434 SECTION IV Pediatric Critical Care Cardiovascular response of peripheral vessels to catecholamines This effect is contrary to the desired effect during CPR In addition, particu larly in patients w[.]
434 S E C T I O N I V Pediatric Critical Care: Cardiovascular response of peripheral vessels to catecholamines This effect is contrary to the desired effect during CPR In addition, particularly in patients with a reactive pulmonary vascular bed, pulmonary vascular resistance is inversely related to pH Rudolph and Yuan observed a twofold increase in pulmonary vascular resistance in calves when pH was lowered from 7.4 to 7.2 under normoxic conditions.201 Therefore, correction of even mild acidosis may be helpful in resuscitating patients who have the potential for increased right-to-left shunting through a cardiac septal defect, patent ductus arteriosus, or aortic-to-pulmonary shunt during periods of elevated pulmonary vascular resistance Multiple adverse effects of bicarbonate administration include metabolic alkalosis, hypercapnia, hypernatremia, and hyperosmolality All of these adverse effects are associated with a high mortality rate Alkalosis causes a leftward shift of the oxyhemoglobin dissociation curve, thus, impairing release of oxygen from hemoglobin to tissues at a time when oxygen delivery already may be low Alkalosis can result in hypokalemia, by enhancing potassium influx into cells, and ionic hypocalcemia, by increasing protein binding of ionized calcium Hypernatremia and hyperosmolality may decrease tissue perfusion by increasing interstitial edema in microvascular beds The marked hypercapnic acidosis that occurs during CPR on the venous side of the circulation, including the coronary sinus, may be worsened by administration of bicarbonate.202,203 Myocardial acidosis during cardiac arrest is associated with decreased myocardial contractility The mean venoarterial partial pressure of carbon dioxide difference was 24 15 mm Hg in patients during CPR and actually increased from 16 to 69 mm Hg in patient after administration of bicarbonate.204 Another group showed a mean difference of 42 mm Hg between partial pressure of carbon dioxide in mixed venous blood and partial pressure of arterial carbon dioxide (Paco2) during CPR Paradoxical intracellular acidosis after bicarbonate administration is possible because of rapid entry of carbon dioxide into cells with a slow egress of hydrogen ion out of cells Paradoxical intracellular acidosis in the central nervous system after bicarbonate administration has been proposed but not definitively shown In neonatal rabbits recovering from hypoxic acidosis, bicarbonate administration increased both arterial pH and intracellular brain pH as measured by nuclear magnetic resonance spectroscopy.205 In another study, intracellular brain ATP concentration in rats did not change during severe intracellular acidosis in the brain produced by extreme hypercapnia.206 The rats who maintained ATP concentration even in the face of severe brain acidosis had no functional or histologic differences from normal control subjects Using nuclear magnetic resonance spectroscopy of the brain in dogs during cardiac arrest and CPR, intracellular brain pH decreased to 6.29, with total depletion of brain ATP after minutes of cardiac arrest Following effective CPR, ATP levels rose to 86% of prearrest levels and to normal by 35 minutes of CPR despite ongoing peripheral arterial acidosis (Fig 38.12).105 However, cerebral pH decreased in parallel with blood pH when CPR was started immediately after arrest Bicarbonate administration ameliorated and did not worsen the cerebral acidosis, indicating that the blood-brain pH gradient is maintained during CPR.207 A Cochrane study looking at the use of empirical sodium bicarbonate administration versus placebo in out-of-hospital cardiac arrests in 874 adults found no difference in survival to the hospital.208 Levy reviewed more than 30 animal studies evaluating the efficacy of sodium bicarbonate administration during CPR.209 Among studies with survival as the primary outcome, four showed Minute 35 of CPR D Minute of CPR C Minute of V-Fib B PCr Pi PME PDE Control A 10 –10 –20 PPM P • Fig 38.12 31 magnetic resonance spectroscopy spectra from in situ dog brain during vest cardiopulmonary resuscitation (CPR) after a 6-minute delay in the onset of CPR from time of arrest Each spectrum was acquired in minute The frequency of the inorganic phosphate (Pi) peak is pH dependent Note complete absence of adenosine triphosphate (ATP) and phosphocreatine (PCr), and pHi 6.28 in trace B after minutes of ventricular fibrillation (v-fib) without CPR After minutes of CPR (trace C), ATP is more than 85% recovered, but pH is only 6.61 After 35 minutes of CPR (trace D), pHi has returned to PDE, phosphodiesters; PME, phosphomonoesters; PPM, parts per million (Modified from Eleff