H's and T's

A checklist of the reversible causes of cardiac arrest (especially pulseless electrical activity and asystole) that rescuers hunt for and treat during CPR: five H causes and five T causes.

H — Hypovolemia

Too little blood volume (hemorrhage, dehydration) - treat with fluids/blood

Hypovolemia from hemorrhage, trauma, dehydration, burns, or fluid shifts is a leading reversible cause of PEA. The heart shows organized electrical activity but no pulse because there is inadequate preload to fill the ventricles.

Physiology. Cardiac output = stroke volume x heart rate, and stroke volume depends on preload. Critically low volume collapses ventricular filling, dropping stroke volume to ~0 (PEA) even while the conduction system fires.

Safety. Give fluids judiciously if the arrest may be cardiac in origin; indiscriminate volume can worsen cardiogenic failure. Use history and bedside ultrasound (empty vs. full heart).

H — Hypoxia

Too little oxygen - treat with airway management and ventilation/oxygenation

Hypoxia from airway obstruction, respiratory failure, drowning, or aspiration is a fundamental reversible cause of arrest. Address the A and B of the ABCs: open the airway, ventilate with 100% oxygen, and place an advanced airway if needed.

Physiology. Severe hypoxemia causes myocardial ischemia and acidosis, suppressing contractility and conduction, progressing to bradycardia, PEA, or asystole.

Safety. Verify airway patency and advanced airway placement with waveform capnography; ensure compressions provide adequate perfusion.

H — Hydrogen ion (acidosis)

Blood too acidic (metabolic or respiratory) - treat by ventilation and addressing the cause

Severe metabolic or respiratory acidosis depresses contractility and blunts catecholamine response. Management is primarily ventilation (blow off CO2); sodium bicarbonate is reserved for specific indications (severe pre-existing metabolic acidosis, hyperkalemia, tricyclic antidepressant overdose).

Physiology. Hydrogen ions interfere with calcium handling and enzyme function in myocytes and reduce catecholamine receptor sensitivity, weakening contraction and vasopressor response.

Safety. Do not reflexively push bicarbonate during routine arrest; it can cause paradoxical intracellular acidosis and hypernatremia.

H — Hypo-/Hyperkalemia

Potassium too low or too high - replace potassium or give calcium plus shift/remove it

Both hypokalemia and hyperkalemia cause lethal dysrhythmias. Hyperkalemia (peaked T waves, widened QRS, sine wave) is treated with IV calcium, insulin + glucose, beta-agonists, and bicarbonate/dialysis; hypokalemia (U waves, PVCs, ventricular dysrhythmias) is treated with replacement.

Physiology. Resting membrane potential and repolarization depend on the potassium gradient. Hyperkalemia depolarizes myocytes (conduction slows to blocks to arrest); hypokalemia prolongs repolarization (early afterdepolarizations to ventricular dysrhythmias).

Safety. Never give IV potassium as a rapid push - it can itself cause arrest. Suspect hyperkalemia in dialysis patients and give calcium for hyperkalemic ECG changes.

H — Hypothermia

Body too cold - treat with active rewarming and prolonged resuscitation

Severe hypothermia (core < 28-30 C) causes bradycardia, Osborne (J) waves, and progression to VF, PEA, or asystole. Resuscitation requires active rewarming (warm IV fluids, warm humidified oxygen, external/internal rewarming, ECMO in severe cases); a cold arrested patient may survive prolonged resuscitation.

Physiology. Hypothermia slows conduction, reduces automaticity, and makes the myocardium irritable; drugs and defibrillation are less effective below ~30 C.

Safety. Handle the patient gently (jostling can trigger VF), obtain a true core temperature, and continue resuscitation longer while rewarming.

T — Tension pneumothorax

Trapped air compressing the heart and lungs - treat with needle decompression then chest tube

A one-way valve lets air into the pleural space but not out, collapsing the lung and shifting the mediastinum, compressing the great vessels and heart (reduced venous return to obstructive shock to PEA). Immediate treatment is needle decompression followed by chest tube.

Physiology. Rising intrathoracic pressure compresses the vena cavae and right heart, cutting preload (obstructive shock) and collapsing the opposite lung (hypoxia).

Safety. Decompress a crashing patient immediately - do not wait for imaging confirmation. Needle decompression is temporizing; definitive chest tube follows.

