Caregiver or parent activation of a medical emergency team or rapid response team in response to changes in a patient’s condition may prevent cardiac or respiratory arrest.
Pediatric medical emergency team/rapid response team systems may be considered in facilities where children with high-risk illnesses are cared for on general in-patient units. (Class IIb, LOE C-LD) (2015 Part 12)
There is no evidence that use of PEWS outside of the critical care unit setting reduces mortality, but one series suggested that it may reduce the cardiac arrest rate.
Respiratory failure is characterized by inadequate ventilation, insufficient oxygenation, or both.
Respiratory failure may be present if you observe any of the following signs:
If the patient has a perfusing rhythm, monitor oxyhemoglobin saturation continuously with a pulse oximeter because clinical recognition of hypoxemia is not reliable.
Pulse oximetry may be unreliable in patients with
Bradycardia commonly occurs during emergency pediatric intubation
The available evidence does not support the routine use of atropine pre-intubation of critically ill infants and children. It may be reasonable for practitioners to use atropine as a premedication in specific emergency intubations when there is higher risk of bradycardia (eg, when giving succinylcholine as a neuromuscular blocker to facilitate intubation). (Class IIb, LOE C-LD) (2015 Part 12)
This recommendation applies only to the use of atropine as a premedication for infants and children during emergency intubation.
Shock results from inadequate blood flow and oxygen delivery to meet tissue metabolic demands.
Hypovolemic shock (including hemorrhagic shock associated with trauma) is the most common type of shock in children. Distributive, cardiogenic, and obstructive shock occur less frequently.
Shock progresses over a continuum of severity, from a compensated to a decompensated state.
Typical signs of compensated shock include:
As compensatory mechanisms fail, signs of inadequate end-organ perfusion develop. In addition to the above, these signs include:
Hypotensive (decompensated) shock is characterized by signs and symptoms consistent with
Note that no single sign confirms the diagnosis of shock.
Tachycardia is a common sign of shock, but it can also result from other causes, such as pain, anxiety, and fever.
Pulses are weak in hypovolemic and cardiogenic shock, but may be bounding in anaphylactic, neurogenic, and septic shock.
Blood pressure may be normal in a child with compensated shock but may decline rapidly when the child decompensates. Like the other signs, hypotension must be interpreted within the context of the entire clinical picture.
For purposes of these guidelines, hypotension is defined as a systolic blood pressure:
Infection-related shock appears to respond differently to fluid bolus than hypovolemic shock. Although there was no benefit demonstrated when restricting fluid therapy in most studies of septic shock, a notable exception was in the Fluid Expansion As Supportive Therapy study conducted in sub-Saharan Africa that reported a survival benefit to fluid restriction in those with severe febrile illness complicated by impaired consciousness, respiratory distress or both, and impaired perfusion. In this population, critical care resources including inotropic support and mechanical ventilation were limited.
These recommendations continue to emphasize appropriate fluid resuscitation for both compensated (detected by physical examination) and decompensated (hypotensive) septic shock.
Before the administration of intravenous fluid boluses, individualized patient evaluation is needed, including physical examination by a clinician and frequent reassessment to determine the appropriate volume of fluid resuscitation.
Integrate clinical signs with patient and locality-specific information about prevalent diseases, vulnerabilities (such as severe anemia and malnutrition), and available critical care resources.
Administration of an initial fluid bolus of 20 mL/kg to infants and children with shock is reasonable, including those with conditions such as severe sepsis (Class IIa, LOE C-LD), severe malaria and Dengue. (Class IIb, LOE B-R) (2015 Part 12)
When caring for children with severe febrile illness (such as those included in the FEAST [Fluid Expansion As Supportive Therapy] trial) in settings with limited access to critical care resources (ie, mechanical ventilation and inotropic support), administration of bolus intravenous fluids should be undertaken with extreme caution because it may be harmful. (Class IIb, LOE B-R) (2015 Part 12)
Etomidate has been shown to facilitate endotracheal intubation in infants and children with minimal hemodynamic effect, but do not use it routinely in pediatric patients with evidence of septic shock. (Class III, LOE B) (2010 Part 14)
There is no added benefit in using colloid (eg, albumin) during the early phase of resuscitation.
Give additional boluses (20 mL/kg) if systemic perfusion fails to improve.
There is no evidence to support the use of a specific isotonic crystalloid. There is insufficient data to make a recommendation for or against use of hypertonic saline for shock associated with head injuries or hypovolemia. (2010 Part 14)
There is insufficient evidence in infants and children to make a recommendation about the best timing or extent of volume resuscitation for children with hemorrhagic shock following trauma. (2010 Part 14)
Children with cardiomyopathy or acute myocarditis who demonstrate high-risk ECG changes (arrhythmias, heart block, ST-segment changes) and/or low cardiac output, are at high-risk for cardiac arrest.
Optimal outcomes from ECMO are achieved in settings with existing ECMO protocols, expertise, and equipment.
Common errors in pediatric trauma resuscitation include:
Involve a qualified surgeon early and, if possible, transport a child with multisystem trauma to a trauma center with pediatric expertise.
The following are special aspects of trauma resuscitation:
Intentional brief hyperventilation may be used as a temporizing rescue therapy if there are signs of impending brain herniation (eg, sudden rise in measured intracranial pressure, dilation of one or both pupils with decreased response to light, bradycardia, and hypertension). However, because hyperventilation and hypocarbia cause cerebral vasoconstriction, they can cause cerebral ischemia.
Suspect thoracic injury in all thoraco-abdominal trauma, even in the absence of external injuries. Tension pneumothorax, hemothorax, or pulmonary contusion may impair oxygenation and ventilation.
Consider intra-abdominal hemorrhage, tension pneumothorax, pericardial tamponade, and spinal cord injury in infants and children, and intracranial hemorrhage in infants, as causes of shock.
For additional information, please refer to the 2018 publication, “Cardiopulmonary Resuscitation in Infants and Children With Cardiac Disease; A Scientific Statement From the American Heart Association.” (2018 AHA Scientific Statement)
Standard prearrest and arrest resuscitation procedures should be followed for infants and children with single ventricle anatomy following Stage I palliation or in the infant or neonate with a univentricular heart and a shunt to augment pulmonary blood flow.
Following resuscitation from cardiac arrest, oxygen administration should be adjusted to balance systemic and pulmonary blood flow, targeting an oxyhemoglobin saturation (SpO2) of approximately 80%.
End-tidal CO2 (ETCO2) during cardiac arrest in the patient with single-ventricle may not be a reliable indicator of CPR quality because pulmonary blood flow and, hence, carbon dioxide brought to the lungs changes rapidly and does not necessarily trend with cardiac output during CPR.
The following recommendations refer to the neonate with single ventricle:
Neonates in a prearrest state due to elevated pulmonary-to-systemic flow ratio prior to Stage I repair might benefit from a PaCO2 of 50 to 60 mm Hg, which can be achieved during mechanical ventilation by reducing minute ventilation, increasing the inspired fraction of CO2, or administering opioids with or without chemical paralysis. (Class IIb, LOE B) (2010 Part 14)
Neonates in a low cardiac output state following stage I repair may benefit from systemic vasodilators such as alpha-adrenergic antagonists (eg, phenoxybenzamine) to treat or ameliorate increased systemic vascular resistance, improve systemic oxygen delivery, and reduce the likelihood of cardiac arrest. (Class IIa, LOE B) (2010 Part 14)
Other drugs that reduce systemic vascular resistance (eg, milrinone or nipride) may also be considered for patients with excessive [pulmonary to systemic flow ratio] Qp:Qs. (Class IIa, LOE B) (2010 Part 14)
Following Stage I repair, evaluation of oxygen delivery and extraction (eg, using central venous oxygen saturation [ScvO2] and near-infrared spectroscopy) may help identify evolving changes in hemodynamics that may herald impending cardiac arrest.
