Hs and Ts: identifying and treating reversible causes of cardiac arrest

When a patient goes into cardiac arrest, the resuscitation team must do more than perform chest compressions and deliver shocks. Clinicians need to actively search for a treatable underlying cause. The Hs and Ts mnemonic provides a structured framework for recalling the most common reversible etiologies of cardiac arrest. Identifying these conditions quickly—and intervening appropriately—can mean the difference between successful resuscitation and death.

In the United States, sudden cardiac arrest claims an estimated 350,000 lives each year.¹ The European Resuscitation Council (ERC) and the American Heart Association (AHA) both emphasize that high-quality CPR, early defibrillation, and systematic evaluation for reversible causes are the cornerstones of effective resuscitation.²

The sections below walk through each of the Hs and Ts, discuss how each condition leads to cardiac arrest, and outline current management strategies.

The “H” causes

Hypoxia very common

Hypoxia refers to inadequate oxygen delivery at the tissue level. Low blood oxygen (hypoxemia) is one of the most frequent non-cardiac triggers of arrest, usually stemming from airway compromise or respiratory failure.²

Common conditions that produce hypoxemia include:

• Airway obstruction — foreign body, soft tissue collapse in an unconscious patient, laryngospasm, or aspiration
• Respiratory diseases — asthma, COPD, pneumonia, and tension pneumothorax
• Environmental exposure — drowning, avalanche burial, high altitude, or traumatic asphyxia (such as a crowd crush)
• Neurologic causes — central hypoventilation from brain or spinal cord injury, or impaired ventilation due to neuromuscular disease
• Reduced oxygen-carrying capacity — severe anemia

Management. Secure the airway, provide supplemental oxygen, and initiate positive-pressure ventilation. Address the specific cause (e.g., needle decompression for tension pneumothorax, bronchodilators for severe bronchospasm). Because tissue hypoxia rapidly becomes irreversible, speed is critical.

Hypovolemia common

A severe reduction in circulating blood volume can deprive the heart of adequate preload, ultimately leading to PEA arrest. Hemorrhagic causes, such as trauma, gastrointestinal bleeding, ruptured aortic aneurysm, or postpartum hemorrhage, are the most immediately life-threatening. Non-hemorrhagic hypovolemia from severe dehydration, burns, or third-spacing of fluid can also precipitate arrest.²

Clinical clues. External bleeding is usually obvious, but occult hemorrhage (retroperitoneal, intra-abdominal, pelvic fracture) can be harder to recognize. Flat neck veins, tachycardia progressing to PEA, and a narrow pulse pressure suggest volume depletion.

Management. Administer warmed crystalloid or blood products rapidly through large-bore IV access while simultaneously controlling the source of bleeding. In traumatic cardiac arrest, damage-control surgery or interventional radiology may be required.

Hypothermia uncommon

Accidental hypothermia—defined as a core body temperature below 35 °C—causes progressive cardiac conduction abnormalities.³ As temperature falls, sinus bradycardia gives way to atrial fibrillation, then to ventricular fibrillation (VF), and finally to asystole.⁴ Approximately 1,500 deaths from accidental hypothermia occur in the United States annually.³

The Swiss staging system classifies hypothermia by severity:⁵

Management. Arrhythmias other than VF typically resolve as core temperature rises and do not require immediate pharmacologic treatment.² Active external rewarming (e.g., forced warm air blankets) combined with warmed IV fluids is the standard approach. For patients in cardiac arrest with severe hypothermia, extracorporeal rewarming (ECMO) should be considered when available. A key clinical principle: do not declare death until the patient is warm and still unresponsive to resuscitation.

Hydrogen ion excess (acidosis) common

Both metabolic and respiratory acidosis impair cardiac function by reducing myocardial contractility, causing vasodilation, and shifting the oxyhemoglobin dissociation curve.⁶

Respiratory acidosis results from inadequate ventilation and is corrected by optimizing airway management and ventilation. Metabolic acidosis has a wide differential—diabetic ketoacidosis, lactic acidosis from shock, renal failure, and toxic ingestions are among the most common causes in arrested patients.

