11.1 Reversible Causes: The H's and T's

Why Reversible Causes Matter in Pediatric Arrest

High-quality CPR, defibrillation for shockable rhythms, and correctly timed epinephrine buy time—but many children will not achieve durable ROSC until the driver of arrest is fixed. Pediatric cardiac arrest is usually secondary to progressive respiratory failure or shock, not primary atherosclerotic coronary disease. That physiology makes the reversible-cause list more than a mnemonic: it is a parallel workstream that runs during every 2-minute cycle.

While compressions continue, the team should:

1. Maintain airway, oxygen, and effective ventilation
2. Ensure IV/IO access and rhythm-appropriate drugs
3. Name and treat reversible causes using history, exam clues, monitors, and limited bedside tests

On the exam and in megacode testing, a team that only recites the algorithm without ever treating hypoxia, giving volume for massive fluid loss, decompressing a tension pneumothorax, or reversing an opioid overdose is incomplete—even if compression rate looks perfect.

The official 2025 list (memorize cold)

The Reversible Causes box on the 2025 AHA/AAP Pediatric Cardiac Arrest Algorithm prints six H's and five T's:

Two differences from the adult ACLS list are worth memorizing because they generate exam distractors:

1. Hypoglycemia is a printed pediatric H. It is not an optional extra or a "some courses also mention it" footnote—check a bedside glucose early in every pediatric arrest and treat documented hypoglycemia with weight-based dextrose.
2. Thrombosis appears twice (pulmonary and coronary), and "trauma" is not printed as its own T. Trauma still matters enormously, but as the context that bundles hemorrhagic hypovolemia, hypoxia, tension pneumothorax, and tamponade together (Section 11.2)—not as a separate letter you can recite instead of the five real T's.

Pediatric emphasis: hypoxia and hypovolemia first among equals

You still treat every H and T when suggested—but if you only remember two pediatric priorities under stress, make them oxygenate/ventilate and restore circulating volume when volume loss or distributive collapse is plausible.

The H's: Recognition and First Interventions During Arrest

Treat these in parallel with CPR—never as a reason to stop compressions for leisurely workups.

Hypovolemia

Clues: History of diarrhea/vomiting, burns, third-spacing, trauma with bleeding, anaphylaxis/sepsis with relative hypovolemia; PEA with flat neck veins (when assessable); empty-appearing chambers on brief ultrasound if used; poor response until volume restored.

First interventions during arrest: Rapid IV/IO access; give isotonic crystalloid boluses (commonly taught 10–20 mL/kg, then reassess) while CPR continues. For hemorrhagic arrest, prioritize hemorrhage control and blood products per trauma protocols rather than endless crystalloid alone. Do not let fluid preparation create long hands-off intervals.

Hypoxia

Clues: Respiratory illness, aspiration, drowning, airway obstruction, failed intubation, progressive cyanosis before collapse, asystole/PEA after respiratory failure.

First interventions: Ensure patent airway; high-concentration oxygen; effective ventilation with chest rise; suction; correct foreign-body or other obstruction; confirm advanced-airway position if already placed (waveform capnography when available). Hypoxia is both a cause of arrest and a reason pediatric BLS stresses ventilations with compressions.

Hydrogen ion (acidosis)

Clues: Prolonged arrest or shock, known DKA or other severe metabolic acidosis, poor ventilation with rising CO₂ (respiratory acidosis).

First interventions: Restore perfusion with high-quality CPR and effective ventilation—these are the primary acid-base therapies during arrest. Sodium bicarbonate is not routine for every pediatric arrest; consider only for specific indications (e.g., certain toxin contexts, documented severe hyperkalemia pathways, or other protocol-directed situations) under expert guidance. Exam trap: automatic bicarb for every PEA.

Hypoglycemia

Clues: Infants and neonates (small glycogen stores), sepsis, prolonged fasting or poor feeding, liver disease, inborn errors of metabolism, insulin or oral hypoglycemic ingestion, and any child whose mental status or perfusion fails to match the rest of the picture. Glucose is the one reversible cause you can confirm in under a minute at the bedside.

First interventions: Send or run a point-of-care glucose early—during CPR, not after ROSC. Treat documented hypoglycemia with weight-based IV/IO dextrose per your provider materials and institutional concentration chart (younger infants receive more dilute dextrose to avoid osmotic injury from concentrated solutions through small veins), then recheck. Do not push concentrated dextrose empirically into every arrest without a measured value; and do not defer the glucose check because "we are busy running the algorithm"—hypoglycemia is a printed pediatric H precisely because it is common, silent, and instantly fixable.

Hypokalemia / Hyperkalemia

Clues: Renal failure, dialysis delay, massive cell lysis, digoxin or other toxin context, ECG changes before or between cycles (peaked T waves, wide QRS, sine-wave pattern for severe hyperkalemia; U waves/arrhythmias for severe hypokalemia when relevant).

First interventions: For life-threatening hyperkalemia in arrest or near-arrest, follow emergency hyperkalemia steps per protocol—calcium to stabilize the myocardium when indicated, plus measures that shift potassium (insulin with glucose when appropriate, beta-agonists, bicarbonate in selected pathways) and remove potassium after ROSC. Correct severe hypokalemia with careful potassium replacement when it is the driver—usually post-identification, not blind bolusing without a reason. Do not give calcium or insulin/glucose empirically to every child without a hyperkalemia story.