SM, Schleien CL, Koehler RC et al: Brain bioenergetics during cardiopulmonary resuscitation in dogs, Anesthesiology 1992;76:77.) benefit and seven did not When assessing myocardial performance, 12 studies concluded that sodium bicarbonate worsened performance, studies showed no difference, and no study showed benefit When reviewing 19 retrospective human adult studies examining mortality rates, suggested a deleterious effect of sodium bicarbonate, 11 showed no difference in outcomes, and none showed benefit.209 A large prospectively conducted observational study of adult out-of-hospital cardiac arrest patients demonstrated outcomes for those who received sodium bicarbonate during resuscitation.210 Out of 13,865 patients, 5165 (37%) received sodium bicarbonate Using 1:1 propensity matching to account for confounding variables, sodium bicarbonate administration was associated with worse survival to discharge and with a lower likelihood of achieving a favorable neurologic outcome In a large retrospective study of pediatric patients with inhospital cardiac arrest, it was found that survivors were less likely to receive sodium bicarbonate than nonsurvivors However, nonsurvivors were also observed to have a longer CPR duration as well as more doses of calcium, vasopressin, and epinephrine.9 A subsequent retrospective study by Raymond et al examined sodium bicarbonate use after the institution of the 2010 AHA guidelines While they found that sodium bicarbonate use for inhospital cardiac arrest had been decreasing, its use was still associated with decreased survival at 24 hours and hospital discharge when given outside current PALS recommendations.211 Due to potential adverse effects of bicarbonate, the indications for its use are limited to cardiac arrest associated with hyperkalemia, patients with preexisting metabolic acidosis, and after approximately 10 minutes of CPR When Paco2 and pH are known, CHAPTER 38 Physiologic Foundations of Cardiopulmonary Resuscitation the dose of bicarbonate to correct the pH to 7.4 is calculated using the following equation: Sodium bicarbonate (mEq) 0.3 weight (kg) Base deficit Because of its possible adverse effects and the large venous to arterial carbon dioxide gradient that develops during CPR, we recommend giving half the dose that would be given based on a volume of distribution of 0.6 If blood gases are not available, the initial dose is mEq/kg, followed by 0.5 mEq/kg every 10 minutes of ongoing arrest Alveolar ventilation must be maintained because of the generation of carbon dioxide and can be assessed only by serial measurements of arterial blood gases and pH ETCO2 monitoring is useful during CPR because it provides important information regarding both pulmonary and cardiac function ETCO2 is measured instantaneously in the exhaled gas of every breath In the absence of lung disease, ETCO2 correlates closely with Paco2 provided that pulmonary blood flow is at least 20% to 25% of normal As a respiratory monitor, ETCO2 analyzers accurately distinguish a tracheal (ETCO2 10) from an esophageal (ETCO2 ,5) intubation in infants and children.212–217 Because measurements are made with every breath, dislodgment of the endotracheal tube from the trachea can be identified immediately When cardiac output is extremely low, as occurs during ineffective CPR, delivery of carbon dioxide to the lungs is so limited that the total amount exchanged across the alveolar-capillary membrane is markedly reduced In this situation, the measured ETCO2 is very low even when Paco2 is elevated As cardiac output increases, ETCO2 increases and the difference between end-tidal and arterial CO2 becomes smaller.218 ETCO2 has been correlated with CPP, the critical parameter for resuscitation of the heart.218 However, a low ETCO2 may occur in the presence of adequate cardiac output during CPR after the administration of epinephrine because of its ability to increase intrapulmonary shunting.191,219,220 In this case, a low ETCO2 underestimates cardiac output Other causes of low ETCO2 include airway obstruction, tension pneumothorax, pericardial tamponade, pulmonary embolism, hypothermia, severe hypocapnia (which occurs commonly with overaggressive hand ventilation), and esophageal intubation In a large prospective observational study of adult in-hospital arrests, Sutton et al showed that an ETCO2 greater than 10 mm Hg was associated with improved ROSC and survival.221 Levine et al monitored ETCO2 in 150 adults with an out-of-hospital cardiac arrest who had electrical activity but no pulse.222 They found that after 20 minutes of ACLS, an ETCO2 level of 10 mm Hg successfully predicted survival to hospital admission with a sensitivity, specificity, and positive- and negative-predictive value of 100% Grmec and Klemen prospectively studied ETCO2 as a prognostic indicator for outcomes in adult resuscitation and found that using