Reversible Causes of Cardiac Arrest: The 5 H's and 5 T's

Resuscitation following standardized algorithms – chest compressions, ventilation, defibrillation, epinephrine – is the foundation of every cardiopulmonary resuscitation. However, even technically flawless CPR will not succeed if the underlying cause of the cardiac arrest remains unrecognized. This is exactly where the concept of reversible causes comes in: the systematic search for treatable triggers during ongoing resuscitation is a decisive factor in patient outcome. The AHA guidelines organize these causes into two easy-to-remember groups – the 5 H's and the 5 T's. This article provides you with a practical breakdown of each individual cause, including specific diagnostic clues and treatment measures.

Why Systematic Cause Identification Is Critical for Survival

In cardiac arrest without an identifiable cardiac etiology – or in an arrest that does not respond to initial interventions – there is a high probability that a treatable cause is present. Identifying and treating this cause is often the only chance for Return of Spontaneous Circulation (ROSC).

The AHA recommends actively and repeatedly searching for reversible causes during every resuscitation – regardless of the initial rhythm. This is especially important in:

• PEA (pulseless electrical activity), where a treatable cause is almost always present
• Asystole without an identifiable cardiac trigger
• Refractory ventricular fibrillation that does not respond to defibrillation
• Traumatic cardiac arrest

The challenge in practice: under the time pressure of resuscitation, differential diagnostic considerations are quickly pushed to the background. This is precisely why a structured framework is essential – one that you can work through aloud as a team.

The 5 H's in Detail

Hypoxia

Hypoxia is one of the most common causes of cardiac arrest worldwide – and at the same time one of the most rapidly treatable. Oxygen deprivation leads to cardiac arrest via myocardial ischemia and electrical instability.

What to consider?

• Pre-existing respiratory diseases (COPD, asthma, pneumonia)
• Airway obstruction (foreign body, swelling, laryngospasm)
• Inadequate ventilation (tube misplacement, equipment malfunction)
• Drowning, strangulation

Treatment measures:

• Prioritize airway management: endotracheal intubation or supraglottic airway
• Verify tube placement: capnography (etCO₂) is the gold standard
• FiO₂ 1.0 during resuscitation
• Auscultate the chest bilaterally – unilaterally absent breath sounds → consider pneumothorax or tube misplacement
• If foreign body aspiration is suspected: direct laryngoscopy and extraction

Hypovolemia

Severe volume depletion – whether from hemorrhage or dehydration – leads to cardiac arrest via a critical drop in preload. PEA is the typical arrest rhythm in hypovolemia.

What to consider?

• Trauma (visible or occult hemorrhage: thorax, abdomen, pelvis, retroperitoneum)
• Gastrointestinal bleeding
• Ruptured aortic aneurysm
• Severe dehydration (sepsis, burns, diarrhea)
• Ectopic pregnancy

Treatment measures:

• Aggressive volume resuscitation: initial crystalloid solution (e.g., balanced electrolyte solution) via pressure infusion
• In hemorrhagic shock: initiate blood products early (packed red blood cells, FFP, platelet concentrates) aiming for a 1:1:1 ratio
• Organize surgical or interventional bleeding control in parallel with resuscitation
• Tranexamic acid 1 g IV for trauma-related hemorrhage
• Pelvic binder if pelvic fracture is suspected

Hydrogen Ions (Acidosis)

Severe metabolic acidosis impairs myocardial contractility, reduces catecholamine effectiveness, and promotes malignant cardiac arrhythmias. A pH drop below 7.1 is associated with significantly reduced defibrillation success rates.

What to consider?

• Diabetic ketoacidosis
• Renal failure (uremic acidosis)
• Lactic acidosis from prolonged shock or sepsis
• Intoxications (methanol, ethylene glycol, salicylates)
• Prolonged resuscitation per se

Treatment measures:

• Sodium bicarbonate 50 mmol (50 ml of 8.4% solution) IV for known or highly probable severe acidosis
• Obtain a blood gas analysis (BGA) as early as possible – also feasible via intraosseous access (venous BGA)
• Ensure adequate ventilation (respiratory compensation)
• Treat the underlying condition (e.g., insulin for DKA, dialysis for renal failure)

Hypo-/Hyperkalemia

Electrolyte disturbances – particularly potassium shifts – are potent triggers of lethal cardiac arrhythmias. Both hypokalemia and hyperkalemia can lead to cardiac arrest.

What to consider?

