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Background
I) Definition
Ventricular fibrillation (VF) is a life-threatening arrhythmia characterized by rapid, chaotic, and disorganized electrical activity in the ventricles, resulting in ineffective myocardial contraction and immediate cessation of cardiac output. VF is a form of pulseless cardiac arrest and the most common arrhythmia associated with sudden cardiac death (SCD). Without rapid defibrillation, it is uniformly fatal.
I) Classification/Types
By Duration:
- Primary VF: Occurs within the first hour of acute myocardial infarction (AMI), not preceded by hemodynamic deterioration.
- Secondary VF: Occurs in response to profound ischemia or metabolic derangement, often with preceding hemodynamic compromise.
By Association:
- Ischemic VF: Commonly related to acute coronary syndromes
- Non-ischemic VF: Due to structural heart disease, electrolyte imbalance, or inherited arrhythmias
- Idiopathic VF: No identifiable cause, often suspected in survivors of unexplained cardiac arrest
Pathophysiology
VF arises from multiple, disorganized reentrant wavelets of electrical activity that circulate within the ventricular myocardium. This disorganized excitation prevents coordinated contraction, leading to no effective cardiac output. Common initiating factors include ischemia-induced dispersion of repolarization, reentrant circuits in scarred myocardium, or early afterdepolarizations (especially in long QT syndromes). Without rapid intervention, VF progresses to asystole.
Epidemiology
- VF is the leading cause of sudden cardiac death (SCD) globally
- Occurs most commonly in adult males >45 years, especially those with coronary artery disease
- Major cause of out-of-hospital cardiac arrest
- Rare in children unless due to congenital cardiac or electrical disorders
Etiology
I) Causes
- Acute myocardial infarction (most common)
- Cardiomyopathies (dilated, hypertrophic)
- Electrolyte abnormalities (hypokalemia, hypomagnesemia)
- Drug toxicity (e.g., digoxin, QT-prolonging agents)
- Inherited channelopathies: Long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT
- Severe heart failure
- Commotio cordis (blunt chest trauma during vulnerable repolarization phase)
II) Risk Factors
- History of coronary artery disease or MI
- Prior episode of VT or VF
- Reduced left ventricular ejection fraction (LVEF)
- Family history of sudden cardiac death
- Use of QT-prolonging drugs
- Electrolyte imbalance or renal dysfunction
Clinical Presentation
I) History (Symptoms)
- Sudden collapse (primary presentation)
- Witnessed syncope or cardiac arrest
- Preceding symptoms may include palpitations, chest pain, lightheadedness, or dyspnea (rarely lasts more than seconds before arrest)
- No pulse or respiration at time of presentation
II) Physical Exam (Signs)
- Unresponsiveness
- Pulselessness
- Apnea
- Cyanosis and cardiac arrest without preceding signs in most cases
Differential Diagnosis (DDx)
- Pulseless VT
- Asystole
- Pulseless electrical activity (PEA)
- Torsades de pointes (form of polymorphic VT)
- High-grade AV block with bradyasystole
- Massive pulmonary embolism or cardiac tamponade (nonarrhythmic arrest)
Diagnostic Tests
Initial Work-Up (in resuscitated patients or survivors)
- ECG (post-resuscitation): ST-elevation or Q waves suggest MI
- Cardiac enzymes: Assess for myocardial injury
- Electrolytes and renal function: Evaluate for correctable triggers
- Toxicology screen: Rule out drug-induced causes
- Echocardiography: Assess for structural disease
- Coronary angiography: If ACS suspected
- Cardiac MRI: Evaluate for scar, myocarditis, or cardiomyopathy
- Genetic testing: If inherited arrhythmia suspected
- EPS: In select cases for arrhythmia source identification
Treatment
I) Initial Approach (ACLS protocol)
- Immediate CPR
- Early defibrillation (biphasic: 120–200 J; monophasic: 360 J)
- Epinephrine 1 mg IV every 3–5 minutes
- Amiodarone 300 mg IV bolus (repeat 150 mg if needed)
- Treat reversible causes (5 Hs and 5 Ts)
II)Post-Resuscitation Management
- Therapeutic hypothermia (targeted temperature management if comatose)
- Hemodynamic support (vasopressors/inotropes)
- Coronary revascularization if ACS is identified
- ICD placement for secondary prevention
- Beta-blockers and antiarrhythmics to prevent recurrence
Medications
Drug Class | Examples | Notes |
Antiarrhythmics | Amiodarone, Lidocaine | Used acutely post-VF; amiodarone preferred |
Beta-blockers | Metoprolol, Carvedilol | Reduce sympathetic tone and arrhythmic risk |
ACE inhibitors/ARBs | Lisinopril, Losartan | Mortality benefit in structural heart disease |
Magnesium sulfate | IV | For torsades de pointes or suspected deficiency |
Device Therapy
- Implantable Cardioverter-Defibrillator (ICD): Gold standard for survivors of VF or those at high risk (EF ≤35%, prior VT/VF)
- Wearable Cardioverter-Defibrillator (WCD): Temporary option while awaiting further evaluation
Consults/Referrals
- Cardiology: For long-term rhythm management
- Electrophysiology: For ICD evaluation and ablation if needed
- Emergency Medicine: For acute arrest response
- Genetics: If inherited arrhythmia suspected
- Critical Care: For post-resuscitation care
Patient Education, Screening, Vaccines, Education
- Recognize warning signs of arrhythmias (palpitations, dizziness)
- Understand ICD use and what to expect with shocks
- Importance of medication adherence and avoiding triggers
- CPR training for family members
Screening/Prevention
- ECG or Holter in high-risk individuals
- Family screening if genetic arrhythmia suspected
- Avoid QT-prolonging drugs in susceptible patients
Vaccinations
- Influenza and pneumococcal vaccines recommended for patients with structural heart disease or ICD
- No VF-specific vaccines
Prognosis
- VF without prompt defibrillation: 100% fatal
- Survival with good neurologic outcome possible if CPR and defibrillation occur within minutes
- ICD therapy reduces risk of sudden cardiac death
- Long-term prognosis depends on underlying cause and management
- Recurrence risk high without ICD or addressing etiology