During cardiopulmonary arrest, it is reasonable to consider extracorporeal membrane oxygenation (ECMO) for patients with single ventricle anatomy who have undergone Stage I procedure. (Class IIa, LOE B) (2010 Part 14)
It is unclear whether patients with hemi-Fontan/bi-directional Glenn physiology in cardiac arrest might benefit from ECMO.
For additional information, the reader is referred to the recent scientific statements, “Cardiopulmonary Resuscitation in the Infant or Child with Congenital Heart Disease; A Scientific Statement From the American Heart Association” by Marino et al, and the Guidelines statement “Pediatric Pulmonary Hypertension; Guidelines From the American Heart Association and American Thoracic Society” by Abman et al.
Patients with pulmonary hypertension and a cardiopulmonary arrest require standard PALS therapy, including oxygenation and ventilation.
It may be beneficial to attempt to correct hypercarbia.
Administration of a bolus of isotonic fluid may be useful to maintain preload to the systemic ventricle.
Overdose with local anesthetics, cocaine, narcotics, tricyclic antidepressants, calcium channel blockers, and beta-adrenergic blockers may require specific treatment modalities in addition to the usual resuscitative measures.
Local anesthetics may cause changes in mental status, seizures, arrhythmias, or even cardiac arrest in settings of overdose or inadvertent vascular administration.
Successful treatment of local anesthetic toxicity with intravenous lipid emulsion has been described.
Cocaine may cause chest pain and cardiac rhythm disturbances (including VT and VF), may prolong the action potential and QRS duration, and impairs myocardial contractility.
Treat elevated temperature aggressively because hyperthermia, which may result from cocaine-induced hypermetabolism, is associated with an increase in toxicity.
For coronary vasospasm consider nitroglycerin. (Class IIa, LOE C) (2010 Part 14) A benzodiazepine, and phentolamine (an alpha-adrenergic antagonist) may be considered. (Class IIb, LOE C) (2010 Part 14)
Toxic doses cause cardiovascular abnormalities, including intraventricular conduction delays, heart block, bradycardia, prolongation of the QT interval, ventricular arrhythmias (including torsades de pointes, ventricular tachycardia and ventricular fibrillation), hypotension, seizures, and depressed level of consciousness.
Give 1 to 2 mEq/kg intravenous boluses of sodium bicarbonate (NaHCO3) until arterial pH is >7.45; then provide an infusion of 150 mEq NaHCO3 per liter of D5W to maintain alkalosis.
In cases of severe intoxication increase the pH to 7.50 to 7.55.
For hypotension, give boluses (10 mL/kg each) of normal saline.
If hypotension persists, epinephrine and norepinephrine are more effective than dopamine in raising blood pressure.
Consider Extracorporeal Membrane Oxygenation (ECMO) if high-dose vasopressors do not maintain blood pressure.
Do not administer Class IA (quinidine, procainamide), Class IC (flecainide, propafenone), or Class III (amiodarone and sotalol) antiarrhythmics, which may exacerbate cardiac toxicity. (Class III, LOE C) (2010 Part 14)
Manifestations of toxicity include:
Mild hypotension can be treated with small boluses (5 to 10 mL/kg) of normal saline because myocardial depression may limit the volume of fluid boluses the patient can tolerate.
Infuse 20 mg/kg (0.2 mL/kg) of 10% calcium chloride intravenously over 5 to 10 minutes; if there is a beneficial effect, give an infusion of 20 to 50 mg/kg per hour.
There is insufficient data to recommend for or against an infusion of insulin and glucose or sodium bicarbonate. (2010 Part 14)
Toxic doses of beta-adrenergic blockers cause:
Some beta-adrenergic blockers (eg, propranolol and sotalol) may also prolong the QRS and the QT interval.
Narcotics may cause:
Naloxone reverses the respiratory depression of narcotic overdose (Class I, LOE B) (2010 Part 14) , but in persons with long-term addictions or cardiovascular disease, naloxone may markedly increase heart rate and blood pressure and cause acute pulmonary edema, cardiac arrhythmias (including asystole), and seizures.
Provision of ventilation before administration of naloxone appears to reduce adverse effects.
Intramuscular (rather than intravenous) administration of naloxone may lower the risk of adverse effects by slowing the onset of drug effect.
In the setting of an organized response in an advanced healthcare environment. multiple responders are rapidly mobilized and are capable of simultaneous coordinated action. Resuscitation teams may also have access to invasive patient monitoring that may provide additional information during the performance of basic life support (BLS). Thus, while recommended steps are presented as a sequence, many steps can be performed simultaneously.
The effectiveness of PALS is dependent on high-quality CPR. High quality CPR requires:
Reasons for not performing high-quality CPR may include:
Optimal chest compressions are best delivered with the victim on a firm surface.
Chest compressions should be immediately started by one rescuer, while a second rescuer prepares to provide ventilation with a bag and mask.
Ventilation is extremely important because most cardiac arrests in children are asphyxial, and for such arrests. best results are obtained with a combination of chest compressions and ventilation.
Ventilation is sometimes delayed while rescuers mobilize and assemble equipment (bag, mask, oxygen, airway).
Chest compressions require only the hands of a willing rescuer. Therefore, start CPR with chest compressions immediately, while a second rescuer prepares to provide ventilations. (Class I, LOE C) (2010 Part 14)
While one rescuer performs chest compressions and another provides ventilation, other rescuers should:
The effectiveness of PALS is dependent on high-quality CPR (see below).
In a monitored patient with an indwelling arterial catheter, providers can use an arterial waveform as feedback regarding effectiveness of chest compressions (ie, to evaluate hand position and chest compression depth) and to identify return of spontaneous circulation (ROSC).
When end-tidal CO2 (ETCO2) is monitored, providers can use the ETCO2 to provide indirect evidence of the quality of chest compressions (ie, the ETCO2 can track linearly with cardiac output and pulmonary blood flow generated with chest compressions) and to assist in identification of possible return of spontaneous circulation.
Oropharyngeal and nasopharyngeal airways help maintain an open airway by displacing the tongue or soft palate from the pharyngeal air passages.
It is reasonable to ventilate with 100% oxygen during CPR because there is insufficient information on the optimal inspired oxygen concentration. (Class IIa, LOE C) (2010 Part 14) Note: for information regarding recommended initial inspired oxygen concentration for newborns at birth, see Neonatal Resuscitation, Part 13.
Once the circulation is restored, monitor systemic oxygen saturation.