An arterial blood gas provides a rapid assessment. Although severe acidemia is common during and after cardiac arrest, its independent prognostic value for neurologic outcomes remains unclear.⁷

Management. Treat the underlying cause. Routine sodium bicarbonate administration during cardiac arrest is not recommended. Sodium bicarbonate (1 mEq/kg IV) may be considered for specific indications, such as hyperkalemia, sodium channel blocker overdose, or pre-existing severe metabolic acidosis when clinically appropriate.⁸

Hyperkalemia and hypokalemia very common

Potassium disorders—especially hyperkalemia—are strongly associated with cardiac arrest. Disturbances in serum potassium alter the resting membrane potential of cardiomyocytes, predisposing to arrhythmias ranging from bradycardia to VF and asystole.²

Hyperkalemia

Hyperkalemia (generally defined as serum potassium above 5.5 mmol/L) is the electrolyte abnormality most commonly linked to cardiac arrest and occurs in up to 10% of hospitalized patients.⁹ Causes include:

• Impaired renal excretion — acute kidney injury, chronic kidney disease
• Medications — ACE inhibitors, angiotensin receptor blockers, potassium-sparing diuretics, NSAIDs, beta-blockers, trimethoprim
• Cellular release — rhabdomyolysis, tumor lysis syndrome, hemolysis
• Acidosis — renal failure, diabetic ketoacidosis
• Endocrine — adrenal insufficiency (Addison disease)

ECG changes progress from peaked T waves through widened QRS complexes to a sine wave pattern. Treatment follows a stepwise approach:¹⁰

1. Stabilize the myocardium — calcium chloride or calcium gluconate IV
2. Shift potassium intracellularly — insulin with dextrose, inhaled beta-2 agonists, sodium bicarbonate
3. Remove potassium from the body — loop diuretics (when appropriate) or hemodialysis. Potassium-binding agents have a delayed onset and are not appropriate for immediate treatment of life-threatening hyperkalemia.
4. Monitor serum potassium and blood glucose closely
5. Prevent recurrence — adjust medications, dietary counseling

Hypokalemia

Hypokalemia (serum potassium below 3.5 mmol/L) affects up to 20% of hospitalized patients and increases the risk of ventricular arrhythmias and sudden death.^{11, 12} Gastrointestinal losses, diuretic therapy, and renal tubular disorders are the most frequent causes. Many hypokalemic patients are also magnesium-depleted, and correcting the magnesium deficit accelerates potassium repletion.¹³

Management. Replace potassium intravenously in urgent situations using appropriate infusion rates and cardiac monitoring. Concurrent magnesium replacement is recommended in severe cases.

The “T” causes

Tension pneumothorax uncommon

A tension pneumothorax develops when air enters the pleural space through a one-way valve mechanism and cannot escape, causing progressive mediastinal shift that compresses the great vessels and obstructs venous return to the heart.¹⁴

This condition arises in trauma patients, as a complication of mechanical ventilation, or iatrogenically after procedures such as central line placement or thoracentesis. During CPR, it should be actively excluded because it is immediately treatable.²

Diagnosis in an arrested patient is clinical: absent breath sounds on one side, tracheal deviation, distended neck veins, and subcutaneous emphysema.¹⁵ Imaging is not required before intervention.

Management. Perform immediate needle decompression (preferably at the fourth or fifth intercostal space at the anterior or mid-axillary line; the second intercostal space midclavicular approach may also be used depending on local protocol) followed by chest tube thoracostomy. In cardiac arrest, some guidelines recommend proceeding directly to finger thoracostomy.

Tamponade (cardiac) rare

Cardiac tamponade occurs when fluid (blood, effusion, or pus) accumulates in the pericardial sac under pressure, compressing the heart chambers and impairing filling.² Traumatic tamponade typically follows penetrating chest injuries, while non-traumatic causes include pericarditis, malignancy, and uremia.

Diagnosis. The classic Beck triad (hypotension, muffled heart sounds, distended neck veins) is often absent and is not reliable for diagnosis during cardiac arrest. Bedside POCUS can rapidly identify pericardial fluid.

Management. Pericardiocentesis—ideally with ultrasound guidance—is the primary intervention for non-traumatic tamponade. For traumatic tamponade, emergency thoracotomy may be necessary.

