020
12.Neivens EJ, Bird NTE, Malk HZ, Mercer SJ, Shahzad K, Lunevicius R, Taylor JV, Misra N. A systematic review of 3251 emergency department thora-cotomies: is it time for a national database? Eur J Trauma Emerg Surg.2019;45:231-243 doi: 10.1007/s00068-018-0982-z
13. Moskowitz EE, Burlew CC, Kulungowski AM, Bensard DD. Survival af-ter emergency department thoracotomy in the pediatric trauma popula-tion: a review of published data. Pediatr Surg Int. 2018;34:857-860. doi: 10.1007/s00383-018-45290-9
14.Seamon MJ, Haut ER, Van Arendonk K, Barbosa RR, Chiu WC, Dente CJ, Fox N, Java RS, Khwaja K, Lee JK, et al. An evidence-based ap-proach to patient selection for emergency department thoracotomy: a 10-269 of literature. J Trumioy Res. Early Surg. 2015;79:159-173. doi:10.1016/j.resuscitation.2007;79:2000.00000000000000000000000000000000000000000000000000000000
15.Moore HB, Moore EE, Bensard DD. Pediatric emergency department thoracotomy: A-40 year review. J Pediatr Surg. 2016;51:315-318. doi:10.1016/j.jpedsurg.2015.10.040
16. Flynn-OBrien KT, Stewart BT, Fallat ME, Maier RV, Arbabi S, Rivana FP,McIntyre L.K. Mortality after emergency department thoracotomy for pediat-ric blunt trauma: analysis of the National Trauma Data Bank 2007-2012.J Pediatr Surg.2016;51:163-167. doi:10.1016/j.jpedsurg.2015.10.034
17.Nicolson NG, Schwustl S, Esposito TA, Crandall ML. Resuscitation tho-racotomy for pediatric trauma in Illinois, 1999 to 2009. Am J Surg.2015;210:720-723. doi:10.1016/j.jamsurg.2015.05.007
18.Easter JS, Vinton DT, Haukoos JS. Emergent pediatric thoracotomy to following traumatic arrest. Resuscitation. 2012;83:1521-1524. doi:10.1016/j.resuscitation.2012.05.024
19.Duron V,Burke RV,Bliss D,Ford HR,Upperman JS.Survival of pediatric blunt trauma patients presenting with no signs of life in the field. J Trauma Acute Care Surg.2014;77:422-426. doi:10.1097/TA.0000000000000394
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Pediatric Advanced Life Support: 2025 AHA/AAP Guidelines for CPR and ECC
CRITICAL KNOWLEDGE GAPS AND ONGOING RESEARCH
During the literature review process, we identified sev-eral critical knowledge gaps related to PALS. These top-ics are either current areas of ongoing research or lack significant pediatric evidence to support evidence-based recommendations.
The causes of pediatric cardiac arrest are very different from cardiac arrest in adults, and pediatric studies are critically needed. As often occurs in the development of pediatric medical guidelines, some recommendations are extrapolated from adult data.However, infants and children are distinct patient pop-ulations and dedicated pediatric resuscitation research is a priority given the more than 20000 cardiac arrests that occur in infants and children in the United States
each year. These critical knowledge gaps are identi-fied areas that, when addressed, will be the founda-tional future knowledge to advance how we care for patients.
Critical knowledge gaps are summarized in Table 2.
ARTICLE INFORMATION
The American Heart Association requests that this document be cited as follows:Lasa JJ, Dhillon GS, Duff JP, Hayes J, Kamath-Rayne BD, Levy A, Mahgoub M,Morgan RW, McCormick T, Roberts JS, Ross CE, Schexnayder SM, Sweberg T,Valdes SO, Topjian AA. Part 8: pediatric advanced life support: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation.2025;152(suppl 2):S479-S537. doi: 10.1161/CIR.0000000000001368
This article has been published in Pediatrics.
Contributor
Rebecca N. Ichord, MD.
Disclosures
Appendix 1. Writing Group Disclosures
|Writing group member|Employment|Research grant|Other research support|Speakers bureau/noraria|Expert witness|Ownership interest|Consultant/ advisory board|Other| |---|---|---|---|---|---|---|---|---| |Javier J. Lasa|Children's Health Systems of Texas, UT Southwestern Medical Center|None|None|None|None|None|None|Edwards Life Sciences Corporation*| |Alexis A. Topjian|The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine|NIHt; Marinus Pharmaceuticalst|None|None|None|None|Elsevier, Associate Editor, Resuscitationt|None| |Gurpreet S. Dhillon|Lucile Packard Children's Hospital at Stanford Medical Center|None|AHA Young Investigator's Seed Grant Award 2019*|None|None|None|None|Kiniksa Pharmaceuticals International*| |Jonathan P. Duff|University of Alberta and Stollery Children's Hospital|None|None|None|None|None|None|None| |Jennifer Hayes|Children's Hospital Orange County|None|None|ZOLL Medical*|None|None|None|None| |Beena D. Kamath-Rayne|American Academy of Pediatrics|None|None|None|None|None|Cerebral Palsy Alliance Research Foundation*|Lurie Children's Hospital; Children's Healthcare of Atlantat| |Arielle Levy|University of Montreal|None|None|None|None|None|None|None| |Melissa Mahgoub|American Heart Association|None|None|None|None|None|None|None| |Ryan W. Morgan|The Children's Hospital of Philadelphia|NIHt|None|None|None|None|None|None| |Taylor McCormick|Denver Health|AHRQt|None|None|None|None|None|None| |Joan S. Roberts|University of Washington|PEDICA study"; SAMURAI studyt|None|None|None|None|None|Seattle Children's Hospital| |Catherine E. Ross|Boston Children's Hospital|NHLBlt|None|None|None|None|None|Abbvie*|
(Continued)
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Appendix 1. Continued
|Writing group member|Employment|Research grant|Other research support|Speakers bureau/nonoraria|Expert witness|Ownership interest|Consultant/ advisory board|Other| |---|---|---|---|---|---|---|---|---| |Stephen M. Schexnayer|University of Arkansas/Arkansas Children's Hospital Pediatric Critical Care|None|None|None|Love& Kirschenbaum LLLCt|None|American Heart Associationt|None| |Todd Sweberg|Northwell Health/ Cohen Children's Medical Center|None|None|None|None|None|None|Nonin Medical*; Abbott Laboratories*| |Santiago O. Valdes|Texas Children's Hospital -Baylor College of Medicine|Milestone Pharmaceuticals*|None|None|None|None|None|Abbott Laboratories*; AltaThera Pharmaceuticals*;|
This table represents the relationships of writing group members that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure Questionnaire, which all members of the writing group are required to complete and submit. A relationship is considered to be“significant” if(a) the person receives$5000 or more during any 12-month period, or 5% or more of the person's gross income; or(b) the person owns 5% or more of the voting stock or share of the entity, or owns$5000 or more of the fair market value of the entity. A relationship is considered to be"modest" if it is less than"significant" under the preceding definition.