Provided appropriate equipment is available, once ROSC is achieved, adjust the FiO2 to the minimum concentration needed to achieve an arterial oxyhemoglobin saturation at least 94% with the goal of avoiding hyperoxia while ensuring adequate oxygen delivery. Since an arterial oxyhemoglobin saturation of 100% may correspond to a PaO2 anywhere between ~80 and 500 mmHg, in general it is appropriate to wean the FIO2 when saturation is 100%, provided the oxyhemoglobin saturation can be maintained ≥94%. (Class IIb, LOE C) (2010 Part 14)
Of course, if the infant or child has unrepaired single ventricle or cyanotic congenital heart disease, the target oxygen saturation should be tailored to that appropriate to the infant or child.
Adequate oxygen delivery requires not only adequate arterial oxyhemoglobin saturation but also adequate hemoglobin concentration and cardiac output.
Bag-mask ventilation requires training and periodic retraining in:
Bag mask ventilation is reasonable compared with advanced airway interventions (endotracheal intubation or supraglottic airway) in the management of children during cardiac arrest in the out-of-hospital setting (Class IIa, LOE C-LD) (2019 PALS)
We cannot make a recommendation for or against the use of an advanced airway for in-hospital cardiac arrest management. In addition, no recommendation can be made about which advanced airway intervention is superior in either out-of-hospital or in-hospital cardiac arrest. (2019 PALS)
During CPR in the infant or child who is intubated, ventilate at a rate of about 1 breath every 6 seconds (10 times per minute) without interrupting chest compressions. (Class I, LOE C) (2010 Part 14) It may be reasonable to do the same if an LMA is in place. (Class IIb, LOE C) (2010 Part 14) Note: In 2016, to improve consistency with ACLS recommendations and to simplify the recommendations for providers, the PALS writing group simplified this 2010 recommendation from “1 breath every 6 to 8 seconds (8-10 times per minute)” to 1 breath every 6 seconds (10 times per minute)” as listed here.
In the victim with a perfusing rhythm but absent or inadequate respiratory effort, give 1 breath every 3 to 5 seconds (12 to 20 breaths per minute), using the higher rate for the younger child. (Class I, LOE C) (2010 Part 14). Note: To better match ventilation and perfusion when the infant or child has a perfusing rhythm, a more rapid ventilation rate is recommended than the rate used during CPR.
One way to achieve the correct rate during bag-mask ventilation is to use the mnemonic “squeeze-release-release” at a normal speaking rate.
If an advanced airway is not in place during CPR, pause after each set of 30 chest compressions (1 rescuer) or after each set of 15 chest compressions (2 rescuers) to give 2 breaths.
Deliver each breath with an inspiratory time of approximately 1 second.
Use only the force and tidal volume needed to just make the chest rise visibly (Class I, LOE C) (2010 Part 14); avoid delivering excessive ventilation during cardiac arrest. (Class III, LOE C) (2010 Part 14)
Gastric inflation may cause regurgitation and aspiration of stomach contents, with further compromise oxygenation and ventilation.
The risk of gastric inflation can be decreased by avoiding excessive peak inspiratory pressures, by ventilating slowly and giving only enough tidal volume to just achieve visible chest rise.
If cricoid pressure cannot be applied by the rescuer who is securing the bag to the face, the application of cricoid pressure will require a third rescuer.
Pass a nasogastric or orogastric tube to relieve gastric inflation, especially if oxygenation and ventilation are compromised.
Pass the tube after intubation because a gastric tube interferes with gastroesophageal sphincter function, allowing regurgitation during intubation.
If a gastrostomy tube is present, vent it during bag-mask ventilation to allow gastric decompression.
If skilled rescuers are available, a 2-person technique may provide more effective bag-mask-ventilation than a single-person technique, particularly if there is significant airway obstruction, poor lung compliance or difficulty creating a tight seal between the mask and the face. To provide 2-rescuer ventilation with bag and mask:
Everyone involved with the care of a child with a tracheostomy (parents, school nurses, and home healthcare providers) should know how to:
Parents and providers should be able to ventilate via a tracheostomy tube and verify effectiveness by assessing chest expansion.
The tracheostomy tube is used for ventilation during CPR and manual ventilation, provided the airway is patent and adequate ventilation can be achieved as demonstrated by chest expansion.
If the tracheostomy tube does not allow effective ventilation, quickly suction the lumen. If effective ventilation still cannot be achieved after suctioning, replace it with a tracheostomy tube of the same size. If a clean tube is unavailable, perform mouth-to-stoma or mask-to-stoma ventilations.
If, after replacing the tracheostomy tube providers are still unable to achieve chest rise, the tracheostomy tube must be removed and alternative ventilation methods are needed, such as mouth-to-stoma ventilation or bag-mask ventilation through the nose and mouth (while a rescuer occludes the tracheal stoma).
If the upper airway is patent, bag-mask ventilation via the nose and mouth may be effective if the tracheal stoma is manually occluded.
Endotracheal intubation in infants and children requires special training because the pediatric airway anatomy differs from that of the adult. The likelihood of successful endotracheal tube placement with minimal complications is related to the provider’s length of training, supervised experience in the operating room and in the field, adequate ongoing experience, and the use of rapid sequence intubation (RSI).
Bag mask ventilation is reasonable compared with advanced airway interventions (endotracheal intubation or supraglottic airway) in the management of children during cardiac arrest in the out-of-hospital setting (Class IIa, LOE C-LD) (2019 PALS)
We cannot make a recommendation for or against the use of an advanced airway for in-hospital cardiac arrest management. In addition, no recommendation can be made about which advanced airway intervention is superior in either out-of-hospital or in-hospital cardiac arrest. (2019 PALS)
When bag-mask ventilation (see “Bag-Mask Ventilation,” above) is unsuccessful and when endotracheal intubation is not possible, the LMA is acceptable when used by experienced providers to provide a patent airway and support ventilation. (Class IIa, LOE C) (2010 Part 14)
LMA insertion is associated with a higher incidence of complications in young children compared with complication rates in older children and adults.
To facilitate emergency intubation and reduce the incidence of complications, skilled, experienced providers may use sedatives, neuromuscular blocking agents, and other medications to provide rapid sedation and neuromuscular blockade.
Use RSI only if you are trained, and have experience using these medications and are proficient in the evaluation and management of the pediatric airway in an environment with appropriate monitoring.
If you use RSI you must have a secondary plan to manage the airway in the event that you cannot achieve intubation.
Actual body weight (or if actual weight cannot be determined in an emergency, the weight estimated using a color-coded length-based tape), rather than ideal/predicted body weight for age, should be used for some non-resuscitation medications used for RSI (eg, succinylcholine).
There is insufficient evidence to recommend routine application of cricoid pressure to prevent aspiration during endotracheal intubation in children. (2010 Part 14)
In certain circumstances (eg, poor lung compliance, high airway resistance, or a large glottic air leak) a cuffed endotracheal tube may be preferable to an uncuffed tube, provided that attention is paid to [ensuring appropriate] endotracheal tube size, position, and cuff inflation pressure. (Class IIa, LOE B) (2010 Part 14)
For children up to approximately 35 kg, color-coded, length-based resuscitation tapes enable more accurate estimates of equipment sizes, including endotracheal tube sizes and medication doses than age-based formula estimates. These tapes are accurate even for children of short stature.
In preparation for intubation with either a cuffed or an uncuffed endotracheal tube, confirm availability of tubes with an internal diameter (ID) 0.5 mm smaller and 0.5 mm larger than the estimated size.
