445CHAPTER 39 Performance of Cardiopulmonary Resuscitation in Infants and Children early recognition of the cardiac arrest and initiate basic and advanced life support Effective CPR optimizes coronary[.]
CHAPTER 39 Performance of Cardiopulmonary Resuscitation in Infants and Children • BOX 39.1 Phases of Cardiac Arrest and Targeted Interventions Prearrest Phase: Protect • • • • Optimize community education regarding child safety Optimize patient monitoring Prioritize interventions to prevent progression to cardiac arrest Early recognition and activation of medical emergency response teams Arrest (No-Flow): Preserve • • • • Minimize interval to BLS and ACLS phase Organized 911/code blue response system Preserve cardiac and cerebral substrate Minimize interval to defibrillation, when indicated Low-Flow (CPR): Resuscitate • High-quality CPR • Consider adjuncts to improve organ perfusion during CPR • Consider E-CPR if standard CPR not promptly successful Postarrest: Regenerate Short Term • Monitor for and aggressively prevent: • Hypotension • Fever • Monitor for seizures • Avoid extremes of: • Oxygenation • Ventilation • Glucose • Continue to address underlying arrest etiology to prevent recurrent arrest Long Term • Early intervention with occupational and physical therapy ACLS, Advanced cardiac life support; BLS, basic life support; CPR, cardiopulmonary resuscitation; E-CPR, extracorporeal membrane oxygenation cardiopulmonary resuscitation TABLE 2015 Cardiopulmonary Resuscitation 39.1 Quality Targets Metric Evidence-Based Target Depth: Infants/children PUSH HARD At least one-third the anteroposterior diameter of the chest (4 cm in infants and 5 cm in children) Depth: Adolescents PUSH HARD At least cm but no more than cm Rate PUSH FAST 100–120 compressions/min Chest compression fraction Minimize interruptions Compressions provided for at least 80% of the arrest duration Ventilation rate Avoid excessive ventilation 10 breaths/min Chest recoil FULL chest recoil between all compressions a a Evidence of pubertal development 445 early recognition of the cardiac arrest and initiate basic and advanced life support Effective CPR optimizes coronary perfusion pressure (CoPP) and cardiac output to support vital organ viability during the low-flow phase.16 Important tenets of basic life support are: PUSH HARD,17,18 PUSH FAST, allow full chest recoil between compressions,19–21 and minimize interruptions in chest compressions.22–24 For ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT), rapid rhythm identification and prompt defibrillation are vital for successful resuscitation.25,26 For all cardiac arrests, it is vital to provide adequate myocardial perfusion, to restore myocardial oxygen delivery, and to assess and reverse the underlying arrest etiology.27,28 Postarrest Most deaths in children receiving CPR in the hospital occur after initially successful resuscitation Thus, the immediate postarrest period should be considered a critical time of ongoing intervention Patients remain at risk for ventricular arrhythmias and critical organ reperfusion injuries Interventions during the immediate postarrest stage should focus on minimizing secondary injury Current evidence-based goals include the following: (1) avoid hypotension (i.e., ,5th percentile systolic blood pressure for age),29,30 (2) avoid fever by proactively providing targeted temperature management,31–33 and (3) recognize and promptly treat seizures.34,35 This postarrest phase may have the greatest potential for innovative advances to improve functional outcomes and facilitate reintegration of the patient back into society The specific phase of resuscitation dictates the focus of care Interventions that improve outcome during one phase may be deleterious during another For instance, the administration of vasopressors during the low-flow phase of cardiac arrest raises systemic vascular resistance with the goal of increasing CoPP and the probability of event survival (return of spontaneous circulation [ROSC]) The persistence of this vasoconstriction into the postarrest phase may worsen myocardial strain and dysfunction and negatively impact cerebral perfusion Current understanding of the physiology of cardiac arrest and recovery allows us to only crudely manipulate blood pressure, oxygen delivery and consumption, body temperature, and other physiologic parameters in our attempts to optimize outcome Future strategies likely will take advantage of increasing knowledge of mitochondrial bioenergetics, cellular metabolism, and