Conceptual Overview

Pediatric cardiac arrest is fundamentally different from adult cardiac arrest. While adults most commonly arrest from primary cardiac causes (VF/pVT), children most commonly arrest from respiratory failure or shock that progresses to bradycardia and then pulseless electrical activity (PEA) or asystole. This means the etiology is usually hypoxia, and many pediatric arrests are preventable with early recognition and intervention.

The survival-to-discharge rate for out-of-hospital pediatric cardiac arrest (OHCA) is approximately 8-12%, and for in-hospital (IHCA) approximately 38-44%. The difference reflects the ability to intervene earlier in the deterioration cascade. If you recognize respiratory failure or shock and treat it before the child arrests, outcomes are dramatically better.

The most important PALS intervention is preventing the arrest: By the time a child is in full cardiac arrest, outcomes are significantly worse than if you had intervened during respiratory failure or compensated shock. The PALS algorithm matters, but recognizing the pre-arrest child and intervening aggressively is where lives are saved. Assess → Recognize → Intervene. Don't wait for the rhythm to flatline.
Shockable Rhythms: VF / Pulseless VT

VF and pulseless VT account for only 5-15% of pediatric arrests but have the best prognosis when identified and treated rapidly. Immediate defibrillation is the priority.

PALS Shockable Rhythm Algorithm

  1. Confirm cardiac arrest: Unresponsive, no breathing (or gasping), no pulse within 10 seconds
  2. Begin high-quality CPR:
    • Infant: two-thumb encircling technique (preferred) or two-finger technique
    • Child: one or two hands on lower half of sternum
    • Depth: at least 1/3 AP diameter (infant ~1.5 inches, child ~2 inches)
    • Rate: 100-120 compressions/min
    • Full chest recoil; minimize interruptions (<10 sec)
  3. Shock #1: 2 J/kg
  4. Resume CPR immediately × 2 minutes
  5. Rhythm check: Still shockable?
  6. Shock #2: 4 J/kg
  7. Resume CPR × 2 minutes
  8. Epinephrine: 0.01 mg/kg (0.1 mL/kg of 1:10,000) IV/IO — give after 2nd shock, repeat every 3-5 minutes
  9. Shock #3: 4 J/kg (max 10 J/kg or adult dose)
  10. Resume CPR × 2 minutes
  11. Amiodarone: 5 mg/kg IV/IO bolus (max 300 mg) — OR — Lidocaine: 1 mg/kg IV/IO
  12. Continue cycle: CPR → rhythm check → shock if indicated → epi every 3-5 min → consider amiodarone × 2 more doses (max total 15 mg/kg)
Shock energy escalation: First shock = 2 J/kg. All subsequent shocks = 4 J/kg. Maximum = 10 J/kg or the adult maximum dose, whichever is lower. If a specific dose of 4 J/kg is not effective, you may increase up to 10 J/kg for refractory VF. Do NOT exceed the adult maximum energy setting on your defibrillator.
Non-Shockable Rhythms: PEA / Asystole

PEA and asystole account for 85-95% of pediatric arrests. These rhythms are treated with CPR and epinephrine while aggressively seeking and treating reversible causes. There is no role for defibrillation.

PALS Non-Shockable Rhythm Algorithm

  1. Confirm cardiac arrest
  2. Begin high-quality CPR
  3. Epinephrine ASAP: 0.01 mg/kg (0.1 mL/kg of 1:10,000) IV/IO as soon as vascular access obtained
  4. CPR × 2 minutes → rhythm check
  5. Repeat epinephrine every 3-5 minutes
  6. Search for and treat reversible causes (H's and T's)
  7. If rhythm changes to VF/pVT → switch to shockable algorithm
Epinephrine timing matters: In non-shockable rhythms, give epinephrine as early as possible. Studies show that earlier epinephrine administration in non-shockable rhythms is associated with improved ROSC and survival. Don't wait for the 2-minute CPR cycle to complete if you already have IV/IO access - give it immediately. For shockable rhythms, give the first dose after the second shock.
H's & T's: Reversible Causes

Identifying and treating reversible causes is the most important cognitive task during pediatric resuscitation. Unlike adult arrest where you can often continue the algorithm and hope for ROSC, pediatric arrest is frequently caused by something fixable.

