Part 14: Pediatric Advanced Life Support
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
- BLS Considerations During PALS
- Emergency Fluids and Medications
- Medications (See Table 1)
- Pulseless Arrest
- Special Resuscitation Situations
- Children With Special Healthcare Needs
- Postresuscitation Stabilization (Post Cardiac Arrest Care)
- Interhospital Transport
- Family Presence During Resuscitation
- Termination of Resuscitative Efforts
- Sudden Unexplained Deaths
- Figures & Tables
- Info & Metrics
In contrast to adults, cardiac arrest in infants and children does not usually result from a primary cardiac cause. More often it is the terminal result of progressive respiratory failure or shock, also called an asphyxial arrest. Asphyxia begins with a variable period of systemic hypoxemia, hypercapnea, and acidosis, progresses to bradycardia and hypotension, and culminates with cardiac arrest.1
Another mechanism of cardiac arrest, ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), is the initial cardiac rhythm in approximately 5% to 15% of pediatric in-hospital and out-of-hospital cardiac arrests;2,–,9 it is reported in up to 27% of pediatric in-hospital arrests at some point during the resuscitation.6 The incidence of VF/pulseless VT cardiac arrest rises with age.2,4 Increasing evidence suggests that sudden unexpected death in young people can be associated with genetic abnormalities in myocyte ion channels resulting in abnormalities in ion flow (see “Sudden Unexplained Deaths,” below).
Since 2010 marks the 50th anniversary of the introduction of cardiopulmonary resuscitation (CPR),10 it seems appropriate to review the progressive improvement in outcome of pediatric resuscitation from cardiac arrest. Survival from in-hospital cardiac arrest in infants and children in the 1980s was around 9%.11,12 Approximately 20 years later, that figure had increased to 17%,13,14 and by 2006, to 27%.15,–,17 In contrast to those favorable results from in-hospital cardiac arrest, overall survival to discharge from out-of-hospital cardiac arrest in infants and children has not changed substantially in 20 years and remains at about 6% (3% for infants and 9% for children and adolescents).7,9
It is unclear why the improvement in outcome from in-hospital cardiac arrest has occurred, although earlier recognition and management of at-risk patients on general inpatient units and more aggressive implementation of evidence-based resuscitation guidelines may have played a role. Implementation of a formal pediatric medical emergency team (MET) or rapid response team (RRT) as part of an emergency response system for a deteriorating inpatient has been shown to significantly decrease the incidence of cardiac and respiratory arrests, as well as hospital mortality rates in some large children's hospitals.18,–,21 Such teams, often consisting of providers with expertise in assessment and initial management of acutely ill patients (critical-care nurses, respiratory therapists, and critical-care physicians), decreased the number of cardiac and respiratory arrests by as much as 72%18 and hospital mortality by as much as 35% in institutions where the effect was studied.19 Although it is possible that most of the impact is due to a decrease in respiratory arrests, this cannot be confirmed by the available published data. Implementation of a pediatric MET/RRT may be beneficial in facilities where children with high risk illnesses are present on general inpatient units (Class IIa, LOE B).
Despite the improved outcome of in-hospital CPR, a majority of children with in-hospital cardiac arrest and an even larger percentage of children with out-of-hospital cardiac arrest do not survive, or they are severely incapacitated if they do. Several studies, discussed later in this document, showed that the presence of family members during resuscitation has helped them deal with the inevitable trauma and grief following the death of a child. Therefore, whenever possible, provide family members with the option of being present during resuscitation of an infant or child (Class I, LOE B).
BLS Considerations During PALS
Pediatric advanced life support (PALS) usually takes place in the setting of an organized response in an advanced healthcare environment. In these circumstances, 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).
BLS (whether for a child or adult) is presented as a series of sequential events with the assumption that there is only one responder, but PALS usually takes place in an environment where many rescuers are rapidly mobilized and actions are performed simultaneously. The challenge is to organize the rescuers into an efficient team. Important considerations for the greatest chance of a successful resuscitation from cardiac arrest include the following:
Chest compressions should be immediately started by one rescuer, while a second rescuer prepares to start ventilations with a bag and mask. Ventilation is extremely important in pediatrics because of the large percentage of asphyxial arrests in which best results are obtained by a combination of chest compressions and ventilations.8 Unfortunately ventilations are sometimes delayed because equipment (bag, mask, oxygen, airway) must be mobilized. 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).
The effectiveness of PALS is dependent on high-quality CPR, which requires an adequate compression rate (at least 100 compressions/min), an adequate compression depth (at least one third of the AP diameter of the chest or approximately 1 ½ inches [4 cm] in infants and approximately 2 inches [5 cm] in children), allowing complete recoil of the chest after each compression, minimizing interruptions in compressions, and avoiding excessive ventilation. Reasons for not performing high-quality CPR include rescuer inattention to detail, rescuer fatigue, and long or frequent interruptions to secure the airway, check the heart rhythm, and move the patient.22 Optimal chest compressions are best delivered with the victim on a firm surface.23,24
While one rescuer performs chest compressions and another performs ventilations, other rescuers should obtain a monitor/defibrillator, establish vascular access, and calculate and prepare the anticipated medications.
Many in-hospital patients, especially if they are in an ICU, are monitored and some have an advanced airway and are receiving mechanical ventilation. If the patient has an indwelling arterial catheter, use the waveform as feedback to evaluate hand position and chest compression depth. A minor adjustment of hand position or depth of compression can significantly improve the amplitude of the arterial waveform, reflecting better chest compression-induced stroke volume. The arterial waveform may also be useful in identification of return of spontaneous circulation (ROSC). If the patient's end-tidal CO2 (Petco2) is being monitored, it can be used to evaluate the quality of chest compressions; it can also provide an indication of ROSC (see below).
Respiratory failure is characterized by inadequate ventilation, insufficient oxygenation, or both. Anticipate respiratory failure if any of the following signs is present:
An increased respiratory rate, particularly with signs of distress (eg, increased respiratory effort including nasal flaring, retractions, seesaw breathing, or grunting)
An inadequate respiratory rate, effort, or chest excursion (eg, diminished breath sounds or gasping), especially if mental status is depressed
Cyanosis with abnormal breathing despite supplementary oxygen
Shock results from inadequate blood flow and oxygen delivery to meet tissue metabolic demands. The most common type of shock in children is hypovolemic, including shock due to hemorrhage. Distributive, cardiogenic, and obstructive shock occur less frequently. Shock progresses over a continuum of severity, from a compensated to a decompensated state. Compensatory mechanisms include tachycardia and increased systemic vascular resistance (vasoconstriction) in an effort to maintain cardiac output and perfusion pressure respectively. Decompensation occurs when compensatory mechanisms fail and results in hypotensive shock.
Typical signs of compensated shock include
Cool and pale distal extremities
Prolonged (>2 seconds) capillary refill (despite warm ambient temperature)
Weak peripheral pulses compared with central pulses
Normal systolic blood pressure
As compensatory mechanisms fail, signs of inadequate end-organ perfusion develop. In addition to the above, these signs include
Depressed mental status
Decreased urine output
Weak central pulses
Deterioration in color (eg, mottling, see below)
Decompensated shock is characterized by signs and symptoms consistent with inadequate delivery of oxygen to tissues (pallor, peripheral cyanosis, tachypnea, mottling of the skin, decreased urine output, metabolic acidosis, depressed mental status), weak or absent peripheral pulses, weak central pulses, and hypotension.
Learn to integrate the signs of shock because no single sign confirms the diagnosis. For example:
Capillary refill time alone is not a good indicator of circulatory volume, but a capillary refill time >2 seconds is a useful indicator of moderate dehydration when combined with decreased urine output, absent tears, dry mucous membranes, and a generally ill appearance. Capillary refill time is influenced by ambient temperature,25 site, and age and its interpretation can be influenced by lighting.26
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.
