What causes ventricular fibrillation (V Fib) arrest?

Causes of Ventricular Fibrillation Arrest

Coronary artery disease is the leading cause of ventricular fibrillation arrest, accounting for 50-60% of all cardiac arrests in adults, with acute coronary ischemia being the predominant underlying mechanism. 1

Primary Etiologies by Age

Adults Over 40 Years

• Acute coronary thrombosis with occlusion of major coronary arteries represents the primary mechanism 1
• Coronary ischemia remains the predominant pathology in the estimated 290,000-350,000 annual cardiac arrests in the United States 1

Young Adults (Under 40 Years)

• Hypertrophic cardiomyopathy is the most common cause, affecting approximately 1 in 500 persons in the general population 1
• Channelopathies and cardiomyopathies predominate in younger patients 2

Secondary and Precipitating Causes

Acute Myocardial Infarction

• VF complicates approximately 10% of hospitalized patients receiving fibrinolytic therapy 3
• Primary VF during acute MI carries high short-term mortality, though survivors of Q-wave MI without new Q waves have significantly higher late cardiac arrest risk 3
• Transient ischemia from coronary artery spasm can trigger polymorphic VT or VF 3

Electrolyte Abnormalities

• Hypokalemia and hypomagnesemia facilitate VF development, particularly in patients on antiarrhythmic agents 3
• However, electrolyte abnormalities discovered after cardiac arrest should not be assumed to be the sole cause unless proven, as hypokalemia can result from the arrest itself 3
• Correction of hypokalemia does not affect inducibility of monomorphic VT after MI 3

Drug-Induced Arrhythmias

• QT-prolonging medications (antiarrhythmics, antibiotics, antipsychotics, antihistamines, prokinetic drugs) can induce torsades de pointes that degenerates into VF 3
• Almost all implicated drugs block the repolarizing potassium current IKr encoded by the HERG gene 3
• Proarrhythmic effects of antiarrhythmic drugs themselves are common putative causes 3
• Drug-induced polymorphic VT requires avoidance of all QT-prolonging agents (www.qtdrugs.org, www.torsades.org) 3

Structural Heart Disease

• Nonischemic dilated cardiomyopathy with significant LV dysfunction increases VF risk 3
• Right ventricular cardiomyopathy (particularly in Italy) 3
• Anomalous coronary artery origin from wrong aortic sinus 3

Accessory Pathways (WPW Syndrome)

• Transition of AV reentry into AF can produce very rapid ventricular response leading to sudden cardiac death 3
• Drugs that slow AV nodal conduction (digitalis, calcium channel blockers, beta-blockers) may paradoxically enhance accessory pathway conduction, resulting in hypotension or cardiac arrest 3

Idiopathic Ventricular Fibrillation

• Occurs in 1% of cardiac arrest survivors and up to 8% of SCD victims when no structural disease, electrolyte abnormalities, or heritable conditions are identified 3
• Carries 30% risk of recurrence at 5 years 3

Other Precipitating Factors

• Hypothermia 3
• Toxic agents requiring specific therapy 3
• Commotio cordis (blunt chest trauma during sports in young individuals with compliant chest walls) 3
• Atrial fibrillation independently increases VF risk 3-fold, even after adjusting for comorbidities, drugs, and acute MI 4

Critical Clinical Pitfall

Do not assume modest troponin elevations after sustained VT/VF indicate acute MI as the cause—prolonged arrhythmias elevate cardiac biomarkers through supply-demand mismatch without acute coronary occlusion 1. Similarly, antiarrhythmic drugs or electrolyte abnormalities should not be assumed to be the sole cause of sustained monomorphic VT, as these patients typically have inducible VT even without these factors 3.

Diagnostic Approach After Arrest

• Obtain 12-lead ECG immediately after return of spontaneous circulation to detect ST elevation or new left bundle-branch block 1
• The presenting rhythm provides diagnostic clues: VF is the most common initial rhythm in sudden, unheralded cardiac arrest from coronary disease 1
• Evaluate for reversible causes systematically: acute ischemia, electrolyte imbalance, drug effects, hypothermia, and toxic agents 3