Disclosures are reviewed and mitigated through a conflict-of-interest process that consists of reviewing pertinent information which is then used to decide what action is re-quired to maintain content integrity. Disclosures may include salary, wages or other remuneration of any kind(including but not limited to consulting or advising fees, speaking fees,research funding, ownership interests, honoraria, participation in pension or benefit plans or programs or other perquisites, and reimbursement for travel, lodging, and meals) given for services rendered or other activities for which remuneration is received or expected, whether that compensation or other remuneration is paid directly to the individual or to the individual's employer or another third party.
*Modest.
tSignificant.
Appendix 2. Reviewer Disclosures
|Reviewer|Employment|Research grant|Other research support|Speakers bureau/ honoraria|Expert witness|Ownership interest|Consultant/ advisory board|Other| |---|---|---|---|---|---|---|---|---| |Erica Andrist|University of Michigan, Mott Children's Hospital|NHLBI(Administrative supplemental award to R01HL15319)↑;SCCM (Research support to fund an SCCM-endorsed project about brain death/death by neurologic criteria)*|None|None|None|None|None|None| |Andrew Cheng|USC|None|None|None|None|None|None|None| |Anne-Marie Guerguerian|The Hospital for Sick Children(Canada)|None|None|None|None|None|None|None| |Rudy Kink|Le Bonheur Children's Hospital|None|None|None|None|None|None|None| |Alan Leonard Nager|Division of Emergency and Transport Medicine, Keck School of Medicine|None|None|None|None|None|None|None| |Gene Yong- Kwang Ong|KK Women's and Children's Hospital(Singapore)|None|None|None|None|None|None|None| |Sylvia Owsu- Ansah|University of Pittsburgh|None|None|None|None|None|Prodigy EMS*;"The Pitt" medical drama series*|None| |Alyssa Smith|Washington University School of Medicine|None|None|None|None|None|None|None| |Vijay Srinivasan|Critical Care Medicine, Children's Hospital of Atlanta|None|None|None|None|None|None|None| |Muhammad Waseem|Lincoln Medical Center|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.
| Recommendations for Ventilation and Advanced Airway Strategies During CPR | ||
|---|---|---|
| COR | LOE | Recommendations |
| 2a | C-LD | 1. In infants and children with out-of-hospital cardiac arrest, it is reasonable to perform bag -mask ventilation rather than advanced airway interventions (tracheal intubation or supraglottic airway [SGA] placement). |
| 2b | C-LD | 2. In infants and children with in-hospital cardiac arrest who do not have an advanced airway in place, it may be reasonable to perform bag -mask ventilation or advanced airway interventions (tracheal intubation or supraglottic airway [SGA] placement). |
| 2b | C-LD | 3. When performing CPR in infants and children with an advanced airway in place, it may be reasonable to perform bag -mask ventilation rate range of 20-30 breaths/ min(1 breath every 2-3 s), accounting for age and clinical characteristics. Hyperventilation may compromise hemodynamics. |
| Recommendations for Drug Administration Methods During Cardiac Arrest | ||
|---|---|---|
| COR | LOE | Recommendations |
| 1 | C-LD | 1. Rapid initiation of vascular access IV or IO is recommended for drug administration in infants and children with cardiac arrest. |
| Recommendations for Drug Administration Methods During Cardiac Arrestst(Continued) | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | C-EO | Health care professionals caring for infants and children with cardiac arrest should choose the initial type of vascular access route(IV or IO) based on availability, expertise, and timeliness. |
| Recommendations for Drug Administration During Cardiac Arrest | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 2a | C-LD | 1. For infants and children in cardiac arrest with initial nonshockable rhythm, it is reasonable to administer the initial dose of epinephrine as early as possible. | |
| 2b | C-LD | 2. For infants and children in cardiac arrest with initial shockable rhythm, it may be reasonable to administer epinephrine after 2 attempts at defibrillation or sooner, only when rapid defibrillation is not possible. | |
| 2b | any-ends setting, it may be reasonable to administer epinephrine every 3-5 min until ROSC is achieved. |
| Recommendations for Drug Administration During Cardiac Arrest (Continued) | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 2b | C-LD | 4. For infants and children with shock-refractory VF/VT, either amodiradone or lidocaine may be considered. | |
| 3:No Benefit | B-NR | 5. Routine administration of sodium bicarbonate is not recommended for infants and children in cardiac arrest,except in special circumstances(eg,sodium channel blocker toxicity or hyperkalemia). | |
| 3:No Benefit | B-NR | 6. Routine administration of calcium is not recommended for infants and children in cardiac arrest,except for special circumstances(eg, hypocalcemia, calcium channel blocker overdose, or hyperkalemia). |
| Recommendations for Weight-Based Dosing of Resuscitation Medications | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | C-EO | 1. For resuscitation medication dosing, it is recommended to use the infant or child's body weight to calculate resuscitation drug doses while not exceeding the recommended dose for adults. | |
| 2b | B-NR | 2. It may be reasonable to use both habitus or anthropomorphic measurements to improve the accuracy of length-based estimated weight in infants or children, when possible. | |
| 2b | C-LD | 3. If the infant or child's weight is unknown, a body length for estimating weight and other cognitive aids to calculate resuscitation drug dosing and administration may be considered. |
| Recommendations for Energy Doses for Defibrillation in Cardiac Arrest | ||
|---|---|---|
| COR | LOE | Recommendations |
| 2a | C-LD | 1. In infants and children experiencing cardiac arrest with VF/pVT, it is reasonable to use an initial dose of 2-4 J/kg of monophasic or biphasic energy for defibrillation; for ease of teaching, it is reasonable to use an initial dose of 2 J/kg. |
| 2b | C-LD | 2. In infants and children experiencing cardiac arrest with refractory VF/pVT, it may be reasonable to attempt subsequent defibrillation doses of 4 J/kg of monophasic or biphasic energy, and higher levels may be considered, though not to exceed 10 J/kg or the adult maximum dose. |
| 2b | C-LD | 3. In infants and children experiencing cardiac arrest with refractory VF/pVT, a single defibrillation dose of monophasic or biphasic energy may be considered over sequential (stacked) shocks, followed by resumption of chest compressions. |
| Recommendations for Measuring CPR Physiology and Quality | ||