Hypothermia

Clues: Environmental exposure, drowning in cold water, inadequate warming of infants, core temperature markedly low.

First interventions: High-quality CPR; prevent further heat loss; active rewarming per protocol for severe hypothermia; handle gently; continue resuscitation efforts longer than you might in normothermic arrest because the hypothermic brain may be more protected and ROSC can occur late with rewarming. Do not declare futility based solely on cold presentation without appropriate rewarming attempts in recoverable scenarios. Drug metabolism and defibrillation response may be altered—follow specialized hypothermia/arrest guidance while CPR quality stays high.

The T's: Recognition and First Interventions During Arrest

Tension pneumothorax

Clues: Trauma or positive-pressure ventilation; unilateral absent/decreased breath sounds; tracheal deviation away from the affected side (late); hypoxemia; PEA/shock physiology; difficult ventilation.

First intervention: Immediate needle decompression of the affected side per training, then definitive chest drainage when available. Do not delay for chest radiograph when the clinical picture is classic. Fluids alone will not fix mediastinal obstruction.

Cardiac tamponade

Clues: Penetrating or blunt chest trauma, post-cardiac surgery, pericardial disease; muffled heart sounds; elevated venous pressure signs; PEA with equal breath sounds; brief ultrasound showing pericardial effusion with chamber collapse when used without long CPR pauses.

First interventions: Support ABCs and CPR; careful volume may temporarily improve filling; definitive therapy is pericardial drainage (pericardiocentesis or surgical drainage) when indicated by trained providers. Do not keep stacking undifferentiated PEA cycles forever when tamponade is obvious and drainage is available.

Toxins

Clues: Known ingestion/overdose, empty pill bottles, toxidrome (opioids: miosis + respiratory arrest; sodium-channel blockers: wide QRS; etc.), access to household products or caregiver medications.

First interventions: Supportive care is foundational—airway, ventilation, CPR as indicated. Give specific antidotes when appropriate (classic PALS-level example: naloxone for opioid-induced respiratory depression/arrest with a pulse; see Section 11.2 for the cardiac-arrest vs respiratory-arrest distinction). Contact poison control/toxicology early. Some toxins require tailored ACLS/PALS modifications (e.g., sodium bicarbonate pathways for certain wide-complex toxicities)—know that toxins change the algorithm, not that you invent doses without a framework.

Thrombosis (pulmonary and coronary)

Pulmonary thrombosis/embolism: Massive PE can cause obstructive PEA. Clues include sudden collapse with risk factors (hypercoagulable state, central lines, congenital heart disease with thrombosis risk, prolonged immobility). Management is expert-level (supportive CPR, oxygen/ventilation, consideration of reperfusion strategies per specialty protocols). Exam-level point: include PE in the differential for sudden obstructive PEA when the history fits.

Coronary thrombosis: Common driver of adult VF arrest; rare in children. Still consider in special populations (Kawasaki disease with giant aneurysms, anomalous coronary arteries, hypercoagulable adolescents, substance-related coronary events). Do not default every pediatric arrest to “adult ACS care,” but do not refuse to think about coronary causes when the story is cardiac and primary.

Trauma context (not a printed T)

Trauma does not appear as its own letter in the 2025 algorithm's Reversible Causes box. It is less a single letter than a bundle of reversible problems: hypovolemia/hemorrhage, hypoxia, tension pneumothorax, tamponade, and sometimes neurogenic physiology. Prioritize hemorrhage control, airway/ventilation with C-spine precautions when indicated, bilateral breath-sound checks, and rapid transport to definitive trauma care while CPR and PALS fundamentals continue (Section 11.2).

Point-of-Care Ultrasound (POCUS) During Arrest

Bedside ultrasound can identify tamponade, a profoundly underfilled heart (hypovolemia), right-heart strain suggestive of massive PE, cardiac standstill vs fine VF questions in some settings, and—with skilled users—signs supporting pneumothorax. 2025-era PALS teaching allows POCUS only when it does not substantially interrupt high-quality CPR.

Practical rules:

• Plan a very brief look during a scheduled rhythm-check pause; hands back on the chest immediately
• One trained operator, one question ("effusion? empty LV?"), not a full echo curriculum mid-code
• Never extend hands-off time for perfect images
• Ultrasound informs cause treatment; it does not replace compressions, epinephrine, or defibrillation

Clinical scenario (synthesis)

A 3-year-old with days of gastroenteritis becomes unresponsive; the monitor shows PEA. The team starts CPR, bag-mask with oxygen, places IO access, and gives epinephrine 0.01 mg/kg. History screams hypovolemia and possible hypoxia from fatigue/aspiration risk. While CPR continues they give isotonic fluid boluses, ensure chest rise, check glucose, and reassess. Breath sounds are equal—no tension physiology. No toxin history. This is classic pediatric reversible-cause care: algorithm plus volume and oxygenation, not algorithm alone.

Bottom line for 11.1: Run H's and T's every cycle. Prioritize hypoxia and hypovolemia in children. Match each cause to a first intervention (ventilate, volume/blood, decompress, drain, antidote, rewarm, treat K+). Use POCUS only if it does not wreck CPR quality. Coronary thrombosis is rare—do not adult-ify every code, but do not miss special cardiac populations.