cellular markers of injury and recovery Epidemiology of Pediatric Cardiac Arrest The true incidence of pediatric cardiac arrest is difficult to determine owing to inconsistencies in reporting However, the best data suggest that over 20,000 American children receive CPR each year (15,000 in hospital and 7000 out of hospital).1–4 Owing in part to the widespread implementation of rapid response systems in most children’s hospitals, more than 95% of in-hospital CPR events in the United States occur in ICUs.36 Despite improvements in survival over the past 20 years— survival-to-discharge rates now approach or exceed 40% after inhospital cardiac arrest (IHCA) in most contemporary series— most children receiving CPR still die before discharge, and many survivors sustain neurologic injury as a result of their cardiac arrest.3 As a specific example, in a recent study by the National Institute of Child Health and Human Development–funded Collaborative Pediatric Critical Care Research Network (CPCCRN), S E C T I O N I V Pediatric Critical Care: Cardiovascular nearly 30% of pediatric survivors of cardiac arrest suffered a significant decline in functional neurologic status.3 In short, pediatric cardiac arrest is an important public health problem Factors that influence outcome from pediatric cardiac arrest include (1) the preexisting condition of the child,37 (2) the initial electrocardiographic rhythm detected,38 (3) the duration of no-flow time (the time during an arrest when there is no spontaneous circulation or provision of CPR), and (4) the quality of the life-supporting therapies provided during and after the resuscitation.17 With this knowledge, it is no surprise that pediatric out-of-hospital cardiac arrests (OHCAs) have worse outcomes than IHCAs As many of these out-of-hospital events are not witnessed and bystander CPR is not common (30% to 40% of children receive bystander CPR), the duration of noflow time can be prolonged As a result, less than 25% of these children survive their initial event28,39 as compared with more than 80% of children who receive CPR while in an ICU.3 These findings are especially troublesome given that bystander CPR more than doubles patient survival rates28 and points to public health and community outreach interventions as means of improving outcomes Pediatric cardiac arrest characteristics differ from those observed in adults in several ways Adult cardiac arrests in and out of the hospital are likely to be associated with coronary artery disease and therefore frequently have shockable rhythms, whereas pediatric cardiac arrests are usually secondary to respiratory failure or shock and less than 15% have an initial shockable rhythm.38,40,41 Despite shockable rhythms being more favorable for survival, more children will survive their cardiac arrest relative to adults These superior outcomes in children are partly driven by higher survival rates among children with asystole or pulseless electrical activity (PEA) compared with adults (24% vs 11%).38 Additionally, CPR is recommended for children with bradycardia with poor perfusion, a common predecessor to pulseless cardiac arrest.42 Children who receive CPR for bradycardia with poor perfusion have greater chances of survival than those with a pulseless initial CPR rhythm.43 Importantly, observational studies of in-hospital cardiac arrest have consistently identified higher survival rates in infants as compared with older children.44 Optimizing Blood Flow During Cardiopulmonary Resuscitation When the heart arrests, the provision of high-quality CPR is the only source of blood flow to organs A primary goal of CPR is the maximization of myocardial blood flow to facilitate ROSC.45 The primary driver of myocardial blood flow is CoPP, mathematically defined by the following equation: CoPP Aortic Pressure – Right Atrial Pressure Myocardial blood flow improves as the gradient between aortic and right atrial pressures increases During the downward compression phase, aortic pressure rises at the same time as right atrial pressure with little change in CoPP However, during the decompression phase of chest compressions, the right atrial pressure falls faster and lower than the aortic pressure, which generates a pressure gradient that perfuses the heart with oxygenated blood during this artificial period of “diastole” (Fig 39.1) Several human and animal studies in both VF and asphyxial models have demonstrated the importance of achieving Aortic pressure Right atrial pressure Coronary perfusion pressure 