There are several sources of data that use large populations to identify the 5th percentile for systolic blood pressure at various ages.27,28 For purposes of these guidelines, hypotension is defined as a systolic blood pressure:
<60 mm Hg in term neonates (0 to 28 days)
<70 mm Hg in infants (1 month to 12 months)
<70 mm Hg + (2 × age in years) in children 1 to 10 years
<90 mm Hg in children ≥10 years of age
Oropharyngeal and Nasopharyngeal Airways
Oropharyngeal and nasopharyngeal airways help maintain an open airway by displacing the tongue or soft palate from the pharyngeal air passages. Oropharyngeal airways are used in unresponsive victims who do not have a gag reflex. Make sure to select the correct size: an oropharyngeal airway that is too small may push the base of the tongue farther into the airway; one that is too large may obstruct the airway.
Nasopharyngeal airways can be used in children who do have a gag reflex. Pay careful attention to proper diameter and length. A nasopharyngeal airway that is too short may not maintain an open airway, while one that is too long may obstruct it. A small-diameter nasopharyngeal airway may be obstructed easily by secretions. It may therefore require frequent suctioning.
Laryngeal Mask Airway (LMA)
Although several supraglottic devices have been used in children, clinical studies of devices other than the LMA in pediatric patients are limited. When bag-mask ventilation (see “Bag-Mask Ventilation,” below) 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).29,–,37 LMA insertion is associated with a higher incidence of complications in young children compared with older children and adults.38,–,43
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). Once the circulation is restored, monitor systemic oxygen saturation. It may be reasonable, when the appropriate equipment is available, to titrate oxygen administration to maintain the oxyhemoglobin saturation ≥94%. 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). Remember that adequate oxygen delivery requires not only adequate arterial oxyhemoglobin saturation but also adequate hemoglobin concentration and cardiac output.
If the patient has a perfusing rhythm, monitor oxyhemoglobin saturation continuously with a pulse oximeter because clinical recognition of hypoxemia is not reliable.44 Pulse oximetry may, however, also be unreliable in patients with poor peripheral perfusion, carbon monoxide poisoning, or methemoglobinemia.
Bag-mask ventilation can be as effective, and may be safer, than endotracheal tube ventilation for short periods during out-of-hospital resuscitation.45,–,52 In the prehospital setting it is reasonable to ventilate and oxygenate infants and children with a bag-mask device, especially if transport time is short (Class IIa, LOE B). Bag-mask ventilation requires training and periodic retraining in selecting a correct mask size, maintaining an open airway, providing a tight seal between mask and face, providing ventilation, and assessing effectiveness of ventilation (see Part 13, “Pediatric Basic Life Support”).
Use only the force and tidal volume needed to just make the chest rise visibly (Class I, LOE C); avoid delivering excessive ventilation during cardiac arrest (Class III, LOE C). Evidence shows that cardiac arrest victims frequently receive excessive ventilation.22,53,–,55 Excessive ventilation during cardiac arrest increases intrathoracic pressure, which impedes venous return, thus reducing cardiac output and cerebral and coronary blood flow. These effects will reduce the likelihood of ROSC.54 In addition, excessive ventilation may cause air trapping and barotrauma in patients with small airway obstruction. It also increases the risk of stomach inflation, regurgitation, and aspiration.
If the infant or child is not intubated, pause after 30 chest compressions (1 rescuer) or after 15 chest compressions (2 rescuers) to give 2 ventilations (mouth-to-mouth, mouth-to-mask, or bag-mask). Deliver each breath with an inspiratory time of approximately 1 second. If the infant or child is intubated, ventilate at a rate of about 1 breath every 6 to 8 seconds (8 to 10 times per minute) without interrupting chest compressions (Class I, LOE C). It may be reasonable to do the same if an LMA is in place (Class IIb, LOE C).
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). One way to achieve that rate with a ventilating bag is to use the mnemonic “squeeze-release-release” at a normal speaking rate.45,56
Two-Person Bag-Mask Ventilation
A 2-person ventilation technique may be preferable when personnel are available and may be more effective than ventilation by a single rescuer if the patient has significant airway obstruction, poor lung compliance, or the rescuer has difficulty in creating a tight mask-to-face seal.57,58 One rescuer uses both hands to maintain an open airway with a jaw thrust and a tight mask-to-face seal while the other compresses the ventilation bag. Both rescuers should observe the victim's chest to ensure chest rise.
Gastric inflation may interfere with effective ventilation59 and cause regurgitation, aspiration of stomach contents, and further ventilatory compromise. 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.45
Applying cricoid pressure in an unresponsive victim to reduce air entry into the stomach (Class IIa, LOE B).60,–,62 This may require a third rescuer if cricoid pressure cannot be applied by the rescuer who is securing the bag to the face. Avoid excessive cricoid pressure so as not to obstruct the trachea (Class III, LOE B).63
Passing 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.
Ventilation With an Endotracheal Tube
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 length of training, supervised experience in the operating room and in the field,64,65 adequate ongoing experience,66 and use of rapid sequence intubation (RSI).67,68
Rapid Sequence Intubation (RSI)
To facilitate emergency intubation and reduce the incidence of complications, skilled, experienced providers may use sedatives, neuromuscular blocking agents, and other medications to rapidly sedate and neuromuscularly block the pediatric patient.69
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. If you use RSI you must have a secondary plan to manage the airway in the event that you cannot achieve intubation.
Cricoid Pressure During Intubation
There is insufficient evidence to recommend routine cricoid pressure application to prevent aspiration during endotracheal intubation in children. Do not continue cricoid pressure if it interferes with ventilation or the speed or ease of intubation (Class III, LOE C).86,87
Cuffed Versus Uncuffed Endotracheal Tubes
Both cuffed and uncuffed endotracheal tubes are acceptable for intubating infants and children (Class IIa, LOE C). In the operating room, cuffed endotracheal tubes are associated with a higher likelihood of correct selection of tube size, thus achieving a lower reintubation rate with no increased risk of perioperative complications.88,–,90 In intensive care settings the risk of complications in infants and in children is no greater with cuffed tubes than with noncuffed tubes.91,–,93 Cuffed endotracheal tubes may decrease the risk of aspiration.94 If cuffed endotracheal tubes are used, cuff inflating pressure should be monitored and limited according to manufacturer's instruction (usually less than 20 to 25 cm H2O).
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 endotracheal tube size, position, and cuff inflation pressure (Class IIa, LOE B).88,91,92
Endotracheal Tube Size
Length-based resuscitation tapes are helpful and more accurate than age-based formula estimates of endotracheal tube size for children up to approximately 35 kg,77,95,96 even for children with short stature.97
In preparation for intubation with either a cuffed or an uncuffed endotracheal tube, confirm that tubes with an internal diameter (ID) 0.5 mm smaller and 0.5 mm larger than the estimated size are available. During intubation, if the endotracheal tube meets resistance, place 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 place a cuffed tube of the same size if an uncuffed tube was used originally. Note that replacement of a functional endotracheal tube is associated with risk; the procedure should be undertaken in an appropriate setting by experienced personnel.
If an uncuffed endotracheal tube is used for emergency intubation, it is reasonable to select a 3.5-mm ID tube for infants up to one year of age and a 4.0-mm ID tube for patients between 1 and 2 years of age. After age 2, uncuffed endotracheal tube size can be estimated by the following formula: 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).89,98,–,100 After age 2 it is reasonable to estimate tube size with the following formula (Class IIa, LOE B:89,98,–,101):
Verification of Endotracheal Tube Placement
There is a risk of endotracheal tube misplacement (ie, in the esophagus, the pharynx above the vocal cords, or a mainstem bronchus) and an ongoing risk of displacement or obstruction,45,102 especially during patient transport.103 Since no single confirmation technique, including clinical signs104 or the presence of water vapor in the tube,105 is completely reliable, use both clinical assessment and confirmatory devices to verify proper tube placement immediately after intubation, again after securing the endotracheal tube, during transport, and each time the patient is moved (eg, from gurney to bed) (Class I, LOE B).
The following are methods for confirming correct position:
Look for bilateral chest movement and listen for equal breath sounds over both lung fields, especially over the axillae.
Listen for gastric insufflation sounds over the stomach. They should not be present if the tube is in the trachea.104
Check for exhaled CO2 (see “Exhaled or End-Tidal CO2 Monitoring,” below).
If there is a perfusing rhythm, check oxyhemoglobin saturation with a pulse oximeter. Remember that following hyperoxygenation, the oxyhemoglobin saturation detected by pulse oximetry may not decline for as long as 3 minutes even without effective ventilation.106,107
If you are still uncertain, 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 that the tube is not in a bronchus and to identify proper position in the midtrachea.