|---|---|---|
| COR | LOE | Recommendations |
| 2a | 8.BN | 1. For infants and children with continuous invasive arterial blood pressure monitoring in place during CPR, it is reasonable for health care professionals to use diastolic blood pressure to assess the child's response to resuscitation efforts. |
| 2b | B-NR | 2. For infants and children with invasive airways in place during CPR,ETCO, monitoring may be considered to monitor CPR quality. |
| 2b | B-NR | 3. For infants and children with continuous invasive arterial blood pressure monitoring in place for arterial blood pressure monitoring in place chronic S78, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, EAC, |
| Recommendation for the Use of Extracorporeal Cardiopulmonary Resuscitation | |
|---|---|
| COR | LOE |
| 2b | C-LD |
| Recommendations for Post-Cardiac Arrest Targeted Temperature Management | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | A | 1. For infants and children who remain comatose following cardiac arrest, continuous central temperature monitoring is recommended. | |
| 1 | B-NR | 2. For infants and children who remain comatose following cardiac arrest, avoiding central temperatures>37.5℃ is recommended. | |
| 2a | B-R | 3. For infants and children between 24 h and 18 y of age who remain comatose after IHCA or OHCA, it is reasonable to use a 5-d course of targeted temperature management (TTM), either 32°C-34 °C followed by TTM of 36°C-37.5°C, or only TTM of 36°C-37.5°C. |
| Recommendations for Post-Cardiac Arrest Blood Pressure Management | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | 1. After cardiac arrest in infants and children, it is recommended to maintain systolic and mean arterial blood pressure greater than the 10th percentile for age. | ||
| 1 | B-NR | 2. After cardiac arrest in infants and children, it is recommended to maintain systolic and mean arterial blood pressure greater than the 10th percentile for age. | |
| 1 | C-EO | 2. After cardiac arrest in infants and children, it is continuous arterial pressure monitoring is recommended to identify and treat hypotension when appropriate resources are available. |
| Recommendations for Post-Cardiac Arrest Oxygenation and Ventilation Management | Recommendations | Recommendations | |
|---|---|---|---|
| COR | LOE | Recommendations | |
| 2b | C-LD | 1. After cardiac arrest in infants and children, it may be reasonable to target nomoxemia that is appropriate to the specific patient's underlying condition. | |
| 2b | C-LD | 2. After cardiac arrest in infants and children, it may be reasonable to wean oxygen to target an oxyhemoglobin saturation between 94% and 99%. |
| Recommendations for Post-Cardiac Arrest Oxygenation and Ventilation Management (Continued) | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 2b | C-LD | 3. After cardiac arrest in infants and children, it may be reasonable to target a Paco2, that is appropriate to the specific patient's underlying condition and limit exposure to hypercapnia or hypocapnia. |
| Recommendations for Post-Cardiac Arrest Electroencephalography Monitoring and Seizure Treatment | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | C-LD | 1. When resources are available, continuous electroencephalography and exceptional research (EEG) monitoring is recommended for the detection of seizures after cardiac arrest in infants and children with persistent encephalopathy. | 1. When resources are available, continuous electroencephalography (EEG) monitoring is recommended for the detection of seizures after cardiac arrest in infants and children with persistent encephalopathy. |
| 1 | C-LD | 2. It is recommended to treat clinical seizures after cardiac arrest in infants and children. | 3. It is recommended to treat nonconvulsive status epilepticus after cardiac arrest in infants and children. |
| 2a | C-EO | 3. It is reasonable to treat nonconvulsive status epilepticus after cardiac arrest in infants and children. | 4.3. It is reasonable to treat nonconvulsive status epilepticus after cardiac arrest in infants and children. |
| Components of Post-Cardiac Arrest Care | Check |
|---|---|
| Ensure normoxia and normocapnia | |
| Monitor Spo2 and target 94%-99%(or child's normal/appropriate oxygen saturation). | □ |
| Measure and target Paco2 appropriate to the patient's underlying condition and limit exposure to severe hypercapnia or hypocapnia. | □ |
| Optimize cardiac function and end-organ perfusion. | |
| Monitor with cardiac telemetry. | □ |
| Monitor arterial blood pressure. | □ |
| Review hemodynamic goals daily. | □ |
| Monitor serum lactate and urine output to help guide therapies. | □ |
| Use parenteral fluid bolus with or without inotropes or vasopressors to maintain a systolic blood pressure and mean arterial blood pressure greater than the 10th percentile for age. | □ |
| Consider echocardiography to assess for myocardial dysfunction. | □ |
| Maintain electrolytes within normal ranges to avoid possible life-threatening arrhythmias. | □ |
| Apply targeted temperature management(TTM). | |
| Continuously monitor core temperature. | □ |
| Prevent and treat fever immediately after cardiac arrest and after rewarming. | □ |
| If patient is comatose, apply TTM(32°C-34°C) followed by (36°C-37.5°C) or only TTM(36°C-37.5°C) for up to 5 days. | □ |
| Prevent shivering. | □ |
| Remember that rewarming is a high-risk time for hypotension, electrolyte abnormalities, hypoglycemia, and seizures. | □ |
| Provide neuromonitoring. | |
| If patient is not at neurologic baseline and resources are available, monitor with continuous electroencephalography. | □ |
| Treat seizures. | □ |
| Measure glucose. | |
| Measure blood glucose and avoid hypoglycemia. | □ |
| Prevent agitation and pain. | |
| Treat with sedatives, anxiolytics, and analgesics to a sedation score target. | □ |
| Consider prognosis. | □ |
| Always consider multiple modalities(clinical and other) over any single predictive factor. | □ |
| Delay prognostication until at least 72 hours after cardiac arrest. | □ |
| Remember that prognostics assessments may be modified by TTM. | □ |
| Recommendation for Multimodal Prognostication Following Cardiac Arrest | |
|---|---|
| COR | LOE |
| 1 | 1. It is recommended that health care professionals consider multiple modalities when predicting neurological outcomes (favorable or unfavorable) after resuscitation from cardiac arrest in infants and children. |
| Recommendations for Prognostication Using Clinical Examination Following Cardiac Arrest | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 2b | C-LD | 1. The usefulness of cough or gag reflexes or response to pain to support a favorable or unfavorable neurological prognosis at any timepoint after cardiac arrest in infants and children is not well established. | |
