Cardiopulmonary Arrest in Children

Etiology

As of 2015, the AHA estimates that over 20,000 children in the U.S. experience cardiopulmonary arrest annually, with a higher incidence of in-hospital cardiac arrest (IHCA) compared to out-of-hospital cardiac arrest (OHCA). More than 70% of these cases occur in children younger than 1 year, followed by adolescents and older children, with a slightly higher proportion in boys. Survival rates for infants are over 6% lower than for older children and adolescents. Because survival rates and neurologic outcomes vary significantly depending on the location of the arrest, IHCA and OHCA represent distinct clinical entities that require tailored approaches.

IHCA occurs in approximately 2% to 6% of children admitted to pediatric intensive care units, predominantly in patients with preexisting comorbidities such as pulmonary, cardiac, oncologic, and gastrointestinal conditions. The majority of presenting rhythms in these cases are asystole and PEA, with ventricular fibrillation and pulseless ventricular tachycardia occurring less frequently. Survival to hospital discharge following IHCA is approximately twice that observed in OHCA, likely reflecting the benefit of immediate initiation of CPR in the hospital setting.

By comparison, OHCA affects between 7.5 and 11.2 children per 100,000 annually, with infants constituting the majority and experiencing the lowest survival rates. Outcomes depend on factors such as whether the arrest was witnessed, whether early bystander CPR was provided, and whether ROSC was achieved prior to hospital transport. Over 80% of OHCA cases present with asystole or PEA, while ventricular fibrillation accounts for approximately 10% of cases.[8]

Causes of pediatric cardiopulmonary arrest fall into several categories: respiratory, cardiac, infectious, and traumatic. Respiratory causes predominate in both IHCA and OHCA, followed by circulatory shock. Respiratory distress leading to arrest includes respiratory infections such as bronchiolitis and pneumonia, asthma, aspiration, tracheal foreign bodies, smoke inhalation, and drowning.

Cardiac causes encompass congenital lesions, arrhythmias, and cardiomyopathies. Infectious causes beyond the respiratory system include sepsis and meningitis. Traumatic causes involve blunt trauma to the head or chest (commotio cordis), drowning, and child abuse. Sudden infant death syndrome (SIDS) and sudden unexpected infant death syndrome (SUID) also contribute to sudden death in children younger than 1 year.

When identifying the underlying cause of cardiopulmonary arrest, the AHA recommends considering the Hs and Ts. These reversible conditions guide targeted interventions during resuscitation.

The Hs include the following:

• Hypoxia: Oxygen deprivation, eg, from respiratory infections or asthma, contributes to cardiac arrest. Airway patency, chest rise, breath sounds, and the delivery of supplemental oxygen must be assessed.
• Hypovolemia: Loss of circulatory volume can precipitate hypovolemic shock, leading to cardiac arrest. Etiologies include acute blood loss (hemorrhagic shock) and severe dehydration (hypovolemic shock).
• Hypokalemia or hyperkalemia: Both low and high potassium levels may cause cardiac arrest. The underlying conditions causing potassium imbalances must be considered, such as gastrointestinal or renal disorders. Electrocardiogram (ECG) findings of hyperkalemia include peaked T waves, widening of the QRS complex, and sine wave patterns. Hypokalemia manifests as flattened T waves, prominent U waves, and possible QRS widening on ECG.
• Hydrogen ions (acidemia): Respiratory and metabolic acidosis, eg, from upper airway obstruction or diabetic ketoacidosis, can precipitate cardiac arrest. Acid-base status should be evaluated through arterial blood gas (ABG) analysis. Adequate ventilation must be ensured, and the causes of metabolic acidosis should be identified.
• Hypothermia: Severe hypothermia may cause cardiac arrest unresponsive to PALS medications or defibrillation. Rapid rewarming should be initiated, and early consideration of extracorporeal membrane oxygenation (ECMO) is recommended.
• Hypoglycemia: Although removed from the traditional Hs and Ts, rapid assessment of blood glucose via finger-stick testing is essential. In patients with impaired consciousness, dextrose should be administered promptly through intravenous or intraosseous routes.

