The goals of postresuscitation care are to preserve neurologic function, prevent secondary organ injury, diagnose and treat the cause of illness, and enable the patient to arrive at a pediatric tertiary-care facility in an optimal physiologic state. Frequent reassessment of the patient is necessary because cardiorespiratory status may deteriorate.
Animal studies suggest that elevated levels of tissue Po2 after ROSC (hyperoxia) contribute to oxidative stress that may potentiate the postresuscitation syndrome, while some adult studies show associations between hyperoxemia and increased mortality.1,2
Three small observational studies of pediatric IHCA and OHCA survivors3-5 did not show an association between elevated Pao2 and outcome. In a larger observational study of 1427 pediatric IHCA and OHCA victims who survived to pediatric ICU admission,6after adjustment of confounders, the presence of normoxemia (defined as a Pao2 60 mmHg or greater and less than 300 mmHg) when compared with hyperoxemia (Pao2 greater than 300 mmHg) after ROSC was associated with improved survival to pediatric ICU discharge.
It may be reasonable for rescuers to target normoxemia after ROSC. (Class IIb, LOE B-NR)
Because an arterial oxyhemoglobin saturation of 100% may correspond to a Pao2 anywhere between 80 and approximately 500 mmHg, it may be reasonable—when the necessary equipment is available—for rescuers to wean oxygen to target an oxyhemoglobin saturation of less than 100%, but 94% or greater. The goal of such an approach is to achieve normoxemia while ensuring that hypoxemia is strictly avoided. Ideally, oxygen is titrated to a value appropriate to the specific patient condition.
Cerebral vascular autoregulation may be abnormal after ROSC. Adult data show an association between post-ROSC hypocapnia and worse patient outcomes.7,8 In other types of pediatric brain injury, hypocapnia is associated with worse clinical outcomes.9-12
There were no studies in children after cardiac arrest specifically comparing ventilation with a predetermined Paco2 target. One small observational study of both pediatric IHCA and OHCA3 demonstrated no association between hypercapnia (Paco2 greater than 50 mmHg) or hypocapnia (Paco2 less than 30 mmHg) and outcome. However, in an observational study of pediatric IHCA,5hypercapnia (Paco2 50 mmHg or greater) was associated with worse survival to hospital discharge.
It is reasonable for practitioners to target a Paco2 after ROSC that is appropriate to the specific patient condition, and limit exposure to severe hypercapnia or hypocapnia. (Class IIb, LOE C-LD)
Monitor exhaled CO2 (ETCO2), especially during transport and diagnostic procedures. (Class IIa, LOE B)
Monitor exhaled CO2 (ETCO2), especially during transport and diagnostic procedures. (Class IIa, LOE B)
Monitor heart rate and blood pressure. Repeat clinical evaluations at frequent intervals until the patient is stable. Consider monitoring urine output with an indwelling catheter. A 12-lead ECG may be helpful in establishing the cause of the cardiac arrest.
Remove the IO access after alternative (preferably 2) secure venous catheters are placed. Monitor venous or arterial blood gas analysis and serum electrolytes, glucose, and calcium concentrations. A chest x-ray should be performed to evaluate endotracheal tube position, heart size, and pulmonary status. Consider obtaining arterial lactate and central venous oxygen saturation to assess adequacy of tissue oxygen delivery.
Three small observational studies involving pediatric IHCA and OHCA20-22 demonstrated worse survival to hospital discharge when children were exposed to post-ROSC hypotension. One of these studies20 associated post-ROSC hypotension (defined as a systolic blood pressure less than fifth percentile for age) after IHCA with lower likelihood of survival to discharge with favorable neurologic outcome. There are no studies evaluating the benefit of specific vasoactive agents after ROSC in infants and children.
After ROSC, we recommend that parenteral fluids and/or inotropes or vasoactive drugs be used to maintain a systolic blood pressure greater than fifth percentile for age. (Class I, LOE C-LD)
When appropriate resources are available, continuous arterial pressure monitoring is recommended to identify and treat hypotension. (Class I, LOE C-EO)
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Systemic and pulmonary vascular resistances are often increased initially, except in some cases of septic shock.23The postarrest effects on the cardiovascular system may evolve over time, with an initial hyperdynamic state replaced by worsening cardiac function. Therefore in infants and children with documented or suspected cardiovascular dysfunction after cardiac arrest, it is reasonable to administer vasoactive drugs titrated to improve myocardial function and organ perfusion.