| 2b | C-LD | 2. The usefulness of motor response to any stimulus to support a favorable or unfavorable neurological prognosis at any timepoint after cardiac arrest in infants and children is not well established. | |
| 2b | C-LD | 3. The usefulness of total Glasgow Coma Scale (GCS) score or GCS motor score to support a favorable neurological prognosis at any timepoint after cardiac arrest in infants and children is not well established. | |
| 2b | C-LD | 4. When interpreted in the context of other prognostic criteria, it may be reasonable to use the presence of bilateral pupillary light reflexes in the first 12 h after cardiac arrest in infants and children to support a favorable neurological prognosis. | |
| 2b | C-LD | 5. When interpreted in the context of other prognostic criteria, it may be reasonable to use the absence of bilateral pupillary light reflexes between 48 and 72 h after cardiac arrest in infants and children to support an unfavorable neurological prognosis. |
| Recommendations for Prognostication Using Clinical Examination Following Cardiac Arrest(Continued) | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 3:No Benefit | B-NR | 6. The absence of pupillary light reflex in the first 24 h after cardiac arrest in infants and children to support an unfavorable neurological prognosis is not recommended. | |
| 3:No Benefit | B-NR | 7. The GCS score in the first 24 h after cardiac arrest in infants and children to support an unfavorable neurological prognosis is not recommended. |
| Recommendations for Prognostication Using Biomarkers Following Cardiac Arrest | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 2b | B-NR | 1. When interpreted in the context of other prognostic criteria, it may be reasonable to use a plasma lactate value <2 mmol/L up to 12 h after cardiac arrest in infants and children to support a favorable neurological prognosis. | |
| 2b | C-LD | 2. The usefulness of neuronal biomarkers (eg, S100B, neuron-specific enolase) to support a favorable or unfavorable neurological prognosis at any timepoint after cardiac arrest in infants and children is not well established. | |
| 3: No Benefit | B-NR | 3. The use of blood lactate after cardiac arrest in infants and children to support an unfavorable neurological prognosis is not recommended. | |
| 3: No Benefit | B-NR | 4. The use of blood pH after cardiac arrest in infants and children to support a favorable or unfavorable neurological prognosis is not recommended. |
| Recommendations for Prognostication Using Electrophysiology Following Cardiac Arrest | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 2a | B-NR | 1. When interpreted in the context of other prognostic criteria, it is reasonable to use EEG up to 72 h after cardiac arrest in infants and children to support a favorable or unfavorable neurological prognosis. | |
| 2b | B-NR | 2. When interpreted in the context of other prognostic criteria, it may be reasonable to use the presence of continuous or normal EEG background in the first 72 h after cardiac arrest in infants and children to support a favorable prognosis. | |
| 2b | C-LD | 3. When interpreted in the context of other prognostic criteria, it may be reasonable to use the presence of sleep spindles or stage ll sleep architecture on EEG between 12 and 24 h after cardiac arrest in infants and children to support a favorable neurological prognosis. | |
| 2b | C-LD | 4. When interpreted in the context of other prognostic criteria, it may be reasonable to use the presence of EEG reactivity between 6 and 24 h after cardiac arrest in infants and children to support a support a favorable neurological prognosis. | |
| 2b | C-LD | 5. When interpreted in the context of other prognostic criteria, it may be reasonable to use the presence of status epilepticus, or the presence of burst suppression, burst attenuation or generalized periodic epileptiform discharges between 24 and 72 h after cardiac arrest in infants and children to support an unfavorable neurological prognosis. | |
| 2b | C-LD | 6. The usefulness of the presence of attenuated isoelectric or flat EEG, or presence of myoclonic status epilepticus at any timepoint after cardiac arrest in infants and children to support an unfavorable neurological prognosis is not well established. | |
| 3: No Benefit | B-NR | 7. The presence of clinical or electrographic seizures, absence of sleep spindles and stage ll sleep architecture, absence of continuous or normal EEG background, absence of EEG reactivity, and absence of EEG variability at any timepoint after cardiac arrest in infants and children is not recommended to support an unfavorable neurological prognosis. | |
| 3: No Benefit | B-NR | 8. The absence of burst suppression, burst attenuation, generalized periodic epileptiform discharges, attenuated, isoelectric, or flat EEG at any timepoint after cardiac arrest in infants and children to support a favorable neurological prognosis. | |
| 3: No Benefit | B-NR | 9. The absence of clinical or electrographic seizures, absence of status epilepticus, or absence of myoclonic seizures in infants and children is not recommended | |
| 3: No Benefit | B-NR | myoclonic seizures in infants and children is not recommended to support a favorable neurological prognosis. |
| COR | LOE | Recommendations |
|---|---|---|
| 2b | B-NR | 1. When interpreted in the context of other prognostic criteria, it may be reasonable to use normal brain magnetic resonance imaging (MRI) between 72 h and 2 wk after cardiac arrest in infants and children to support a favorable neurological prognosis. |
| 2b | C-LD | 2. When interpreted in the context of other prognostic criteria, it may be reasonable to use an abnormal brain MRI showing high ischemic burden at 72 h or later after cardiac arrest in infants and children to support an unfavorable neurological prognosis. |
| 2b | C-LD | 3. When interpreted in the context of other prognostic criteria, it may be reasonable to use a CT with loss of gray-white matter differentiation within 24 h after cardiac arrest in infants and children to support an unfavorable neurological prognosis. |
| 3: No Benefit | C-LD | 4. A normal brain CT scan within the first 48 h after cardiac arrest in infants and children is not recommended to support a favorable neurological prognosis. |
| Day 1 | Day 1 | Day 2 | Day 2 | Day 3 | Day 4 | Day 5-2 weeks |
|---|---|---|---|---|---|---|
| 0-12h | 13-24 h | 25-48 h | 49-72 h | 73-96 h | 42-72 h | Day 5-2 weeks |
| Presence of bilateral pupillary light reflex 0-12 hours | Normal MRI≥72 hours | |||||
| Plasma lactate <2 mmol/L within 12 hours | ||||||
| Presence of EEG reactivity 6-24 hours | ||||||