The Ts include the following:

• Tension pneumothorax: This condition occurs when air accumulates in the pleural space, increasing pressure within the intrathoracic cavity and causing cardiopulmonary collapse. In children, tension pneumothorax commonly results from trauma or aggressive mechanical ventilation. Primary spontaneous pneumothorax is rare.[9][10] Clinical signs include tachycardia, jugular venous distension (JVD), unequal breath sounds, and tracheal deviation. Definitive treatment involves needle decompression of the chest, followed by chest tube catheter placement.
• Tamponade (cardiac): Cardiac tamponade occurs when fluid accumulates within the pericardium, leading to cardiac arrest. Typical findings include narrow-complex tachycardia, JVD, and muffled heart sounds. The definitive treatment is pericardiocentesis. History may reveal trauma, recent cardiac surgery, or cardiac disorders like pericarditis.
• Toxins: Poisoning from accidental or intentional ingestion of medications and illicit drugs can precipitate cardiac arrest. Common causative agents include tricyclic antidepressants, calcium channel blockers, β-blockers, and digoxin. Overdose of street drugs such as opiates and cocaine also poses a significant risk. Consultation with poison control services is advised during management.
• Thrombosis, coronary: Coronary thrombosis involves occlusion of 1 or more coronary arteries, resulting in myocardial infarction and potential cardiac arrest. This condition is rare in the pediatric population but may occur in the setting of congenital cardiac disorders, inherited thrombophilias, or Kawasaki disease. Treatment options include fibrinolytic therapy and percutaneous coronary intervention.
• Thrombosis, pulmonary: Pulmonary thrombosis refers to the acute obstruction of 1 or both pulmonary arteries, causing rapid cardiopulmonary collapse. This condition is rare in children but may occur in adolescents with clotting disorders. Clinical features include tachycardia, respiratory distress, and JVD. Right heart strain is evident on echocardiogram. Definitive management consists of fibrinolytic therapy and, when indicated, pulmonary thrombectomy.

The etiology of pediatric cardiac arrest differs from that of adults, where approximately 70% of cases result from ischemic coronary disease, followed by congestive heart failure and left ventricular hypertrophy. In the U.S., over 400,000 adults experience cardiac arrest annually, with a survival rate of around 10%, many of whom sustain poor neurologic outcomes.

Epidemiology

The AHA estimates that over 20,000 children experience cardiopulmonary arrest annually in the U.S., with IHCA occurring more frequently than OHCA. According to AHA data, outcomes for unwitnessed cardiopulmonary arrest in infants and children remain poor. Only 8.4% of pediatric patients with OHCA survive to discharge, many with neurological impairments. The in-hospital survival rate is approximately 24%, with better neurological outcomes. The best-reported outcomes occur in children who receive immediate high-quality CPR, ensuring adequate ventilation and coronary perfusion, and in those with witnessed sudden arrest presenting with ventricular rhythm disturbances that respond to early defibrillation.

A retrospective cohort study analyzed data from the Nationwide Emergency Department Sample (NEDS), encompassing emergency department cardiac arrest (EDCA) and inpatient cardiac arrest (IPCA) events from 2016 to 2018. During this period, 15,348 pediatric cardiac arrest events were recorded, including 13,239 EDCA and 2,109 IPCA cases. The causes of arrest varied. However, respiratory etiologies predominated, accounting for 75.8%.

Other contributing factors included acidosis (43.9%), acute kidney injury (27.2%), trauma (27.1%), and sepsis (22.5%). Several cases lacked a definitive associated diagnosis. Survival rates differed significantly, with 19% for EDCA and 40.4% for IPCA. This study underscores the survival gap between pediatric patients experiencing cardiopulmonary arrest in inpatient settings versus emergency departments or out-of-hospital environments.