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 farther into the airway, and extension may pull the tube out of the airway.108,109
If an intubated patient's condition deteriorates, consider the following possibilities (mnemonic DOPE):
Displacement of the tube
Obstruction of the tube
Exhaled or End-Tidal CO2 Monitoring
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], ICU, ward, operating room) (Class I, LOE C)110,–,114 and during intrahospital or interhospital transport (Class IIb, LOE C).115,116 Remember that 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 (Class IIa, LOE C)110,117,–,120 because the absence of CO2 may reflect very low pulmonary blood flow rather than tube misplacement.
Confirmation of endotracheal tube position by colorimetric end-tidal CO2 detector may be altered by the following:
If the detector is contaminated with gastric contents or acidic drugs (eg, endotracheally administered epinephrine), a consistent color rather than a breath-to-breath color change may be seen.
A large glottic air leak may reduce exhaled tidal volume through the tube and dilute CO2 concentration.
Esophageal Detector Device (EDD)
If capnography is not available, an esophageal detector device (EDD) may be considered to confirm endotracheal tube placement in children weighing >20 kg with a perfusing rhythm (Class IIb, LOE B),125,126 but the data are insufficient to make a recommendation for or against its use in children during cardiac arrest.
Transtracheal Catheter Oxygenation and Ventilation
Transtracheal catheter oxygenation and ventilation may be considered for patients with severe airway obstruction above the level of the cricoid cartilage if standard methods to manage the airway are unsuccessful. Note that transtracheal ventilation primarily supports oxygenation as tidal volumes are usually too small to effectively remove carbon dioxide. This technique 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).127
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 noncollapsible suction tubing and semirigid pharyngeal tips are used to suction the mouth and pharynx.
CPR Guidelines for Newborns With Cardiac Arrest of Cardiac Origin
Recommendations for infants differ from those for the newly born (ie, in the delivery room and during the first hours after birth) and newborns (during their initial hospitalization and in the NICU). The compression-to-ventilation ratio differs (newly born and newborns – 3:1; infant two rescuer - 15:2) and how to provide ventilations in the presence of an advanced airway differs (newly born and newborns – pause after 3 compressions; infants – no pauses for ventilations). This presents a dilemma for healthcare providers who may also care for newborns outside the NICU. Because there are no definitive scientific data to help resolve this dilemma, for ease of training we recommend that newborns (intubated or not) who require CPR in the newborn nursery or NICU receive CPR using the same technique as for the newly born in the delivery room (ie, 3:1 compression-to-ventilation ratio with a pause for ventilation). Newborns who require CPR in other settings (eg, prehospital, ED, pediatric intensive care unit [PICU], etc.), should receive CPR according to infant guidelines: 2 rescuers provide continuous chest compressions with asynchronous ventilations if an advanced airway is in place and a 15:2 ventilation-to-compression ratio if no advanced airway is in place (Class IIb, LOE C). It is reasonable to resuscitate newborns with a primary cardiac etiology of arrest, regardless of location, according to infant guidelines, with emphasis on chest compressions (Class IIa, LOE C). For further information, please refer to Part 13, “Pediatric Basic Life Support,” and Part 15, “Neonatal Resuscitation.”
Extracorporeal Life Support (ECLS)
Extracorporeal life support (ECLS) is a modified form of cardiopulmonary bypass used to provide prolonged delivery of oxygen to tissues. Consider early activation of ECLS for a cardiac arrest that occurs in a highly supervised environment, such as an ICU, with the clinical protocols in place and the expertise and equipment available to initiate it rapidly. ECLS should be considered only for children in cardiac arrest refractory to standard resuscitation attempts, with a potentially reversible cause of arrest (Class IIa, LOE C).128,–,154 When ECLS is employed during cardiac arrest, outcome for children with underlying cardiac disease is better than the outcome for children with noncardiac disease. With underlying cardiac disease, long-term survival when ECLS is initiated in a critical-care setting has been reported even after >50 minutes of standard CPR.128,129,139,147
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.
There is insufficient evidence for or against the routine use of echocardiography in pediatric cardiac arrest. 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).155,–,162 Minimize interruption of CPR while performing echocardiography.
End-Tidal CO2 (Petco2)
Continuous capnography or capnometry monitoring, if available, may be beneficial during CPR, to help guide therapy, especially the effectiveness of chest compressions (Class IIa, LOE C). Animal and adult studies show a strong correlation between Petco2 and interventions that increase cardiac output during CPR or shock.53,163,–,169 If the Petco2 is consistently <10 to 15 mm Hg, focus efforts on improving chest compressions and make sure that the victim does not receive excessive ventilation. An abrupt and sustained rise in Petco2 in adults170,171 and animals110 is observed just prior to clinical identification of ROSC, so use of Petco2 may spare the rescuer from interrupting chest compressions for a pulse check. Petco2 must be interpreted with caution for 1 to 2 minutes after administration of epinephrine or other vasoconstrictive medications because these medications may decrease the end-tidal CO2 level by reducing pulmonary blood flow.
Vascular access is essential for administering medications and drawing blood samples. Obtaining peripheral venous access can be challenging in infants and children during an emergency; intraosseous (IO) access can be quickly established with minimal complications by providers with varied levels of training.172,–,179 Limit the time spent attempting to establish peripheral venous access in a critically ill or injured child.180
Intraosseous (IO) Access
IO access is a rapid, safe, effective, and acceptable route for vascular access in children,172,–,179,181 and it is useful as the initial vascular access in cases of cardiac arrest (Class I, LOE C). All intravenous medications can be administered intraosseously, including epinephrine, adenosine, fluids, blood products,182,183 and catecholamines.184 Onset of action and drug levels for most drugs are comparable to venous administration.185 IO access can be used to obtain blood samples for analysis including for type and cross match and blood gases during CPR,186 but acid-base analysis is inaccurate after sodium bicarbonate administration via the IO cannula.187 Use manual pressure or an infusion pump to administer viscous drugs or rapid fluid boluses;188,189 follow each medication with a saline flush to promote entry into the central circulation.
Peripheral IV access is acceptable during resuscitation if it can be placed rapidly, but placement may be difficult in a critically ill child. 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. Therefore central venous access is not recommended as the initial route of vascular access during an emergency. 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 multilumen central than a peripheral catheter.
Endotracheal Drug Administration
Vascular access (IO or IV) is the preferred method for drug delivery during CPR, but if it is not possible, lipid-soluble drugs, such as lidocaine, epinephrine, atropine, and naloxone (mnemonic “LEAN”)190,191 can be administered via an endotracheal tube.192 However, the effects may not be uniform with tracheal as compared with intravenous administration. One study of children in cardiac arrest193 demonstrated similar ROSC and survival rates regardless of the method of drug delivery, while three studies of adults in cardiac arrest194,–,196 demonstrated reduced ROSC and survival to hospital discharge with tracheal administration of epinephrine compared to vascular delivery. If CPR is in progress, stop chest compressions briefly, administer the medications, and follow with a flush of at least 5 mL of normal saline and 5 consecutive positive-pressure ventilations.197 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 ETT. For epinephrine, a dose ten times the intravenous dose (0.1 mg/kg or 0.1 mL/kg of 1:1000 concentration) is recommended (see Table 1).
The effectiveness of endotracheal epinephrine during cardiac arrest is controversial. Some studies showed it to be as effective as vascular administration193,198,199 while other studies have not found it to be as effective.194,–,196,200 Animal studies201,–,206 suggested that a higher dose of epinephrine is required for endotracheal than for intravascular administration because the lower epinephrine concentrations achieved when the drug is delivered by the endotracheal route may produce predominant transient peripheral β2-adrenergic vasodilating effects. These effects can be detrimental, and cause hypotension, lower coronary artery perfusion pressure and flow, and a reduced potential for ROSC.
Non-lipid-soluble drugs (eg, sodium bicarbonate and calcium) may injure the airway; they should not be administered via the endotracheal route.