During intubation, if the endotracheal tube meets resistance, use a tube 0.5 mm smaller instead.
Following intubation, if there is a large glottic air leak that interferes with oxygenation or ventilation, consider replacing the tube with one that is 0.5 mm larger, or, if an uncuffed tube was used originally, place a cuffed tube of the same size.
Elective replacement of a functional endotracheal tube is associated with risk; the procedure should be undertaken in an appropriate setting by experienced personnel.
An uncuffed endotracheal tube is used for emergency intubation.
Estimates of uncuffed tube sizes are as follows:
If a cuffed tube is used for emergency intubation of an infant less than 1 year of age, it is reasonable to select a 3.0 mm ID tube. For children between 1 and 2 years of age, it is reasonable to use a cuffed endotracheal tube with an internal diameter of 3.5 mm.
(Class IIa, LOE B) (2010 Part 14)
Since no single confirmation technique, including clinical signs or the presence of water vapor in the tube, is completely reliable, use both clinical assessment and confirmatory devices to verify proper tube placement immediately after intubation, [and] again after securing the endotracheal tube, during transport, and each time the patient is moved (eg, from gurney to bed). (Class I, LOE B) (2010 Part 14)
Methods for confirming correct position:
If you are still uncertain of the tube position, perform direct laryngoscopy and visualize the endotracheal tube to confirm that it lies between the vocal cords.
In hospital settings, perform a chest x-ray to verify depth of insertion (ie that the tube is not in a bronchus) and to identify proper position in the mid trachea.
After intubation, secure the tube; there is insufficient evidence to recommend any single method.
After securing the tube, maintain the patient’s head in a neutral position; neck flexion may push the tube deeper into the airway, and neck extension may pull the tube out of the airway.
If an intubated patient’s condition deteriorates, consider the following possibilities (mnemonic DOPE):
When available, exhaled CO2 detection (capnography or colorimetry) is recommended as confirmation of tracheal tube position for neonates, infants, and children with a perfusing cardiac rhythm in all settings (eg, prehospital, emergency department [ED], intensive care unit, ward, operating room) (Class I, LOE C) (2010 Part 14) and during intrahospital or interhospital transport. (Class IIb, LOE C) (2010 Part 14)
A color change or the presence of a capnography waveform confirms tube position in the airway but does not rule out right mainstem bronchus intubation.
During cardiac arrest, if exhaled CO2 is not detected, confirm tube position with direct laryngoscopy, because the absence of [exhaled] CO2 may reflect very low pulmonary blood flow rather than tube misplacement. (Class IIa, LOE C) (2010 Part 14)
Accuracy of colorimetric end-tidal CO2 detector may be affected by the following:
If capnography is not available, an esophageal detector device may be considered to confirm endotracheal tube placement in children weighing >20 kg with a perfusing rhythm), but the data are insufficient to make a recommendation for or against its use in children during cardiac arrest. (Class IIb, LOE B) (2010 Part 14)
For patients with severe airway obstruction above the level of the cricoid cartilage, transtracheal catheter oxygenation and ventilation may be considered if standard methods to manage the airway are unsuccessful.
Note that transtracheal ventilation primarily supports oxygenation, because delivered tidal volumes are usually too small to effectively remove carbon dioxide.
This technique [transtracheal catheter oxygenation and ventilation] is intended for temporary use while a more effective airway is obtained. Attempt this procedure only after proper training and with appropriate equipment. (Class IIb, LOE C) (2010 Part 14)
A properly sized suction device with an adjustable suction regulator should be available.
Do not insert the suction catheter beyond the end of the endotracheal tube
To avoid injuring the mucosa, use a maximum suction force of -80 to -120 mm Hg for suctioning the airway via an endotracheal tube. Higher suction pressures applied through large-bore non-collapsible suction tubing and semirigid pharyngeal tips are used to suction the mouth and pharynx.
PBLS and PALS recommendations for infants differ from those for the newly born (ie, in the delivery room and during the transition to extrauterine life occurring during the first hours after birth) and neonates during the initial hospitalization in the NICU.
There are no definitive scientific data to identify the optimal compression to ventilation ratio, so the following expert consensus recommendation is made for ease of teaching.
For newborns who require CPR in settings other than the delivery room or NICU (eg, prehospital, ED, pediatric intensive care unit, cardiac intensive care unit etc.), it may be reasonable to use [PBLS] infant CPR guidelines: 2 rescuers provide continuous chest compressions with asynchronous ventilation if an advanced airway is in place, or use a 15:2 compression to ventilation ratio if no advanced airway is in place. (Class IIb, LOE C) (2010 Part 14)
It is reasonable to resuscitate newborns with a primary cardiac etiology of arrest, regardless of location, according to [PBLS] infant guidelines, with emphasis on [high-quality] chest compressions. (Class IIa, LOE C) (2010 Part 14)
Extracorporeal CPR (ie, extracorporeal membrane oxygenation [ECMO] as a form of mechanical circulatory rescue for failed CPR) may be considered for pediatric patients with cardiac diagnoses who have in-hospital cardiac arrest in settings with existing extracorporeal membrane oxygenation protocols, expertise and equipment. (Class IIb, LOE C-LD) (2019 PALS)
There is insufficient evidence to recommend for or against the use of extracorporeal CPR for pediatric patients experiencing out-of-hospital cardiac arrest or for pediatric patients with noncardiac disease experiencing in-hospital cardiac arrest refractory to conventional CPR. (2019 PALS)
In the text below, box numbers identify the corresponding step in the algorithm (Figure 1).
Step 1: As soon as the child is found to be unresponsive with no breathing or only gasping, call for help, send for a defibrillator (manual or AED), and start CPR (with supplementary oxygen if available). Attach ECG monitor or AED pads as soon as available.
During resuscitation, place emphasis on the provision of high-quality CPR including:
While CPR is provided, determine the cardiac rhythm from the ECG or, if you are using an AED, the device will tell you whether the rhythm is “shockable” (eg, ventricular fibrillation [VF] or pulseless ventricular tachycardia [pVT]) or “non-shockable” (eg, asystole or PEA).
It may be necessary to temporarily interrupt chest compressions to determine the child’s rhythm.
Step 10: While 2 minutes of high-quality CPR is provided, another rescuer obtains vascular access and delivers epinephrine, 0.01 mg/kg (0.1 mL/kg of 1:10 000 solution); maximum of 1 mg (10 mL). Epinephrine should be administered promptly.
CPR by two or more rescuers once an advanced airway is in place:
Check rhythm every 2 minutes with minimal interruptions in chest compressions.
If the rhythm is “non-shockable,” continue with cycles of CPR and epinephrine administration every 3-5 minutes until there is evidence of ROSC or you decide to terminate the effort.
If at any time the rhythm becomes “shockable,” give a shock (go to Step 5 if epinephrine has not been administered in previous 2 minutes of CPR, or Step 7 if epinephrine was administered in previous 2 minutes of CPR) and immediately resume chest compressions for 2 minutes before rechecking the rhythm (see “Shockable Rhythm,” Steps 5 and 7, below).
Search for and treat reversible causes (see “Reversible Causes” in the Doses/Details box in Figure 1).
In adults with sudden VF/pulseless VT OHCA, the probability of survival declines by 7% to 10% for each minute of arrest without CPR and defibrillation.