Among cardiovascular deaths in athletes younger than 18, 29% of patients were Black, while 54% were high school students. Additionally, 82% occurred during physical exertion in competition or training. These findings suggest specific groups and conditions that may benefit from focused cardiovascular risk assessment and intervention.

Pathophysiology

During cardiopulmonary arrest, global ischemia results in cellular-level organ damage that may continue even after resuscitation. Ischemia causes cellular edema, which damages all organs but is particularly detrimental to the brain. Due to this organ’s limited capacity for expansion, swelling increases intracranial pressure and decreases perfusion, leading to poor neurological outcomes.

Cardiac arrest progresses through 4 phases: prearrest, no-flow, low-flow, and postresuscitation. The duration and management of each phase significantly affect neurological recovery.

The prearrest phase encompasses events preceding arrest, including underlying pathologies such as acute illness and comorbidities, as well as environmental factors like trauma. Early recognition during this phase allows timely intervention to prevent arrest. Environmental factors have a greater impact on OHCA, where caregiver education on infant safe sleep and swimming safety plays a vital role in reducing pediatric deaths. In contrast, IHCA outcomes improve with early provider recognition and management of prearrest conditions such as hypoxia, hypotension, tachycardia, and acidosis.

The no-flow phase represents the interval from cardiac arrest onset to recognition by a bystander or healthcare provider. During this period, circulation and cerebral perfusion cease entirely. OHCA cases generally experience longer no-flow times, contributing to poorer outcomes in this group.

Following recognition, the low-flow phase begins with the initiation of CPR and continues until ROSC is achieved. Although high-quality chest compressions restore some blood flow, cerebral perfusion during low-flow remains approximately 20% of baseline and declines further with longer no-flow intervals.[11] This phase also involves identifying and treating the arrest rhythm according to PALS guidelines.

Once ROSC is achieved, the postarrest phase begins, during which children may experience varying degrees of postarrest syndrome. The clinical focus shifts to neuroprotection and treating the underlying cause of arrest. This phase encompasses the immediate postarrest period (the first 20 minutes after ROSC), the early postarrest period (20 minutes to 6-12 hours), the intermediate period (6-12 to 72 hours), and the recovery phase (starting 3 days after ROSC).

History and Physical

The history and physical examination of a child in cardiopulmonary arrest differ between OHCA and IHCA. In OHCA, signs of impending arrest may include loss of consciousness, abnormal breathing patterns, cyanosis, agitation, and seizure-like activity. The initial physical examination should follow the ABCDE approach: airway, breathing, circulation, disability, and exposure. While assessing these domains, the clinician should gather history from a parent or guardian, focusing on events leading to the arrest and any underlying conditions, such as congenital heart disease, prematurity, epilepsy, or recent illness. Environmental factors warrant careful consideration—electrocution, extreme weather, and potential chemical exposures may compromise the safety of the child and rescuers. A bystander should be immediately tasked with contacting emergency medical services (EMS).

In IHCA, the ABCDE framework remains central to the initial evaluation. History should be obtained from parents, the primary nurse, and documentation, detailing the reason for admission, relevant laboratory data, and recent clinical deterioration. Signs of impending cardiac arrest in hospitalized children often include bradycardia, hypoxia, respiratory distress, agitation, confusion, somnolence, and skin changes such as pallor or cyanosis.

ABCDE Rapid Assessment

The ABCDE rapid assessment begins with airway evaluation. Patency should be assessed, and foreign body aspiration considered if arrest occurred during eating or if a small object was in the child’s mouth. In intubated patients, the DOPE mnemonic—dislodgement, obstruction, pneumothorax, equipment failure—should be applied to guide troubleshooting.