• Hyperkalemia: Renal failure (especially dialysis patients), ACE inhibitors/ARBs, potassium-sparing diuretics, rhabdomyolysis, tumor lysis syndrome, burns, crush syndrome
• Hypokalemia: Diuretic therapy, vomiting, diarrhea, alcoholism

Diagnostic clues:

• ECG changes (if available prior to arrest): in hyperkalemia – peaked (tented) T-waves, widened QRS complexes, sine wave pattern; in hypokalemia – U-waves, ST depression, flattened T-waves
• Point-of-care blood gas analysis with electrolyte measurement delivers results in under 2 minutes

Treatment for hyperkalemia (the more common arrest cause):

• Calcium gluconate 10% – 30 ml IV (or calcium chloride 10% – 10 ml IV via central access): membrane stabilization, onset of action within minutes
• Sodium bicarbonate 50 mmol IV
• Insulin 10 IU + glucose 25 g (50 ml of 50% glucose) IV: intracellular potassium shift
• Nebulized salbutamol 10–20 mg (off-label dosing in emergency)
• Goal: initiate dialysis as soon as possible in known renal failure

Treatment for hypokalemia:

• Potassium chloride 20–40 mmol IV over 10–20 minutes (caution: never as a bolus; maximum infusion rate 20 mmol/h under monitor surveillance – in the arrest setting, faster administration may be considered under strict monitoring)
• Magnesium sulfate 2 g IV (hypomagnesemia is frequently a concomitant finding)

Hypothermia

Severe hypothermia (core temperature < 30 °C) can trigger cardiac arrest while simultaneously providing a degree of neuroprotection – the well-known principle: "Nobody is dead until warm and dead."

What to consider?

• Avalanche accidents, water immersion
• Exposure in homeless individuals or intoxicated patients
• Elderly patients with reduced thermoregulation

Treatment measures:

• Measure core temperature (esophageal or rectal, not tympanic)
• At core temperature < 30 °C: limit defibrillation to a maximum of 3 attempts until core temperature > 30 °C
• Extend epinephrine administration intervals (every 6–10 minutes) at core temperature < 30 °C
• Active rewarming: warm infusions (38–42 °C), forced-air warming (Bair Hugger), in severe hypothermia aim for extracorporeal rewarming (ECMO/ECLS)
• Continue CPR until rewarming is achieved or until an ECMO center is reached
• Transport to an ECMO-capable center is the highest priority

The 5 T's in Detail

Tension Pneumothorax

A tension pneumothorax leads rapidly to obstructive shock and cardiac arrest via mediastinal shift and decreased venous return.

What to consider?

• Chest trauma (blunt or penetrating)
• After central venous catheter placement (subclavian vein, internal jugular vein)
• Mechanically ventilated patients (barotrauma)
• Pre-existing lung disease (COPD with bullae)

Diagnostic clues:

• Unilaterally absent breath sounds
• Distended neck veins (may be absent in hypovolemia)
• Tracheal deviation (late sign)
• Bedside ultrasound (absent lung sliding, absent "seashore sign")

Treatment measures:

• Immediate needle decompression: 2nd intercostal space midclavicular line or 4th–5th intercostal space anterior axillary line, long needle (at least 8 cm in obese patients)
• Definitive management: chest tube (tube thoracostomy, 28–32 Fr)
• Bilateral decompression if there is no response to unilateral decompression

Tamponade (Cardiac Tamponade)

Pericardial tamponade compresses the cardiac chambers and prevents diastolic filling. As little as 150–200 ml of fluid can be hemodynamically significant when it accumulates acutely.

What to consider?

• Penetrating chest trauma
• Aortic dissection
• Pericarditis, malignancy
• After cardiac surgery or catheter-based interventions

Diagnostic clues:

• Beck's triad: muffled heart sounds, hypotension, distended neck veins (rarely fully present in the resuscitation setting)
• Bedside echocardiography (Focused Cardiac Ultrasound): pericardial effusion and right ventricular diastolic collapse

Treatment measures:

• Pericardiocentesis: subxiphoid approach under ultrasound guidance; aspiration of even small volumes (20–50 ml) can be hemodynamically effective
• In traumatic tamponade: consider emergency thoracotomy (resuscitative thoracotomy)
• Volume resuscitation to maintain preload

Thrombosis – Pulmonary Embolism

Massive pulmonary embolism is one of the most common non-cardiac causes of cardiac arrest. The massive obstruction of the pulmonary arteries leads to acute right heart failure.

What to consider?