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H's Pediatric Considerations Intervention
Hypoxia #1 cause of pediatric arrest; respiratory failure → cardiac arrest Oxygenate, ventilate, secure airway; confirm ETT placement
Hypovolemia Hemorrhage, dehydration, sepsis; children compensate then crash 20 mL/kg NS bolus (repeat up to 60 mL/kg); blood products if hemorrhagic
Hydrogen ion (acidosis) DKA, inborn errors of metabolism, prolonged arrest Ventilation to correct respiratory acidosis; NaHCO3 1 mEq/kg for refractory metabolic acidosis
Hypo/Hyperkalemia Renal failure, DKA, crush injuries, tumor lysis Calcium chloride 20 mg/kg IV; glucose + insulin; albuterol for hyperK
Hypothermia Submersion injury, environmental exposure, neonatal Active rewarming; "not dead until warm and dead"
Hypoglycemia Neonates, diabetics, sepsis, limited glycogen stores in children D10W 5 mL/kg IV; check glucose in ALL pediatric arrests
T's Pediatric Considerations Intervention
Tension pneumothorax Trauma, asthma, positive pressure ventilation Needle decompression → chest tube; look for absent breath sounds, tracheal deviation, JVD
Tamponade (cardiac) Trauma, post-cardiac surgery, malignancy Pericardiocentesis; Beck's triad (muffled hearts, JVD, hypotension)
Toxins Accidental ingestion (#1 in toddlers); intentional in adolescents Specific antidotes; activated charcoal if appropriate; sodium bicarb for TCA overdose; lipid emulsion for local anesthetic toxicity
Thrombosis (pulmonary) Rare but increasing; central lines, immobility, hypercoagulable states Consider tPA (fibrinolysis) for massive PE causing arrest
Thrombosis (coronary) Kawasaki disease, congenital anomalies (very rare primary MI in kids) Cardiology consultation
Think respiratory first: When running through the H's and T's in a pediatric arrest, start with Hypoxia. Confirm the ETT is correctly placed (waveform ETCO2), bilateral breath sounds are present, and the child is being adequately ventilated with 100% O2. Fix the breathing problem before anything else. In pediatric arrest, this single intervention addresses the #1 cause.
Medication Dosing
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Medication Dose Route Notes
Epinephrine 0.01 mg/kg (0.1 mL/kg of 1:10,000) IV/IO Every 3-5 min; max single dose 1 mg
Amiodarone 5 mg/kg IV/IO bolus IV/IO For refractory VF/pVT; may repeat × 2 (max total 15 mg/kg)
Lidocaine 1 mg/kg IV/IO IV/IO Alternative to amiodarone for VF/pVT
Atropine 0.02 mg/kg IV/IO IV/IO For vagal-mediated bradycardia; min dose 0.1 mg; max single dose 0.5 mg
Adenosine 0.1 mg/kg (1st), 0.2 mg/kg (2nd) Rapid IV push For SVT; max 1st dose 6 mg, max 2nd dose 12 mg; rapid flush after
Calcium chloride 10% 20 mg/kg IV/IO IV/IO (slow push) For hyperkalemia, hypocalcemia, Ca-channel blocker OD
Sodium bicarbonate 1 mEq/kg IV/IO IV/IO For refractory metabolic acidosis, hyperkalemia, TCA overdose
Dextrose (D10W) 5 mL/kg IV/IO IV/IO For documented hypoglycemia; check glucose in ALL arrests
NEVER use adult-concentration epinephrine (1:1,000) IV: The IV/IO dose uses 1:10,000 concentration (0.1 mg/mL). The 1:1,000 concentration (1 mg/mL) is 10× more concentrated and is reserved for IM use in anaphylaxis. Giving 1:1,000 IV can cause lethal hypertension, arrhythmias, and myocardial ischemia. Always verify the concentration. Many institutions now use "cardiac epi" labeling to prevent this error.
IO is as good as IV: If you can't get peripheral IV access within 60 seconds of a pediatric arrest, go directly to IO access. IO delivers medications to the central circulation as quickly as peripheral IV. Don't waste critical minutes on repeated IV attempts in a pulseless child. Proximal tibia is the preferred site in children under 6; distal tibia or proximal humerus for older children.
Post-ROSC Care

Achieving ROSC is only the beginning. Post-cardiac arrest syndrome includes myocardial dysfunction, neurologic injury, systemic ischemia-reperfusion, and the precipitating cause that hasn't gone away. Meticulous post-ROSC care improves neurologic outcomes.