an initial, average, and final ETCO2 level of 10 mm Hg identified 100% of patients who were successfully resuscitated, with specificities of 74%, 90%, and 81%, respectively.223 The 2015 AHA guidelines state that the use of ETCO2 as an indicator of cardiac output may be useful in adults (evidence class IIb).112 Pediatric data are limited at this time One small prospective study of pediatric arrests evaluated whether an ETCO2 greater than 20 mm Hg during resuscitation was associated with survival but found no difference.224 There have been no human trials studying whether titrating resuscitation efforts to a specific number can affect clinical outcomes In a piglet model of CPR, it was found that CPR guided by a target ETCO2 was as effective as CPR guided by depth monitor, video monitor, and verbal feedback While no specific 435 value has yet to be established, given the noninvasive nature of ETCO2 monitoring and extrapolating from adult data,225 maintaining an ETCO2 of greater than 10 to 15 mm Hg through the use of ETCO2 monitoring is recommended during pediatric arrests.159 Other Alkalinizing Agents A number of other alkalinizing agents have been used experimentally in animals and humans However, none have demonstrated any real advantages over sodium bicarbonate Carbicarb, a solution of equimolar amounts of sodium bicarbonate and sodium carbonate, corrects metabolic acidosis without many of the adverse effects of sodium bicarbonate.76 The buffering action of sodium carbonate occurs by consumption of carbon dioxide with generation of bicarbonate ion, as illustrated in the following equation: Na2CO3 CO2 H2O 2HCO32 2Na1 During CPR, Carbicarb administration resulted in a greater increase in arterial pH and smaller increases in Paco2, lactate, and serum osmolality in animals.76,226,227 However, Carbicarb was not superior to sodium bicarbonate when used for hypovolemic shock in rats.228 Dichloroacetate (DCA) increases the activity of pyruvate dehydrogenase, which facilitates the conversion of lactate to pyruvate.229 When administered to patients with lactic acidosis, DCA decreased lactate concentration by half and increased bicarbonate concentration and pH.230 DCA improved cardiac output in other studies, possibly by increasing myocardial metabolism of lactate and carbohydrate.231,232 DCA did not improve outcome when compared with sodium bicarbonate in a multicenter trial of patients with lactic acidosis.233 Tromethamine (THAM; tris-hydroxymethyl-aminomethane) is an organic amine that combines with hydrogen ion, causing CO2 and H2O to combine to form bicarbonate and hydrogen ion A dose of mL/kg should raise the bicarbonate concentration by mEq/L Adverse effects of THAM include hyperkalemia, hypoglycemia, and acute hypocarbia, resulting in apnea In addition, peripheral vasodilatation may occur after administration of THAM during CPR, which is an undesirable effect THAM is contraindicated in patients with renal failure Calcium Recommendations for the use of calcium in CPR are restricted to a few specific situations: hypocalcemia, hyperkalemia, hypermagnesemia, and calcium channel blocker overdose These restrictions are based on the possibility that exogenously administered calcium may worsen ischemia/reperfusion injury Intracellular calcium overload occurs during cerebral ischemia by the influx of calcium through voltage- and agonist-dependent (e.g., N-methyl-d-aspartate) calcium channels Calcium plays an important role in the process of cell death in many organs, possibly by activating intracellular enzymes such as nitric oxide synthase, phospholipases A and C, and others.234,235 Calcium channel blockers improve blood flow and function after ischemia to the heart, kidney, and brain.236–238 Calcium channel blockers also raise the threshold of the ischemic heart to VF.239 For these reasons, it appears that the recommended restrictions for use of calcium during CPR are well founded On the other hand, no studies have shown that elevation of plasma calcium concentration, which occurs after calcium administration, 436 S E C T I O N I V Pediatric Critical Care: Cardiovascular worsens outcome of cardiac arrest Because the normal ratio of extracellular to intracellular calcium is on the order of 1000:1 to 10,000:1, it seems unlikely that the rate of influx of calcium into cells would be influenced by a relatively small increase in its extracellular concentration The calcium ion is essential in myocardial excitation-contraction coupling, in increasing ventricular contractility, and in enhancing ventricular automaticity during asystole Ionized hypocalcemia is associated with decreased ventricular performance and peripheral blunting of the hemodynamic response to catecholamines.240,241 In addition, severe ionized hypocalcemia has been documented in adults experiencing out-of-hospital cardiac arrest (mean Ca, 0.67 mmol/L), during