100 90 80 70 Pressure (mm Hg) 446 60 50 40 30 20 10 –10 –20 0.2 0.4 0.6 0.8 Time (seconds) • Fig 39.1 Hemodynamics during cardiopulmonary resuscitation Depic- tion of the hemodynamic response to high-quality chest compressions during pediatric cardiac arrest Yellow line, Aortic pressure; blue line, right atrial pressure; and black line, coronary perfusion pressure, depicted as the mathematical difference between aortic and right atrial pressure During the compression phase (systole), right aortic and right atrial pressure rise simultaneously, generating negligible coronary perfusion pressure (a negative value in this example) and likely minimal myocardial blood flow During the relaxation phase (diastole), aortic pressure exceeds right atrial pressure, allowing for the generation of coronary perfusion pressure and myocardial blood flow The dashed line at 20 mm Hg represents coronary perfusion pressure threshold associated with improved outcomes in animal and adult human literature and maintaining CoPP thresholds to the attainment of shortterm survival (i.e., ROSC).16,46–51 Based on the preceding equation, CoPP can be improved by strategies that increase the pressure gradient between the aorta and right atrium This is principally accomplished by the provision of vasopressors during CPR to increase systemic vascular resistance and aortic diastolic pressure Other interventions can target right atrial pressure by augmenting negative intrathoracic pressure—these include the impedance threshold device (ITD) and active compression-decompression device (ACD) The ITD is a small, disposable valve that can be connected directly to the tracheal tube or facemask to augment negative intrathoracic pressure during the inspiratory phase of spontaneous breathing and the decompression phase of CPR by impeding airflow into the lungs The ACD is a handheld device that is fixed to the anterior chest of the patient by means of suction and is used to apply active decompression forces during the release phase of chest compressions By actively generating negative intrathoracic pressure during the relaxation phase, cardiac preload is augmented, potentially increasing the cardiac output generated with CPR While neither device has a clear survival benefit when applied broadly to all patients, animal and adult studies have demonstrated that the ITD and ACD, either alone or in combination, improve organ perfusion pressures during CPR.52–57 CHAPTER 39 Performance of Cardiopulmonary Resuscitation in Infants and Children Pediatric Cardiopulmonary Resuscitation Targets Chest Compression Depth Pediatric chest compression depth recommendations are largely based on expert clinical consensus using data extrapolated from animal, adult, and limited pediatric studies Supported by two computer-automated tomography studies suggesting that depths of one-half anteroposterior (AP) chest depth are unattainable in most children,58,59 the most recent change to the pediatric depth recommendation occurred in 2015 when the American Heart Association (AHA) Guidelines60,61 recommended a compression depth of “at least one-third AP chest depth” rather than “onethird to one-half.” This subtle change acknowledged the potential difficulty (or even potential harm) of trying to provide chest compressions to one-half AP depth.62,63 These recommendations correspond to approximately cm in infants and cm in children Once children reach puberty, the adult CPR depth of “at least cm, but no more than cm” is recommended Again, an upper limit is placed to acknowledge the potential harm of compressions that are too deep Future studies that collect data from pediatric patients and that associate quantitatively measured CPR mechanics with physiologic measurements and clinical outcomes (e.g., arterial blood pressure, end-tidal carbon dioxide [Etco2], ROSC, survival) are needed Chest Compression Rate Over the last 20 years, there have been minimal changes to the recommended chest compression rate, which has hovered around 100 per minute for adults, children, and infants These recommendations were initially based primarily on animal models of cardiac arrest showing improved hemodynamic measures and short-term survival outcomes when rates were increased from 60 to greater than 100 per minute.64 The most recent refinement to the chest compression rate recommendation occurred in 2015, at which time an upper rate limit (120/minute) was added.60,61 This change acknowledged animal work dating back to the 1980s establishing that higher rates can have