• Known deep vein thrombosis
• Immobilization, postoperative state
• Malignancy
• Oral contraceptives, pregnancy/postpartum period
• Sudden dyspnea prior to arrest

Diagnostic clues:

• PEA with marked right ventricular dilation on bedside echocardiography
• Persistently low etCO₂ (< 10 mmHg) despite good CPR quality (indicating absent pulmonary blood flow)

Treatment measures:

• Systemic thrombolysis during CPR: weight-adjusted tenecteplase as a bolus or alteplase 50 mg IV as a bolus (for highly probable or confirmed pulmonary embolism)
• After thrombolysis: continue CPR for at least 60–90 minutes before considering termination
• Alternative: interventional or surgical thrombectomy, if available
• Heparin 5,000 IU IV as a bolus (if thrombolysis has not already been administered)

Thrombosis – Coronary Thrombosis (Myocardial Infarction)

Acute ST-elevation myocardial infarction (STEMI) is the most common cause of sudden cardiac death. Ventricular fibrillation and pulseless ventricular tachycardia are the typical initial rhythms.

What to consider?

• Chest pain prior to arrest
• Known coronary artery disease, cardiovascular risk factors
• ST elevations on 12-lead ECG (if available before arrest or after ROSC)

Treatment measures:

• Aim for early coronary angiography after ROSC (PCI-capable center)
• Heparin 5,000 IU IV as a bolus
• Aspirin 250–500 mg IV
• If PCI access is unavailable and STEMI is present: consider fibrinolysis
• Even without ROSC: in selected cases, consider transport under ongoing resuscitation to the catheterization lab or ECPR

Toxins (Intoxications)

Poisoning with cardiodepressant or arrhythmogenic substances can trigger cardiac arrest. The range is enormous – from medication overdoses to recreational drug intoxications.

What to consider?

• Empty medication packages, suicide note
• Known psychiatric disorders
• Substance abuse (opioids, cocaine, amphetamines)
• Occupational exposure (organophosphates, cyanides)

Specific antidotes in cardiac arrest:

Toxin	Antidote	Dosing
Opioids	Naloxone	2 mg IV/IN, repeatable
Beta-blockers	Glucagon	5–10 mg IV bolus
Calcium channel blockers	Calcium gluconate 10%	30–60 ml IV
Local anesthetics	Lipid emulsion 20%	1.5 ml/kg IV bolus, then 0.25 ml/kg/min
Tricyclic antidepressants	Sodium bicarbonate 8.4%	1–2 mmol/kg IV
Digitalis	Digitalis-specific antibody (Fab)	Weight-adjusted
Cyanides	Hydroxocobalamin	5 g IV over 15 min

• For unknown substances: supportive therapy, consider lipid rescue
• Involve toxicology consultation (poison control center)

Practical Tips for Structured Cause Identification

The following approach has proven effective in the resuscitation setting:

1. Team leader role: The search for reversible causes is primarily the responsibility of the team leader. While the team performs CPR, the team leader systematically works through the H's and T's.
2. Obtain history in parallel: Interview family members, review medication lists, read the prehospital documentation.
3. Point-of-care ultrasound (POCUS): During the rhythm analysis pause, perform a subxiphoid view: pericardial effusion? RV dilation? Hypovolemia? Absent cardiac activity?
4. Immediate blood gas analysis: Potassium, pH, lactate, and hemoglobin provide essential information in under 2 minutes.
5. Think out loud: Verbalize the H's and T's within the team: "Have we ruled out hypoxia? Could this be a pulmonary embolism?"
6. Use a checklist: Many teams work with laminated cards or cognitive aids that are available at the resuscitation station.

Summary as Quick Reference

The 5 H's:

• Hypoxia → Secure the airway, FiO₂ 1.0
• Hypovolemia → Volume resuscitation, bleeding control
• Hydrogen ions (acidosis) → Sodium bicarbonate, ventilation
• Hypo-/hyperkalemia → Calcium, insulin/glucose, potassium replacement
• Hypothermia → Rewarming, consider ECMO

The 5 T's:

• Tension pneumothorax → Needle decompression, chest tube
• Tamponade → Pericardiocentesis
• Thrombosis (pulmonary embolism) → Thrombolysis
• Thrombosis (coronary) → Aim for PCI
• Toxins → Specific antidotes

Practical Training

The systematic search for reversible causes during ongoing resuscitation is a competency that can only be internalized through repeated training. Theoretical knowledge alone is not enough – what matters is that you can recall the right diagnostic and therapeutic steps under stress. In the ACLS course by Simulation Tirol, you train exactly these scenarios: realistic megacode simulations with reversible causes, structured team leading, and the targeted use of cognitive aids. The AHA-certified courses give you the opportunity to apply your knowledge practically in a safe learning environment, ensuring you are prepared for real-life emergencies.

---