Ventricular Tachycardia

Epidemiology and Etiology

Epidemiology

• Half of cardiac mortality in the United States is caused by ventricular tachycardia.
• Incidence ↑ with age
• More common in men
• Torsades de pointes more common in women

Etiology

• Heart disease:
  • Coronary artery disease (most common), especially with prior MI
  • Atherosclerosis
  • Smoking
  • Diabetes mellitus
• Structural disease:
  • Congestive heart failure
  • Cardiomyopathy
  • Myocarditis
• Congenital disorders:
  • Long-QT syndrome
  • Wolff-Parkinson-White syndrome
• Electrolyte derangement:
  • Hypokalemia
  • Hypomagnesemia
  • Hypocalcemia
• QT-prolonging agents:
  • Antibiotics
  • Macrolides
  • Fluoroquinolones
  • Antiarrhythmics
  • Amiodarone
  • Quinidine
  • Digitalis toxicity
  • 1st-generation antipsychotic agent such as haloperidol
  • Tricyclic antidepressants
• Idiopathic: right ventricular outflow tract (RVOT) tachycardia

Pathophysiology

• Ventricular tachycardia is due to abnormal ectopic contractions in the ventricle:
  • Benign ventricular tachycardia 
    • Ectopic signal is regular and stationary.
    • Cardiac output is maintained.
  • Life-threatening ventricular tachycardia: if ectopic signal has a variable location or rate
• Myocardial scar formation → slows conduction of cardiac electrical impulses
  • Usually from ischemic damage
  • Unexcitable scar tissue is surrounded by hyperirritable myocardial cells:
    • Electrical impulses slow as they pass through the scar.
    • Rest of the ventricle has time to repolarize.
  • Remaining ventricular tissue depolarizes again as the impulse exits the scar (known as reentry).
  • Ventricular contractions are rapid and out of sync with the atria:
    • If tolerated, the arrhythmia may cause cardiomyopathy over time.
    • If not tolerated, acute decompensation, including cardiac arrest, may occur.
• Medications and genetic disorders that result in a prolonged or delayed repolarization may result in early afterdepolarizations and torsades de pointes.
• Monomorphic ventricular tachycardia is caused primarily by abnormal reentry circuits, leading to ↑ automaticity.
• Polymorphic ventricular tachycardia is caused primarily by abnormal ventricular repolarization:
  • Electrolyte abnormalities
  • Long-QT syndrome

Clinical Presentation

Family history

• Premature sudden death (< 40 years old)
• Long-QT syndrome
• Short-QT syndrome
• Brugada syndrome
• Arrhythmogenic right ventricular dysplasia
• Catecholaminergic polymorphic ventricular tachycardia
• Hypertrophic cardiomyopathy

Symptoms

• May be asymptomatic
• Chest pain
• Hypotension 
• Syncope
• Fatigue
• Confusion
• Palpitations
• Dizziness
• Dyspnea
• Sudden death

Exam

• Hypotension
• Tachypnea
• Signs of diminished perfusion:
  • Diminished level of consciousness
  • Pallor
  • Diaphoresis
  • ↑ Jugular venous pressure
  • S1 may vary in intensity.

Diagnosis

Diagnosis is by ECG or cardiac monitoring.

There are 2 primary types of ventricular tachycardia:

1. Monomorphic:
   • Wide QRS complexes (often > 200 msec)
   • Uniform QRS morphology
2. Polymorphic:
   • Wide QRS complexes (> 120 msec)
   • Torsades de pointes: beat-to-beat axis deviation of the QRS complexes around the baseline

Management

Management of ventricular tachycardia is based on whether a pulse is present and, if it is, whether the individual is hemodynamically stable.

For pulseless ventricular tachycardia

Follow the adult cardiac arrest algorithm.