Toxins common

Poisoning and drug overdose cause cardiac arrest through multiple mechanisms: respiratory depression and airway loss, direct myocardial toxicity, and vasodilation leading to distributive shock.¹⁶ Identifying the specific agent is important because targeted antidotes exist for several drug classes.

General principles. Secure the airway early, as loss of consciousness from sedative overdose is a leading cause of aspiration death. Drug-induced hypotension usually responds to IV crystalloid, though vasopressors such as norepinephrine may be needed.

Opioids

Opioid overdose suppresses respiratory drive, leading to apnea and hypoxic arrest. Naloxone reverses the effects and can be given through IV, intramuscular, subcutaneous, intraosseous, or intranasal routes.¹⁷ Initial dosing should be titrated to effect, starting with 0.04–0.4 mg IV (or 2 mg intranasal), with repeat or escalating doses as needed to restore adequate ventilation. Repeat doses may be needed every 2–3 minutes because naloxone’s duration of action is shorter than that of most opioids.²

Benzodiazepines

Benzodiazepine overdose produces sedation, respiratory depression, and hypotension. Flumazenil, a competitive antagonist, can reverse these effects but is contraindicated in patients with chronic benzodiazepine use, seizure disorders, or suspected mixed/unknown overdoses due to the risk of precipitating seizures.²

Tricyclic antidepressants

Tricyclic toxicity causes sodium channel blockade, leading to QRS prolongation and wide-complex ventricular tachycardia, along with anticholinergic effects.² Sodium bicarbonate (1–2 mEq/kg IV bolus) is the primary treatment for tricyclic-induced cardiac toxicity, as it both overcomes sodium channel blockade and corrects acidosis.¹⁸

Local anesthetics

LAST occurs from inadvertent intravascular injection or excessive absorption during regional anesthesia. Manifestations include seizures, cardiovascular collapse, and cardiac arrest.¹⁹ IV lipid emulsion (20% intralipid) is the specific rescue therapy and should be administered alongside standard ACLS measures.

Beta-blockers

Beta-blocker overdose produces profound bradycardia and negative inotropy. Treatment options include high-dose glucagon (3–10 mg IV bolus), high-dose insulin-euglycemia therapy, IV calcium, and lipid emulsion.²⁰ Refractory cases may require mechanical circulatory support.

Calcium channel blockers

Calcium channel blocker poisoning is one of the most lethal categories of prescription drug overdose.²¹ Sustained-release formulations can cause delayed-onset cardiovascular collapse hours after ingestion. Treatment includes IV calcium (calcium chloride 10% in 10–20 mL IV boluses, repeated as needed based on clinical response and ionized calcium levels), high-dose insulin-euglycemia therapy, and vasopressors.²²

Thrombosis (pulmonary) common

Massive pulmonary embolism is one of the most common non-cardiac causes of sudden arrest, usually originating from deep vein thrombosis (DVT).²³ Patients may present with sudden dyspnea, pleuritic chest pain, hemoptysis, or syncope immediately before arrest, though the embolism can also be the first manifestation of thrombotic disease.²⁴

Management. When pulmonary embolism is the suspected cause of cardiac arrest, systemic fibrinolysis should be considered when pulmonary embolism is suspected as the cause of cardiac arrest. If fibrinolytics are administered during CPR, prolonged resuscitation should be considered after fibrinolytic administration, as ROSC may be delayed.² Surgical embolectomy and catheter-directed thrombectomy are alternatives when available.

Thrombosis (coronary) very common

Acute coronary occlusion is the single most common cause of out-of-hospital cardiac arrest. When the presenting rhythm is VF, an occluded coronary artery is the likely etiology.² For more detailed information, see our article on myocardial infarction.

Management. Emergent coronary angiography with primary percutaneous coronary intervention (PCI) is the definitive treatment. Transport to a cardiac catheterization laboratory during ongoing CPR may be considered in selected cases at experienced centers with mechanical CPR and resuscitation protocols.²

Putting it together

During any cardiac arrest, the resuscitation team should systematically work through the Hs and Ts while performing high-quality CPR. History from bystanders, the patient’s medical record, point-of-care labs (blood gas, electrolytes, glucose), bedside ultrasound, and the presenting cardiac rhythm all provide clues that narrow the differential.

Rapid identification and treatment of a reversible cause gives the patient the best chance of meaningful survival.

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