Pediatric advanced life support (PALS)

INTRODUCTION — This topic will discuss the advanced components of recognition and treatment of respiratory failure, shock, cardiopulmonary failure, and cardiac arrhythmias in children.

Basic life support in children and guidelines for cardiac resuscitation in adults are discussed separately. (See "Pediatric basic life support (BLS) for health care providers" and "Advanced cardiac life support (ACLS) in adults".)

BACKGROUND — The American Heart Association (AHA) PALS program provides a structured approach to the assessment and treatment of the critically ill pediatric patient [1-4]. The AHA guidelines are based upon the International Liaison Committee on Resuscitation (ILCOR) consensus on science, which has transitioned to a continuous evidence evaluation process. As a result, periodic focused updates to the AHA PALS guidelines are anticipated as new science is published and reviewed.

The PALS content includes:

●Overview of assessment

●Recognition and management of respiratory distress and failure

●Recognition and management of shock

●Recognition and management of cardiac arrhythmias

●Recognition and management of cardiac arrest

●Postresuscitation management of patients with pulmonary and cardiac arrest

●Review of pharmacology

The clinician should primarily focus on prevention of cardiopulmonary failure through early recognition and management of respiratory distress, respiratory failure, and shock that can lead to cardiac arrest from hypoxia, acidosis, and ischemia.

ASSESSMENT — The assessment of respiratory distress and circulatory compromise in children, including the common findings, is covered in greater detail separately. (See "Initial assessment and stabilization of children with respiratory or circulatory compromise".)

PALS uses an assessment model that facilitates rapid evaluation and intervention for life-threatening conditions. In infants and children, most cardiac arrests result from progressive respiratory failure and/or shock, and one of the aims of this rapid assessment model is to prevent progression to cardiac arrest.

The evaluation includes:

●Initial impression (brief visual and auditory observation of child's overall appearance, work of breathing, circulation) (see "Initial assessment and stabilization of children with respiratory or circulatory compromise", section on 'Pediatric assessment triangle')

●Primary assessment – The clinician should in rapid sequence assess:

•Airway (patent, patent with maneuvers/adjuncts, partially or completely obstructed)

•Breathing (respiratory rate, effort, tidal volume, lung sounds, pulse oximetry)

•Circulation (skin color and temperature, heart rate and rhythm, blood pressure, peripheral and central pulses, capillary refill time)

•Disability

-AVPU pediatric response scale: Alert, Voice, Pain, Unresponsive

-Pupillary response to light

-Presence of hypoglycemia (rapid bedside glucose or response to empiric administration of dextrose)

-Glasgow Coma Scale: Eye Opening, Verbal Response, Motor Response (table 1) (for trauma patients)

•Exposure (fever or hypothermia, skin findings, evidence of trauma)

●Secondary assessment – This portion of the evaluation includes a thorough head to toe physical examination, as well as a focused medical history that consists of the "SAMPLE" history:

•S: Signs and symptoms

•A: Allergies

•M: Medications

•P: Past medical history

•L: Last meal

•E: Events leading to current illness

●Tertiary assessment – Injury and infection are common causes of life-threatening illness in children. Thus, ancillary studies are frequently directed towards identifying the extent of trauma or an infectious focus. (See "Trauma management: Approach to the unstable child", section on 'Adjuncts to the primary survey' and "Trauma management: Approach to the unstable child", section on 'Adjuncts to the secondary survey' and "Initial evaluation of shock in children", section on 'Evaluation' and "Approach to the ill-appearing infant (younger than 90 days of age)", section on 'Ancillary studies for infectious etiologies'.)

Respiratory distress and failure — Recognition and treatment of respiratory conditions that respond to simple measures (eg, supplemental oxygen or inhaled bronchodilators) are major goals of PALS [5]. The clinician may also have to treat rapidly progressive conditions and intervene with advanced therapies to avoid cardiopulmonary arrest in patients with respiratory failure. Early detection and treatment improve overall outcome.

There are many causes of acute respiratory compromise in children (table 2). The clinician should strive to categorize respiratory distress or failure into one or more of the following [5] (see "Acute respiratory distress in children: Emergency evaluation and initial stabilization"):

●Upper airway obstruction (eg, croup, epiglottitis)

●Lower airway obstruction (eg, bronchiolitis, status asthmaticus)

●Lung tissue (parenchymal) disease (eg, bronchopneumonia)

●Disordered control of breathing (eg, seizure, coma, muscle weakness)

Initial management supports airway, breathing, and circulation:

●Airway – Key steps in basic airway management include (see "Basic airway management in children"):

•Provide 100 percent inspired oxygen

•Allow the child to assume a position of comfort or manually open the airway

•Clear the airway (suction)

•Insert an airway adjunct if consciousness is impaired (eg, nasopharyngeal airway or, if gag reflex absent, oropharyngeal airway)

•If the patient is unresponsive without signs of life, begin chest compressions immediately

●Breathing – The clinician should:

•Assist ventilation manually in patients not responding to basic airway maneuvers or with inadequate or ineffective respiratory effort

•Monitor oxygenation by pulse oximetry

•Monitor ventilation by end-tidal carbon dioxide (EtCO₂) if available

•Administer medications as needed (eg, albuterol for status asthmaticus, inhaled racemic epinephrine for croup)

In preparation for intubation, 100 percent oxygen should be applied via non-rebreather mask or other high concentration device. If the patient has evidence of respiratory failure, positive pressure ventilation should be initiated with a bag-valve-mask or flow-inflating device to oxygenate and improve ventilation. (See "Basic airway management in children".)

Children who cannot maintain their airway, oxygenation, or ventilatory requirements should undergo placement of an artificial airway, usually via endotracheal intubation and, less commonly, with a supraglottic airway or alternative device. Certain populations of patients with upper airway obstruction and/or respiratory failure may respond to noninvasive ventilation (CPAP or BiPAP) if airway reflexes are preserved. A rapid overview describes the steps in performing rapid sequence intubation (table 3). (See "Noninvasive ventilation for acute and impending respiratory failure in children" and "Emergency endotracheal intubation in children" and "Rapid sequence intubation (RSI) outside the operating room in children: Approach".)

●Circulation – Key interventions consist of monitoring heart rate and rhythm and establishing vascular access to provide volume administration and/or medications for resuscitation. (See "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies".)

Shock — The goal is to recognize and categorize the type of shock in order to prioritize treatment options (algorithm 1). Early treatment of shock may prevent the progression to cardiopulmonary failure (algorithm 2). The management of shock is discussed separately. (See "Initial management of shock in children" and "Septic shock in children: Rapid recognition and initial resuscitation (first hour)".)

Shock may occur with normal, increased, or decreased systolic blood pressure. Shock in children is usually related to low cardiac output, but some patients may have high cardiac output, such as with sepsis or severe anemia. (See "Initial evaluation of shock in children".)

Shock severity is usually categorized by its effect on systolic blood pressure [6]:

●Compensated shock – Compensated shock occurs when compensatory mechanisms (including tachycardia, increased systemic vascular resistance, increased inotropy, and increased venous tone) maintain a systolic blood pressure within a normal range (table 4 and table 5).

●Hypotensive shock (or decompensated shock) – Hypotensive shock occurs when compensatory mechanisms fail to maintain systolic blood pressure.