Survival is better if early, high-quality CPR and defibrillation are provided as soon as possible.
The outcome of shock delivery is best if rescuers minimize the time between last compression and shock delivery, and between shock delivery and resumption of compressions, so training, practice, and coordination are required to minimize interruptions in chest compressions.
Please refer to Figure 1 for the Steps referenced below.
Step 2: When a shockable rhythm is detected, provide CPR until the defibrillator is charged and ready to deliver a shock.
Step 3: “Clear” the victim and give 1 shock (2 J/kg) as quickly as possible after compressions are interrupted.
Step 4: After shock delivery, resume CPR immediately, beginning with chest compressions. Provide 2 minutes of CPR. Note: In in-hospital settings with continuous invasive monitoring, this sequence may be modified at the expert provider’s discretion.
If a sufficient number of rescuers is present, establish vascular (IO or IV) access.
Step 5: After 2 minutes of CPR, check the rhythm.
Step 6: Administer epinephrine during chest compressions (to help circulate the drug), but the timing of drug administration is less important than the need to minimize interruptions in chest compressions.
Providers typically administer epinephrine during every other 2-minute period of CPR; this will result in doses administered slightly more than 4 minutes apart.
When multiple rescuers are present, it is helpful if a dedicated rescuer prepares drug doses before the rhythm is checked so the appropriate drug can be administered soon after CPR is resumed.
Just prior to the next rhythm check, the rescuer operating the defibrillator should prepare to recharge the defibrillator (to 4 J/kg dose or more with a maximum dose not to exceed 10 J/kg or the adult dose, whichever is lower).
Step 7: After 2 minutes of CPR, check the rhythm.
Step 8: During CPR after shock delivery give either amiodarone or lidocaine. It is helpful if the drug has been prepared before the previous rhythm check, so it can be administered soon after CPR is resumed.
Note: If at any time the rhythm check reveals a “non-shockable” rhythm, determine if an organized rhythm is present. If an organized rhythm is present, check a pulse.
If defibrillation is successful but VF or pulseless VT recurs, resume CPR and give another bolus of amiodarone (or of lidocaine if lidocaine was previously given) before trying to defibrillate with the previously successful shock dose.
During resuscitation, the delivery of high-quality CPR is critical. Components of high-quality CPR are:
Note: When two or more rescuers are present, they should switch the compressor role approximately every 2 minutes to prevent compressor fatigue and deterioration in quality and rate of chest compressions.
Search for and treat reversible causes. See “Reversible Causes” in Grey and White column of boxes on the right side of Figure 1.
Defibrillators are either manual or automated (AED), with monophasic or biphasic waveforms.
AEDs in institutions caring for children at risk for arrhythmias and cardiac arrest (eg, hospitals, EDs) must be capable of recognizing pediatric cardiac rhythms and should ideally have a method of adjusting the energy level for children.
Use the largest paddles or self-adhering electrodes that will fit on the child’s chest without touching. When possible, leave about 3 cm between the paddles or electrodes.
Paddles and self- adhering pads appear to be equally effective.
Self-adhering pads should be pressed firmly on the chest so that the gel on the pad completely touches the child’s chest.
An appropriate paddle or self-adhesive pad size is:
The electrode-chest wall interface is part of the self-adhesive pad.
When using paddles, apply electrode gel liberally to the paddles. Do not use saline-soaked pads, ultrasound gel, bare paddles, or alcohol pads.
Follow package directions for placement of self-adhesive AED or monitor/defibrillator pads.
Place manual paddles over the right side of the upper chest and the apex of the heart (to the left of the nipple over the left lower ribs) so the heart is between the two paddles. Apply firm pressure.
There is no advantage to use of an anterior-posterior position of the paddles.
It is reasonable to use an initial dose of 2 to 4 J/kg of monophasic or biphasic energy for defibrillation (Class IIa, LOE C-LD) (2015 Part 12), but for ease of teaching, an initial dose of 2 J/kg may be considered. (Class IIb, LOE C-EO) (2015 Part 12)
For subsequent energy levels, a dose of 4 J/kg may be reasonable and higher energy levels may be considered, though not to exceed 10 J/kg or the adult maximum dose. (Class IIb, LOE C-LD) (2015 Part 12)
In addition to AEDs that deliver shock doses appropriate for adolescents and adults, systems and institutions that have AED programs and that care for children should use AEDs with a high specificity to recognize pediatric shockable rhythms and a pediatric attenuating system that can be used for infants and children up to approximately 25 kg (approximately 8 years of age).
In infants <1 year of age, use of a manual defibrillator is preferred to use of an AED, because the manual defibrillator will allow adjustment of shock dose to smaller doses (and smaller incremental increases in subsequent doses if needed). If a manual defibrillator is not available, an AED with a dose attenuator may be used.
This polymorphic VT is associated with a long QT interval. Prolonged QT interval may be congenital or may result from toxicity with type IA antiarrhythmics (eg, procainamide, quinidine, and disopyramide) or type III antiarrhythmics (eg, sotalol and amiodarone), tricyclic antidepressants (see below), digitalis, or drug interactions.
Polymorphic VT quickly deteriorates to pulseless VT. Initiate CPR and proceed with defibrillation when pulseless “shockable” arrest develops.
Regardless of the cause, treat torsades de pointes with a rapid (over several minutes) IV infusion of magnesium sulfate (25 to 50 mg/kg; maximum single dose 2 g).
If the partial pressure of ETCO2 is consistently less than 15 mmHg, efforts should focus on improving CPR quality, particularly improving chest compressions and ensuring that the victim does not receive excessive ventilation.
Monitor cardiac rhythm as soon as possible so both normal and abnormal cardiac rhythms are identified and followed. Continuous monitoring is helpful in tracking responses to treatment and changes in clinical condition.
When appropriately trained personnel are available, echocardiography may be considered to identify patients with potentially treatable causes of the arrest, particularly pericardial tamponade, and inadequate ventricular filling. (Class IIb, LOE C) (2010 Part 14)
Minimize interruption of CPR while performing echocardiography.
Limit the time spent attempting to establish peripheral venous access in a critically ill or injured child.
IO access is a rapid, safe, effective, and acceptable route for vascular access in children, and it is useful as the initial vascular access in cases of cardiac arrest. (Class I, LOE C) (2010 Part 14)
Peripheral IV access is an acceptable route for drug and fluid administration during resuscitation, provided it can be placed rapidly.
Placement of a central venous catheter is not recommended as the initial route of vascular access during an emergency. Although a central venous catheter can provide more secure long-term access, its placement requires training and experience, and the procedure can be time-consuming.
If both central and peripheral accesses are available, administer medications into the central circulation since some medications (eg, adenosine) are more effective when administered closer to the heart, and others (eg, calcium, amiodarone, procainamide, sympathomimetics) may be irritating when infused into a peripheral vein.
The length of a central catheter can contribute to increased resistance, making it more difficult to push boluses of fluid rapidly through a multi-lumen central catheter than a peripheral catheter.
Lipid- soluble drugs, such as lidocaine, epinephrine, atropine, and naloxone (mnemonic “LEAN”) can be administered via an endotracheal tube if vascular access (IO or IV) is not possible.
Non-lipid-soluble drugs (eg, sodium bicarbonate and calcium) may injure the airway; they should not be administered via the endotracheal route.