| Presence of continuous or normal EEG background 1-72 hours | ||||||
| Presence of sleep spindles or stage II sleep on EEG 12-24 hours |
| COR | LOE | Recommendations |
|---|---|---|
| 1 | 1 | 1. It is recommended that infants and children who survive cardiac arrest be evaluated for rehabilitation services. |
| 2a | C-LD | 2. It is reasonable that infants and children who survive cardiac arrest be evaluated for physical, cognitive, and emotional needs to guide follow-up care within the first year following cardiac arrest. |
| Recommendations for Family Presence During Resuscitation | ||
|---|---|---|
| COR | LOE | Recommendations |
| 1 | B-NR | 1. Family members should be provided the option of being present during the resuscitation of their infant or child. |
| 1 | B-NR | 2. When family members are present during resuscitation of their infant or child, it is recommended for a designated team member to provide comfort, answer questions, and support the family. |
| Recommendations for Family Presence During Resuscitation (Continued) | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | C-LD | 3. If the presence of family members is considered detrimental to the resuscitation of the infant or child, family members should be respectfully asked to leave. |
| Recommendations for the Evaluation of Sudden Unexplained Cardiac Arrest | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | B-NR | 1. A complete unrestricted autopsy of infants and children with sudden unexplained death is recommended, preferably performed by a pathologist with training and experience in cardiovascular pathology with preservation of biological material for further genetic analysis to determine the presence of inherited cardiac disease. | |
| 1 | B-NR | 2. When conventional autopsy does not identify a cause of death or diagnosis in infants and children with sudden unexplained death, a postmortem genetic evaluation is recommended, when resources allow, especially if clinical evidence suggests the diagnosis of an inherited cardiac disease. | |
| 1 | B-NR | 3. When autopsy does not identify a cause of death or is not performed in infants and children with sudden unexplained death, it is recommended that first-degree family members be referred to a health care professional or center with expertise in inherited cardiac disease and cardiac genetic counseling. | |
| 1 | C-EO | 4. For infants and children who survive sudden unexplained cardiac arrest, obtain a complete past medical and family history(including a history of syncopal episodes, seizures, unexplained accidents or drowning or sudden unexpected death before 50 y of age), review previous electrocardiograms, and refer to a cardiologist with expertise in inherited cardiac disease. |
| Recommendations for Fluid Resuscitation and Management of Septic Shock | ||
|---|---|---|
| COR | LOE | Recommendations |
| 1 | C-LD | 1. Health care professionals should reassess infants and children after every third bolus to assess for fluid responsiveness and signs of volume overload. |
| 2a | B-R | 2. Either isotonic crystalloids or colloids can be effective as the initial fluid choice for resuscitation in infants and children. |
| 2a | B-NR | 3. Either balanced or unbalanced solutions can be effective as the fluid choice for resuscitation in infants and children. |
| 2a | C-LD | 4. In infants and children with septic shock, it is reasonable to administer fluid in 10-mL/kg or 20- mL/kg aliquots with frequent reassessment. |
| 2a | C-LD | 5. In infants and children with fluid-refractory septic shock, it is reasonable to enter using bienephrine or norepinephrine as an initial vasoactive infusion. |
| 2a | C-EO | 6. For infants and children with cardiac arrest and sepsis, it is reasonable to apply the standard PALS algorithm compared with any unique approach for sepsis-associated cardiac arrest. |
| 2b | B-NR | 7. For infants and children with septic shock unresponsive to fluids and requiring vasoactive support, it may be reasonable to consider stress- dose corticosteroids. |
| 2b | C-LD | 8. In infants and children with fluid-refractory septic shock, if epinephrine or norepinephrine are unavailable, dopamine may be considered. |
| Recommendations for Management of Cardiogenic Shock | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | C-EO | 1. For infants and children with cardiogenic shock,early expert consultation is recommended. | |
| 2b | C-EO | 2. For infants and children with cardiogenic shock,it may be reasonable to use epinephrine, dopamine, dobutamine, or nilrinone as an inotropic infusion. |
| Recommendation for Management of Traumatic Hemorrhagic Shock | |||
|---|---|---|---|
| COR | LOE | Recommendation | $$\begin{array}{l}\\ 2a\\ \\ \end{array}$$ |
| 2a | C-EO | 1. Among infants and children with hypotensive hemorrhagic shock following trauma, it is reasonable to administer blood products, when available, instead of crystalloid for ongoing volume resuscitation. |
| Recommendations for the Use of Cuffed Endotracheal Tubes for Intubation | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | C-EO | 1. When a cuffed endotracheal tube(ETT) is used in infants and children, attention should be paid to ETT size, position, and cuff inflation pressure (usually<20-25 cm $H_{2}O)$). | |
| 2a | B-NR | 2. It is reasonable to choose cuffed ETTs over uncuffed ETTs for intubating infants and children. |
| Recommendations for the Use of Cricoid Pressure During Intubation | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 3:No Benefit | C-LD | 1. Routine use of cricoid pressure to reduce the risk of regurgitation is not recommended during bag- mass ventilation of infants and children. | |
| 3:No Benefit | C-LD | 2. Routine use of cricoid pressure is not recommended during tracheal intubation of infants and children. | |
| 3: Harm | C-LD | 3. If cricoid pressure is used, discontinue if it interferes with ventilation or the speed or ease of tracheal intubation in infants and children. |
| Recommendations for Atropine Use for Emergency Intubation | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 2b | C-LD | 1. It may be reasonable to use atropine as a premedication to prevent bradycardia in infants and children during emergency intubation. | |
| 2b | C-LD | 2. When atropine is used as a premedication for emergency intubation of infants and children, a dose of 0.02 mg/kg with no minimum dose may be considered. |
| Recommendations for Monitoring Exhaled CO2 in Patients With Advanced Airways | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | C-LD | 1. In all settings, for infants and children with a perfusing rhythm,exhaled CO2 detection (colorimetric detector or capnography) should be used for confirmation of ETT placement. | |