The definition of hypotension varies by age [6]:

•In term infants 0 to 1 month of age, systolic pressure <60 mmHg

•For infants 1 to 12 months of age, hypotension is defined by systolic pressure <70 mmHg

•In children 1 to 10 years of age, hypotension is defined as:

•In children over 10 years of age, systolic blood pressure <90 mmHg

Hypotensive shock may rapidly progress to cardiopulmonary failure.

●Shock categorization – There are four major categories of shock [6] (see "Initial evaluation of shock in children"):

•Hypovolemic shock – Hypovolemic shock is characterized by inadequate circulating blood volume. Common causes of fluid loss include diarrhea, hemorrhage (internal and external), vomiting, inadequate fluid intake, osmotic diuresis (eg, diabetic ketoacidosis), third-space losses, and burns.

•Distributive shock – Distributive shock describes inappropriately distributed blood volume typically associated with decreased systemic vascular resistance. Common causes include septic shock, anaphylactic shock, and neurogenic shock (eg, head injury, spinal injury).

•Cardiogenic shock – Cardiogenic shock refers to impairment of heart contractility. Common causes include congenital heart disease, myocarditis, cardiomyopathy, arrhythmias, sepsis, poisoning or drug toxicity, and myocardial injury (trauma).

•Obstructive shock – In this form of shock, hypotension arises from obstructed blood flow to the heart or great vessels. Common causes include cardiac tamponade, tension pneumothorax, ductal dependent congenital heart lesions, and massive pulmonary embolism.

Any given patient may suffer from more than one type of shock. For example, a child in septic shock may develop hypovolemia during the prodrome phase, distributive shock during the early phase of sepsis, and cardiogenic shock later in the course.

Cardiopulmonary failure — Respiratory failure and hypotensive shock are the most common conditions preceding cardiac arrest.

●Causes of respiratory failure include:

•Upper airway obstruction (choking, infection)

•Lower airway obstruction (asthma, foreign body aspiration)

•Parenchymal disease (pneumonia, acute pulmonary edema)

•Disordered control of breathing (coma, toxic ingestion, status epilepticus)

●Causes of hypotensive shock include:

•Hypovolemia (dehydration, hemorrhage)

•Cardiac failure (eg, due to myocarditis or valvular disease)

•Distributive shock (septic, neurogenic)

•Metabolic/electrolyte disturbances

•Acute myocardial infarction/ischemia

•Toxicologic ingestions

•Pulmonary embolism

●The following physical findings often precede cardiopulmonary failure:

•Airway – Stridor, stertor, drooling, and/or severe retractions

•Breathing – Bradypnea, irregular, ineffective respiration, gasping, and/or cyanosis

•Circulation – Bradycardia, capillary refill >5 seconds, weak central pulses, no peripheral pulses, hypotension, cool extremities, and/or mottled/cyanotic skin

•Disability – Diminished level of consciousness

The patient in cardiopulmonary failure will progress rapidly to cardiac arrest without aggressive intervention. Positive pressure ventilations with 100 percent inspired oxygen, chest compressions for heart rate <60 beats per minute in patients with poor perfusion, and administration of intravenous fluids and medications tailored to treat the underlying cause are indicated. (See "Basic airway management in children" and "Pediatric basic life support (BLS) for health care providers".)

Heart rate and rhythm — In children, the heart rate is classified as bradycardia, tachycardia, and pulseless arrest. Interpretation of the cardiac rhythm requires knowledge of the child's typical heart rate (table 6) and baseline rhythm as well as level of activity and clinical condition.

Bradycardia — Bradyarrhythmias are common pre-arrest rhythms in children and are often due to hypoxia. Bradycardia with symptoms of shock (eg, poor systemic perfusion, hypotension, altered consciousness) requires urgent treatment to prevent cardiac arrest (algorithm 3). (See 'Bradycardia algorithm' below.)

Bradycardia is defined as a heart rate that is slow compared with normal heart rates for the patient's age (table 6) [7].

Primary bradycardia is the result of congenital and acquired heart conditions that directly slow the spontaneous depolarization rate of the heart's pacemaker or slow conduction through the heart's conduction system.

Secondary bradycardia is the result of conditions that alter the normal function of the heart, including hypoxia, acidosis, hypotension, hypothermia, and drug effects.

●Signs and symptoms – Pathologic bradycardia frequently causes a change in the level of consciousness, lightheadedness, dizziness, syncope, or fatigue. Shock associated with bradycardia can manifest with hypotension, poor end-organ perfusion, altered consciousness, and/or sudden collapse.

Electrocardiogram (ECG) findings associated with bradycardia include (see "Bradycardia in children"):

•Slow heart rate relative to normal rates (table 6)

•P waves that may or may not be visible

•QRS complex that is narrow (electrical conduction arising from the atrium or high nodal area) or wide (electrical conduction from low nodal or ventricular region)

•P wave and QRS complex may be unrelated (ie, atrioventricular dissociation) or have an abnormally long period between them (atrioventricular block)

Typical bradyarrhythmias include:

●Sinus bradycardia – Sinus bradycardia is commonly an incidental finding in healthy children as a normal consequence of reduced metabolic demand (sleep, rest) or increased stroke volume (well-conditioned athlete) (waveform 1). Pathologic causes include hypoxia, hypothermia, poisoning, electrolyte disorders, infection, sleep apnea, drug effects, hypoglycemia, hypothyroidism, and increased intracranial pressure. (See "Bradycardia in children", section on 'Sinus bradycardia'.)

●Atrioventricular block – Atrioventricular (AV) block is defined as a delay or interruption in the transmission of an atrial impulse to the ventricles due to an anatomical or functional impairment in the conduction system. Heart block is categorized into three types:

•First degree – First degree AV block is characterized by a prolonged PR interval for age caused by slow conduction through the AV node without missed ventricular beats (waveform 2). Of note, first degree AV block does not cause bradycardia. In general, the normal PR-intervals are: 70 to 170 msec in newborns, and 80 to 200 msec in young children and adults. (See "Bradycardia in children", section on 'First-degree atrioventricular block'.)

•Second degree – In second degree AV block, the organized atrial impulse fails to be conducted to the ventricle in a 1:1 ratio. There are two types of second degree AV block (see "Bradycardia in children", section on 'Second-degree atrioventricular block'):

-Mobitz type I (Wenckebach phenomenon) – On ECG, there is progressive prolongation of the PR-interval until a P wave fails to be conducted (waveform 3). The block is located at the level of the AV node and is usually not associated with other significant conduction system disease or symptoms.

-Mobitz type II – This block occurs below the AV node and has consistent inhibition of a specific proportion of atrial impulses, usually with a 2:1 atrial to ventricular rate (waveform 4). It has a less predictable course and frequently progresses to complete heart block.

•Third degree – In third-degree AV block, also referred to as complete heart block, there is complete failure of the atrial impulse to be conducted to the ventricles (waveform 5). The atrial and ventricular activity is independent of one another. The ventricular escape rhythm that is generated is dictated by the location of the block. It is usually slower than the lower limits of normal for age, resulting in clinically significant bradycardia. (See "Bradycardia in children", section on 'Third-degree atrioventricular block'.)

Tachycardia — Relative tachycardia is a heart rate that is too fast for the child's age, level of activity, and clinical condition (table 6). In children, sinus tachycardia usually represents hypovolemia, fever, physiologic response to stress, pain, or fear, or drug effect (such as with beta agonists). (See "Approach to the child with tachycardia".)