Breathing should be examined by checking for spontaneous respirations, evaluating respiratory effort, determining respiratory rate, and auscultating for bilateral breath sounds. Circulation must be inspected by checking for a central pulse, measuring capillary refill, identifying active bleeding, and, when available, recording blood pressure. Disability should be assessed by evaluating consciousness, pupillary response, and reactivity to verbal or tactile stimuli. A full-body inspection must be performed to look for signs of illness, such as trauma, rash, or cyanosis, while thermoregulation is maintained.

Evaluation

The evaluation of a child in cardiopulmonary arrest differs between OHCA and IHCA settings. In OHCA without an AED, a nonwitnessed cardiac arrest warrants brief CPR before calling for help and an AED. In the event of sudden collapse, the rescuer should call for help and retrieve an AED before initiating CPR. A lone rescuer uses a 30:2 compression–ventilation ratio for all pediatric age groups, while 2-person CPR uses a 15:2 ratio for infants and children (3:1 for neonates). For infants, the 2-thumb-encircling technique is preferred for 2-person CPR, while the 2-finger technique is used for a lone rescuer. For children, both 1- and 2-handed techniques are acceptable. Compressions should target the lower 3rd of the sternum at a depth of 1/3 the anterior-posterior chest diameter.

In OHCA with an AED, CPR should begin immediately with AED pads applied. For children at least 8 years of age, pads are placed as in adults (right upper chest and left lower chest). Anterior-posterior placement is recommended for children younger than 8 or if pads overlap. The AED determines the rhythm and guides shock delivery or continued CPR. CPR should be extended as instructed until EMS arrives.

In IHCA with a code blue team, a rapid physical exam and ABCDE assessment should be initiated. Additionally, a code blue should be called, CPR should be started, and a defibrillator should be attached to assess the cardiac rhythm.

Treatment / Management

When OHCA is anticipated, preparation should occur before the patient’s arrival. A code team must be activated, a resuscitation room prepared, and age-appropriate equipment readied. Team members should be assigned specific roles, including the following:

• Team leader
• Airway provider
• Chest compressor
• Vascular access provider (intravenous or intraosseous)
• Medication administrator
• History taker (from family and EMS)
• Family liaison
• Recorder/timekeeper
• Security officer (for crowd control, if available)

Initial treatment of cardiopulmonary arrest involves delivering quality chest compressions at a rate of 100 to 120 compressions per minute, with a depth of approximately 1/3 the chest diameter, ensuring interruptions last less than 10 seconds. Advanced airway management should include rescue breathing at a rate of 1 breath every 2 to 3 seconds and placement of an advanced airway. Early defibrillation must be administered for shockable rhythms, starting at 2 J/kg for the 1st shock, increasing to 4 J/kg for the 2nd, and greater than 4 J/kg for subsequent shocks up to a maximum of 10 J/kg. Epinephrine should be administered every 3 to 5 minutes. Reversible and underlying causes of cardiopulmonary arrest must be considered, as well as the potential use of extracorporeal circulation with extracorporeal membrane oxygenation.

In cases of IHCA, rapid assessment and recognition of the arrest state are required, followed by immediate initiation of CPR and alerting the code blue team. Once the cardiac rhythm is determined, management should follow PALS guidelines.

Cardiac rhythms during arrest are identified on the cardiac monitor or defibrillator. Asystole indicates no cardiac activity. PEA shows electrical activity without a detectable pulse. Ventricular tachycardia presents as monomorphic wide-complex tachycardia. Ventricular fibrillation appears as polymorphic fibrillatory waves. Torsades de Pointes is characterized by polymorphic wide-complex tachycardia with a heart rate exceeding 300 bpm. For further details on arrhythmia identification during arrest, refer to the StatPearls learning activity on arrhythmias.[12]

The Broselow system, a length-based resuscitation tape and code cart, assists in determining appropriate medication doses and equipment sizes. However, the accuracy of this system is limited, as several studies indicate suboptimal precision, requiring consideration of the child’s body habitus in addition to age and length. A 2017 meta-analysis showed that the Broselow tape accurately estimated weight within 10% only slightly more than 50% of the time. Inaccuracies in weight estimation may lead to critical medication dosing errors, risking patient harm.