| 2a | C-LD | 2. In infants and children with a perfusing rhythm and ETT in place, it is beneficial to monitor exhaled CO2(colorimetric detector or capnography) during out-of-hospital and intra-hospital transport. |
| Recommendations for the Management of Bradycardia With Cardiopulmonary Compromise | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | C-LD | 1. In infants and children with bradycardia and cardiopulmonary compromise due to increased vagal tone or atrioventricular conduction block not due to factors such as hypoxia, atropine is recommended. | |
| 2 | C-EO | 2. In infants and children with heart rate<60 beats/ min and cardiopulmonary compromise despite effective ventilation with oxygen, start CPR. | |
| 1 | C-EO | 3. In infants and children with bradycardia and cardiopulmonary compromise that persists after correction of other factors(eg, hypoxia), give epinephrine IV/IO. | |
| 2b | C-EO | 4. Emergency transcutaneous pacing may be considered for infants and children with bradycardia and cardiopulmonary compromise due to complete heart block or sinus node dysfunction unresponsive to CPR. |
| Recommendations for Treatment of Supraventricular Tachycardia With a Pulse | ||
|---|---|---|
| COR | LOE | Recommendations |
| 1 | C-LD | 1. In infants and children with SVT without cardiopulmonary compromise, it is useful to attempt vagal stimulation first. |
| 1 | C-LD | 2. If IV/IO access is readily available, adenosine is recommended for the treatment of SVT in infants and children. |
| 1 | C-EO | 3. For infants and children without cardiopulmonary compromise whose SVT is unresponsive to vagal maneuvers and IV adenosine, expert consultation is recommended. |
| 2a | C-LD | 4. In infants and children with SVT and cardiopulmonary compromise, it is reasonable to perform electrical synchronized cardioversion starting with a dose of 0.5 to 1 J/kg. If unsuccessful, increase the dose to 2 J/kg. |
| 2b | C-LD | 5. For infants and children with SVT and cardiopulmonary compromise unresponsive to vagal maneuvers, adenosine, and electrical synchronized cardioversion and for whom expert consultation is not available, it may be reasonable to consider either IV procainamide, amiodarone, or sotalol. |
| Recommendations for Treatment of Wide-Complex Tachycardia With a Pulse | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 1 | C-LD | 1. In infants and children with wide-complex tachycardia without cardiopulmonary compromise, expert consultation is recommended prior to administration of antiarrhythmic agents. | |
| 2a | C-EO | 2. In infants and children with wide-complex tachycardia with regular and monomorphic QRS without cardiopulmonary compromise, adenosine administration can be useful in conjunction with expert consultation. | |
| 2a | C-EO | 3. In infants and children with wide-complex tachycardia and cardiopulmonary compromise, it is reasonable to perform electrical synchronized cardioversion starting with a dose of 0.5-1 J/kg. If unsuccessful, increase the dose to 2 J/kg. |
| Recommendations for Treatment of Myocarditis and Cardiomyopathy | ||
|---|---|---|
| COR | LOE | Recommendations |
| 1 | B.-NR | 1. Given the high risk of cardiac arrest in infants or children with myocarditis who demonstrate arrhythmias, heart block, ST-segment changes, or low cardiac output, early consideration of transfer to an ICU for monitoring and therapy is recommended. |
| 2a | B-NR | 2. For infants and children with myocarditis or cardiomyopathy with refractory low cardiac output, ECMO/mechanical cardiac support(MCS) can be beneficial to provide end-organ support and to prevent cardiac arrest. |
| 2a | B-NR | 3. In infants and children with myocarditis or cardiomyopathy experiencing cardiac arrest, early deployment of ECPR is reasonable. |
| 2a | C-LD | 4. For infants and children with myocarditis or cardiomyopathy experiencing cardiac arrest, early deployment of ECPR is reasonable. |
| Recommendations for the Resuscitation of Patients With Single Ventricle Congenital Heart Disease | ||
|---|---|---|
| COR | LOE | Recommendations |
| 1 | C-EO | 1. For infants and children with aortopulmonary shunt-dependent congenital heart disease with known or suspected shunt obstruction, early consideration for transfer to a center with advanced cardiac therapy capabilities (ie, cardiac catheterization, cardiac surgery,ECMO) is recommended if these services are not available. |
| Recommendations for the Resuscitation of Patients With Single Ventricle Congenital Heart Disease (Continued) | ||
|---|---|---|
| COR | LOE | Recommendations |
| 2a | C-LD | 2. In infants and children with single ventricle congenital heart disease following initial palliative procedures(eg, Stage I Norwood, Hybrid procedure, Blalock-Thomas-Taussig shunt), timely ECMO deployment can be useful to treat low cardiac output syndrome. |
| 2a | C-EO | 3. For infants and children with aortopulmonary shunt-dependent congenital heart disease with known or suspected shunt obstruction, it is reasonable to administer oxygen, vasoactive agents, and heparin while preparing for catheter-based or surgical intervention. |
| 2b | C-LD | 4. In infants and children with single ventricle congenital heart disease following initial palliative procedures(eg, Stage I Norwood, Hybrid procedure, Blalock-Thomas-Taussig shunt) experiencing cardiac arrest, timely ECPR deployment may be a useful rescue strategy to achieve ROC. |
| 2b | C-LD | 5. In infants and children with single ventricle congenital heart disease following Stage II (bidirectional Glenn, fiem-Fontan) or Stage III (Fontan) palliation, timely ECMO deployment may be considered to treat low cardiac output syndrome. |
| Recommendations for the Management of Infants and Children at Risk for Pulmonary Hypertensive Crises | ||
|---|---|---|
| COR | LOE | Recommendations |
| COR | 1. For infants and children who are at risk for pulmonary hypertensive crises, provide careful respiratory management and monitoring to avoid hypoxia and acidosis. | |
| 1 | C-EO | |
| 1 | 2. For infants and children who are mechanically ventilated and at risk for pulmonary hypertensive crises, provide adequate analgesics, sedatives, and neuromuscular blocking agents. | |
| 1 | C-EO |
| Recommendations for the Treatment of Infants and Children With Pulmonary Hypertensive Crises | ||
|---|---|---|
| COR | LOE | Recommendations |
| 1 | B-R | 1. In infants and children with pulmonary hypertensive crises or acute right-sided heart failure secondary to increased pulmonary vascular resistance, inhaled nitric oxide or prostacyclin should be used as the initial pulmonary vasodilator therapy. |