• CPR to help maintain blood flow through the body
• Defibrillation:
  • Delivery of an electrical shock to the heart
  • Can use manual defibrillator or automated external defibrillator (AED)
• Consider the addition of antiarrhythmics, if needed:
  • Amiodarone
  • Lidocaine
• IV/intraosseous access 
• Advanced airway

For ventricular tachycardia with a pulse

• If hemodynamically unstable:
  • 1st-line treatment of unstable individuals is synchronized direct-current cardioversion.
  • Usually starts at 100 J
• If hemodynamically stable:
  • Sustained monomorphic ventricular tachycardia without signs of end-organ damage should receive medication-induced cardioversion with:
    • Procainamide
    • Amiodarone
    • Sotalol
    • Lidocaine
  • Polymorphic ventricular tachycardia should be treated with:
    • IV magnesium sulfate
    • Isoproterenol
    • Pacing
    • Antiarrhythmic agent that will not prolong the QT interval (procainamide and amiodarone are contraindicated)
    • Synchronized cardioversion if medical therapy is unsuccessful at 50–200 J monophasic.
    • Correction of electrolyte abnormalities
• If left ventricular dysfunction is present, cardioversion should be undertaken with amiodarone or lidocaine.
• If ventricular tachycardia is the result of digitalis toxicity, manage with antidigitalis antibody and electrocardiovert to achieve normal sinus rhythm.
• Most effective long-term therapy for ↓ mortality is an implantable cardioverter-defibrillator (ICD).

Evaluating for underlying causes

• Cardiac enzymes: ↑ after MI
• Coronary angiography to evaluate myocardial ischemia
• Electrolytes
  • Hypokalemia
  • Hypomagnesemia
  • Hypocalcemia
• Urine drug screen for medications or stimulants that may affect heart rate
• Echocardiography if structural cause is suspected
• Holter monitor can be used to detect intermittent ventricular tachycardia not detected by regular ECG.

Differential Diagnosis

• Hypokalemia: plasma potassium concentration < 3.5 mEq/L. Hypokalemia can be due to renal losses, GI losses, transcellular shifts, or poor dietary intake. Hypokalemia is usually asymptomatic if minor; however, it can lead to cardiac arrhythmias, muscle weakness, rhabdomyolysis, paralysis, and respiratory failure. Diagnosis is by history and lab testing. Management is by correcting the potassium deficit and treating the underlying cause.
• Coronary artery disease: inadequate supply of blood to the myocardium, typically caused by atherosclerosis. The myocardium becomes ischemic when oxygen supply does not meet oxygen demand. Diagnosis is based on history and ECG findings, cardiac stress tests, or heart catheterization. Management is primarily based on reducing oxygen demand of the heart and increasing the delivery of oxygen.
• Myocardial infarction: ischemia of an area of myocardial tissue due to insufficient blood flow and oxygenation. The clinical presentation of MI is with chest pain. Diagnosis is by history, ECG changes, increases in cardiac enzymes, and evidence of wall-motion abnormalities. Management is with thrombolytic therapy rather than percutaneous intervention. All individuals receive nitrates, pain control, aspirin, anticoagulation, and beta-blockers.
• Long-QT syndrome: disorder of the heart’s electrical activity. Long-QT syndrome affects the repolarization of the heart after a heartbeat and may be congenital or acquired. The syndrome is typically characterized by a prolongation of the QT interval on the ECG and by the occurrence of syncope or cardiac arrest.
• Ventricular fibrillation: type of ventricular tachyarrhythmia (> 300/min) often preceded by V-fib. In this arrhythmia, the ventricle beats rapidly and sporadically. The ventricular contraction is uncoordinated, leading to a decrease in cardiac output and immediate hemodynamic collapse. Ventricular fibrillation is most commonly caused by underlying ischemic heart disease. 
• Cardiac arrest: sudden complete cessation of cardiac output with hemodynamic collapse. Individuals with cardiac arrest present in a pulseless, unresponsive, and apneic state. Rhythms associated with cardiac arrest are V-fib/tachycardia, asystole, or pulseless electrical activity. Management of cardiac arrest starts with BLS outside the hospital and advanced cardiac life support (ACLS) when in the hospital.