Ventricular Fibrillation

Epidemiology and Etiology

Epidemiology

Ventricular fibrillation (VF) secondary to myocardial infarction (MI) is the most common cause of sudden cardiac death (leading cause of death in developed countries).

• Patients are monitored in the intensive care unit (ICU) after an acute MI due to the risk of VF.
• Patients with a reduced left ventricular ejection fraction are at highest risk for VF following MI.
• Half of all deaths due to coronary artery disease are caused by VF.
• More common in men than in women

Etiology

• Underlying cardiovascular disease:
  • Coronary artery disease (most common)
  • Congestive heart failure
  • MI
  • Cardiomyopathy
  • Myocarditis
  • Valvular stenosis or insufficiency
• Cardiac conduction disorders:
  • Long QT syndrome
  • Wolff-Parkinson-White syndrome
  • Torsade de pointes
• Electrolyte imbalance (e.g., hypokalemia)
• Autonomic nervous system dysfunction (e.g., increased sympathetic activity from drugs such as dobutamine and albuterol)
• Idiopathic (rare)

Pathophysiology

Ventricular tachyarrhythmias are caused by abnormal ectopic contractions in the ventricle.

• Benign if the ectopic signal is regular and stationary and cardiac output is maintained
• May lead to hemodynamic collapse and death if the ectopic signal has a variable location or rate

Detailed process

• Myocardial scar formation (most commonly due to previous ischemic damage) causes slowing of the conduction of cardiac electrical impulses.
• This unexcitable scar tissue is surrounded by hyperirritable myocardial cells.
• Electrical impulse slows as it passes through the scar; the rest of the ventricle then has time to repolarize and it depolarizes again as the impulse exits the scar (known as re-entry).
• Ventricular contractions are rapid and out of sync with the atria. 
• Cardiac output decreases significantly → hemodynamic collapse occurs → loss of consciousness due to drop in cerebral oxygenation → cardiac arrest → sudden death
• If the rapid ventricular contraction rate is tolerated, arrhythmia may cause cardiomyopathy over time.
• Any medications and genetic disorders that result in a prolonged or delayed repolarization may result in early afterdepolarizations and torsade de pointes.

Mnemonic

Sustained VF after an MI results from: Myocardial ischemia → Necrosis → Reperfusion → Healing → Scar formation → Autonomic changes (mnemonic device: My Nephew Really Hates Scary Aliens!)

Clinical Manifestations

• Chest pain
• Hypotension and respective signs and symptoms (e.g., syncope, fatigue, pallor, cold extremities, heat intolerance, blurry vision) 
• Confusion
• Palpitations
• Dizziness
• Shortness of breath 
• Loss of consciousness
• Sudden death

Diagnosis

Electrocardiogram (ECG) confirms the diagnosis.

• Disorganized/deranged electrical activity originating in the ventricles
• Increased heart rate (> 300/min)
  • Ventricular flutter: heart rate of 240–300/min; frequently transitions to VF (300–400/min)
• Loss of P waves
• Indiscernible QRS complexes
  • Fibrillatory waves

Evaluation of underlying conditions:

• Cardiac enzymes (elevated after MI)
• Coronary angiography to evaluate myocardial ischemia
• Electrolytes (abnormally high or low levels of potassium, calcium, or magnesium)
• Urine drug screen for medications or stimulants that may affect the heart rate
• Echocardiogram if structural cause is suspected

Treatment

• Follow advanced cardiac life support algorithm.
• Management:
  • Cardiopulmonary resuscitation to help maintain blood flow through the body
  • Defibrillation: delivery of electrical shock  to the heart (momentarily stops the electrical activity and chaotic beats); start at 200 joules
  • Epinephrine after 2 attempts at defibrillation; makes next attempt at defibrillation more likely to succeed
  • Consider antiarrhythmics: Amiodarone is superior to lidocaine in VF.
  • IV/IO access 
  • Advanced airway
• Correct reversible causes (e.g., metabolic acidosis, electrolyte disturbances)
• Implantable cardioverter-defibrillator should be used if no reversible cause is found and/or if there is recurrence of hemodynamically unstable ventricular fibrillation at a later time.

Clinical Relevance

• Ventricular tachycardia: a group of arrhythmias that can originate from anywhere in the ventricle and that result in a heartbeat > 100 bpm. There are 3 main types of ventricular tachyarrhythmias: ventricular fibrillation, monomorphic ventricular tachycardia, and polymorphic ventricular tachycardia (also known as torsades de pointes).
• Coronary artery disease: the leading cause of death worldwide. It occurs as a result of atherosclerotic changes of the coronary arteries with subsequent narrowing of the vessels, preventing their dilation. 
• Congestive heart failure: also called cardiac insufficiency; refers to the inability of the heart to supply the body with normal cardiac minute volume under normal end-diastolic pressure conditions
• Myocardial infarction: refers to ischemia of the myocardial tissue due to a complete obstruction or drastic constriction of the coronary artery. This is usually accompanied by an increase in cardiac enzymes, typical ECG changes (ST elevations), and pain.
• Cardiomyopathy: refers to a group of myocardial diseases associated with impaired systolic and diastolic function. The World Health Organization classifies 5 types based on cardiac changes:
  • Dilated cardiomyopathy
  • Hypertrophic nonobstructive or obstructive cardiomyopathy
  • Restrictive cardiomyopathy
  • Arrhythmogenic right ventricular cardiomyopathy
  • Unclassified cardiomyopathy
• Myocarditis: an inflammatory disease of the heart muscle that mostly arises due to infections with cardiotropic viruses, especially infections with the coxsackievirus
• Long QT syndrome: a condition that affects repolarization of the heart after a contraction. It results in an increased risk of an irregular heartbeat and ventricular tachyarrhythmias, which can result in sudden death.