| 2a | C-LD | 2. For the initial treatment of infants and children with pulmonary hypertensive crises, oxygen administration and induction of alkalosis through hyperventilation or alkali administration can be useful while pulmonary vasodilators are administered. |
| Recommendations for the Treatment of Infants and Children With Pulmonary Hypertensive Crises(Continued) | |||
|---|---|---|---|
| COR | LOE | Recommendations | |
| 2b | C-LD | 3. For infants and children with refractory pulmonary hypertension, including signs of low cardiac output or profound respiratory failure despite optimal medical therapy,ECMO may be considered. |
| Recommendation for Pulmonary Hypertension-Specific Therapies and Interventions for the Treatment of Infants and Children in Cardiac Arrest | ||
|---|---|---|
| COR | LOE | Recommendation |
| 2b | C-EO | 1. In infants and children with pulmonary hypertension experiencing cardiac arrest, it is unknown whether the addition of pulmonary hypertension-specific therapies improves CPR outcomes compared to standard CPR. |
| Recommendations for the Management of Traumatic Cardiac Arrest | |||
|---|---|---|---|
| COR | LOE | Recommendations | 1. In infants and children with traumatic cardiac arrest, evaluation and treatment for potentially reversible causes such as hemorrhage, tension pneumothorax, and pericardial tamponade are recommended. |
| 2b | C-EO | Infants and children with traumatic cardiac arrest | 2. In infants and children with traumatic cardiac arrest with traumatic chronic injury with a short transport time, it may be reasonable to perform resusitative thoracotomy. |
| Topic | Knowledge gap |
|---|---|
| Guidelines development | What is the appropriate age and setting to transition from(1) neonatal resuscitation protocols to pediatric resuscitation protocols and(2) from pediatric resuscitation protocols to adult resuscitation protocols? |
| Drug administration | What is the optimal method(ie, age, weight, or physiology) to estimate body weight for medication administration? |
| Drug administration | What is the optimal method to transition from weight-based dosing to fixed-dose medication administration during cardiac arrest in adolescents or children with high BMI? |
| Drug administration | With what frequency should subsequent doses of epinephrine be administered? |
| Drug administration | Should epinephrine dosing strategies be individualized to patients based on hemodynamic response, blood pressure targets, or both? |
| Drug administration | With what frequency should epinephrine be administered in infants and children during CPR who are undergoing ECMO cannulation? |
| Drug administration | What are special circumstances in which sodium bicarbonate and calcium are beneficial to administer during pediatric cardiac arrest? are There circumstances where these medications are harmful? |
| CPR techniques | Are alternative compression techniques (cough CPR, precordial thump,fist pacing, interposed abdominal compression CPR, mechanical CPR devices) equally or more effective than conventional CPR? |
| CPR techniques | What are the optimal chest compression techniques for patients immediately postestomy? |
| CPR techniques | Is double sequential defibrillation, vector change, or stacked shocks more effective to achieve ROSC than traditional single defibrillation? When are these strategies appropriate in defibrillation sequences when single shocks have failed? |
| CPR techniques | What is the optimal timing and dosing of initial defibrillation for VF/vT or subsequent defibrillation for refractory VF/vT? |
| Airway management, ventilation, oxygenation during cardiac arrest | Are there specific situations in which advanced airway placement is beneficial or harmful in OHCA? |
| Airway management, ventilation, oxygenation during cardiac arrest | What is the appropriate timing of advanced airway placement in IHCA? |
| Airway management, ventilation, oxygenation during cardiac arrest | What is the optimal Fio2 to administer during CPR? |
| Airway management, ventilation, oxygenation during cardiac arrest | What is the optimal ventilation rate during CPR in patients with or without an advanced airway? Is it age dependent? |
| Airway management, ventilation, oxygenation during cardiac arrest | What is the optimal PEEP, PIP, and tidal volume to administer during CPR? |
| Airway management, ventilation, oxygenation during cardiac arrest | For mechanically ventilated infants and children with IHCA, does manual ventilation versus remaining on the ventilator impact the efficacy of ventilation or outcomes? |
| Airway management, ventilation, oxygenation during cardiac arrest | Is there an ETCO2 value that health care professionals should target during CPR? |
| Monitoring during cardiac arrest | What are the optimal blood pressure targets during CPR? Is it age dependent? |
| Monitoring during cardiac arrest | Can transthoracic or transesophageal echocardiography diagnose reversible causes/contributors to cardiac arrest? |
| Monitoring during cardiac arrest | Can transesophageal echocardiography during cardiac arrest guide and improve CPR quality? |
| Monitoring during cardiac arrest | Can NIRS or other cerebral perfusion monitoring technologies improve CPR quality or outcomes when used during cardiac arrest? |
| Monitoring during cardiac arrest | Should specific heart rate, blood pressure or other factors be used as the threshold for performing CPR in children with poor perfusion? |
| Monitoring during cardiac arrest | Mechanical circulatory support(ECPR/VAD) |
| What other patient/arrest factors should be considered in determining ECPR candidacy? | Mechanical circulatory support(ECPR/VAD) |
| Should the optimal dosing frequency of vasoactive medications be modified for ECPR? | Mechanical circulatory support(ECPR/VAD) |
| What approach to minimizing chest compression pauses during cannulation is optimal during ECPR? | Mechanical circulatory support(ECPR/VAD) |
| What is the role of ECPR deployment in patients with single ventricle heart disease at each stage of palliation(Stage I, II, III)? | Mechanical circulatory support(ECPR/VAD) |
| Should post-cardiac arrest care hemodynamic, oxygenation, ventilation targets be similar for ECPR patients when compared to conventional CPR patients? | Mechanical circulatory support(ECPR/VAD) |
| What are optimal CPR practices for patients with intra- or extracorporeal ventricular assist devices (continuous flow or pulsatile) experiencing low-flow alarm, absent pulse, hypotension, with or without evidence of VAD malfunction? | Mechanical circulatory support(ECPR/VAD) |
| Termination of resuscitation | What clinical tools can be used to help in the decision to terminate pediatric IHCA and OHCA resuscitation? |