Tachyarrhythmias are fast abnormal rhythms originating in the atria or the ventricles. Certain arrhythmias, such as supraventricular tachycardia and ventricular tachycardia, can lead to shock and cardiac arrest. Unstable rhythms lead to poor tissue perfusion with a fall in cardiac output, poor coronary artery perfusion, and increased myocardial oxygen demand, which can all lead to cardiogenic shock.

Signs and symptoms in children with tachycardia are often nonspecific and vary by age. They may include palpitations, lightheadedness, dizziness, fatigue and syncope. In infants, prolonged tachycardia may cause poor feeding, tachypnea, and irritability with signs of heart failure. (See "Approach to the child with palpitations" and "Emergency evaluation of syncope in children and adolescents".)

Important ECG findings include:

●Heart rate that is fast compared with normal rates (table 6)

●P waves that may or may not be visible

●QRS interval that is narrow or wide

Treatment priorities in managing tachycardias rely on whether hemodynamic instability is present and differentiating between tachycardia with narrow QRS complex (sinus tachycardia, supraventricular tachycardia, atrial flutter) and wide QRS complex tachycardias (ventricular tachycardia, supraventricular tachycardia with aberrant intraventricular conduction) (algorithm 4):

●Sinus tachycardia – Sinus tachycardia is characterized by a rate of sinus node discharge that is faster than normal for the patient's age (table 6). This rhythm usually represents the body's increased need for cardiac output or oxygen delivery. The heart rate is not fixed and varies with other factors, including fever, stress, and level of activity. Causes include tissue hypoxia, hypovolemia, fever, metabolic stress, injury, pain, anxiety, toxins/poisons/drugs, and anemia. Less common causes include cardiac tamponade, tension pneumothorax, and thromboembolism. (See "Approach to the child with tachycardia".)

Typical ECG findings in patients with sinus tachycardia include:

•Heart rate is usually <220/min in infants, <180/min in children, and exhibits beat to beat variability in rate.

•P waves are present with normal appearance.

•PR interval is constant and exhibits a normal duration for age.

•R-R interval is variable.

•QRS complex is narrow.

●Supraventricular tachycardia – Supraventricular tachycardia (SVT) can be defined as an abnormally rapid heart rhythm originating above the ventricles, often (but not always) with a narrow QRS complex; it conventionally excludes atrial flutter and atrial fibrillation. The two most common forms of SVT in children are atrioventricular reentrant tachycardia (AVRT), including the Wolff-Parkinson-White (WPW) syndrome (waveform 6), and atrioventricular nodal reentrant tachycardia (AVNRT).

•Signs and symptoms – SVT typically has an abrupt onset and intermittent presentation. Signs and symptoms in infants include poor feeding, tachypnea, irritability, increased sleepiness, diaphoresis, pallor, and/or vomiting. Older children may have palpitations, shortness of breath, chest pain/discomfort, dizziness, lightheadedness, and/or fainting. Infants and children with prolonged SVT may display clinical findings of heart failure. (See "Clinical features and diagnosis of supraventricular tachycardia (SVT) in children", section on 'Clinical features'.)

Typical ECG findings in patients with SVT include [7]:

-Heart rate that is usually >220/min in infants, >180/min in children, and has no or minimal beat to beat variability.

-P waves are absent or abnormal.

-PR interval may not be present or short PR interval with ectopic atrial tachycardia.

-R-R interval is usually constant.

-QRS is usually narrow. Conduction delay along the ventricular system may lead to an appearance of wide complex tachycardia, known as SVT with aberrant conduction.

●Ventricular tachycardia – Ventricular tachycardia (VT) originates from the ventricular myocardium or Purkinje cells below the bifurcation of the bundle of His (waveform 7). VT may present with or without pulses. VT is associated with sudden cardiac death. As a result, patients who develop VT or are at risk for developing VT must be identified, evaluated, and treated, if necessary.

VT with pulses can vary in rate from near normal to >200 beats per minute. Faster rates can compromise stroke volume and cardiac output leading to pulseless VT or ventricular fibrillation (VF). Causes of VT include underlying heart disease or cardiac surgery, prolonged QT syndrome or other channelopathies, or myocarditis/cardiomyopathy. Other causes include hyperkalemia and toxic ingestions (eg, tricyclic antidepressants, cocaine) (table 7).

Findings of ventricular tachycardia on ECG include (waveform 7):

•Ventricular rate is >120 beats per minute and regular.

•P waves are often not identifiable, may have AV dissociation, or may have retrograde depolarization.

•QRS is typically wide (>0.09 seconds).

•T waves are often opposite in polarity from the QRS complex.

Ventricular fibrillation, causes of wide complex QRS, and treatment of pulseless arrest are discussed separately. (See 'Pulseless arrest' below and "Causes of wide QRS complex tachycardia in children", section on 'Ventricular tachycardia' and 'Pulseless arrest algorithm' below.)

Pulseless arrest — Pulseless arrest refers to the cessation of blood circulation caused by absent or ineffective cardiac mechanical activity. Most pediatric cardiac arrests are hypoxic/asphyxial arrests that result from a progression of respiratory distress, respiratory failure, or shock rather than from primary cardiac arrhythmias ("sudden cardiac arrest").

Children with pulseless arrest appear apneic or display a few agonal gasps. They have no palpable pulses, and are unresponsive.

The arrest rhythms consist of:

●Shockable rhythms:

•Ventricular fibrillation – Ventricular fibrillation is characterized by no organized rhythm and no coordinated contractions (waveform 8). Electrical activity is chaotic. Causes overlap with etiologies of ventricular tachycardia, including hyperkalemia, congenital or acquired heart disease, toxic exposures, electrical or lightning shocks, and submersion.

•Pulseless ventricular tachycardia – Pulseless VT is a cardiac arrest of ventricular origin characterized by organized, wide QRS complexes (waveform 7). Any cause of VT with pulses can lead to pulseless VT. (See 'Tachycardia' above.)

•Torsades de pointes – Torsades de pointes or polymorphic VT displays a QRS complex that changes in polarity and amplitude, appearing to rotate around the ECG isoelectric line (translation: "twisting of the points") (waveform 9). This arrhythmia is associated with markedly prolonged QTc interval from congenital conditions (long QT syndrome), drug toxicity (antiarrhythmic drugs, tricyclic antidepressants, calcium channel blockers, phenothiazine), and electrolyte disturbances (eg, hypomagnesemia arising from anorexia nervosa). Ventricular tachycardia, including torsades de pointes, can deteriorate into ventricular fibrillation.

●Asystole – Children with asystole have cardiac standstill with no discernible electrical activity (waveform 8). The most common cause is respiratory failure progressing to critical hypoxemia, bradycardia, and then cardiac standstill. Underlying conditions include airway obstruction, pneumonia, submersion, hypothermia, sepsis, and poisoning (eg, carbon monoxide poisoning, sedative-hypnotics) leading to hypoxia and acidosis.