Emergency Fluids and Medications
In the out-of-hospital setting, a child's weight is often unknown, and even experienced personnel may not be able to estimate it accurately.74 Tapes with precalculated doses printed at various patient lengths have been clinically validated74,77,95 and are more accurate than age-based or observer (parent or provider) estimate-based methods in the prediction of body weight.70,–,77 Body habitus may also be an important consideration.70,72,78,79
Medication Dose Calculation
To calculate the dose of resuscitation medications, use the child's weight if it is known. If the child's weight is unknown, it is reasonable to use a body length tape with precalculated doses (Class IIa, LOE C).70,–,77
It is unclear if an adjustment in the calculation of resuscitation medications is needed in obese children. Use of the actual body weight in calculation of drug doses in obese patients may result in potentially toxic doses. Length-based tapes estimate the 50th percentile weight for length (ie, ideal body weight), which may, theoretically, result in inadequate doses of some medications in obese patients. Despite these theoretical considerations, there are no data regarding the safety or efficacy of adjusting the doses of resuscitation medications in obese patients. 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).
For subsequent doses of resuscitation drugs in both nonobese and obese patients, expert providers may consider adjusting doses to achieve the desired therapeutic effect. In general, the dose administered to a child should not exceed the standard dose recommended for adult patients.
Medications (See Table 1)
Adenosine causes a temporary atrioventricular (AV) nodal 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 drug delivery to the central circulation. If adenosine is given IV, it should be administered as close to the heart as possible. (See also “Arrhythmia.”)
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. (See also “Arrhythmia.”)
Monitor blood pressure and electrocardiograph (ECG) during intravenous administration of amiodarone. If the patient has a perfusing rhythm, administer the drug as slowly (over 20 to 60 minutes) as the patient's clinical condition allows; if the patient is in VF/pulseless VT, give the drug as a rapid bolus. Amiodarone causes hypotension through its vasodilatory property, and the severity is related to the infusion rate; hypotension is less common with the aqueous form of amiodarone.207 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. 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.
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). Routine calcium administration in cardiac arrest provides no benefit210,–,221 and may be harmful.210,–,212
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.222 In critically ill children, calcium chloride may be preferred because it results in a greater increase in ionized calcium during the treatment of hypocalcemia.222A In the nonarrest setting, if the only venous access is peripheral, calcium gluconate is recommended because it has a lower osmolality than calcium chloride and is therefore less irritating to the vein.
The α-adrenergic-mediated vasoconstriction of epinephrine increases aortic diastolic pressure and thus coronary perfusion pressure, a critical determinant of successful resuscitation from cardiac arrest.223,224 At low doses, the β-adrenergic effects may predominate, leading to decreased systemic vascular resistance; in the doses used during cardiac arrest, the vasoconstrictive α-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.225 Check blood glucose concentration during the resuscitation and treat hypoglycemia promptly (Class I, LOE C).226
Lidocaine decreases automaticity and suppresses ventricular arrhythmias,227 but is not as effective as amiodarone for improving ROSC or survival to hospital admission among adult patients with VF refractory to shocks and epinephrine.228 Neither lidocaine nor amiodarone has been shown to improve survival to hospital discharge.
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.231,–,233
Magnesium produces vasodilation and may cause hypotension if administered rapidly.
Procainamide prolongs the refractory period of the atria and ventricles and depresses conduction velocity.
There is limited clinical data on using procainamide in infants and children.234,–,236 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. Prior to using procainamide for a hemodynamically stable patient, expert consultation is strongly recommended.
Routine administration of sodium bicarbonate is not recommended in cardiac arrest (Class III, LOE B).212,237,238 Sodium bicarbonate may be administered for treatment of some toxidromes (see “Toxicological Emergencies,” below) 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.239,240 Excessive sodium bicarbonate may impair tissue oxygen delivery;241 cause hypokalemia, hypocalcemia, hypernatremia, and hyperosmolality;242,243 decrease the VF threshold;244 and impair cardiac function.
There is insufficient evidence to make a recommendation for or against the routine use of vasopressin during cardiac arrest. Pediatric245,–,247 and adult248,249 case series/reports suggested that vasopressin245 or its long-acting analog, terlipressin,246,247 may be effective in refractory cardiac arrest when standard therapy fails. A large pediatric NRCPR case series, however, suggested that vasopressin is associated with lower ROSC, and a trend toward lower 24-hour and discharge survival.250 A preponderance of controlled trials in adults do not demonstrate a benefit.251,–,256
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, 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. Throughout resuscitation, emphasis should be placed on provision of high-quality CPR (providing chest compressions of adequate rate and depth, allowing complete chest recoil after each compression, minimizing interruptions in compressions and avoiding excessive ventilation).
While CPR is being given, determine the child's cardiac rhythm from the ECG or, if you are using an AED, the device will tell you whether the rhythm is “shockable” (eg, VF or rapid VT) or “not shockable” (eg, asystole or PEA). It may be necessary to temporarily interrupt chest compressions to determine the child's rhythm. Asystole and bradycardia with a wide QRS are most common in asphyxial arrest.1 VF and PEA are less common13 but VF is more likely to be present in older children with sudden witnessed arrest.
“Nonshockable Rhythm”: Asystole/PEA (Step 9)
PEA is an organized electric activity—most commonly slow, wide QRS complexes—without palpable pulses. Less frequently there is a sudden impairment of cardiac output with an initially normal rhythm but without pulses and with poor perfusion. This subcategory, formerly known as electromechanical dissociation (EMD), may be more reversible than asystole. For asystole and PEA:
(Step 10) Continue CPR with as few interruptions in chest compressions as possible. A second 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), while CPR is continued. The same epinephrine dose is repeated every 3 to 5 minutes (Class I, LOE B). There is no survival benefit from high-dose epinephrine, and it may be harmful, particularly in asphyxia (Class III, LOE B).257,–,261 High-dose epinephrine may be considered in exceptional circumstances, such as β-blocker overdose (Class IIb, LOE C).
Once an advanced airway is in place, 1 rescuer should give continuous chest compressions at a rate of at least 100 per minute without pause for ventilation. The second rescuer delivers ventilations at a rate of 1 breath every 6 to 8 seconds (about 8 to 10 breaths per minute). Rotate the compressor role approximately every 2 minutes to prevent compressor fatigue and deterioration in quality and rate of chest compressions. Check rhythm every 2 minutes with minimal interruptions in chest compressions. If the rhythm is “nonshockable” continue with cycles of CPR and epinephrine administration until there is evidence of ROSC or you decide to terminate the effort. If at any time the rhythm becomes “shockable,” give a shock (Step 7) and immediately resume chest compressions for 2 minutes before rechecking the rhythm. Minimize time between chest compressions and shock delivery (ie, check rhythm and deliver shocks immediately after compressions rather than after rescue breaths, if possible) and between shock delivery and resumption of chest compressions.
Search for and treat reversible causes.
“Shockable Rhythm”: VF/Pulseless VT (Step 2)
Defibrillation is the definitive treatment for VF (Class I, LOE B) with an overall survival rate of 17% to 20%.4,262,263 Survival is better in primary than in secondary VF.6 In adults, the probability of survival declines by 7% to 10% for each minute of arrest without CPR and defibrillation.264 Survival is better if early, high-quality CPR is provided with minimal interruptions. Outcome of shock delivery is best if rescuers minimize the time between last compression and shock delivery, so rescuers should be prepared to coordinate (brief) interruptions in chest compressions to deliver shocks, and should resume compressions immediately after shock delivery.
Defibrillators are either manual or automated (AED), with monophasic or biphasic waveforms. For further information see Part 6, “Electrical Therapies: Automated External Defibrillators, Defibrillation, Cardioversion, and Pacing.”
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.
The following should be considered when using a manual defibrillator:
In general, manual defibrillators have two sizes of hand-held paddles: adult and infant. The infant paddles may slide over or be located under the adult paddles. Manual defibrillators can also be used with hands-free pads that are self adhesive. Use the largest paddles or self-adhering electrodes265,–,267 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.268 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
“Adult” size (8 to 10 cm) for children >10 kg (> approximately 1 year)
“Infant” size for infants <10 kg
The electrode–chest wall interface is part of the self-adhesive pad; in contrast, electrode gel must be applied liberally on manually applied 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 in an anterior-posterior position of the paddles.268
The lowest energy dose for effective defibrillation and the upper limit for safe defibrillation in infants and children are not known; more data are needed. It has been observed that in children with VF, an initial monophasic dose of 2 J/kg is only effective in terminating ventricular fibrillation 18% to 50% of the time,269,270 while similar doses of biphasic shocks are effective 48% of the time.268 Children with out-of-hospital VF cardiac arrest often receive more than 2 J/kg,271,272 and one in-hospital cardiac arrest study268 showed that children received doses between 2.5 and 3.2 J/kg to achieve ROSC. Energy doses >4 J/kg (up to 9 J/kg) have effectively defibrillated children272,–,274 and pediatric animals275 with negligible adverse effects. Based on data from adult studies276,277 and pediatric animal models,278,–,280 biphasic shocks appear to be at least as effective as monophasic shocks and less harmful.