Airway management during pediatric resuscitation prioritizes establishing a definitive airway via endotracheal intubation, which remains the gold standard. For OHCA with short transport times, bag-valve-mask ventilation is preferred until arrival at the hospital for definitive airway placement. When transport times are prolonged, paramedics should place a supraglottic airway or endotracheal tube.

In IHCA, endotracheal intubation is standard. Cuffed endotracheal tubes are recommended for all children except neonates. Tube size should be estimated by the formula [(age/4) + 3.5] for cuffed tubes and [(age/4) + 4] for uncuffed tubes, with tube depth set at 3 times the tube size. The Broselow tape may assist with sizing if the child’s age is unknown. Continuous end-tidal carbon dioxide (ETCO2) monitoring plays a critical role not only in verifying tube placement and ventilation but also in detecting ROSC earlier than pulse checks.[13] For a more detailed discussion on pediatric and neonatal resuscitation, clinicians may refer to the StatPearls learning activity on the subject.[14]

Differential Diagnosis

In pediatric cardiopulmonary arrest, noncardiac causes often predominate and should be prioritized during the initial assessment. Respiratory etiologies such as infection, airway obstruction, and drowning frequently lead to hypoxia and PEA or asystole. Trauma, particularly to the head or chest, may cause respiratory failure, hemorrhage, or direct cardiac injury.

Sepsis is another critical consideration, especially in children presenting with fever and poor perfusion. Myocarditis can lead to arrhythmias or pump failure in previously healthy patients, while cardiac tamponade should be suspected in trauma or known pericardial disease. Pulmonary embolism, though uncommon, may occur in adolescents with risk factors such as central lines or hypercoagulable states.

Cardiac causes should also be considered, especially in sudden collapse without preceding respiratory compromise. Structural heart defects, including Tetralogy of Fallot, Ebstein anomaly, and transposition of the great arteries, may present undiagnosed in infancy. Coronary artery anomalies and aortic dissection (eg, in Marfan syndrome) may lead to ischemia or rupture. Arrhythmogenic conditions such as hypertrophic cardiomyopathy, long QT syndrome, Brugada syndrome, Wolff-Parkinson-White syndrome, dilated cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy can cause ventricular tachycardia or ventricular fibrillation as the initial arrest rhythm.

A broad differential should be maintained. Still, reversible and common causes should be considered first to optimize resuscitation outcomes.

Prognosis

According to an observational study conducted by the AHA from January 2000 to December 2018, survival rates for pediatric patients with IHCA have increased from 19% to 32%. In contrast, survival for pediatric patients with OHCA remains significantly lower, ranging from 5% to 6%.

Over 50% of pediatric cardiac arrests present with pulseless bradycardic rhythms, including PEA, asystole, and bradycardia with poor perfusion. Ventricular fibrillation and pulseless ventricular tachycardia account for approximately 10% of initial arrest rhythms and are associated with more favorable outcomes than PEA or asystole. However, ventricular fibrillation or pulseless ventricular tachycardia occurring as secondary rhythms during CPR are linked to the poorest outcomes, likely reflecting progressive myocardial injury during resuscitation.

Survival rates for children with IHCA have improved most notably in intensive care settings, where these figures range from 78% to 90%. Nevertheless, the overall survival rate to hospital discharge remains 32%. Although favorable neurologic outcomes are reported in approximately 90% of children who survive to discharge, data on long-term global neurologic function are limited.[15]

Complications

Many survivors experience neurologic impairments that affect speech, memory, motor function, and decision-making. Factors associated with improved survival outcomes include a witnessed cardiac arrest, shorter duration of CPR, a shockable presenting rhythm, younger patient age, and an in-hospital location at the time of arrest.