●Pulseless electrical activity – Pulseless electrical activity (PEA) consists of any organized electrical activity observed on ECG in a patient with no central palpable pulse. Reversible conditions may underlie PEA, including:

•Hypovolemia

•Hypoxia

•Hydrogen ion (acidosis)

•Hypo-/hyperkalemia

•Hypoglycemia

•Hypothermia

•Toxins

•Tamponade, cardiac

•Tension pneumothorax

•Thrombosis (coronary or pulmonary)

•Trauma

These can be remembered as the H's and T's of PEA [8].

COVID-19 PATIENTS (SUSPECTED OR CONFIRMED) — The American Heart Association (AHA) in collaboration with several other major medical organizations has published guidance, including updated algorithms for basic and advanced life support for children with suspected or confirmed COVID-19 [9] with additional focused, pediatric-specific guidance from the American Academy of Pediatrics [10].

For in-hospital pediatric cardiac arrest, modifications to advanced life support include (algorithm 5) [10]:

●Locate patients at risk for cardiac arrest in negative pressure rooms whenever possible.

●Don personal protective equipment (PPE) (eg, gown, N95 face mask, tight-fitting eye goggles or face shield, gloves) prior to entering the patient room and ensure that all members of the resuscitation team have the necessary PPE or immediately excuse them and replace them with properly protected providers.

●Keep the door to the resuscitation room closed.

●Limit personnel who are performing cardiopulmonary resuscitation (CPR). In general, a minimum of four providers is needed for high-quality pediatric advanced resuscitation. Video monitors, if available, can be used so that one team member may remain outside the room to monitor and record the resuscitation.

●Securely attach a high-efficiency particulate air (HEPA) filter with a low dead space to any ventilation device:

•For unintubated patients:

-Rapidly begin ventilating with a bag-mask and HEPA filter with a tight seal, ideally with a two-person technique (picture 1). Consider use of a supraglottic airway to optimize chest compression fraction prior to intubation.

-Determine the need for endotracheal intubation based upon the overall clinical picture and per usual care standards.

-If performed, ensure endotracheal intubation with a cuffed endotracheal tube by the person most likely to achieve success on the first pass (table 8) using a videolaryngoscope, if available.

-Pause chest compression to perform endotracheal intubation.

-Connect the patient to a ventilator with inline HEPA filter and minimize any subsequent ventilator disconnections.

•For patients intubated and ventilated before arrest:

-To reduce aerosol exposure, ensure that the endotracheal tube is connected, patent, and in proper position, and leave the patient connected to a closed ventilator system with an in-line HEPA filter.

-For patients in the prone position at the time of arrest, initiate compressions with the hand centered over the T7 to T10 vertebral bodies, arrange sufficient numbers of trained personnel in PPE to safely turn the patient to the supine position, and then reinitiate CPR in the supine position.

•Ventilator settings during pediatric CPR:

-Increase FiO₂ to 1 (100 percent).

-Based upon patient age and size, use either volume-controlled (table 9) or pressure-controlled (table 10) ventilator settings that produce adequate chest wall rise.

-Initially set positive end-expiratory pressure (PEEP) to physiologic (3 to 5 cmH₂O); adjust as needed to optimize lung volume while maintaining adequate venous return.

-Adjust trigger settings so that chest compressions do not cause the ventilator to initiate a breath.

-Set the ventilation rate to 20 to 30 breaths per minute in infants and children.

Health care providers can significantly reduce their risk of infection, especially severe infection and death by, receiving the SARS CoV-2 vaccine and recommended boosters.

AHA RESUSCITATION GUIDELINES — The approach to pediatric advanced life support presented in this topic is based on the 2020 American Heart Association (AHA) Guidelines on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care [3,4].

Bradycardia algorithm — The management of bradycardia focuses on (algorithm 3):

●Reestablishing or optimizing oxygenation and ventilation (see "Basic airway management in children")

●Supporting circulation with chest compressions for patients with poor perfusion and a heart rate <60 beats per minute

●Using medications (ie, epinephrine or atropine) to increase heart rate and cardiac output

If these measures fail, transcutaneous pacing can be attempted; however, the same factors that are producing refractory bradycardia (eg, hypoxia, hypothermia, electrolyte disturbance, or drug overdose) may prevent effective electrical capture. (See "Bradycardia in children", section on 'Acute management of patients with poor perfusion'.)

Tachycardia algorithm — The management of sinus tachycardia focuses on treatment of the underlying physiologic derangement and is largely supportive.

The management of tachyarrhythmias that are not sinus in origin is guided by the appearance of the QRS complex, and by the patient's status, whether unstable or stable (algorithm 4) [3,4]:

●Unstable – Patients with a pulse and either narrow or wide complex tachycardia who have significantly impaired consciousness and hypotensive shock should be treated with synchronized cardioversion (initial dose: 0.5 to 1 J/kg) (algorithm 4). (See "Defibrillation and cardioversion in children (including automated external defibrillation)", section on 'Methods: Manual defibrillator use'.)

●Stable – For patients who are mentating and not hypotensive, treatment is determined by the QRS complex:

•Narrow QRS (≤0.09 seconds) – For narrow complex tachycardia suggestive of supraventricular tachycardia (SVT), vagal maneuvers may be attempted while preparing for medication administration. Appropriate vagal maneuvers include application of ice to the face or, in a cooperative child, a Valsalva maneuver by bearing down or blowing into an occluded straw.

The first recommended medication for SVT is adenosine, 0.1 mg/kg (maximum dose 6 mg) administered rapidly IV/IO and followed by a rapid saline flush (table 11). (See "Management of supraventricular tachycardia (SVT) in children", section on 'Supraventricular tachycardia refractory to vagal maneuvers'.)

•Wide QRS (>0.09 seconds) – If the wide-complex rhythm is monomorphic and regular, it is acceptable to administer a dose of adenosine to determine if the rhythm is actually supraventricular tachycardia with aberrant conduction.

Antiarrhythmic therapy of wide-complex tachycardia involves agents with significant side effects (eg, amiodarone or procainamide) and consultation with a pediatric cardiology specialist is strongly recommended. (See "Management and evaluation of wide QRS complex tachycardia in children", section on 'Management'.)

Pulseless arrest algorithm — Treatment of a pediatric cardiac arrest is provided in the algorithm (algorithm 6) and summarized below [1,2]. The epidemiology of cardiac arrest in children is discussed separately. (See "Pediatric basic life support (BLS) for health care providers", section on 'Epidemiology and survival'.)

Start CPR — The first step is to initiate cardiopulmonary resuscitation according to the algorithms for a single rescuer (algorithm 7) or two or more rescuers (algorithm 8) [11,12].

Pediatric basic life support by health care providers is discussed in detail separately. (See "Pediatric basic life support (BLS) for health care providers".)

Shockable rhythm — Patients with ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT) should receive immediate CPR and defibrillation at 2 J/kg as soon as a device is available (algorithm 6). After delivering the shock, perform approximately two minutes of CPR (10 cycles for two person CPR or 5 cycles for one person CPR) before checking the rhythm [1,2].

If the rhythm has not converted with defibrillation, then the patient should receive repeated defibrillation at a higher dose (4 J/kg) followed by additional cycles of CPR [1,2]. Subsequent defibrillations should be provided at a minimum of 4 J/kg, up to 10 J/kg or the adult energy dose (typically 120 to 200 J for a biphasic defibrillator and 360 J for a monophasic defibrillator).

