What can cause ventricular fibrillation (V Fib)?

Causes of Ventricular Fibrillation

Ischemic heart disease is the definitive primary cause of ventricular fibrillation in adults, accounting for the majority of sudden cardiac arrest cases, with acute myocardial ischemia and infarction representing the predominant trigger. 1

Primary Cardiac Causes

Acute Coronary Syndromes

• Acute myocardial infarction and ongoing ischemia are the most common underlying substrates for VF, with the majority of individuals dying from acute coronary syndrome before reaching the hospital 1
• VF is the most common primary arrhythmia in adult cardiac arrest, often preceded by a brief period of ventricular tachycardia that deteriorates into VF 1
• Coronary artery spasm can cause polymorphic VT or VF, and treatment of the spasm may be sufficient to prevent recurrent arrhythmia 2
• Recurrent polymorphic VT degenerating into VF may indicate incomplete reperfusion or recurrence of acute ischemia 2

Structural Heart Disease

• Cardiomyopathies (hypertrophic, dilated, restrictive) create arrhythmogenic substrates that predispose to VF 2, 1
• Tachycardia-induced cardiomyopathy from atrial fibrillation can lead to ventricular dysfunction that predisposes to VF 1
• Valvular heart disease, particularly when causing ventricular dysfunction, increases VF risk 1
• Left ventricular hypertrophy increases pro-arrhythmic risk, especially with certain antiarrhythmic drugs 2

Electrolyte Abnormalities

Hypokalemia

• Serum potassium <3.5 mEq/L is an independent predictor of primary VF during myocardial infarction (OR 2.28,95% CI: 1.6-3.3) 3
• Low serum potassium concentrations are associated with increased frequency of ventricular fibrillation, particularly in acute myocardial infarction 4
• Hypokalemia facilitates development of VT in predisposed patients, especially those receiving antiarrhythmic agents and drugs associated with long QT syndrome 2
• Acute catecholamine-induced shifts of potassium into cells may occur during acute myocardial ischemia 4

Hypomagnesemia

• Diuretic-induced magnesium deficiency may favor emergence of ventricular arrhythmias in patients with ischemic heart disease 4
• Hypomagnesemia facilitates development of VT in predisposed patients receiving antiarrhythmic agents 2

Hyperkalaemia

• Unrecognized hyperkalaemia, particularly with combination of renin-angiotensin system inhibitors and antibiotics like co-trimoxazole, has been associated with increased risk of sudden death 2
• Hyperkalaemia may trigger arrhythmic death in heart transplant patients during hemodialysis or plasmapheresis 2

Drug-Induced Causes

Antiarrhythmic Drugs

• Sodium channel-blocking drugs (flecainide, propafenone, quinidine) increased mortality in patients with previous myocardial infarction in large trials like CAST and CASH 2
• D-sotalol slightly increased mortality in patients with remote infarction 2
• QT-prolonging agents can cause torsades de pointes and VF, with dofetilide causing TdP in 3.3% of severe heart failure patients during first 72 hours 2
• Amiodarone causes TdP much less commonly than other QT-prolonging antiarrhythmics 2

Non-Cardiac Medications

• Many non-cardiac medications inhibit potassium channels and are associated with risk for torsades de pointes (www.crediblemeds.org) 2
• Antibiotics (quinolones, azithromycin, erythromycin, clarithromycin) significantly increase risk of death and cardiac arrhythmia 2
• Tricyclic antidepressants may produce QRS prolongation and typical Brugada syndrome ECG pattern 2
• 5-fluorouracil may cause VF due to coronary spasm 2
• Anthracycline cardiotoxicity is dose-dependent, with higher cumulative doses increasing risk of lethal arrhythmias 2

Drug-Drug Interactions

• Bradyarrhythmias are common with digoxin, verapamil, diltiazem, and beta-blockers 2
• Digitalis toxicity causes enhanced atrial, junctional, or ventricular automaticity often combined with AV block 2

Other Precipitating Factors

Hemodynamic and Metabolic

• Low systolic blood pressure at presentation is an independent predictor of primary VF (OR 0.982 per mm Hg) 3
• Hypoxia and acid-base disturbances can trigger ventricular arrhythmias 2
• Hypothermia can cause VF 2

Patient-Specific Risk Factors

• Family history of sudden death is an independent predictor (OR 1.80,95% CI: 1.1-3.0) 3
• Physical inactivity is an independent predictor (OR 1.73,95% CI: 1.1-2.8) 3
• Anterior MI location increases VF risk (OR 1.52,95% CI: 1.1-2.1) 3

Post-Transplant

• Sudden death is frequent after heart transplantation (>10% of cardiac transplant recipients) 2
• Acute rejection can damage the conduction system, leading to VA and sudden death 2
• These hearts may be at increased risk during hemodynamic stresses of hemodialysis or plasmapheresis 2

Critical Clinical Pitfalls

Do not assume VF is purely electrical—always search for underlying acute coronary syndrome, as this is the most common reversible cause requiring immediate revascularization. 1, 2

• Do not assume electrolyte abnormalities are the sole cause of sustained monomorphic VT; patients should be evaluated and treated similarly to those without electrolyte abnormalities 2
• Hypokalemia can result from cardiac arrest itself and should not be assumed to be the cause except under unusual circumstances 2
• In patients with structural heart disease and abnormal serum potassium at time of initial VF episode, the risk of recurrent arrhythmia remains high (82% at 5 years) despite correction, suggesting defibrillator therapy may be reasonable 5
• Atrial fibrillation on admission with acute MI is independently associated with increased risk of VF and subsequent mortality 6