It is acceptable to use an initial dose of 2 to 4 J/kg (Class IIa, LOE C), but for ease of teaching an initial dose of 2 J/kg may be considered (Class IIb, LOE C). For refractory VF, it is reasonable to increase the dose to 4 J/kg (Class IIa, LOE C). Subsequent energy levels should be at least 4 J/kg, and higher energy levels may be considered, not to exceed 10 J/kg or the adult maximum dose (Class IIb, LOE C).
Many AEDs can accurately detect VF in children of all ages.271,281,–,283 They can differentiate “shockable” from “nonshockable” rhythms with a high degree of sensitivity and specificity.281,282 It is recommended that 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).274,284 If an AED with an attenuator is not available, use an AED with standard electrodes (Class IIa, LOE C).
In infants <1 year of age a manual defibrillator is preferred. If a manual defibrillator is not available, an AED with a dose attenuator may be used. An AED without a dose attenuator may be used if neither a manual defibrillator nor one with a dose attenuator is available (Class IIb, LOE C).
Integration of Defibrillation With Resuscitation Sequence
The following are important considerations:
Provide CPR until the defibrillator is ready to deliver a shock; after shock delivery, resume CPR, beginning with chest compressions. Minimize interruptions of chest compressions. In adults with prolonged arrest285,286 and in animal models,287 defibrillation is more likely to be successful after a period of effective chest compressions. Ideally chest compressions should be interrupted only for ventilations (until an advanced airway is in place), rhythm check, and shock delivery. If a “shockable” rhythm is still present, continue chest compressions after a rhythm check (when possible) while the defibrillator is charging (so chest compressions are delivered until shock delivery).
(Step 3) Give 1 shock (2 J/kg) as quickly as possible and immediately resume CPR, beginning with chest compressions. If 1 shock fails to eliminate VF, the incremental benefit of another immediate shock is low, and resumption of CPR is likely to confer a greater value than another shock. CPR may provide coronary perfusion, increasing the likelihood of defibrillation with a subsequent shock. It is important to minimize the time between chest compressions and shock delivery and between shock delivery and resumption of postshock compressions.
(Step 4) Continue CPR for about 2 minutes. In in-hospital settings with continuous invasive monitoring, this sequence may be modified at the expert provider's discretion (see, also Part 8.2: “Management of Cardiac Arrest”). If sufficient rescuers are present, obtain vascular (IO or IV) access.
After 2 minutes of CPR, check the rhythm; recharge the defibrillator to a higher dose (4 J/kg).
(Step 5) If a “shockable” rhythm persists, give another shock (4 J/kg). If rhythm is “nonshockable,” continue with the asystole/PEA algorithm (Steps 10 and 11).
(Step 6) Immediately resume chest compressions. Continue CPR for approximately 2 minutes. During CPR give epinephrine 0.01 mg/kg (0.1 mL/kg of 1:10 000 concentration), maximum of 1 mg (Class I, LOE B) every 3 to 5 minutes. It is helpful if a third rescuer prepares the drug doses before the rhythm is checked so epinephrine can be administered as soon as possible. Epinephrine should be administered during chest compressions, but the timing of drug administration is less important than the need to minimize interruptions in chest compressions. Just prior to the rhythm check, the rescuer operating the defibrillator should prepare to recharge the defibrillator (4 J/kg or more with a maximum dose not to exceed 10 J/kg or the adult dose, whichever is lower).
Check the rhythm
(Step 7) If the rhythm is “shockable,” deliver another shock (4 J/kg or more with a maximum dose not to exceed 10 J/kg or the adult dose, whichever is lower) and immediately resume CPR (beginning with chest compressions).
If at any time the rhythm check shows a “nonshockable” rhythm, proceed to the “Pulseless Arrest” sequence (Steps 10 or 11).
Once an advanced airway is in place, 2 rescuers no longer deliver cycles of CPR (ie, compressions interrupted by pauses for ventilation). Instead, the compressing rescuer gives continuous chest compressions at a rate of at least 100 per minute without pause for ventilation. The rescuer delivering ventilation provides about 1 breath every 6 to 8 seconds (8 to 10 breaths per minute). Two or more rescuers should rotate the compressor role approximately every 2 minutes to prevent compressor fatigue and deterioration in quality and rate of chest compressions.
If defibrillation successfully restores an organized rhythm (or there is other evidence of ROSC, such as an abrupt rise in Petco2 or visible pulsations on an arterial waveform), check the child's pulse to determine if a perfusing rhythm is present. If a pulse is present, continue with postresuscitation care.
If defibrillation is successful but VF recurs, resume CPR and give another bolus of amiodarone before trying to defibrillate with the previously successful shock dose.
Search for and treat reversible causes
Torsades de Pointes
This polymorphic VT is associated with a long QT interval, which 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.291,292
Torsades de pointes VT typically deteriorates rapidly to VF or pulseless VT, so providers should initiate CPR and proceed with defibrillation when pulseless arrest develops (see above). 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).
Box numbers in the text below refer to the corresponding boxes in the PALS Bradycardia Algorithm (see Figure 2). This algorithm applies to the care of the infant or child with bradycardia and cardiorespiratory compromise, but a palpable pulse. If at any time the patient develops pulseless arrest, see the PALS Pulseless Arrest Algorithm.
Emergency treatment of bradycardia is indicated when the rhythm results in hemodynamic compromise.
(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 and is still causing cardiorespiratory symptoms despite adequate oxygenation and ventilation.
(Box 4a) If pulses, perfusion, and respirations are adequate, no emergency treatment is necessary. Monitor and proceed with evaluation.
(Box 3) If heart rate is <60 beats per minute with poor perfusion despite effective ventilation with oxygen, start CPR.
(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).
(Box 5) Medications and pacing:
– Continue to support airway, ventilation, oxygenation, and chest compressions (Class I, LOE B). 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).
– 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 or an endotracheal dose of 0.04 to 0.06 mg/kg (Class I, LOE C).
– 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).293 Pacing is not useful for asystole293,294 or bradycardia due to postarrest hypoxic/ischemic myocardial insult or respiratory failure.
The box numbers in the text below correspond to the numbered boxes in the Tachycardia Algorithm (see Figure 3).
If there are signs of poor perfusion and pulses are not palpable, proceed with the PALS Pulseless Arrest Algorithm (see Figure 1).
(Box 1) If pulses are palpable and the patient has adequate perfusion
–Assess and support airway, breathing, and circulation
–Obtain vascular access.
–Evaluate 12-lead ECG and assess QRS duration (Box 2).
Narrow-Complex (≤0.09 Second) Tachycardia
Evaluation of a 12-lead ECG (Box 3) and the patient's clinical presentation and history (Boxes 4 and 5) should help differentiate sinus tachycardia from supraventricular tachycardia (SVT). If the rhythm is sinus tachycardia, search for and treat reversible causes.
Supraventricular Tachycardia (Box 5)
Monitor rhythm during therapy to evaluate the effect of interventions. The choice of therapy is determined by the patient's degree of hemodynamic instability.
Attempt vagal stimulation (Box 7) first, unless the patient is hemodynamically unstable or the procedure will unduly delay chemical or electric cardioversion (Class IIa, LOE C). In infants and young children, apply ice to the face without occluding the airway.295,296
One method for performing a Valsalva maneuver is to have the child blow through a narrow straw.298 Do not apply pressure to the eye because this can damage the retina.