a detrimental effect on stroke volume/cardiac output as a result of shorter diastolic filling times, but was also supported by large clinical studies of adult OHCA from the Resuscitation Outcomes Consortium funded by the National Institutes of Health.65,66 Importantly, the guidelines acknowledge that “insufficient data were available for a systematic review of chest compression rate in children” and thereby deferred to the adult guidelines of 100 to 120 chest compressions per minute.61 Chest Compression Fraction/Minimizing Interruptions The avoidance of unnecessary interruptions in chest compressions and minimization of the duration of necessary interruptions remain central tenets of high-quality CPR Laboratory studies have shown that CoPP falls during chest compression interruptions and requires multiple compressions to return to the preinterruption baseline.67 Recent data in pediatric IHCA suggest that these harmful hemodynamic effects can be attenuated by limiting the frequency and duration of interruptions.68 Current guidelines call for a goal of maintaining a chest compression fraction (CCF)— the percentage of time during a CPR event spent actually delivering compressions—of more than 80% However, high-functioning 447 resuscitation teams have reported mean CCFs more than 90%.69 Recent adult studies have revealed counterintuitive data regarding the relationship between CCF and outcome, but interpretation of these is difficult due to their observational nature.70,71 Duty Cycle Duty cycle (DC), the percentage of time spent during the downstroke of a chest compression, remains a relatively understudied aspect of CPR quality The 2002 version of the Pediatric Advanced Life Support (PALS) Guidelines recommended that rescuers provide compressions with “approximately equal compression and relaxation phases (DC 50%).” This approximation was based on the argument that it is difficult for the rescuer to judge or manipulate the DC during compressions when they are provided at rates exceeding 100 per minute However, there are substantial amounts of preclinical data suggesting that a briefer, more “high-impact” compression phase improves organ blood flow.72–74 In a recent single-center clinical study of pediatric inhospital CPR, the mean DC for events was 40%, with only 5% of events having a DC compliant with guideline recommendations.75 Unfortunately, an optimal DC to improve outcomes could not be established, highlighting the need for further study of this element of CPR quality Airway and Breathing Management During Cardiopulmonary Resuscitation It is estimated that even excellent CPR provides only about 25% of normal cardiac output and pulmonary blood flow.76 As such, less minute ventilation may be necessary for adequate gas exchange (i.e., to match ventilation and perfusion) Moreover, animal and adult data indicate that a rapid rate of assisted ventilation (overventilation from exuberant rescue breathing) during CPR is common and may compromise venous return and cardiac output by increasing intrathoracic pressure.77,78 These hemodynamic effects are compounded when considering the deleterious effects of interruptions in CPR to provide airway management and rescue breathing.67 Cumulatively, these physiologic observations provide the justification for the provision of a relatively low ventilation rate during adult and pediatric resuscitation Although overventilation is problematic, because most pediatric arrests are asphyxial in nature, the provision of adequate ventilation is still important The difference between arrhythmogenic and asphyxial arrests lies in the physiology In animal models of sudden VF cardiac arrest, acceptable partial pressure of arterial oxygen (Pao2) and partial pressure of arterial carbon dioxide (Paco2) can persist for to minutes during chest compressions without rescue breathing.79 This is in part because arterial and alveolar oxygen and carbon dioxide concentrations at the onset of the arrest not vary much from the prearrest state As a result, the lungs act as a reservoir of oxygen during CPR, and adequate oxygenation and ventilation can continue without rescue breathing However, when an arrest occurs secondary to a respiratory etiology, there is no pulmonary reservoir of oxygen, and CPR circulates hypoxemic, hypercarbic blood, perpetuating organ hypoxia and acidemia Therefore, even at the onset of resuscitation, arterial hypoxemia and acidemia can be substantial In this circumstance, rescue breathing with controlled ventilation can be lifesaving