Low-dose infusions (<0.3 mcg/kg per minute) generally produce β-adrenergic actions (tachycardia, potent inotropy, and decreased systemic vascular resistance). Higher-dose infusions (>0.3 mcg/kg per minute) cause α-adrenergic vasoconstriction.24,25 Because there is great interpatient variability in response,26,27 titrate the drug to the desired effect. Epinephrine or norepinephrine may be preferable to dopamine in patients (especially infants) with marked circulatory instability and decompensated shock.28
Dopamine can produce direct dopaminergic effects and indirect β- and α-adrenergic effects through stimulation of norepinephrine release.
Titrate dopamine to treat shock that is unresponsive to fluids and when systemic vascular resistance is low. (Class IIb, LOE C)
Titrate dopamine to treat shock that is unresponsive to fluids and when systemic vascular resistance is low (Class IIb, LOE C).420,435
Typically a dose of 2 to 20 mcg/kg per minute is used. Although low-dose dopamine infusion has been frequently recommended to maintain renal blood flow or improve renal function, data do not show benefit from such therapy.29,30 At higher doses (>5 mcg/kg per minute), dopamine stimulates cardiac β-adrenergic receptors, but this effect may be reduced in infants and in patients with chronic congestive heart failure. Infusion rates >20 mcg/kg per minute may result in excessive vasoconstriction.24,25 In one study in single ventricle postoperative cardiac patients, dopamine increased oxygen consumption while not improving blood pressure or cardiac output.31
Dobutamine has a relatively selective effect on β1- and β2-adrenergic receptors due to effects of the two isomers; one is an α-adrenergic agonist, and the other is an α-adrenergic antagonist.32Dobutamine increases myocardial contractility and can decrease peripheral vascular resistance. Titrate the infusion26,33,34 to improve cardiac output and blood pressure due to poor myocardial function.34
Norepinephrine is a potent vasopressor promoting peripheral vasoconstriction. Titrate the infusion to treat shock with low systemic vascular resistance (septic, anaphylactic, spinal, or vasodilatory) unresponsive to fluid.
Sodium nitroprusside increases cardiac output by decreasing vascular resistance (afterload). If hypotension is related to poor myocardial function, consider using a combination of sodium nitroprusside to reduce afterload and an inotrope to improve contractility. Fluid administration may be required secondary to vasodilatory effects.
Inodilators (inamrinone and milrinone) augment cardiac output with little effect on myocardial oxygen demand.
It is reasonable to use an inodilator in a highly monitored setting for treatment of myocardial dysfunction with increased systemic or pulmonary vascular resistance. (Class IIa, LOE B)
Administration of fluids may be required secondary to vasodilatory effects.
Inodilators have a long half-life with a delay in reaching a steady-state hemodynamic effect after the infusion rate is changed (18 hours with inamrinone and 4.5 hours with milrinone). In cases of toxicity the cardiovascular effects may persist for several hours even after the infusion is discontinued.
Data suggest that fever after pediatric cardiac arrest is common and is associated with poor outcomes.35 The 2010 AHA PALS Guidelines suggested a role for targeted temperature management after pediatric cardiac arrest (fever control for all patients, therapeutic hypothermia for some patients), but the recommendations were based predominantly on extrapolation from adult and asphyxiated newborn data.
A large multi-institutional, prospective, randomized study of pediatric patients (aged 2 days to 18 years) with OHCA found no difference in survival with good functional outcome at 1 year and no additional complications in comatose patients who were treated with therapeutic hypothermia (32°C to 34°C), compared to those treated with normothermia (36°C to 37.5°C).36Observational data of pediatric patients resuscitated from IHCA or OHCA37,38 have also shown that ICU duration of stay, neurologic outcomes, and mortality are unchanged with the use of therapeutic hypothermia. Only 1 small study of therapeutic hypothermia in survivors of pediatric asphyxial cardiac arrest39 showed an improvement in mortality at hospital discharge, but with no difference in neurologic outcomes. Results are pending from a large multicenter randomized controlled trial of targeted temperature management for pediatric patients with IHCA (see Therapeutic Hypothermia After Cardiac Arrest).
For infants and children remaining comatose after OHCA, it is reasonable either to maintain 5 days of continuous normothermia (36°C to 37.5°C) or to maintain 2 days of initial continuous hypothermia (32°C to 34°C) followed by 3 days of continuous normothermia. (Class IIa, LOE B-R)
Continuous measurement of temperature during this time period is recommended. (Class I, LOE B-NR)
For infants and children remaining comatose after IHCA, there is insufficient evidence to recommend cooling over normothermia.
Fever (temperature 38°C or higher) should be aggressively treated after ROSC. (Class I, LOE B-NR)
Decreased urine output (<1 mL/kg per hour in infants and children or <30 mL/hour in adolescents) may be caused by prerenal conditions (eg, dehydration, inadequate systemic perfusion), renal ischemic damage, or a combination of factors. Avoid nephrotoxic medications and adjust the dose of medications excreted by the kidneys until you have checked renal function.