The effects of medications may not be uniform with tracheal administration as compared with intravenous administration.
To administer drugs via endotracheal route when CPR is in progress, stop chest compressions briefly, administer the medication, and follow with a flush of at least 5 mL of normal saline and 5 consecutive positive pressure breaths, then resume CPR.
Optimal endotracheal doses of medications are unknown; in general expert consensus recommends doubling or tripling the dose of lidocaine, atropine or naloxone given via the endotracheal tube. For epinephrine, a dose ten times the intravenous dose (0.1 mg/kg or 0.1 mL/kg of 1:1,000 concentration) is recommended (see Table 1).
Tapes with precalculated doses printed at various patient lengths are more accurate than age-based or observer (parent or provider) estimate-based methods in the prediction of body weight.
To calculate the dose of resuscitation medications, use the child’s weight if it is known.
Therefore, regardless of the patient’s habitus, use the actual body weight for calculating initial resuscitation drug doses or use a body length tape with precalculated doses. (Class IIb, LOE C) (2010 Part 14)
There are no data regarding the safety or efficacy of adjusting the doses of resuscitation medications in obese patients. While use of the actual body weight in calculation of drug doses in obese patients may result in potentially toxic doses, use of a length-based tape to estimate drug dose may result in inadequate doses of some medications for obese patients, because length-based tapes estimate the 50th percentile weight for length (ie, ideal body weight), which will be a weight much lower than that of the obese patient.
When administering resuscitation drugs for both nonobese and obese patients, expert providers may consider adjusting doses to achieve the desired therapeutic effect.
In general, the doses of resuscitation drugs administered to a child should not exceed the standard doses of the drugs recommended for adult patients.
During cardiac arrest, vasopressors can help restore spontaneous circulation by increasing coronary perfusion pressure and helping maintain cerebral perfusion (see Table 1). However, they also cause intense vasoconstriction and increase myocardial oxygen consumption, which might be detrimental.
See Table 1
Adenosine causes a temporary atrioventricular (AV) node conduction block and interrupts reentry circuits that involve the AV node.
The drug has a wide safety margin because of its short half-life.
Adenosine should be given only IV or IO, followed by a rapid saline flush to promote rapid drug delivery to the central circulation.
If adenosine is given IV, it should be administered at a vascular access site as close to the heart as possible.
Amiodarone slows AV conduction, prolongs the AV refractory period and QT interval, and slows ventricular conduction (widens the QRS).
Expert consultation is strongly recommended prior to administration of amiodarone to a pediatric patient with a perfusing rhythm.
If the patient is in VF/pulseless VT, give the drug as a rapid bolus.
If the patient has a perfusing rhythm, administer the drug as slowly (over 20 to 60 minutes) as the patient’s clinical condition allows.
Other potential complications of amiodarone include bradycardia and torsades de pointes ventricular tachycardia.
Amiodarone should not be administered together with another drug that causes QT prolongation, such as procainamide, without expert consultation.
Atropine sulfate is a parasympatholytic drug that accelerates sinus or atrial pacemakers and increases the speed of AV conduction. It may be administered for the treatment of symptomatic bradycardia associated with increased vagal tone or primary AV conduction block (ie, not secondary to factors such as hypoxia).
The available evidence does not support the routine use of atropine pre-intubation of critically ill infants and children. It may be reasonable for practitioners to use atropine as a premedication in specific emergency intubations when there is a higher risk of bradycardia (eg, when giving succinylcholine as a neuromuscular blocker to facilitate intubation). (Class IIb, LOE C-LD) (2015 Part 12)
Note: Larger than recommended doses may be required in special circumstances such as organophosphate poisoning or exposure to nerve gas agents.
Routine calcium administration in cardiac arrest provides no benefit and may be harmful.
Calcium administration is not recommended for pediatric cardiopulmonary arrest in the absence of documented hypocalcemia, calcium channel blocker overdose, hypermagnesemia, or hyperkalemia. (Class III, LOE B) (2010 Part 14)
If calcium administration is indicated during cardiac arrest, either calcium chloride or calcium gluconate may be considered.
Hepatic dysfunction does not appear to alter the ability of calcium gluconate to raise serum calcium levels.
The alpha-adrenergic-mediated vasoconstriction of epinephrine increases aortic diastolic pressure and thus coronary perfusion pressure, a critical determinant of successful resuscitation from cardiac arrest.
At low doses, the beta-adrenergic effects may predominate, leading to decreased systemic vascular resistance; in the doses used during cardiac arrest, the vasoconstrictive alpha-effects predominate.
Do not administer catecholamines and sodium bicarbonate simultaneously through an IV catheter or tubing because alkaline solutions such as the bicarbonate inactivate the catecholamines.
In patients with a perfusing rhythm, epinephrine causes tachycardia; it may also cause ventricular ectopy, tachyarrhythmias, vasoconstriction, and hypertension.
Because infants have a relatively high glucose requirement and low glycogen stores, they may develop hypoglycemia when energy requirements rise.
Lidocaine decreases automaticity and suppresses ventricular arrhythmias.
Lidocaine toxicity includes myocardial and circulatory depression, drowsiness, disorientation, muscle twitching, and seizures, especially in patients with poor cardiac output and hepatic or renal failure.
Magnesium is indicated for the treatment of documented hypomagnesemia or for torsades de pointes (polymorphic VT associated with long QT interval). There is insufficient evidence to recommend for or against the routine administration of magnesium during cardiac arrest.
Magnesium produces vasodilation and may cause hypotension if administered rapidly.
Procainamide prolongs the refractory period of the atria and ventricles and depresses conduction velocity.
Prior to using procainamide for a hemodynamically stable patient, expert consultation is strongly recommended.
Infuse procainamide very slowly (over 30 to 60 minutes) while monitoring the ECG and blood pressure.
Decrease the infusion rate if there is prolongation of the QT interval, or heart block.
Stop the infusion if the QRS widens to >50% of baseline or hypotension develops.
Do not administer together with another drug causing QT prolongation, such as amiodarone, without expert consultation.
Sodium bicarbonate may be administered for the treatment of some toxidromes or special resuscitation situations such as hyperkalemic cardiac arrest.
During cardiac arrest or severe shock, arterial blood gas analysis may not accurately reflect tissue and venous acidosis.
Excessive sodium bicarbonate may impair tissue oxygen delivery; cause hypokalemia, hypocalcemia, hypernatremia, and hyperosmolality; decrease the VF threshold; and impair cardiac function.
There is insufficient evidence to make a recommendation for or against the routine use of vasopressin during cardiac arrest.
Although there are factors associated with better or worse outcomes, no single factor studied predicts the outcome with sufficient accuracy to recommend termination or continuation of CPR.
Box numbers in the text below refer to the corresponding boxes in the PALS Bradycardia Algorithm (see Figure 2, PALS Bradycardia with a Pulse and Poor Perfusion Algorithm).
If at any time the patient develops pulseless arrest, see the PALS Pulseless Arrest Algorithm.
Emergency treatment of bradycardia is indicated when the low heart rate results in cardiovascular compromise. Signs of cardiopulmonary compromise include hypotension, acutely altered mental status and signs of shock.