In fact, whereas hands-only CPR without rescue breathing is a validated method of CPR for adult OHCA,80–84 448 S E C T I O N I V Pediatric Critical Care: Cardiovascular children fare worse when bystander CPR does not include the provision of rescue breaths, especially if they have a noncardiac OHCA etiology.27,28,85 Evidence has demonstrated that a compression/ventilation ratio of 15:2 delivers the same minute ventilation and increases the number of delivered chest compressions by 48% compared with CPR at a compression/ventilation ratio of 5:1 in a simulated pediatric arrest model.86,87 This is important because when chest compressions cease, the aortic pressure falls rapidly and coronary perfusion pressure decreases.68,88 Increasing the ratio of compressions to ventilations minimizes these interruptions, optimizing myocardial blood flow These findings are, in part, the reason that the 2015 AHA Guidelines recommend a pediatric compression/ ventilation ratio of 15:2 In reality, more work is necessary to determine ideal ranges of ventilation ratios during CPR for children The best ratio of compressions to ventilations in pediatric patients likely depends on compression rate, tidal volume, blood flow generated by compressions, the time that compressions are interrupted to perform ventilations, and the patient’s underlying physiology We believe that ventilation strategies that are titrated to individual patient characteristics and physiology warrant investigation A discussion of airway management and further discussion of ventilation rates during pediatric cardiac arrest follow in the Controversies section CPR.98,99 In a large multicenter prospective pediatric trial, there was no association between Etco2 and survival, highlighting the need for further pediatric study to establish an Etco2 target to which CPR could be adjusted.100 Irrespective of a specific target to guide CPR, Etco2 remains a useful device for confirmation of invasive airway placement as long as the CPR is sufficient to provide some amount of pulmonary blood flow Despite being recommended by the AHA, providers rarely use physiology to guide the resuscitation effort However, in a propensity-matched cohort, the use of physiologic monitoring was associated with a higher likelihood of ROSC, indicating that more widespread use may be one method to improve pediatric cardiac arrest outcomes.101 Physiologic Targets Vasopressors 89 A 2013 CPR Quality Consensus Statement released by the AHA and the 2015 PALS Guidelines60 recommend physiologic monitoring during CPR with invasive hemodynamics or exhaled Etco2 This recommendation was based on decades of experimental and clinical evidence supporting the physiologic response to CPR as a key determinant of outcome In this updated section, we provide evidence for the use of physiologic targets during CPR Arterial Blood Pressure In preclinical models of pediatric IHCA, titration of vasopressor administration to CoPP and adjustment of compression depth to systolic blood pressure results in higher rates of survival and improved neurologic outcomes.46,48,50,90 While CoPP monitoring requires simultaneous measurement of diastolic blood pressure (DBP) and central venous pressure, DBP alone is a more clinically feasible surrogate marker of CPR quality.89,91 In a large multicenter prospective trial conducted in the CPCCRN, a DBP of 25 mm Hg or higher in infants younger than year and 30 mm Hg or higher in older children was associated with improved survival to hospital discharge and survival with favorable neurologic outcome among children with an ICU arrest.92 End-Tidal Carbon Dioxide Etco2 reflects pulmonary blood flow; thus, it is a marker of cardiac output.93 There are three main themes regarding Etco2 use during CPR: (1) low values (,10 mm Hg) are rarely associated with successful resuscitation,94 (2) Etco2 values are generally higher among patients who achieve ROSC,95 and (3) an abrupt rise in Etco2 can be used to detect underlying ROSC during CPR.96,97 Similar to hemodynamic-directed CPR described earlier, recent animal work in a neonatal model of cardiac arrest has demonstrated that Etco2-guided chest compressions are associated with improved rates of ROSC compared with standard Medications Used to Treat Cardiac Arrest Although animal studies have indicated that epinephrine can improve initial resuscitation success after both asphyxial and VF cardiac arrests, no single medication has been shown to improve survival outcome from pediatric cardiac arrest A variety of