Pharmacologic cardioversion with adenosine (Box 8) is very effective with minimal and transient side effects.300,–,304 If IV/IO access is readily available, adenosine is the drug of choice (Class I, LOE C). Side effects are usually transient.300,–,304 Administer IV/IO adenosine 0.1 mg/kg using 2 syringes connected to a T-connector or stopcock; give adenosine rapidly with 1 syringe and immediately flush with ≥5 mL of normal saline with the other. An IV/IO dose of Verapamil, 0.1 to 0.3 mg/kg is also effective in terminating SVT in older children,305,306 but it should not be used in infants without expert consultation (Class III, LOE C) because it may cause potential myocardial depression, hypotension, and cardiac arrest.306,307
If the patient is hemodynamically unstable or if adenosine is ineffective, perform electric synchronized cardioversion (Box 8). 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). If a second shock is unsuccessful or the tachycardia recurs quickly, consider amiodarone or procainamide before a third shock.
Consider amiodarone 5 mg/kg IO/IV308,309 or procainamide 15 mg/kg IO/IV236 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). Both amiodarone and procainamide must be infused slowly (amiodarone over 20 to 60 minutes and procainamide over 30 to 60 minutes), depending on the urgency, while the ECG and blood pressure are monitored. If there is no effect and there are no signs of toxicity, give additional doses (Table 1). Avoid the simultaneous use of amiodarone and procainamide without expert consultation.
Wide-Complex (>0.09 Second) Tachycardia (Box 9)
Wide-complex tachycardia often originates in the ventricles (ventricular tachycardia) but may be supraventricular in origin.310
Because all arrhythmia 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.
The following are important considerations in treating wide-complex tachycardia in hemodynamically stable patients:
Adenosine may be useful in differentiating SVT from VT and converting wide-complex tachycardia of supraventricular origin (Box 12). Adenosine should be considered only if the rhythm is regular and the QRS is monomorphic. Do not use adenosine in patients with known Wolff-Parkinson-White syndrome and wide-complex tachycardia.
Consider electric cardioversion after sedation using a starting energy dose of 0.5 to 1 J/kg. If that fails, increase the dose to 2 J/kg (Class IIb, LOE C) (Box 11).
Consider pharmacologic conversion 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). Expert consultation is strongly recommended prior to administration.
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).
Special Resuscitation Situations
There appears to be no clinically important difference in survival of children who are treated for septic shock with colloid compared with those who are treated with isotonic crystalloid solutions.311,–,314 Although colloid may be beneficial as part of a protocol-driven strategy,315 it is reasonable to use isotonic crystalloid solution as the initial fluid for the treatment of septic shock (Class IIa, LOE C).
Monitoring the central venous (superior vena cava) oxygen saturation (ScvO2) may be useful to titrate therapy in infants and children with septic shock. Protocol-driven or “goal-directed” therapy, with a target ScvO2 ≥70% appears to improve patient survival in severe sepsis (Class IIb, LOE B).316,–,318
Etomidate has been shown to facilitate endotracheal intubation in infants and children with minimal hemodynamic effect,320,–,322 but do not use it routinely in pediatric patients with evidence of septic shock (Class III, LOE B). Adrenal suppression is seen after administration of etomidate in children323 and adults.324 In children and adults with septic shock, etomidate administration is associated with a higher mortality rate.323,325
Use an isotonic crystalloid solution (eg, lactated Ringer's solution or normal saline)326,327 as the initial fluid for the treatment of shock (Class I, LOE A). There is no added benefit in using colloid (eg, albumin) during the early phase of resuscitation.328,329
Treat signs of shock with a bolus of 20 mL/kg of isotonic crystalloid even if blood pressure is normal (Class IIb, LOE C). Crystalloids may have an associated survival benefit over colloid for children with shock secondary to general trauma, traumatic brain injury, and burns.329,–,332 There is no evidence to support the use of a specific isotonic crystalloid. Give additional boluses (20 mL/kg) if systemic perfusion fails to improve. There are insufficient data to make a recommendation for or against use of hypertonic saline for shock associated with head injuries or hypovolemia.333,334
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.
Some aspects of trauma resuscitation require emphasis because improperly performed resuscitation is a major cause of preventable pediatric deaths.335
Common errors in pediatric trauma resuscitation include failure to open and maintain the airway, failure to provide appropriate fluid resuscitation, and failure to recognize and treat internal bleeding. 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:
When the mechanism of injury is compatible with cervical spinal injury, restrict motion of the cervical spine and avoid traction or movement of the head and neck. Open and maintain the airway with a jaw thrust, and do not tilt the head.
If the airway cannot be opened with a jaw thrust, use a head tilt–chin lift because you must establish a patent airway. Because of the disproportionately large head of infants and young children, optimal positioning may require recessing the occiput336 or elevating the torso to avoid undesirable backboard-induced cervical flexion.336,337
Do not routinely hyperventilate even in case of head injury (Class III, LOE C).338,339 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).
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.
If the patient has maxillofacial trauma or if you suspect a basilar skull fracture, insert an orogastric rather than a nasogastric tube (Class IIa, LOE C).340
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. Heparin may be considered for infants with a systemic-pulmonary artery shunt or right ventricular-pulmonary artery shunt. 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 (Petco2) in the single-ventricle patient during cardiac arrest may not be a reliable indicator of CPR quality because pulmonary blood flow changes rapidly and does not necessarily reflect cardiac output during CPR.345
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).346,347 Neonates in a low cardiac output state following stage I repair may benefit from systemic vasodilators such as α-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).348,–,350 Other drugs that reduce systemic vascular resistance (eg, milrinone or nipride)351 may also be considered for patients with excessive Qp:Qs (Class IIa, LOE B).352 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.353,–,355 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).129,132,152,356,357
Hypoventilation may improve oxygen delivery in patients in a prearrest state with Fontan or hemi-Fontan/bidirectional Glenn (BDG) physiology (Class IIa, LOE B).358,–,361 Negative-pressure ventilation may improve cardiac output (Class IIa, LOE C).362,363 During cardiopulmonary arrest, it is reasonable to consider extracorporeal membrane oxygenation (ECMO) for patients with Fontan physiology (Class IIa, LOE C).364 It is unclear at this time whether patients with hemi-Fontan/BDG physiology in cardiac arrest might benefit from ECMO.
Standard PALS, including oxygenation and ventilation, should be provided to patients with pulmonary hypertension and a cardiopulmonary arrest. 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. If intravenous or inhaled therapy to decrease pulmonary hypertension has been interrupted, reinstitute it (Class IIa, LOE C). Consider administering inhaled nitric oxide (iNO) or aerosolized prostacyclin or analogue to reduce pulmonary vascular resistance (Class IIa, LOE C). If iNO is not available, consider giving an intravenous bolus of prostacyclin (Class IIa, LOE C).365,–,367 ECMO may be beneficial if instituted early in the resuscitation (Class IIa, LOE C).368
Children With Special Healthcare Needs
Children with special healthcare needs369 may require emergency care for chronic conditions (eg, obstruction of a tracheostomy), failure of support technology (eg, ventilator failure), progression of their underlying disease, or events unrelated to those special needs.370
For additional information about CPR see Part 13: “Pediatric Basic Life Support.”
Ventilation With a Tracheostomy or Stoma
Parents, school nurses, and home healthcare providers should know how to assess patency of the airway, clear the airway, replace the tracheostomy tube, and perform CPR using the artificial airway in a child with a tracheostomy.
Parents and providers should be able to ventilate via a tracheostomy tube and verify effectiveness by assessing chest expansion. If, after suctioning, the chest does not expand with ventilation, remove the tracheostomy tube and replace it or insert a same-sized endotracheal tube, if available, into the tracheal stoma. If a clean tube is unavailable, perform mouth-to-stoma or mask-to-stoma ventilations. If the upper airway is patent, bag-mask ventilation via the nose and mouth may be effective if the tracheal stoma is manually occluded.
Overdose with local anesthetics, cocaine, narcotics, tricyclic antidepressants, calcium channel blockers, and β-adrenergic blockers may require specific treatment modalities in addition to the usual resuscitative measures.