Box 1: Support a patent airway, breathing, and circulation as needed. Administer oxygen, attach an ECG monitor/defibrillator, and obtain vascular access.
Box 2: Reassess the patient to determine if bradycardia persists despite verification of adequate airway, oxygenation and ventilation. If cardiorespiratory compromise persists despite adequate oxygenation and ventilation, check heart rate.
Box 3: If heart rate is <60 beats per minute with poor perfusion despite effective ventilation with oxygen, begin CPR.
Box 4a: If, at any time pulses, perfusion, and respirations are adequate, no emergency treatment is necessary.
Continue to monitor the patient and consider expert consultation.
Box 4: After 2 minutes reevaluate the patient to determine if bradycardia and signs of hemodynamic compromise persist. Verify that the support is adequate (eg, check airway, oxygen source, and effectiveness of ventilation). If bradycardia persists, see Box 5 for additional therapy.
Box 5: Recommendations are listed below and include epinephrine. Atropine is indicated only if the bradycardia is associated with increased vagal tone or primary atrioventricular conduction block; it is not effective in the treatment of hypoxia-induced bradycardia. Emergency transcutaneous pacing may be lifesaving (see below) but is not useful for asystole or bradycardia associated with myocardial hypoxic/ischemic insult or respiratory failure.
If bradycardia persists or responds only transiently, give epinephrine IV (or IO) 0.01 mg/kg (0.1 mL/kg of 1:10 000 solution) or if IV/IO access not available, give endotracheally 0.1 mg/kg (0.1 mL/kg of 1:1 000 solution). (Class I, LOE B) (2010 Part 14)
If bradycardia is due to increased vagal tone or primary AV conduction block (ie, not secondary to factors such as hypoxia), give IV/IO atropine 0.02 mg/kg (minimum dose: 0.1 mg; maximum dose: 0.5 mg) or an endotracheal dose of 0.04 to 0.06 mg/kg. (Class I, LOE C) (2010 Part 14)
Emergency transcutaneous pacing may be lifesaving if the bradycardia is due to complete heart block or sinus node dysfunction unresponsive to ventilation, oxygenation, chest compressions, and medications, especially if it is associated with congenital or acquired heart disease. (Class IIb, LOE C) (2010 Part 14)
The Pediatric Tachycardia with a Pulse and Poor Perfusion Algorithm is, as titled, for patients with a pulse and poor perfusion. NOTE: If there are signs of poor perfusion and pulses are not palpable, proceed to the PALS Pulseless Arrest Algorithm (see Figure 1).
The box numbers in the text below correspond to the numbered boxes in the Pediatric Tachycardia with a Pulse and Poor Perfusion Algorithm (see Figure 3).
Box 1: In general, providers begin caring for any infant or child in distress by ensuring that the airway is patent and breathing is adequate, and by administering oxygen. A cardiac monitor can help identify the rhythm and assessment of blood pressure and pulse oximetry will provide additional information to identify and treat the underlying causes of the tachycardia. Establishment of IV/IO access will help treatment, and a 12-lead ECG will be useful in further evaluating the tachycardia, but if severe distress is present, support of airway, oxygenation and ventilation is the first priority.
Box 2: Evaluate 12-lead ECG and assess QRS duration to determine if it is narrow (≤ 0.09 sec) or wide (>0.09 sec).
Box 3: For narrow-complex (QRS ≤ 0.09 Seconds) tachycardia, evaluate rhythm with 12-lead ECG or monitor, and the patient’s clinical presentation and history to differentiate probable sinus tachycardia from probable supraventricular tachycardia (SVT).
Box 4: If there is a known cause for the tachycardia (eg, fever, shock, hypoxemia), the P waves are present and normal, the R-R interval is variable, but the P-R interval is constant, and the rate is <180/min in children and <220/min in infants (these are not absolute thresholds), the rhythm is probable sinus tachycardia. Go to Box 6 for treatment.
Box 5: For treatment of sinus tachycardia, search for and treat reversible causes.
Box 6: If the history is vague and non-specific with a history of abrupt rate changes and no known associated cause such as fever, the P waves are absent or abnormal, the heart rate is not variable, and the rate is ≥180/min in children and ≥220/min in infants (these are not absolute thresholds), the rhythm is probable supraventricular tachycardia. Go to Boxes 7 and 8 for treatment.
Monitor the rhythm during therapy to evaluate the effect of interventions. The choice of therapy is determined by the patient’s degree of hemodynamic instability.
Box 7: Attempt vagal stimulation unless patient hemodynamically unstable, but do not delay chemical or electrical cardioversion.
To perform vagal stimulation:
Box 8: IF IV/IO access is present or immediately available, give adenosine. If IV/IO access not available or adenosine ineffective, provide synchronized cardioversion. If infant or child is extremely unstable, provide immediate synchronized cardioversion.
An IV/IO dose of Verapamil, 0.1 to 0.3 mg/kg is also effective in terminating SVT in older children, but it should not be used in infants without expert consultation because it may cause potential myocardial depression, hypotension, and cardiac arrest. (Class III, LOE C) (2010 Part 14)
If the patient is hemodynamically unstable or if adenosine is ineffective, perform electric synchronized cardioversion. Use sedation, if possible. Start with a dose of 0.5 to 1 J/kg. If unsuccessful, increase the dose to 2 J/kg. (Class IIb, LOE C) (2010 Part 14)
If a second shock is unsuccessful or the tachycardia recurs quickly, consider giving amiodarone or procainamide before a third shock.
Consider amiodarone 5 mg/kg IO/IV [over 20 to 60 minutes ] or procainamide 15 mg/kg IO/IV [over 30 to 60 minutes] for a patient with SVT unresponsive to vagal maneuvers and adenosine and/or electric cardioversion; for hemodynamically stable patients, expert consultation is strongly recommended prior to administration. (Class IIb, LOE C) (2010 Part 14)
Both amiodarone and procainamide must be infused slowly while the ECG and blood pressure are monitored; speed of administration is determined by the level of urgency. If there is no effect and there are no signs of toxicity, give additional doses (see Figure 1).
Avoid the simultaneous use of amiodarone and procainamide without expert consultation.
Box 9: Wide-complex (QRS > 0.09 seconds) tachycardia often originates in the ventricles (ventricular tachycardia) although it may be supraventricular in origin, with aberrant intraventricular conduction causing the widening of the QRS complex.
Because all anti-arrhythmic therapies have a potential for serious adverse effects, consultation with an expert in pediatric arrhythmias is strongly recommended before treating children who are hemodynamically stable.
Box 10: Determine if cardiovascular compromise (hypotension, acutely altered mental status and signs of shock) is present; if so, proceed immediately to synchronized cardioversion. If not, consider further rhythm evaluation (Box 12).
Box 11: Provide synchronized cardioversion. Administer sedation if possible, but do not delay cardioversion.
In hemodynamically unstable patients, electric cardioversion is recommended using a starting energy dose of 0.5 to 1 J/kg. If that fails, increase the dose to 2 J/kg. (Class 1, LOE C) (2010 Part 14) Do not delay cardioversion.
Box 12: If the child with wide-complex tachycardia is hemodynamically stable, adenosine may be useful in differentiating SVT from VT and converting wide-complex tachycardia of supraventricular origin.
