Ventricular tachycardia pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

The underlying mechanism of VT is due to automaticity arising in either the myocardium or in the distal conduction system. The most common underlying substrate for ventricular tachycardia is ischemic heart disease. Myocardial scarring from any process increases the likelihood of electrical reentrant circuits. These circuits generally include a zone where normal electrical propagation is slowed by the scar. Ventricular scar formation from a prior myocardial infarction (MI) is the most common cause of sustained monomorphic VT. The morphology of ventricular tachycardia often depends on its cause. VT in a structurally normal heart typically results from mechanisms such as triggered activity and enhanced automaticity. If VT is hemodynamically tolerated, the incessant tachyarrhythmia may cause a dilated cardiomyopathy. This may develop over a period of weeks to years and may resolve with successful suppression of the VT.

Pathophysiology of ventricular tachycardia can be better studied depending upon the subclass:^[1][2][3][4]

• Electrical reentry or abnormal automaticity is the main reason behind ventricular tachycardia.
  • Myocardial scarring from any process increases the likelihood of electrical reentrant circuits.
  • These circuits generally include a zone where normal electrical propagation is slowed by the scar.
  • Ventricular scar formation from a prior myocardial infarction (MI) is the most common cause of sustained monomorphic VT.

• VT in a structurally normal heart typically results from mechanisms such as triggered activity and enhanced automaticity.
• Torsade de pointes seen in the long QT syndromes is likely a combination of triggered activity and ventricular reentry.

• During VT, cardiac output is reduced as a consequence of decreased [[ventricular] filling from the rapid heart rate and the lack of properly timed or coordinated atrial contraction.
• Ischemia and mitral insufficiency may also contribute to decreased ventricular stroke output and hemodynamic intolerance.
• Hemodynamic collapse is more likely when underlying left ventricular dysfunction is present or when heart rates are very rapid.
• Diminished cardiac output may result in diminished myocardial perfusion, worsening inotropic response, and degeneration to ventricular fibrillation (VF), resulting in sudden death.
• In patients with monomorphic VT, mortality risk correlates with the degree of structural heart disease. Underlying structural heart diseases such as ischemic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, Chagas disease, and right ventricular dysplasia have all been associated with degeneration of monomorphic or polymorphic VT to VF.
• Even without such degeneration, VT can also produce congestive heart failure and hemodynamic compromise, with subsequent morbidity and mortality.
• If VT is hemodynamically tolerated, the incessant tachyarrhythmia may cause a dilated cardiomyopathy. This may develop over a period of weeks to years and may resolve with successful suppression of the VT.

• There are two reasons the morphology of the QRS does not vary in monomorphic ventricular tachycardia:
  • A single site that generates automaticity of a single point in either the left or right ventricle.
  • A reentry circuit within the ventricle.

• Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization.
• The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval.
• QT prolongation may be congenital or acquired.
• Congenital problems include long QT syndrome and catecholaminergic polymorphic ventricular tachycardia.
• Acquired problems are usually related to drug toxicity or electrolyte abnormalities, but can occur as a result of myocardial ischemia.
• Class III anti-arrhythmic drugs such as sotalol and amiodarone prolong the QT interval and may in some circumstances be pro-arrhythmic.
• Other relatively common drugs including some antibiotics and antihistamines may also be a danger, particularly in combination with one another.
• Problems with blood levels of potassium, magnesium and calcium may also contribute. High dose magnesium is often used as an antidote in cardiac arrest protocols.

• Bundle branch reentry ventricular tachycardia usually occurs either in patients with structural heart disease or in patients with conduction disturbances with a structurally normal heart.
• Bundle branch reentry is a macro-reentrant tachycardia that incorporates the His-Purkinje system, the bundle branches, and trans-septal myocardial conduction in the circuit.
• Typical bundle branch reentry tachycardia uses the right bundle as the anterograde limb and the left bundle as the retrograde limb.
• Atypical bundle branch reentry uses the left bundle (anterior fascicle, posterior fascicle, or both) as the antegrade limb and the right bundle as the retrograde limb.
• The tachycardia appears as a typical left bundle branch block or right bundle branch block.

• Accelerated idioventricular rhythm commonly seen in the setting of reperfusion following myocardial ischemia or infarction. However, spontaneous coronary artery dissection should be considered when the atherosclotic disease is unlikely. ^[5]

• The Known mechanism is automaticity and can be seen in patients with digoxin toxicity and rarely seen in structurally normal heart.
• Self-limited condition, resolved spontaneously

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