sepsis, and in animals during prolonged CPR.241–243 Thus, patients at risk for ionized hypocalcemia should be identified and treated expeditiously Both total and ionized hypocalcemia may occur in patients with chronic or acute disease Total body calcium depletion leading to total serum hypocalcemia occurs in patients with hypoparathyroidism, DiGeorge syndrome, renal failure, pancreatitis, and long-term use of loop diuretics Ionized hypocalcemia occurs after massive or rapid transfusion of blood products, a result of citrate and other preservatives in stored blood products binding calcium The magnitude of hypocalcemia in this setting depends on the rate of blood administration, total dose, and hepatic and renal function of the patient Administration of mL/kg per minute of citrated whole blood causes a significant decrease in ionized calcium concentration in anesthetized patients The pediatric dose of calcium chloride for resuscitation is 20 mg/kg The adult dose is 500 to 1000 mg Calcium gluconate is as effective as calcium chloride in raising ionized calcium concentration during CPR Calcium gluconate is given at a dose of 60 mg/kg, with a maximum dose of g in pediatric patients Calcium should be given slowly through a large-bore, free-flowing intravenous line, preferably a central venous line Severe tissue necrosis occurs when calcium infiltrates into subcutaneous tissue When administered too rapidly, calcium may cause bradycardia, heart block, or ventricular standstill Srinivasan et al reviewed 1477 consecutive pediatric cardiopulmonary events submitted to the National Registry of Cardiopulmonary Resuscitation and reported on the prevalence of calcium administration.244 Calcium was given in 659 of these events Calcium was more likely to be used in pediatric facilities, ICUs, in the setting of recent cardiac surgery, CPR performed for more than 15 minutes, asystole, and concurrently with other advanced life support medications After controlling for confounding factors, calcium administration during CPR was independently associated with poor survival to discharge and unfavorable neurologic outcomes They found that 21% of patients survived to hospital discharge when calcium was used, compared with 44% who survived when calcium was not used Only 15% of patients had a favorable neurologic outcome when calcium was used, compared with 35% with a favorable outcome when calcium was not administered.244 Glucose Administration of glucose during CPR should be restricted to patients with documented hypoglycemia because of the possible detrimental effects of hyperglycemia on the brain during or following ischemia Myers found that infant monkeys receiving glucose before cardiac arrest were more likely to develop seizures, prolonged coma, and brain death with cerebral necrosis than were those that received saline solution.245 Siemkowicz and Hansen confirmed this finding when they demonstrated that after 10 minutes of global brain ischemia, the neurologic recovery of hyperglycemic rats was worse than that of normoglycemic control subjects.246 The mechanism by which hyperglycemia exacerbates ischemic neurologic injury may be increased production of lactic acid in the brain by anaerobic metabolism During ischemia under normoglycemic conditions, brain lactate concentration reaches a plateau In a hyperglycemic milieu, however, brain lactate concentration continues to rise for the duration of the ischemic period The severity of intracellular acidosis during ischemia is directly proportional to the preischemic glucose concentration.247 The negative effect of hyperglycemia during brain ischemia is predicated on the presence of at least a small amount of blood flow to brain tissue In one study, collaterally perfused but not end-arterial brain tissue had greater neuronal damage during hyperglycemic focal ischemia (Fig 38.13).248 Clinical studies show a direct correlation between the initial post–cardiac arrest serum glucose concentration and poor neurologic outcome.237,249 However, a higher glucose concentration may simply reflect an endogenous response to severe stress and not the proximate cause of more severe brain injury.77 In piglets, postischemic administration of glucose did not worsen neurologic outcome after global hypoxia-ischemia.250 However, given the likelihood of additional ischemic and hypoxic events in the postresuscitation period, it seems prudent to maintain serum glucose in the normal range Administration of insulin Glucose NADH +2Pi NAD+ 2ATP NADH NADH NAD+ Pyruvate− Ischemia Hypoxia − Lactate−+2H+ PDH +/− O2 Ca2+ 36 ATP CO2 • Fig 38.13 Schematic diagram illustrating the aerobic/anaerobic metabolism of glucose Oxidation of pyruvate to CO2 (and H2O) by pyruvate dehydrogenase and citric acid cycle enzymes is retarded to blocked by oxygen deficiency, causing a reduction of pyruvate to lactate If the adenosine triphosphate (ATP) formed during glycolysis is hydrolyzed (i.e., if the ATP concentration stays constant), one molecule of H1 is released for each molecule of lactate formed If the mitochondria retain a membrane potential, they will sequester excess calcium entering the cell However, if they deenergized (with collapse of their membrane potential), they will release their calcium content ADP, Adenosine diphosphate; NAD, nicotinamide adenine dinucleotide; NADH, reduced nicotinamide adenine dinucleotide; Pi, intracellular phosphorus; PDH, pyruvate dehydrogenase CHAPTER 38 Physiologic Foundations of Cardiopulmonary Resuscitation to hyperglycemic rats after global brain ischemia improved neurologic outcome.251 The effect of insulin may be independent of its ability to lower blood glucose, because these investigators later showed that normoglycemic insulin-treated rats had a better outcome than normoglycemic placebo-treated control subjects.252 Using intensive insulin therapy, Van den Berghe et al strictly controlled the blood glucose levels of adults in a surgical ICU, maintaining levels between 80 and 110 mg/dL.253,254 This control of blood glucose levels appeared to reduce mortality and protect the central and peripheral nervous systems However, a subsequent study in a medical ICU showed no difference in mortality between the intensive insulin therapy and control groups.255 Another study showed that the use of intensive insulin therapy to maintain normoglycemia was associated with increased episodes of hypoglycemia.256 The HALF-PINT study was a large multicenter randomized controlled trial that assigned critically ill children to one of two different tight glycemic control targets: 80 to 110 mg/dL or 150 to 180 mg/dL.257 The trial was stopped early owing to low likelihood of benefit and possibility of induced harm There was no difference in ICU-free days, mortality, organ dysfunction, or ventilator-free days between groups The lowertarget group had a higher rate of health care–associated infections and more cases of severe hypoglycemia Some groups of patients, including premature infants and debilitated patients with low endogenous glycogen stores, are more prone to the development of hypoglycemia during and after a physiologic stress (e.g., surgery).258 Hypoglycemia poses a higher risk in the immature pediatric brain compared with the adult brain Bedside monitoring of serum glucose is critical during and after a cardiac arrest and allows for intervention before the critical point of low substrate delivery is reached The dose of glucose needed to correct hypoglycemia is 0.5 to 1.0 g/kg given as 10% dextrose in infants The osmolarity of 50% dextrose is approximately 2700 Osm/L and is associated with intraventricular hemorrhage in neonates and infants cardiac arrest.18,259 The incidence increases with age Approximately 25% of children experiencing in-hospital cardiac arrest have ventricular tachycardia or fibrillation.123 Moreover, the growing and aging population of children palliated for complex congenital heart disease in which the occurrence of ventricular arrhythmias may be much higher than in the general pediatric population requires greater attention to ventricular arrhythmias than in the past Other potential causes of ventricular arrhythmias include familial and acquired prolonged QT syndrome, other arrhythmogenic ventricular conditions, cardiomyopathies, myocarditis, drug intoxications (such as illicit and accidental ingestion and therapeutic misadventures), electrolyte derangements (e.g., magnesium, calcium, potassium, or glucose), and hypothermia.260,261 Advances have been made in the management of ventricular arrhythmias Rapid access to defibrillation has been shown to reduce mortality in adults; the development of public access defibrillation and AEDs has flowed from this knowledge Initially, AED devices had little utility for children, but the development of current-reducing electrodes and specific pediatric algorithms has made public access defibrillation a reality for children Consequently, AEDs have been deployed in the many environments in which children would be the primary beneficiaries (e.g., schools and public swimming pools) The wearable cardioverterdefibrillator has been shown to be safe and effective in the pediatric population.262 When automated external defibrillators are used within minutes of adult-witnessed VF in children, longterm survival can occur in more than 70% of cases.263–265 The technique of current delivery has undergone change with the development and deployment of biphasic defibrillators, which may offer increased efficacy with reduced risk of myocardial injury (Fig 38.14) Finally, amiodarone is joined by lidocaine as the drugs of choice for refractory ventricular arrhythmias The role of each of these factors in the resuscitation of pediatric arrest victims is discussed in the following