Local anesthetics are used topically, intravenously, subcutaneously, and in epidural or other catheters for delivery of regional analgesia. The toxicity of local anesthetics is well recognized in children; they may cause changes in mental status, seizures, arrhythmias, or even cardiac arrest in settings of overdose or inadvertent vascular administration. Multiple case reports, including some pediatric reports, have described successful treatment of local anesthetic toxicity with intravenous lipid emulsion.371
Acute coronary syndrome, manifested by chest pain and cardiac rhythm disturbances (including VT and VF), is the most frequent cocaine-related reason for hospitalization in adults.372,373 Cocaine also may prolong the action potential and QRS duration and impairs myocardial contractility.374,375
Hyperthermia, which may result from cocaine-induced hypermetabolism, is associated with an increase in toxicity;376 therefore treat elevated temperature aggressively.
Do not give β-adrenergic blockers (Class III, LOE C),376
To prevent arrhythmias secondary to myocardial infarction, consider a lidocaine bolus followed by a lidocaine infusion (Class IIb, LOE C).
Tricyclic Antidepressants and Other Sodium Channel Blockers
Toxic doses cause cardiovascular abnormalities, including intraventricular conduction delays, heart block, bradycardia, prolongation of the QT interval, ventricular arrhythmias (including torsades de pointes, VT, and VF), hypotension, seizures,375,383 and a depressed level of consciousness.
Give 1 to 2 mEq/kg intravenous boluses of sodium bicarbonate 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 7.55.375,384 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).384
Calcium Channel Blockers
Manifestations of toxicity include hypotension, ECG changes (prolongation of the QT interval, widening of the QRS, and right bundle branch block), arrhythmias (bradycardia, SVT, VT, torsades de pointes, and VF),389 seizures, and altered mental status.
Treat mild hypotension with small boluses (5 to 10 mL/kg) of normal saline because myocardial depression may limit the amount of fluid the patient can tolerate.
The effectiveness of calcium administration is variable (Class IIb, LOE C).389,–,393 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. Monitor serum ionized calcium concentration to prevent hypercalcemia. It is preferable to administer calcium chloride via a central venous catheter; use caution when infusing into a peripheral IV because infiltration can cause severe tissue injury. If no central venous catheter is available, infuse calcium gluconate through a secure peripheral IV. For bradycardia and hypotension, consider vasopressors and inotropes such as norepinephrine or epinephrine (Class IIb, LOE C).392
Toxic doses of β-adrenergic blockers cause bradycardia, heart block, and decreased cardiac contractility, and some (eg, propranolol and sotalol) may also prolong the QRS and the QT intervals.397,–,400
Consider an infusion of glucose and insulin (Class IIb, LOE C).394
Calcium may be considered if glucagon and catecholamines are ineffective (Class IIb, LOE C).
Narcotics may cause hypoventilation, apnea, bradycardia, and hypotension in addition to depressed responsiveness.
Support of oxygenation and ventilation is the initial treatment for severe respiratory depression from any cause (Class I).
Naloxone reverses the respiratory depression of narcotic overdose (Class I, LOE B),406,–,410 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. Ventilation before administration of naloxone appears to reduce these adverse effects.411 Intramuscular administration of naloxone may lower the risk by slowing the onset of drug effect.
Postresuscitation Stabilization (Post Cardiac Arrest Care)
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.
Data suggest that hyperoxemia (ie, a high PaO2) enhances the oxidative injury observed following ischemia-reperfusion. Therefore, one goal of the postresuscitation phase is to reduce the risk of oxidative injury while maintaining adequate oxygen delivery. A practical way to achieve that goal is to reduce the Fio2 to reduce the Pao2 while ensuring adequate arterial oxygen content. Specifically, use the lowest inspired oxygen concentration that will maintain the arterial oxyhemoglobin saturation ≥94%. Provided appropriate equipment is available, once ROSC is achieved, adjust the Fio2 to the minimum concentration needed to achieve transcutaneous or arterial oxygen 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 for a saturation of 100%, provided the oxyhemoglobin saturation can be maintained ≥94%.
In addition to the usual clinical signs of adequate perfusion, laboratory parameters of adequate oxygen delivery over time include resolution of metabolic acidosis, reduced lactate concentration, and normalization of venous oxygen saturation.
Assist ventilation if there is significant respiratory compromise (tachypnea, respiratory distress with agitation or decreased responsiveness, poor air exchange, cyanosis, hypoxemia). If the patient is already intubated, verify tube position, patency, and security. In the hospital setting, consider obtaining arterial blood gases 10 to 15 minutes after establishing the initial mechanical ventilator settings and make appropriate adjustments. Ideally, correlate blood gases with capnographic end-tidal CO2 concentration (Petco2) to enable noninvasive monitoring of ventilation.
Control pain and discomfort with analgesics (eg, fentanyl or morphine) and sedatives (eg, lorazepam or midazolam). Neuromuscular blocking agents (eg, vecuronium or pancuronium) with analgesia or sedation, or both, may improve oxygenation and ventilation in case of patient-ventilator dyssynchrony or severely compromised pulmonary function. Neuromuscular blockers, however, can mask seizures and impede neurologic examinations.
Insert a gastric tube to relieve and help prevent gastric inflation.
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.
Drugs Used to Maintain Cardiac Output (Table 2)
Myocardial dysfunction and vascular instability are common following resuscitation from cardiac arrest.414,–,419 Systemic and pulmonary vascular resistances are often increased initially, except in some cases of septic shock.420 The 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.
There are no studies evaluating the benefit of specific vasoactive agents after ROSC in infants and children. In animal studies after resuscitation from cardiac arrest418,419,421,–,424 and post–cardiac surgical experience in children352 and adults,425,–,428 hemodynamic improvement was associated with administration of selected vasoactive agents. Each drug and dose must be tailored to the patient because clinical response is variable. Infuse all vasoactive drugs into a secure IV line. The potential adverse effects of catecholamines include local ischemia and ulceration, tachycardia, atrial and ventricular tachyarrhythmias, hypertension, and metabolic changes (hyperglycemia, increased lactate concentration,429 and hypokalemia).
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.430,431 Because there is great interpatient variability in response,432,433 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.434
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).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.436,437 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.430,431 In one study in single ventricle postoperative cardiac patients, dopamine increased oxygen consumption while not improving blood pressure or cardiac output.438
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.439 Dobutamine increases myocardial contractility and can decrease peripheral vascular resistance. Titrate the infusion432,440,441 to improve cardiac output and blood pressure due to poor myocardial function.441
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 B352,442,–,444). 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.
A primary goal of resuscitation is to preserve brain function. Limit the risk of secondary neuronal injury by adhering to the following precautions:
Do not routinely provide excessive ventilation or hyperventilation. Hyperventilation has no benefit and may impair neurologic outcome by adversely affecting cardiac output and cerebral perfusion.445 Intentional brief hyperventilation may be used as temporizing rescue therapy in response to signs of impending cerebral herniation (eg, sudden rise in measured intracranial pressure, dilated pupil[s] not responsive to light, bradycardia, hypertension).
Therapeutic hypothermia (32°C to 34°C) may be considered for children who remain comatose after resuscitation from cardiac arrest (Class IIb, LOE C).446,447 It is reasonable for adolescents resuscitated from sudden, witnessed, out-of-hospital VF cardiac arrest (Class IIa, LOE C). Although there are no randomized studies in the pediatric population on the effect of therapeutic hypothermia, it is of benefit in adults following witnessed out-of-hospital VF arrest448,449 and in asphyxiated newborns.450,451
The ideal method and duration of cooling and rewarming are not known. Prevent shivering by providing sedation and, if needed, neuromuscular blockade, recognizing that this can mask seizure activity. Closely watch for signs of infection. Other potential complications of hypothermia include diminished cardiac output, arrhythmia, pancreatitis, coagulopathy, thrombocytopenia, hypophosphatemia, hypovolemia from cold diuresis, hypokalemia, and hypomagnesemia.
Monitor temperature continuously, if possible, and treat fever (>38°C) aggressively with antipyretics and cooling devices because fever adversely influences recovery from ischemic brain injury (Class IIa, LOE C).452,–,458
Treat postischemic seizures aggressively; search for a correctable metabolic cause such as hypoglycemia or electrolyte imbalance.
Avoid rewarming from 32 to 34°C faster than 0.5°C per 2 hours unless the patient requires rapid rewarming for clinical reasons.
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.