Although manual defibrillators operated by advanced life support providers or automated external defibrillators with pediatric attenuating devices are preferred for use in infants and children, automated external defibrillators without pediatric attenuating devices may be used if they are the only option available. (See "Pediatric basic life support (BLS) for health care providers", section on 'Automated external defibrillator' and "Defibrillation and cardioversion in children (including automated external defibrillation)", section on 'Methods: Manual defibrillator use'.)

Persistent VF or pVT requires the addition of medications such as parenteral epinephrine every three to five minutes and antiarrhythmic therapy (eg, amiodarone or lidocaine for VF or pVT (algorithm 6) or magnesium sulfate for torsades de pointes) [1-4,13]. When giving medications, the IO or IV route is always preferred to administration through the endotracheal tube. Attempts at vascular or intraosseous access should not interrupt chest compressions. During CPR, intraosseous access may be pursued initially, or simultaneously with peripheral vascular access. (See "Intraosseous infusion" and "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies", section on 'General approach'.)

Drug doses are as follows (table 11) [1-3]:

●Epinephrine – The IV/IO dose of epinephrine is 0.01 mg/kg (0.1 mL/kg of the 0.1 mg/mL concentration) given every three to five minutes; maximum single dose: 1 mg (10 mL).

When epinephrine is administered via endotracheal tube, use a 10-fold higher dose or 0.1 mg/kg (0.1 mL/kg of the 1 mg/mL concentration) every three to five minutes. (See "Primary drugs in pediatric resuscitation", section on 'Epinephrine'.)

●Amiodarone – The initial IV/IO dose of amiodarone is 5 mg/kg (maximum single dose 300 mg). The 5 mg/kg (maximum 300 mg) dose can be repeated twice. (See "Primary drugs in pediatric resuscitation", section on 'Amiodarone'.)

●Lidocaine – The initial IV/IO bolus dose of lidocaine is 1 mg/kg. This may be followed by an infusion of 20 to 50 mcg/kg/min. The bolus dose should be repeated if the lidocaine infusion is started more than 15 minutes after the initial bolus. Although lidocaine can be given through the endotracheal tube, the optimal dose is unknown. An increase of two- to threefold is suggested. (See "Primary drugs in pediatric resuscitation", section on 'Lidocaine' and "Primary drugs in pediatric resuscitation", section on 'Endotracheal drug administration'.)

●Magnesium sulfate – The IV/IO dose is 25 to 50 mg/kg (maximum dose 2 g) given as an infusion of magnesium sulfate diluted in a 5 percent dextrose solution (D5W) to a concentration of 20 percent or less and, in an arrested patient, infused over one to two minutes. (See "Primary drugs in pediatric resuscitation", section on 'Magnesium sulfate'.)

Resuscitation medications given through an IO or peripheral IV should be followed with a 5 to 10 mL flush of normal saline to move the drug from the peripheral to the central circulation.

Asystole or pulseless electrical activity — Patients with asystole or pulseless electrical activity should receive cardiopulmonary resuscitation and epinephrine as soon as possible after arrest [1-4].

During the course of the resuscitation, the clinician should evaluate for and treat underlying causes (H's and T's) for the pulseless arrest [1,2]. When giving medications, the IO or IV route is always preferred to administration through the endotracheal tube. Attempts at vascular or intraosseous access should NOT interrupt chest compressions. During CPR, intraosseous access may be pursued initially, or simultaneously with peripheral vascular access. (See "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies", section on 'General approach'.)

The IV/IO dose of epinephrine is 0.01 mg/kg (0.1 mL/kg of the 0.1 mg/mL concentration) given every three to five minutes; maximum single dose: 1 mg (10 mL). Epinephrine given through an IO or peripheral IV should be followed with a 5 to 10 mL flush of normal saline to move the drug from the peripheral to the central circulation. IV/IO administration is strongly preferred to endotracheal (ET) administration.

When epinephrine is administered via ET tube, the dose should be increased 10-fold to 0.1 mg/kg (0.1 mL/kg of the 1 mg/mL concentration) every three to five minutes. (See "Primary drugs in pediatric resuscitation", section on 'Epinephrine' and "Primary drugs in pediatric resuscitation", section on 'Endotracheal drug administration'.)

Among children who arrest in an inpatient setting and who do not have rapid return of spontaneous circulation with initiation of basic life support, timely administration of epinephrine is associated with improved survival [14,15]. As an example, in a retrospective review of registry data on 1558 children with inpatient arrest and a documented non-shockable initial rhythm, the median time to the first dose of epinephrine was one minute [14,16]. Adjusted survival to discharge was seen in up to 37 percent of patients receiving epinephrine one minute or less after arrest and decreased 5 percent for every additional minute delay in epinephrine administration. Survival with favorable neurologic outcome at discharge occurred in approximately 16 percent of patients and also decreased 5 percent for every additional minute of delay in epinephrine administration based upon adjusted analysis.

Monitoring — Given the importance of high quality chest compressions, techniques to measure and monitor CPR performance have been developed. Feedback devices for pediatric patients are not widely available, and there are no studies evaluating the effect of their use on outcome. (See "Pediatric basic life support (BLS) for health care providers", section on 'Chest compressions'.)

In adults, end-tidal carbon dioxide (EtCO₂) measurements from continuous waveform capnography also accurately reflect cardiac output and cerebral perfusion pressure, and therefore the quality of CPR. A decline in EtCO₂ during resuscitation may indicate inadequate effectiveness of compressions, dislodgement of an endotracheal tube, or disruption of pulmonary blood flow (eg, massive pulmonary embolus). Whether EtCO₂ has similar ability to identify the quality of CPR during pediatric resuscitations and specific values to guide therapy have not been established [1,2]. (See "Advanced cardiac life support (ACLS) in adults", section on 'Intra-arrest monitoring' and "Carbon dioxide monitoring (capnography)", section on 'Effectiveness of CPR'.)

In pediatric patients with a declining EtCO₂, efforts to improve the quality of compressions and to avoid excessive ventilation are appropriate. Thus, in addition to monitoring rate and clinical effectiveness of ventilation, we use EtCO₂ measurements from continuous waveform capnography whenever possible during pediatric cardiac arrest. Sudden, sustained increases in EtCO₂ during CPR are associated with a return of spontaneous circulation (ROSC). (See "Carbon dioxide monitoring (capnography)", section on 'Return of spontaneous circulation'.)

In adults, measurements of arterial relaxation provide a reasonable approximation of coronary perfusion pressure. During CPR, a reasonable goal is to maintain the arterial relaxation (or "diastole") pressure above 20 mmHg. Similarly, in adult patients, central venous oxygen saturation (SCVO₂) provides information about oxygen delivery and cardiac output. During CPR, a reasonable goal is to maintain SCVO₂ above 30 percent (see "Advanced cardiac life support (ACLS) in adults", section on 'Intra-arrest monitoring'). Data from other physiologic monitors are less likely to be available in children with pulseless arrest, but measurements obtained from arterial and central venous catheters can provide useful feedback about the quality of CPR and the presence of ROSC. Published evidence from analysis of hemodynamic monitoring data during in-hospital pediatric CPR has found an association between a mean diastolic blood pressure (DBP) of >25 mmHg in infants young than one year of age and >30 mmHg in children one year of age and older and survival to discharge, as well as survival to discharge with favorable neurologic outcome [17]. However, specific targets for SCVO₂ have not been established in children during cardiac arrest [1,2].