section Defibrillation Management of Ventricular Fibrillation The management of lethal ventricular arrhythmias traditionally has not played a major role in resuscitation teaching or management for children because of the low incidence of these arrhythmias Newer evidence gathered in the environment of rapid access defibrillation suggests that as many as 19% of the presenting rhythms in pediatric arrests are ventricular in origin, represent as many as 5% to 15% of all pediatric victims of out-of-hospital VF is the chaotic electrical excitation of the ventricle The definitive treatment in accordance with the 2015 AHA guidelines is defibrillation.47,196,266 The electrical mechanism is usually explained as a reentrant depolarization of the myocardium, initially in waves, that then take more circuitous routes and degenerate into smaller reentry circuits resulting in loss of the rhythmic contractile function of the ventricles.267 This changing pattern of reentry circuits corresponds with the change from coarse to fine VF '(),%5,//$7,21:$9()2506 MRXOHVDWRKPV 7LPH PV 7\SLFDOELSKDVLF %LSKDVLFWUXQFDWHGH[SRQHQWLDO &XUUHQW DPSV &XUUHQW DPSV &RQYHQWLRQDOPRQRSKDVLF 'DPSHGVLQHZDYH − − − − MRXOHVDWRKPV 7LPH PV • Fig 38.14 Schematic patterns of current flow for conventional monophasic and typical biphasic defibrillator waveforms 437 438 S E C T I O N I V Pediatric Critical Care: Cardiovascular as the duration of fibrillation persists and may correlate with deterioration in energy stores associated with persistence of fibrillation.5,268,269 Similarly, most cases of ventricular tachycardia (VT) are attributable to reentrant mechanisms, although increased automaticity is the likely mechanism in persons with drug-induced torsades de pointes and electrolyte disturbances, such as hypokalemia and hypomagnesemia.270 Nonpulsatile VT with loss of effective contractile function of the heart rapidly deteriorates into VF Loss of effective ventricular function with these arrhythmias requires emergent management The standard for management of VF and pulseless VT is immediate defibrillation and high-quality CPR Although the lowest energy dose for effective defibrillation and the upper limit for safe defibrillation in infants and children are not known, energy doses greater than J/kg (up to J/kg) have effectively defibrillated children.159 The standard voltage dose for pediatric defibrillation is J/kg If unsuccessful, successive doses of defibrillation are repeated at J/kg or more, not to exceed 10 J/kg or the maximum adult dose.109 This dosage is based on data reported by Gutgesell et al in 1976.271 They reported 71 defibrillation attempts in 27 children Efficacy was 91% with J/kg and 100% with J/kg After initial defibrillation, CPR is performed for minutes, followed by a rhythm check and then repeat shock if required This sequence may then be repeated, with consideration given to initiating vasopressor therapy Rhythms that fail to respond to three rounds are defined as “shock resistant.” In this setting, the standard as defined in the AHA guidelines is amiodarone or lidocaine (or magnesium for torsades de pointes), followed by minutes of CPR and continuation of the rhythm check-shock-CPR/vasopressor cycle (Fig 38.15) Reversible causes of VT/VF should also be investigated It is important to continue to deliver appropriate CPR while gathering defibrillation equipment.272,273 Additional important considerations when delivering shocks include paddle size, position, contact pressure, and use of electrode paste Large paddles reduce thoracic impedance, and infants older than year or weighing more than 10 kg should be treated with adult paddles.274 Adhesive patch electrodes are an acceptable alternative to paddles and can be used when available if their use does not cause a delay in therapy.275–277 Paddles should be positioned to achieve current flow through the heart; an anterior-apex, or anterior-posterior placement is selected Contact pressure has been demonstrated to reduce impedance Firm pressure, which commonly is not properly applied, is required.278 Proper electrode paste or gel is needed Care is required to avoid smearing paste across the chest wall Doing so can lead to arcing of the circuit and a resultant short circuit Bare paddles, ultrasound gel, pads soaked in saline solution, and alcohol pads are not acceptable alternatives to electrode cream or paste.196 The role of immediate defibrillation in pediatric patients has come under question The efficacy of defibrillation declines rapidly as fibrillation persists When an arrest is witnessed and a defibrillator is immediately available, defibrillation likely will be successful With any delay in resuscitation, the success of initial defibrillation declines at a rate estimated at between 7% and 10% per minute of continued fibrillation.160 A number of studies have demonstrated in both animals and adults