| Family presence | What is the long-term emotional and psychological impact on family members who witness resuscitation, including potential trauma, grief processing, or closure? |
| Family presence | What is the impact on health care professionals' emotional well-being when families are present during resuscitation? |
| Family presence | How do cultural, religious, or individual family beliefs influence the perception of FPDR and how should we tailor practices to respect these differences? |
| Post-cardiac arrest care, neuroprognostication | What are the blood pressure targets during post-cardiac arrest period and for what time period post-cardiac arrest should they serve as hemodynamic targets? |
| Post-cardiac arrest care, neuroprognostication | Should seizure prophylaxis be administered post-cardiac arrest? |
| Post-cardiac arrest care, neuroprognostication | Does the treatment of post-cardiac arrest convulsive and nonconvulsive seizure improve outcomes? |
| Post-cardiac arrest care, neuroprognostication | What is the optimal temperature and duration of TTM for post-cardiac arrest care? |
| Post-cardiac arrest care, neuroprognostication | Does TTM benefit subpopulations of cardiac arrest patients? |
| Post-cardiac arrest care, neuroprognostication | What are the reliable methods and optimal timing for post-cardiac arrest prognostication? |
| Post-cardiac arrest care, neuroprognostication | What are the modalities and timing of physical, cognitive, and psychological assessments that should be provided in the year following cardiac arrest? |
| Post-cardiac arrest care, neuroprognostication | Which modalities and their respective timing should be used to predict good and poor neurological outcomes after cardiac arrest? |
| Arrhythmia management | What are the most effective and safest medications for adenosine-refractory SVT? |
| Specific disease etiologies presenting in cardiac arrest- myocardium or cardiomyathy | Are there specific modifications to the cardiac arrest algorithm that should be used when treating a patient with myocarditis/ cardiomyopathy and cardiac arrest? |
| Specific disease etiologies presenting in cardiac arrest-pulmonary hypertension | What intra-arteral therapies are effective to treat pulmonary hypertension-associated cardiac arrest compared to standard resuscitation therapies? |
| Specific disease etiologies presenting in cardiac arrest-pulmonary hypertension | What is the optimal approach to ventilation during the resuscitation of infants and children with pulmonary hypertension? |
| Writing group member | Employment | Research grant | Other research support | Speakers bureau/noraria | Expert witness | Ownership interest | Consultant/ advisory board | Other |
|---|---|---|---|---|---|---|---|---|
| Javier J. Lasa | Children's Health Systems of Texas, UT Southwestern Medical Center | None | None | None | None | None | None | Edwards Life Sciences Corporation* |
| Alexis A. Topjian | The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine | NIHt; Marinus Pharmaceuticalst | None | None | None | None | Elsevier, Associate Editor, Resuscitationt | None |
| Gurpreet S. Dhillon | Lucile Packard Children's Hospital at Stanford Medical Center | None | AHA Young Investigator's Seed Grant Award 2019* | None | None | None | None | Kiniksa Pharmaceuticals International* |
| Jonathan P. Duff | University of Alberta and Stollery Children's Hospital | None | None | None | None | None | None | None |
| Jennifer Hayes | Children's Hospital Orange County | None | None | ZOLL Medical* | None | None | None | None |
| Beena D. Kamath-Rayne | American Academy of Pediatrics | None | None | None | None | None | Cerebral Palsy Alliance Research Foundation* | Lurie Children's Hospital; Children's Healthcare of Atlantat |
| Arielle Levy | University of Montreal | None | None | None | None | None | None | None |
| Melissa Mahgoub | American Heart Association | None | None | None | None | None | None | None |
| Ryan W. Morgan | The Children's Hospital of Philadelphia | NIHt | None | None | None | None | None | None |
| Taylor McCormick | Denver Health | AHRQt | None | None | None | None | None | None |
| Joan S. Roberts | University of Washington | PEDICA study"; SAMURAI studyt | None | None | None | None | None | Seattle Children's Hospital |
| Catherine E. Ross | Boston Children's Hospital | NHLBlt | None | None | None | None | None | Abbvie* |
| Writing group member | Employment | Research grant | Other research support | Speakers bureau/nonoraria | Expert witness | Ownership interest | Consultant/ advisory board | Other |
|---|---|---|---|---|---|---|---|---|
| Stephen M. Schexnayer | University of Arkansas/Arkansas Children's Hospital Pediatric Critical Care | None | None | None | Love& Kirschenbaum LLLCt | None | American Heart Associationt | None |
| Todd Sweberg | Northwell Health/ Cohen Children's Medical Center | None | None | None | None | None | None | Nonin Medical*; Abbott Laboratories* |
| Santiago O. Valdes | Texas Children's Hospital -Baylor College of Medicine | Milestone Pharmaceuticals* | None | None | None | None | None | Abbott Laboratories*; AltaThera Pharmaceuticals*; |
| Reviewer | Employment | Research grant | Other research support | Speakers bureau/ honoraria | Expert witness | Ownership interest | Consultant/ advisory board | Other |
|---|---|---|---|---|---|---|---|---|
| Erica Andrist | University of Michigan, Mott Children's Hospital | NHLBI(Administrative supplemental award to R01HL15319)↑;SCCM (Research support to fund an SCCM-endorsed project about brain death/death by neurologic criteria)* | None | None | None | None | None | None |
| Andrew Cheng | USC | None | None | None | None | None | None | None |
| Anne-Marie Guerguerian | The Hospital for Sick Children(Canada) | None | None | None | None | None | None | None |
| Rudy Kink | Le Bonheur Children's Hospital | None | None | None | None | None | None | None |
| Alan Leonard Nager | Division of Emergency and Transport Medicine, Keck School of Medicine | None | None | None | None | None | None | None |
| Gene Yong- Kwang Ong | KK Women's and Children's Hospital(Singapore) | None | None | None | None | None | None | None |
| Sylvia Owsu- Ansah | University of Pittsburgh | None | None | None | None | None | Prodigy EMS*;"The Pitt" medical drama series* | None |
| Alyssa Smith | Washington University School of Medicine | None | None | None | None | None | None | None |
| Vijay Srinivasan | Critical Care Medicine, Children's Hospital of Atlanta | None | None | None | None | None | None | None |
| Muhammad Waseem | Lincoln Medical Center | None | None | None | None | None | None | None |
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引用 / 出处
2025+AHA心肺复苏与心血管急救指南-第8部分:儿童高级生命支持. 2025.