medications are used during pediatric resuscitation attempts, including vasopressors (epinephrine or vasopressin), antiarrhythmics (amiodarone or lidocaine), and other drugs, such as calcium and sodium bicarbonate Epinephrine Epinephrine (adrenaline) is an endogenous catecholamine with potent a- and b-adrenergic stimulating properties The a-adrenergic action (vasoconstriction) increases systemic and pulmonary vascular resistance The b-adrenergic effect increases myocardial contractility and heart rate Epinephrine (recommended dose of 0.01 mg/kg) primarily helps achieve ROSC by increasing systemic vascular resistance, which leads to a higher DBP and CoPP A recent adult randomized controlled trial has suggested no benefit to epinephrine administration during OHCA resuscitation, though it was more than 20 minutes (median) after the emergency call.102,103 In contrast, delayed administration of epinephrine has been associated with worse outcomes in a recent large in-hospital pediatric registry study of patients with nonshockable rhythms, suggesting that, when needed, early administration is better.104,105 Therefore, the 2015 PALS Guidelines continued to recommend epinephrine as a reasonable therapy during CPR High-dose epinephrine (0.1 mg/kg) is not recommended due to its use being associated with higher mortality in a randomized pediatric cardiac arrest trial.106 In light of clinical pediatric IHCA data that attainment of adequate DBP during CPR is associated with survival,92 it seems reasonable to use epinephrine when needed to attain adequate DBP during CPR Vasopressin Vasopressin is a long-acting endogenous hormone that acts to mediate systemic vasoconstriction (V1 receptor) and reabsorption of water in the renal tubule (V2 receptor) The vasoconstriction is most intense in the skeletal muscle and skin vascular beds Unlike epinephrine, vasopressin does not cause significant pulmonary vasoconstriction The 2015 Advanced Cardiac Life Support (ACLS) Guidelines removed the use of vasopressin owing to a lack of survival advantage over epinephrine alone.107,108 Owing to limited pediatric data and an association with lower rates of ROSC in an in-hospital Get With The Guidelines–Resuscitation CHAPTER 39 Performance of Cardiopulmonary Resuscitation in Infants and Children (GWTG-R) registry study, routine vasopressin use is also not recommended during cardiac arrest in children.109 Experts will still consider administration in select resuscitation circumstances in which adrenergic receptor stimulation may be detrimental (e.g., pulmonary hypertension, arrhythmogenic states) or ineffective (e.g., sepsis with catecholamine-refractory shock).110 Antiarrhythmics Amiodarone Versus Lidocaine The 2005 and 2010 PALS Guidelines recommended amiodarone over lidocaine for shock-refractory VF/pVT based on pediatric case series and adult data Supported by a 2014 pediatric GWTG-R study that demonstrated higher rates of ROSC with lidocaine compared with amiodarone, the 2015 PALS Guidelines removed the preference for amiodarone and simply stated that either amiodarone or lidocaine was an appropriate pharmacologic choice for shock-refractory VF or pVT.111 Publication of the adult out-ofhospital ALPS study (Amiodarone, Lidocaine, or Placebo in Outof-Hospital Arrest) prompted a re-review of this topic for the 2018 PALS update.112,113 While this adult study demonstrated no benefit of either antiarrhythmic compared with placebo, given the differences between pediatric and adult cardiac arrest, the pediatric recommendation remained unchanged (i.e., either amiodarone or lidocaine is reasonable for shock-refractory VF/pVT) Other Medications Calcium In the absence of a documented clinical indication (e.g., hypocalcemia, calcium channel blocker overdose, hypermagnesemia, or hyperkalemia), administration of calcium does not improve outcome from cardiac arrest To the contrary, three observational pediatric studies have associated routine calcium administration with decreased survival rates or worse neurologic outcomes.114–116 Sodium Bicarbonate Similar to calcium, routine use of sodium bicarbonate is also not recommended The 2010 PALS Guidelines state that sodium bicarbonate can be administered in select circumstances (e.g., sodium channel blocker overdose, hyperkalemia, hypermagnesemia) While there are no randomized controlled studies in children examining the use of sodium bicarbonate for management of pediatric cardiac arrest, two multicenter retrospective in-hospital pediatric studies have found that