Extracorporeal membrane oxygenation (ECMO) with CPR (ECPR) — Use of ECPR in settings with existing ECMO protocols, expertise, and equipment may be beneficial for selected patients who fail conventional CPR after inpatient cardiac arrest [18]. Our approach is to activate ECPR after approximately 5 to 10 minutes of failed conventional resuscitation in patients with conditions that may be reversible after a period of mechanical circulatory support (eg, myocarditis, pulmonary or air embolus, sudden arrest after cardiac surgery, poisoning, or primary hypothermic arrest) or who are candidates for the use of ECPR as a bridge to therapies such as cardiac transplantation.

Extracorporeal membrane oxygenation with CPR (ECPR) for infants and children with in-hospital cardiac arrests is used in selected institutions with resources to rapidly deploy ECMO when conventional resuscitation efforts are unsuccessful [1,2,19,20]. A single-institution series of 56 patients undergoing ECPR (almost 80 percent of patients with structural cardiac disease) showed a survival to discharge of 66 percent and a reasonable quality of life at a median of 38 months [21]. Other observational studies also indicate improved outcomes only for patients with underlying cardiac diseases (eg, cardiomyopathy, myocarditis, or congenital cardiac anomalies) [22-24]. For such patients, intact survival approaching 50 percent has been described [23]. Furthermore, intact survival has occurred even after prolonged periods of chest compressions (>60 minutes) in these patients. In addition, in a small observational study of neurocognitive outcomes in 47 pediatric ECPR survivors, 60 percent had no to mild impairment at one year after arrest [25].

In one multicenter prospective cohort study of 3756 children with inpatient cardiac arrests, ECPR was associated with overall increased rates of survival to discharge and favorable neurologic outcomes on adjusted analysis [20]. However, the study pooled patients with cardiac and noncardiac etiologies even though ECPR was much more likely to be used in surgical cardiac patients. When these groups were analyzed separately, only the cardiac patients had statistically significant improved outcomes. Another large registry study that included neonates through adults with cardiac disease looked at over 14,000 admissions of which 3.1 percent underwent at least one ECMO course [26]. Mortality rates for both cardiac surgical and cardiac medical patients receiving ECPR were high (50 and 83 percent, respectively). Special considerations for resuscitation of pediatric patients with cardiac disease have been published in an AHA Scientific Statement and provide additional resuscitation recommendations according to structural and physiologic abnormalities [27].

Termination of resuscitation — Although certain factors are associated with better or worse outcomes after cardiac arrest in infants and children, no single factor is reliable enough to accurately guide whether termination efforts should cease or continue [1,2].

Thus, the decision to terminate resuscitation should be individualized and multiple factors considered including:

●Duration of cardiac arrest, including when the patient was discovered relative to initial presentation (eg, patients with sudden infant death syndrome who are found with evidence of lividity would have CPR discontinued earlier than patients with in hospital arrests)

●Presenting rhythm (eg, shockable versus asystole or pulseless electrical activity)

●Underlying disease or cause, if known (eg, cardiac disease, trauma, respiratory failure, or sepsis)

●Setting and available resources

●Do not resuscitate status

Intact survival after prolonged resuscitation (>30 minutes) has occurred in patients with the following conditions [8]:

●Poisoning

●Primary hypothermic arrest (see "Hypothermia in children: Management", section on 'Nonperfusing cardiac rhythms')

●Patients with cardiac disease resuscitated with ECPR (see 'Extracorporeal membrane oxygenation (ECMO) with CPR (ECPR)' above)

Immediate and early postresuscitation management — The early postresuscitation period involves the time soon after return of spontaneous circulation or recovery from circulatory or respiratory failure up to 12 hours post-event. During this time, the clinician must continue to treat the underlying cause of the life-threatening event and monitor for common respiratory or circulatory problems that may cause secondary morbidity or death [3,4,28].

Maintain airway — All intubated children require continued assessment to ensure proper endotracheal tube positioning, including continuous monitoring of oxygenation (pulse oximetry), and ongoing monitoring of ventilation (eg, continuous EtCO₂ monitoring, if available, and/or intermittent blood gas assessment). Insertion of a gastric tube helps to reduce gastric distension and may prevent vomiting.

The causes of sudden decompensation in a child who has been successfully intubated with an artificial airway is described by the mnemonic "DOPE" [8]:

●D: Dislodged or displaced endotracheal tube (right mainstem or esophageal location)

●O: Obstructed endotracheal tube (eg, mucous plug, kinked endotracheal tube)

●P: Pneumothorax

●E: Equipment failure (eg, ventilator malfunction, oxygen disconnected or off)

Avoid low and high arterial oxygen — Once return of spontaneous circulation has been achieved, the clinician should titrate inspired oxygen to maintain pulse oximetry between 94 and 99 percent to avoid hypo- or hyperoxemia [3,4,29].

Small observational studies have failed to show an association between arterial oxygenation and mortality in resuscitated children [30-32]. However, in one large, retrospective, multicenter observational pediatric study of 1875 infants and children who survived to pediatric intensive care unit (PICU) admission, multivariate analysis showed that both hypoxemia (PaO₂ <60 mmHg) and hyperoxemia (PaO₂ ≥300 mmHg) independently and significantly increased the estimated risk of death by 90 and 25 percent, respectively [29]. Overall mortality prior to PICU discharge was 39 percent in this study.

Monitor ventilation — The 2015 international consensus on science with treatment recommendations suggest that PaCO₂ after return of spontaneous circulation may be targeted based upon the patient's specific condition and that exposure to severe hypocapnia (PaCO₂ <30 mmHg) or hypercapnia (PaCO₂ >50 mmHg) should be limited [1,2,33].

In one prospective, multicenter observational study of 223 infants and children who sustained an in-hospital arrest, hypo- or hypercapnia upon return of spontaneous circulation was associated with a mortality of 50 or 59 percent, respectively, compared with 33 percent mortality if the PaCO₂ was 30 to 50 mmHg [30].

Hypocapnia should also be avoided since indirect evidence suggests that hyperventilation may cause cerebral ischemia in pediatric patients with severe brain injury. (See "Severe traumatic brain injury (TBI) in children: Initial evaluation and management", section on 'Ventilation'.)

Avoid recurrent shock — The 2015 international guidelines recommend that parenteral fluids and vasoactive medications be used to maintain the systolic blood pressure >5^th percentile for age [1,2]. Hypotension after ROSC is associated with decreased survival to hospital discharge [34-37] and, for infants and children with an inpatient arrest, decreased survival with favorable neurologic outcome [34].

After return of spontaneous circulation (ROSC) in a child, circulatory instability may recur as the result of ongoing fluid loss, decreased cardiac function, and/or harmful alterations in systemic vascular resistance. Recurrent shock should be managed according to physiologic endpoints (eg, skin perfusion, quality of pulses, blood pressure, urine output and mental status). Of note, cardiogenic shock occurs frequently in survivors of cardiac arrest. If hypovolemia is suspected in a patient with cardiogenic shock, the clinician should carefully infuse 5 to 10 mL/kg of isotonic fluids (eg, normal saline or Ringer's lactate) over 10 to 20 minutes followed by reevaluation of endpoints (algorithm 2). (See "Initial management of shock in children", section on 'Volume and rate'.)