Ideally postresuscitation 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.459 Transport team members should be trained and experienced in the care of critically ill and injured children103,460 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.461 Monitor exhaled CO2 (qualitative colorimetric detector or capnography) during interhospital or intrahospital transport of intubated patients (Class IIa, LOE B).116,413
Family Presence During Resuscitation
Family presence during CPR is increasingly common, and most parents would like to be given the opportunity to be present during resuscitation of their child.462,–,471 Studies show that family members who are present at a resuscitation would recommend it to others.462,463,465,471,472 Parents of chronically ill children are comfortable with medical equipment and emergency procedures, but even family members with no medical background who were at the side of a loved one to say goodbye during the final moments of life believe that their presence was beneficial to the patient,462,–,464,466,471,–,476 comforting for them,462,–,465,468,–,471,476 and helpful in their adjustment463,–,465,472,473,476,477 and grieving process.477 Standardized psychological examinations suggest that, compared with those not present, family members present during attempted resuscitations have less anxiety and depression and more constructive grieving behavior.477 Parents or family members often fail to ask, but healthcare providers should offer the opportunity in most situations.474,478,479 Whenever possible, provide family members with the option of being present during resuscitation of an infant or child (Class I, LOE B).474,478,479
Family presence during resuscitation, in general, is not disruptive,464,472,475,476,480,481 and does not create stress among staff or negatively affect their performance.462,464,480,482 If the presence of family members creates undue staff stress or is considered detrimental to the resuscitation,483 then family members should be respectfully asked to leave (Class IIa, LOE C). 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.484
Termination of Resuscitative Efforts
There are no reliable predictors of outcome to guide when to terminate resuscitative efforts in children.
Clinical variables associated with survival include length of CPR, number of doses of epinephrine, age, witnessed versus unwitnessed cardiac arrest, and the first and subsequent rhythm.6,7,11,–,13,15,16,151,485,–,489 None of these associations, however, predict outcome. Witnessed collapse, bystander CPR, and a short interval from collapse to arrival of professionals improve the chances of a successful resuscitation. Intact survival has been documented after unusually prolonged in-hospital resuscitation.13,133,134,151,490,491
Sudden Unexplained Deaths
Increasing evidence demonstrates that some cases of sudden infant death syndrome (SIDS) and sudden death in older children and young adults may be associated with genetic mutations causing cardiac ion channelopathies. Channelopathies are dysfunctional myocyte ion channels that result in abnormal movement of electrolytes into and/or out of the cell and predispose the heart to arrhythmia.492,–,501 Mutations causing cardiac ion channelopathies are found in 2% to 10% of victims492,–,498 and in 14% to 20% of young adults with sudden death in whom the cause of death is not evident in a routine autopsy.499,–,501 Clinical and laboratory (eg, ECG, molecular-genetic screening) investigations of first- and second-degree relatives of patients with sudden unexplained death reported inherited, arrhythmogenic disease in 22% to 53% of families.502,–,505
Therefore 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 previous ECGs.
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. Refer families of patients that do not have a cause of death found on autopsy to a healthcare provider or center with expertise in arrhythmias (Class I, LOE C).
The American Heart Association requests that this document be cited as follows: Kleinman ME, Chameides L, Schexnayder SM, Samson RA, Hazinski MF, Atkins DL, Berg MD, de Caen AR, Fink EL, Freid EB, Hickey RW, Marino BS, Nadkarni VM, Proctor LT, Qureshi FA, Sartorelli K, Topjian A, van der Jagt EW, Zaritsky AL. Part 14: pediatric advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(suppl 3):S876–S908.
© 2010 American Heart Association, Inc.
- © 2010 American Heart Association, Inc.
- Atkins DL,
- Everson-Stewart S,
- Sears GK,
- Daya M,
- Osmond MH,
- Warden CR,
- Berg RA
- Kitamura T,
- Iwami T,
- Kawamura T,
- Nagao K,
- Tanaka H,
- Nadkarni VM,
- Berg RA,
- Hiraide A
- Reis AG,
- Nadkarni V,
- Perondi MB,
- Grisi S,
- Berg RA
- Meaney PA,
- Nadkarni VM,
- Cook EF,
- Testa M,
- Helfaer M,
- Kaye W,
- Larkin GL,
- Berg RA
- Brilli RJ,
- Gibson R,
- Luria JW,
- Wheeler TA,
- Shaw J,
- Linam M,
- Kheir J,
- McLain P,
- Lingsch T,
- Hall-Haering A,
- McBride M
- Raju NV,
- Maisels MJ,
- Kring E,
- Schwarz-Warner L
- Carenzi B,
- Corso RM,
- Stellino V,
- Carlino GD,
- Tonini C,
- Rossini L,
- Gentili G
- Gausche M,
- Lewis RJ,
- Stratton SJ,
- Haynes BE,
- Gunter CS,
- Goodrich SM,
- Poore PD,
- McCollough MD,
- Henderson DP,
- Pratt FD,
- Seidel JS
- Wang HE,
- Lave JR,
- Sirio CA,
- Yealy DM
- Aufderheide TP,
- Sigurdsson G,
- Pirrallo RG,
- Yannopoulos D,
- McKnite S,
- von Briesen C,
- Sparks CW,
- Conrad CJ,
- Provo TA,
- Lurie KG
- Black K,
- Barnett P,
- Wolfe R,
- Young S
- Chan GM,
- Moyer-Mileur L,
- Rallison L
- Krieser D,
- Nguyen K,
- Kerr D,
- Jolley D,
- Clooney M,
- Kelly AM
- Hofer CK,
- Ganter M,
- Tucci M,
- Klaghofer R,
- Zollinger A
- Johnson TN
- Gill MA,
- Ueda CT
- Rodriguez W,
- Selen A,
- Avant D,
- Chaurasia C,
- Crescenzi T,
- Gieser G,
- Di Giacinto J,
- Huang SM,
- Lee P,
- Mathis L,
- Murphy D,
- Murphy S,
- Roberts R,
- Sachs HC,
- Suarez S,
- Tandon V,
- Uppoor RS
- Traub SL,
- Kichen L
- Walker RW,
- Ravi R,
- Haylett K
- Weiss M,
- Dullenkopf A,
- Fischer JE,
- Keller C,
- Gerber AC
- O'Donnell CP,
- Kamlin CO,
- Davis PG,
- Morley CJ
- Bhende MS,
- Thompson AE,
- Orr RA
- Bhende MS,
- Thompson AE
- Alsoufi B,
- Al-Radi OO,
- Nazer RI,
- Gruenwald C,
- Foreman C,
- Williams WG,
- Coles JG,
- Caldarone CA,
- Bohn DG,
- Van Arsdell GS
- Duncan BW,
- Ibrahim AE,
- Hraska V,
- del Nido PJ,
- Laussen PC,
- Wessel DL,
- Mayer JE Jr..,
- Bower LK,
- Jonas RA
- Thiagarajan RR,
- Laussen PC,
- Rycus PT,
- Bartlett RH,
- Bratton SL
- Aharon AS,
- Drinkwater DC Jr..,
- Churchwell KB,
- Quisling SV,
- Reddy VS,
- Taylor M,
- Hix S,
- Christian KG,
- Pietsch JB,
- Deshpande JK,
- Kambam J,
- Graham TP,
- Chang PA
- del Nido PJ
- Ghez O,
- Fouilloux V,
- Charpentier A,
- Fesquet P,
- Lion F,
- Lebrun L,
- Commandeur M,
- Fraisse A,
- Metras D,
- Kreitmann B
- Ravishankar C,
- Dominguez TE,
- Kreutzer J,
- Wernovsky G,
- Marino BS,
- Godinez R,
- Priestley MA,
- Gruber PJ,
- Gaynor WJ,
- Nicolson SC,
- Spray TL,
- Tabbutt S
- Thourani VH,
- Kirshbom PM,
- Kanter KR,
- Simsic J,
- Kogon BE,
- Wagoner S,
- Dykes F,
- Fortenberry J,
- Forbess JM
- Guly UM,
- Robertson CE
- Pokorna M,
- Necas E,
- Kratochvil J,
- Skripsky R,
- Andrlik M,
- Franek O
- Seigler RS,
- Tecklenburg FW,
- Shealy R
- Berg RA