T — Tamponade (cardiac)

Fluid around the heart squeezing it - treat with pericardiocentesis or surgical drainage

Fluid (blood from trauma or MI rupture, effusion from malignancy/uremia/pericarditis) accumulates in the pericardial sac, compressing the heart and preventing diastolic filling (obstructive shock to PEA). Treatment is pericardiocentesis or surgical drainage. Beck's triad (hypotension, muffled heart sounds, distended neck veins) and pulsus paradoxus may be present.

Physiology. The stiff pericardial sac limits ventricular filling; as fluid accumulates, stroke volume and cardiac output fall despite preserved electrical activity.

Safety. Suspect in trauma or post-cardiac surgery; assist with pericardiocentesis and avoid treatments that reduce preload.

T — Toxins

Poisoning or drug overdose - treat with specific antidotes and prolonged supportive care

Toxic causes include overdose of tricyclic antidepressants, beta-blockers, calcium-channel blockers, opioids, digoxin, and local anesthetics. Management is agent-specific: sodium bicarbonate for TCA/Na-channel blockade, calcium for calcium-channel blockers, digoxin immune Fab for digoxin, naloxone for opioids, intralipid for local anesthetic toxicity, plus prolonged supportive resuscitation.

Physiology. Toxins disrupt specific channels or receptors (Na, K, Ca, beta, opioid); correcting the molecular target with an antidote reverses the dysrhythmia or vasoplegia.

Safety. Get a history (family, EMS, bottles), consider toxidromes, call poison control, prepare antidotes, and anticipate prolonged resuscitation (toxin-induced arrest can be very reversible).

T — Thrombosis (pulmonary)

Blood clot in the lung (pulmonary embolism) - treat with fibrinolysis and continued CPR

Massive pulmonary embolism obstructs pulmonary flow, causing acute right ventricular failure, obstructive shock, and PEA. In arrest or peri-arrest, treatment is fibrinolytic therapy (alteplase) and/or embolectomy, with high-quality CPR continued for 60-90 minutes after thrombolysis.

Physiology. A clot in the pulmonary arteries abruptly raises right-heart afterload; the thin-walled right ventricle fails and output falls to PEA. Dissolving the clot restores flow.

Safety. If PE is strongly suspected during arrest, facilitate emergent thrombolysis per protocol and continue CPR for an extended period after giving it.

T — Thrombosis (coronary)

Blood clot in the heart (myocardial infarction) - treat with PCI or fibrinolysis

Coronary thrombosis causes acute myocardial infarction (usually STEMI), which can present as VF or PEA/asystole. Reperfusion via percutaneous coronary intervention (PCI) or fibrinolysis is definitive; during arrest, high-quality CPR, defibrillation for shockable rhythms, and early cath-lab activation are key.

Physiology. Coronary occlusion causes ischemia/infarction, electrical instability (VF), and pump failure; restoring flow salvages myocardium and is the definitive reversal.

Safety. Obtain a 12-lead ECG early; for STEMI-related arrest activate the cath lab and continue CPR (mechanical CPR if available); consider thrombolysis if PCI is unavailable.

Memory aids

• H = Hypovolemia
• H = Hypoxia
• H = Hydrogen ion (acidosis)
• H = Hypo-/Hyperkalemia
• H = Hypothermia
• T = Tension pneumothorax
• T = Tamponade (cardiac)
• T = Toxins
• T = Thrombosis (pulmonary)
• T = Thrombosis (coronary)

Quick review

• H = Hypovolemia — Too little blood volume (hemorrhage, dehydration) - treat with fluids/blood
• H = Hypoxia — Too little oxygen - treat with airway management and ventilation/oxygenation
• H = Hydrogen ion (acidosis) — Blood too acidic (metabolic or respiratory) - treat by ventilation and addressing the cause
• H = Hypo-/Hyperkalemia — Potassium too low or too high - replace potassium or give calcium plus shift/remove it
• H = Hypothermia — Body too cold - treat with active rewarming and prolonged resuscitation
• T = Tension pneumothorax — Trapped air compressing the heart and lungs - treat with needle decompression then chest tube
• T = Tamponade (cardiac) — Fluid around the heart squeezing it - treat with pericardiocentesis or surgical drainage
• T = Toxins — Poisoning or drug overdose - treat with specific antidotes and prolonged supportive care
• T = Thrombosis (pulmonary) — Blood clot in the lung (pulmonary embolism) - treat with fibrinolysis and continued CPR
• T = Thrombosis (coronary) — Blood clot in the heart (myocardial infarction) - treat with PCI or fibrinolysis