Maintain normal blood glucose — The clinician should monitor blood glucose levels and promptly treat hypoglycemia. (See "Approach to hypoglycemia in infants and children", section on 'Immediate management'.)

Sustained hyperglycemia (blood glucose >180 mg/dL [10 mmol/L]) is associated with higher mortality in critically ill children and should be avoided [38,39]. Evidence indicates that blood glucose should be maintained below this threshold, but the role of "tight control" that uses insulin to achieve a specified blood glucose range is of uncertain value in children after cardiac arrest [40]. If performed, tight glucose control requires close monitoring of blood glucose and avoidance of hypoglycemia. Intensive insulin therapy in adults to maintain a blood glucose range of 80 to 110 mg/dL (4.4 to 6.1 mmol/L) increases the risk of hypoglycemia without demonstrated benefit. (See "Glycemic control in critically ill adult and pediatric patients", section on 'Our approach'.)

EEG monitoring — Based upon small observational studies, seizures are common following resuscitation from pediatric cardiac arrest occurring in approximately 33 to 50 percent of patients [41-43]. Nonconvulsive status epilepticus has also been described and may affect a significant proportion of patients. As an example, nonconvulsive status epilepticus was found after cardiac arrest in 6 of 19 children in one series [41]. For this reason, infants and children who remain comatose after cardiac arrest should have electroencephalogram (EEG) evaluation for the presence of seizures, with prompt management to reduce the risk of worsening neurologic injury.

The management of nonconvulsive and convulsive status epilepticus are discussed separately. (See "Management of convulsive status epilepticus in children" and "Nonconvulsive status epilepticus: Treatment and prognosis".)

Information from post-arrest EEG monitoring should not be used as the sole criterion for prognostication following pediatric cardiac arrest [3,4].

Targeted temperature management — Targeted temperature management describes measures to keep core body temperature in a pre-defined range after resuscitation. In our institution, we use a target core body temperature of 36 to 37.5°C with the goal of avoiding fever (temperature >38°C) in children following cardiac arrest. Based upon the available evidence and international resuscitation guidelines, it is reasonable to either provide five days of normothermia (temperature 36 to 37.5°C), or to provide two days of therapeutic hypothermia (targeted temperature range 32 to 34°C) followed by three days of continuous normothermia for comatose infants and children after cardiac arrest [1,2,18]. Further studies are needed to establish the optimal temperature target and duration of targeted temperature management.

Regardless of the approach chosen, fever (temperature>38°C) should be strictly avoided. Elevated temperature following resuscitation is associated with worse outcomes in neonates and adult patients and is presumed to be harmful in children as well although there is no direct evidence in this population [44]. Fever is common in children after resuscitation from cardiac arrest; thus, defining the target range for temperature and careful core temperature monitoring are indicated. Prompt availability and anticipatory use of cooling blankets and anti-pyretics are routine in our practice.

Therapeutic hypothermia to maintain core body temperature below normal (typically 32 to 34°C) has been evaluated in children based upon evidence for improved neurologic outcome in neonates and selected adults. (See "Clinical features, diagnosis, and treatment of neonatal encephalopathy", section on 'Therapeutic hypothermia' and "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Temperature management'.)

However, the data for therapeutic hypothermia for 48 hours for both out-of-hospital and in-hospital cardiac arrest have not shown improved outcomes. For example, in a multicenter trial involving children who were resuscitated from an out-of-hospital cardiac arrest, 260 patients (48 hours to 18 years of age) were randomized to either therapeutic hypothermia with a target core body temperature of 33°C or therapeutic normothermia to maintain a target temperature of 36.8°C. One year survival with good neurologic function was not significantly different in patients undergoing therapeutic hypothermia compared with therapeutic normothermia (20 versus 12 percent, respectively, relative likelihood 1.54, 95% CI 0.86-2.76) [44]. The groups also did not significantly differ with respect to incidence of adverse effects including infections or serious arrhythmias and 28-day mortality. Similarly, these investigators, using the same methodology, found no benefit of therapeutic hypothermia compared with therapeutic normothermia in 329 children resuscitated from in-hospital cardiac arrest [45]. This trial was stopped early for futility. Of note, the number of patients randomized in both of these trials was insufficient to exclude an important benefit or harm from therapeutic hypothermia and further study may be warranted. However, pooling of individual patient data from these two trials also did not show a survival benefit from therapeutic hypothermia [46]. The lack of benefit from hypothermia may be related to improved outcomes in the control groups of these two trials, both of whom received active controlled normothermia, which may also be beneficial in patients with cardiac arrest.

Transfer to a pediatric center — If the child is not being treated in a center with pediatric emergency and critical care expertise, the child should be stabilized and rapidly transferred for definitive care at a regional pediatric center. Critically ill or injured children typically benefit from transport by a team with pediatric expertise and advanced pediatric treatment capability, although in some isolated cases (eg, expanding epidural hematoma) more rapid transport by an immediately available non-pediatric team may be advantageous. (See "Prehospital pediatrics and emergency medical services (EMS)", section on 'Inter-facility transport'.)

Prior to transfer, the clinician responsible for the child's care at the transferring hospital should speak directly to the clinician who will be taking charge of the patient at the receiving hospital. All documentation of care (eg, medical chart, medication administration record, laboratory results, copies of ancillary studies [radiographs, ECGs]) should be sent with the patient. (See "Prehospital pediatrics and emergency medical services (EMS)", section on 'Inter-facility transport'.)

Rapid response teams — A rapid response team (RRT), also known as a medical emergency team (MET), consists of personnel from medical, nursing and/or respiratory therapy who have critical care training and are available 24 hours per day, seven days a week for evaluation and treatment of patients who show signs of clinical deterioration and are located in non-critical care settings (eg, medical or surgical inpatient wards. Implementation of an RRT has been promoted as a major strategy for improving patient safety in hospitals [47]. Infants and children with high-risk conditions who are managed on general inpatient units may benefit from rapid response teams that can provide prompt assessment and management if clinical deterioration occurs although results from large studies are not consistent [1,2,48-51]:

●A meta-analysis of five pediatric prospective observational studies with a total of 347,618 patient admissions found that implementation of an RRT was associated with a significant reduction in deaths from cardiac arrest when compared with historical control periods (0.05 versus 0.17 percent, relative risk [RR] 0.6, 95% CI 0.5-0.8) [48]. However, decreased mortality after implementation of an RRT was not found in all studies.

●A cohort study of 29,294 patient admissions (7257 admissions after institution of an RRT) that was included in the meta-analysis compared hospital-wide mortality rates and rates of respiratory and cardiopulmonary arrests outside of the intensive care unit before and after implementation of an RRT in a 264-bed freestanding children's hospital [49]. Major findings included:

•The mean monthly mortality rate decreased from 1 to 0.8 deaths per 100 discharges (18 percent decrease, 95% CI 5-30 percent).

•The mean monthly code rate (respiratory or cardiopulmonary arrest) decreased from 2.5 to 0.7 codes per 1000 patient admissions (RR 0.3, 95% CI 0.1-0.7). A possible explanation for this finding is that early activation of the RRT in a critically ill patient might have prevented codes.

•Over 18 months, the RRT was activated 143 times, most commonly for respiratory distress, hypotension, hypoxemia, altered mental status, and tachycardia. The most common actions by the RRT were respiratory support, fluid resuscitation, airway management, and transfer to the intensive care unit.