Box 13: Expert consultation is strongly advised before further drug administration in the child with wide-complex tachycardia. Pharmacologic conversion may be achieved with either intravenous amiodarone (5 mg/kg over 20 to 60 minutes) or procainamide (15 mg/kg given over 30 to 60 minutes) while monitoring ECG and blood pressure. Stop or slow the infusion if there is a decline in blood pressure or the QRS widens (Box 13).
Most parents would like to be given the opportunity to be present during resuscitation of their child, and some studies suggest that if they are present it can assist in the grieving process. Members of the resuscitation team must be sensitive to the presence of family members, and one person should be assigned to remain with the family to comfort, answer questions, and support the family.
If the presence of family members creates undue staff stress or is considered detrimental to the resuscitation, then family members should be respectfully asked to leave.
(Class IIa, LOE C) (2010 Part 14)
There are no reliable predictors of outcome to guide when to terminate resuscitative efforts in children.
Clinical variables associated with survival include:
None of these associations, however, predict outcome.
The goals of post cardiac arrest care are:
Patients require frequent reassessment during post-cardiac care, because cardiorespiratory status and organ function may deteriorate. For additional information, the reader is referred to the recent scientific statement, “Pediatric Post-Cardiac Arrest Care: A Scientific Statement from the American Heart Association.”
For infants and children between 24 hours and 18 years of age who remain comatose after OHCA or IHCA, it is reasonable to use either Targeted Temperature Management 32°C to 34°C followed by Targeted Temperature Management 36°C to 37.5°C or to use Targeted Temperature Management 36°C to 37.5°C. (Class IIa, LOE B-NR) (2019 PALS)
Provided appropriate equipment is available, once ROSC is achieved, adjust the FiO2 to the minimum concentration needed to achieve an arterial oxyhemoglobin saturation at least 94% with the goal of avoiding hyperoxia while ensuring adequate oxygen delivery. Since an arterial oxyhemoglobin saturation of 100% may correspond to a PaO2 anywhere between ~80 and 500 mmHg, in general it is appropriate to wean the FIO2 when saturation is 100%, provided the oxyhemoglobin saturation can be maintained ≥94%.
(Class IIb, LOE C) (2010 Part 14)
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.
Note that if the patient has a single ventricle or cyanotic heart disease, the target oxygen saturation must be tailored to the range appropriate for that patient. (Cardiopulmonary Resuscitation in the Infant or Child with Congenital Heart Disease; A Scientific Statement From the American Heart Association” by Marino et al)
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) (2015 Part 12)
Consider obtaining arterial lactate and central venous oxygen saturation to assess adequacy of tissue oxygen delivery.
Myocardial dysfunction and vascular instability are common after resuscitation from cardiac arrest.
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) (2015 Part 12)
Initially following return of spontaneous circulation after cardiac arrest other than arrest associated with septic shock, systemic and pulmonary vascular resistances are often increased.
Post-cardiac arrest 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 (see Table 2).
Low-dose epinephrine infusions (<0.3 mcg/kg per minute) generally produce beta-adrenergic actions (tachycardia, potent inotropy, and decreased systemic vascular resistance).
Higher-dose epinephrine infusions (>0.3 mcg/kg per minute) typically cause alpha- adrenergic vasoconstriction.
Because there is great inter-patient variability in response to epinephrine infusion, 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.
Dopamine can produce direct dopaminergic effects and indirect beta- and alpha-adrenergic effects through stimulation of norepinephrine release.
Typically, a dopamine dose of 2 to 20 mcg/kg per minute is used.
At higher doses (>5 mcg/kg per minute), dopamine stimulates cardiac alpha-adrenergic receptors, but this effect may be reduced in infants and in patients with chronic congestive heart failure.
Dopamine infusion doses >20 mcg/kg per minute may result in excessive vasoconstriction.
Dobutamine has a relatively selective effect on beta1- and beta 2-adrenergic receptors as the result of effects of the two dobutamine isomers; one is an alpha-adrenergic agonist, and the other is an alpha-adrenergic antagonist. Dobutamine increases myocardial contractility and can decrease peripheral vascular resistance.
Titrate the infusion to improve cardiac output and blood pressure associated with poor myocardial function.
Norepinephrine is a potent vasopressor that produces peripheral vasoconstriction. Titrate the infusion to treat shock with low systemic vascular resistance (eg, septic, anaphylactic, spinal, 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.
Additional fluid administration may be required to support cardiac output and blood pressure in the presence of vasodilation.
Milrinone is an inodilator that augments cardiac output with little effect on myocardial oxygen demand. It has both inotropic and vasodilatory effects.
Administration of fluids may be required to support cardiac output and blood pressure in the presence of vasodilation.
Inodilators have a long half-life and there may be a delay in reaching steady-state hemodynamic effects after the infusion rate is changed. In cases of toxicity the cardiovascular effects may persist for several hours even after the infusion isdiscontinued.
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.
EEGs performed within the first 7 days after pediatric cardiac arrest may be considered in prognosticating neurologic outcome at the time of hospital discharge but should not be used as the sole criterion. (Class IIb, LOE C-LD) (2015 Part 12)
Ideally post-cardiac arrest care should be provided by a trained team from a pediatric tertiary care facility.
Contact such a team as early as possible during the resuscitation attempt and coordinate transportation with the receiving unit.
Transport team members should be trained and experienced in the care of critically ill and injured children and supervised by a pediatric emergency medicine or pediatric critical care physician.
The mode of transport and composition of the team should be established for each system, based on the care required by each patient.
When sudden unexplained cardiac arrest occurs in children and young adults, obtain a complete past medical and family history (including a history of syncopal episodes, seizures, unexplained accidents or drownings, or sudden unexpected death at <50 years old) and review patient’s previous ECGs.
Channelopathies are dysfunctional myocyte ion channels that result in abnormal depolarization and repolarization of myocardial cells and predispose to arrhythmias. These channelopathies are found in a significant number of children and young adults with sudden cardiac death and no cause of death found with routine autopsy. If channelopathies are identified prior to sudden death or in family members of patients who die as the result of a sudden arrhythmia caused by a channelopathy, appropriate treatment is possible to reduce the risk of sudden death.
All infants, children, and young adults with sudden unexpected death should, where resources allow, have an unrestricted, complete autopsy, preferably performed by a pathologist with training and experience in cardiovascular pathology. Consider appropriate preservation and genetic analysis of tissue to determine the presence of a channelopathy.
Allan R. de Caen, Chair; Marc D. Berg; Leon Chameides; Cheryl K. Gooden; Robert W. Hickey; Halden F. Scott; Robert M. Sutton; Janice A. Tijssen; Alexis Topjian; Élise W. van der Jagt; Stephen M. Schexnayder; Ricardo A. Samson
Monica E. Kleinman, Chair; Leon Chameides; Stephen M. Schexnayder; Ricardo A. Samson; Mary Fran Hazinski; Dianne L. Atkins; Marc D. Berg; Allan R. de Caen; Ericka L. Fink; Eugene B. Freid; Robert W. Hickey; Bradley S. Marino; Vinay M. Nadkarni; Lester T. Proctor; Faiqa A. Qureshi; Kennith Sartorelli; Alexis Topjian; Elise W. van der Jagt; Arno L. Zaritsky
The American Heart Association requests that this document be cited as follows:
© Copyright 2015 American Heart Association, Inc.