  • Oxygenation: Target SpO2 94-99%. Avoid hyperoxia (100% FiO2 for extended periods) - it worsens neurologic injury through oxidative stress. Titrate FiO2 down to maintain SpO2 94-99%
  • Ventilation: Target age-appropriate ETCO2 (35-45 mmHg). Avoid hyperventilation - it causes cerebral vasoconstriction and worsens neurologic outcomes
  • Hemodynamics: Maintain systolic BP >5th percentile for age. Use vasopressors/inotropes as needed (epinephrine infusion 0.1-1 mcg/kg/min or norepinephrine)
  • Temperature management: Avoid hyperthermia aggressively (target 36-37.5°C). Targeted temperature management (TTM) to 32-34°C may be considered for comatose patients per institutional protocol
  • Glucose: Monitor frequently; treat both hypoglycemia and hyperglycemia
  • Seizure monitoring: Treat clinical seizures; continuous EEG monitoring when available
  • Labs: ABG/VBG, lactate, electrolytes, glucose, calcium, coagulation studies
Avoid the post-ROSC "autopilot": The adrenaline of the resuscitation fades after ROSC, and teams sometimes relax. This is the most dangerous phase. Hyperoxia, hyperventilation, hypotension, and hyperthermia during the post-ROSC period can erase any survival benefit you gained from excellent CPR. Assign a team member specifically to manage post-ROSC parameters.
Quick Reference

CPR Parameters

  • Rate: 100-120/min
  • Depth (infant): ≥1.5 inches (1/3 AP diameter)
  • Depth (child): ≥2 inches (1/3 AP diameter)
  • Compression:ventilation ratio: 15:2 (two rescuers) or 30:2 (single rescuer)
  • With advanced airway: Continuous compressions + 1 breath every 2-3 sec (20-30/min)

Shock Doses

  • 1st shock: 2 J/kg
  • Subsequent: 4 J/kg (max 10 J/kg or adult dose)
  • Cardioversion (SVT/VT with pulse): 0.5-1 J/kg → 2 J/kg

Key Meds

  • Epinephrine: 0.01 mg/kg IV/IO q3-5 min (max 1 mg)
  • Amiodarone: 5 mg/kg IV/IO (max 300 mg)
  • Adenosine: 0.1 mg/kg → 0.2 mg/kg rapid push
  • Atropine: 0.02 mg/kg (min 0.1 mg, max 0.5 mg)

H's & T's Mnemonic

  • H's: Hypoxia, Hypovolemia, Hydrogen ion, Hypo/hyperkalemia, Hypothermia, Hypoglycemia
  • T's: Tension pneumothorax, Tamponade, Toxins, Thrombosis (pulmonary), Thrombosis (coronary)
Clinical Pearls
"Push hard, push fast, let it come all the way up": The three pillars of high-quality CPR haven't changed. Adequate depth (at least 1/3 the AP chest diameter), adequate rate (100-120/min), and full chest recoil are the single most important determinants of survival. Poor-quality CPR with the right drugs still fails. Excellent CPR with no drugs can still produce ROSC.
Use ETCO2 to guide CPR quality: Waveform capnography during CPR is the best real-time measure of compression quality and perfusion. Target ETCO2 >10-15 mmHg during CPR. If ETCO2 is <10, improve compression quality before blaming the rhythm. A sudden spike in ETCO2 (typically to >40 mmHg) during CPR is often the first sign of ROSC.
Assign roles before the arrest: The resuscitation team should have pre-assigned roles: team leader, compressor, airway manager, vascular access/medications, monitor/defibrillator, recorder/timer. Use closed-loop communication. The team leader should NOT perform procedures - their job is to think, direct, and watch the big picture.
Think about the family: Current AHA guidelines support family presence during resuscitation when a support person (nurse, social worker, chaplain) is available. Studies show that family presence does not interfere with resuscitation efforts, reduces family anxiety and PTSD, and is desired by the majority of families when asked. Designate someone to be with the family, explain what's happening, and prepare them for possible outcomes.
References
  1. Topjian AA, Raymond TT, Atkins D, et al. Part 4: Pediatric Basic and Advanced Life Support: 2020 AHA Guidelines for CPR and Emergency Cardiovascular Care. Circulation. 2020;142(16_suppl_2):S469-S523.
  2. Ralston M, Hazinski MF, et al. Pediatric Advanced Life Support (PALS) Provider Manual. American Heart Association; 2020.
  3. Holmberg MJ, Ross CE, Fitzmaurice GM, et al. Annual incidence of first-documented pediatric cardiac arrest and outcomes. Resuscitation. 2019;142:135-144.
  4. Andersen LW, Berg KM, Saindon BZ, et al. Time to epinephrine and survival after pediatric in-hospital cardiac arrest. JAMA. 2015;314(8):802-810.
  5. de Caen AR, Berg MD, Chameides L, et al. Part 12: Pediatric Advanced Life Support. Circulation. 2015;132(18 Suppl 2):S526-S542.
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