that if more than to minutes of fibrillation have occurred before institution of defibrillation, use of CPR for 90 to 180 seconds to restore myocardial energy stores will improve the likelihood of conversion to a perfusing rhythm with defibrillation.6,8,279,280 Mitani et al showed that children with out-of-hospital cardiac arrest due to a shockable rhythm had a higher rate of 1-month survival and better neurologic outcome after bystander-initiated AED usage compared with those who received defibrillation by emergency medical services.281 Hunt et al analyzed data obtained from the Get with the Guidelines–Resuscitation national registry to evaluate time to defibrillation and survival in pediatric in-hospital arrest.282 They found that time to first shock, whether less than or greater than minutes, did not impact survival, ROSC, or favorable neurologic outcome Thus, immediate recognition and initiation of CPR in a highly monitored pediatric setting may attenuate the effects of time to the first defibrillation attempt Use of biphasic defibrillators is another important advance in the management of tachyarrhythmias Studies suggest that defibrillation with a biphasic waveform can be achieved with lower energy and less myocardial injury than with a standard monophasic defibrillator current.283,284 The first commercially available devices were approved by the US Food and Drug Administration in 1996 An evidence-based review was undertaken by the AHA and published in 1998.45 The reviewers concluded that “low-energy, non-progressive biphasic waveform defibrillators may be used for both out-of-hospital and in-hospital VF arrest, including persistent or recurrent VF that does not respond to the initial lowenergy shock.” These conclusions were based on observational studies and case reports Subsequently, Schneider et al reported a randomized controlled trial of biphasic versus monophasic defibrillation for out-of-hospital cardiac arrest.285 Of 338 arrests, 115 patients had VF and were shocked with an AED Defibrillation in the initial shock series was successful in 98% of patients receiving biphasic shocks but in only 69% of those receiving monophasic shocks (P , 0001), providing further evidence that biphasic waveforms are more efficacious than monophasic waveforms Biphasic shocks appear to be at least as effective as monophasic shocks and less harmful Published data on children are limited to case reports.286 Animal data are supportive of the use of biphasic defibrillators in infants and children Clark et al demonstrated in a piglet model that low-energy biphasic shocks were superior to monophasic shocks for converting catheter-induced VF.287 Both Tang et al and Berg et al studied the use of AEDs equipped with energy-reducing electrodes and found increased efficacy compared with monophasic waveforms.5,288 Berg et al also demonstrated improved LV function hours after resuscitation According to the 2015 AHA recommendations, with a manual defibrillator, dosage recommendations for children remain J/kg for the first attempt followed by J/kg for subsequent attempts.5,49,289 This dose was increased from the 2005 guidelines, which cited studies that demonstrated the ineffectiveness of J/ kg at achieving ROSC Subsequent to the publication of the 2010 AHA recommendations, a review of the National Registry of Cardiopulmonary Resuscitation data compared the effect of J/ kg with historical controls and a J/kg initial shock dose in VF and pulseless VT The authors found that termination of the arrhythmia with an initial shock dose of J/kg was significantly less effective than historical controls (56% vs 91%) A higher initial dose of J/kg was associated with less successful ROSC than the J/kg dose Based on this conflicting data, they concluded that the optimal initial shock dose has yet to be determined In the early 1990s, as part of an AHA campaign to improve the abysmal rates of resuscitation from out-of-hospital cardiac arrest in adults, the development and deployment of AEDs was initiated Both fixed and escalating dose devices were developed; however, the initial dose usually was at least 150 J in adults Because of the high fixed-energy doses, the devices were not recommended for use in children younger than years Moreover, their ... required This sequence may then be repeated, with consideration given to initiating vasopressor therapy Rhythms that fail to respond to three rounds are defined as “shock resistant.” In this setting,... administration of epinephrine because of its ability to increase intrapulmonary shunting.191,219,220 In this case, a low ETCO2 underestimates cardiac output Other causes of low ETCO2 include airway obstruction,... of cardiac output may be useful in adults (evidence class IIb).112 Pediatric data are limited at this time One small prospective study of pediatric arrests evaluated whether an ETCO2 greater than