●A multicenter, prospective observational study of the implementation of a clinician-led pediatric RRT in four pediatric academic centers found that initiation of an RRT was associated with a significant reduction in pediatric intensive care unit mortality rate after readmission from a medical or surgical unit (0.3 to 0.1 deaths per 1000 hospital admissions) but no significant decline in the rate of cardiopulmonary arrests [50].

However, these observations do not prove that the RRT was responsible for the improvement in outcomes. Support for this concern comes from an observational study in a children's hospital that did not implement an RRT but also found a significant reduction in mortality over the same time period in which other pediatric centers reported decreased mortality in association with RRT implementation [51]. In a separate multicenter study that evaluated predicted versus actual hospital mortality rates in 38 free-standing children's hospitals before and after implementation of an RRT and that controlled for declining mortality over time, RRT implementation was not associated with a reduction in hospital deaths beyond what was predicted by preimplementation trends [52].

Thus, the benefit of an RRT is not consistent across all settings, and it is possible that explanations other than the RRT may be responsible for at least part of the benefit. In addition, the quality and generalizability of the evidence describing the effectiveness of implementing RRTs is limited by features such as before and after observation design, selection of primary and secondary outcome measures, and varied indications for RRT activation. In addition, because the mortality following pediatric intensive care unit (PICU) admission is typically low, its utility as an outcome measure may be limited. Finally, the systems being studied are complex, making it difficult to identify confounding factors such as changes in secular trends or indirect benefits derived from the RRT implementation. However, institutions may choose to implement and maintain RRTs based upon their own safety priorities.

Family presence during resuscitation — Observational studies indicate that caretakers should be given the option of being present during the in-hospital resuscitation of their child [40].

Key findings include:

●Most parents or primary caregivers want the opportunity to remain with their child during resuscitation [40] and believe it is their right [53].

●Caretakers present during the resuscitation of a family member frequently reported that their presence during the resuscitation was beneficial to the patient [53-55].

●Two-thirds of caretakers present during the resuscitation of a child who died reported that their presence helped with their adjustment to the death and the grieving process [55].

●Studies of hospital personnel suggest that the presence of a family member, in most instances, was not stressful to staff and did not negatively impact staff performance [53,54,56].

When family members are present during a pediatric resuscitation, a staff member with clinical knowledge, empathy, and strong interpersonal skills should be present with them to provide support and answer questions.

In the rare instance that family presence is disruptive to team resuscitation efforts, the family members should be respectfully asked to leave.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Basic and advanced cardiac life support in children".)

SUMMARY AND RECOMMENDATIONS

●Early recognition – The principal aim for Pediatric Advanced Life Support (PALS) is to prevent cardiopulmonary failure and arrest through early recognition and management of respiratory distress, respiratory failure, and shock. (See 'Assessment' above and "Initial assessment and stabilization of children with respiratory or circulatory compromise".)

●Respiratory distress and failure – A major goal of pediatric advanced life support is to recognize and treat respiratory conditions amenable to simple measures (eg, supplemental oxygen, inhaled albuterol) (table 2). The clinician may also have to treat rapidly progressive conditions and intervene with advanced therapies to avoid cardiopulmonary arrest in patients with respiratory failure. Early detection and treatment improve overall outcome. (See 'Respiratory distress and failure' above.)

Key steps in basic airway management include (see 'Respiratory distress and failure' above):

•Provide 100 percent inspired oxygen

•Allow child to assume position of comfort or manually open airway

•Clear airway (suction)

•Insert an airway adjunct if consciousness is impaired (eg, nasopharyngeal airway or, if gag reflex absent, oropharyngeal airway)

The clinician should assist ventilation manually in patients not responding to basic airway maneuvers, monitor oxygenation by pulse oximetry, monitor ventilation by end-tidal carbon dioxide (EtCO₂) if available, and administer medications as needed (eg, albuterol or racemic epinephrine). In preparation for intubation, the patient should receive 100 percent oxygen via a high-concentration mask, or if indicated, positive pressure ventilation with a bag-valve-mask to preoxygenate and improve ventilation. (See 'Respiratory distress and failure' above.)

Children who cannot maintain an effective airway, oxygenation, or ventilation should receive noninvasive ventilation (NIV) or undergo endotracheal intubation. A rapid overview provides the steps in performing rapid sequence intubation (table 3). Initiation of NIV is discussed separately. (See "Rapid sequence intubation (RSI) outside the operating room in children: Approach" and "Noninvasive ventilation for acute and impending respiratory failure in children".)

●Shock – Proper treatment of shock in children requires the clinician to recognize and eventually categorize the type of shock in order to prioritize treatment options (algorithm 1). Early treatment of shock may prevent the progression to cardiopulmonary failure (algorithm 2). (See "Initial evaluation of shock in children" and "Initial management of shock in children" and 'Shock' above.)

●Bradycardia – The management of bradycardia focuses on (algorithm 3) (see 'Bradycardia algorithm' above):

•Reestablishing or optimizing oxygenation and ventilation (see "Basic airway management in children")

•Supporting circulation with chest compressions for patients with poor perfusion and a heart rate <60 beats per minute

•Using medications (ie, epinephrine or atropine) to increase heart rate and cardiac output

●Tachycardia – The management of tachyarrhythmias that are not sinus in origin is guided by the appearance of the QRS complex and by the patient's status, whether unstable or stable (algorithm 4). (See 'Tachycardia algorithm' above.)

●Pulseless arrest – Resuscitation of children in cardiopulmonary arrest is determined by the presenting rhythm (shockable versus pulseless electrical activity or asystole) (algorithm 6). (See 'Pulseless arrest algorithm' above.)

Use of extracorporeal membrane oxygenation (ECMO) with CPR (ECPR) in settings with existing ECMO protocols, expertise, and equipment may be beneficial for selected patients who fail conventional CPR after inpatient cardiac arrest. Our approach is to activate ECPR after approximately 10 minutes of failed conventional resuscitation in patients with conditions that may be reversible after a period of ECPR (eg, myocarditis, pulmonary or air embolus, sudden arrest after cardiac surgery, poisoning, or primary hypothermic arrest) or who are candidates for the use of ECPR as a bridge to therapies such as cardiac transplantation. (See 'Extracorporeal membrane oxygenation (ECMO) with CPR (ECPR)' above.)

●Postresuscitation management – Key measures after resuscitation are as follows (see 'Immediate and early postresuscitation management' above):

•Continue specific management of the underlying cause of the life-threatening event

•Titrate inspired oxygen to maintain pulse oximetry between 94 and 99 percent

•In intubated patients, ensure proper endotracheal tube position and ongoing monitoring of ventilation

•Avoid recurrent shock and hypotension (blood pressure <5^th percentile for age) by administering parenteral fluids and vasoactive medications as needed and according to physiologic endpoints and cardiac function

•Avoid hypoglycemia while maintaining blood glucose <180 mg/dL (10 mmol/L)

•Monitor for and treat seizures aggressively if they occur

•Prevent elevated core body temperature (>38°C) using cooling measures, as needed

If the child is not being treated in a center with pediatric emergency and critical care expertise, the child should be stabilized and rapidly transferred for definitive care at a regional pediatric center. (See 'Immediate and early postresuscitation management' above.)