sodium bicarbonate administered during cardiac arrest is associated with decreased survival.115,117 Postarrest Interventions The postarrest phase should focus on limiting secondary injury Management priorities include (1) anticipation of and prevention of hyperthermia (targeted temperature management), (2) avoidance of hypotension, (3) avoidance of extremes of oxygenation and ventilation, (4) monitoring for and treatment of seizures, and (5) ongoing treatment of the underlying arrest etiology and prevention of recurrent arrest Targeted Temperature Management Hyperthermia following cardiac arrest is common in children and is associated with poor neurologic outcome.31 Therefore, proactive 449 avoidance of fever should be a priority However, whether a patient should receive therapeutic hypothermia has been a topic of substantial interest Two large pediatric multicenter trials (https://www.thapca.org) in comatose survivors of OHCA and IHCA have failed to demonstrate a benefit of therapeutic hypothermia (32°C–34°C) compared with targeted normothermia (36°C–37.5°C).32,33 However, it is worth noting that there was a nonsignificant trend toward improved rates of survival with hypothermia in the out-of-hospital study As a result, the most recent PALS Guidelines recommended that for infants and children between 24 hours and 18 years of age who remain comatose after OCHA or ICHA, it is reasonable to use either targeted temperature management (TTM) of 32°C to 34°C followed by TTM of 36°C to 37.5°C or to use TTM of 36°C to 37.5°C In either case, providers should ensure continuous measurement of temperature during the postarrest period and should aggressively avoid and treat fever (temperature of 38°C or more; class I recommendations).60 Anticipation and Prevention of Hypotension Postarrest myocardial dysfunction and arterial hypotension occur commonly after successful resuscitation.29,30,118 This postarrest myocardial stunning is pathophysiologically similar to sepsis-related myocardial dysfunction and postcardiopulmonary bypass myocardial dysfunction, including increases in inflammatory mediators and nitric oxide production.119 Four small observational studies after pediatric cardiac arrest have demonstrated lower rates of survival to hospital discharge when children exhibited hypotension after ROSC.29,30,120,121 One of these studies associated postROSC hypotension (defined as a systolic blood pressure ,5th percentile for age) after IHCA with a lower likelihood of survival to discharge with favorable neurologic outcome Interestingly, only about half of the patients with hypotension in this study were treated, highlighting postarrest hypotension as an underrecognized therapeutic target In response, the most recent iteration of the PALS Guidelines recommended that when appropriate resources are available, providers should both continuously monitor invasive arterial pressure after ROSC and use parenteral fluids, inotropes, and vasopressors to avoid/treat hypotension (class I recommendation).60 Postarrest Oxygenation and Ventilation Management In children, hyperoxia is common and continuous normoxia is rarely achieved in the hours following cardiac arrest One report in pediatrics has demonstrated a survival benefit of normoxia (Pao2 60 and ,300 mm Hg) over hyperoxia (Pao2 300 mm Hg).122 Similarly, hypocapnia (Paco2 ,30 mm Hg) and hypercapnia (Paco2 50 mm Hg) were both associated with mortality in pediatric observational studies.123 As such, the most recent PALS Guidelines made recommendations to avoid extremes of oxygenation and ventilation, with the understanding that avoiding hypoxemia is most important Monitoring for and Treating Seizures Seizures are present in up to 30% of patients after cardiac arrest.124 Moreover, certain electroencephalographic findings (abnormal background, burst suppression, and subclinical status epilepticus) are all associated with worse neurologic outcome.35 ... (AHA) Guidelines60,61 recommended a compression depth of “at least one-third AP chest depth” rather than “onethird to one-half.” This subtle change acknowledged the potential difficulty (or even potential... acidemia can be substantial In this circumstance, rescue breathing with controlled ventilation can be lifesaving In fact, whereas hands-only CPR without rescue breathing is a validated method of... carbon dioxide (Paco2) can persist for to minutes during chest compressions without rescue breathing.79 This is in part because arterial and alveolar oxygen and carbon dioxide concentrations at the