• Clinical science

Ventricular tachycardia (VT…)

Abstract

Ventricular tachycardia (VT) is a potentially life-threatening arrhythmia originating in the cardiac ventricles. Usually, VT results from underlying cardiac diseases such as myocardial infarction or cardiomyopathy, but it can also be idiopathic or iatrogenic. Clinical manifestations range from palpitations and syncope to cardiogenic shock and sudden cardiac death. The characteristic ECG findings of VT are broad QRS complexes (> 120 ms) and tachycardia (> 120 bpm). In the acute setting, management of VT may require immediate cardioversion, defibrillation, or administration of antiarrhythmic drugs. Most patients who develop symptomatic, sustained VT require long-term antiarrhythmic therapy involving medication, intracardiac devices, or catheter ablation.

Etiology

References:[1][2][3][4][5]

Pathophysiology

  • Monomorphic VT (all QRS complexes look similar)
    • Increased automaticity
    • Re-entry circuit
  • Polymorphic VT (dissimilar QRS complexes): caused by abnormal ventricular repolarization (e.g., long QT syndrome, drug toxicity, electrolyte abnormalities)
  • Decreased cardiac output: asynchronous atrial and ventricular beats + rapid ventricular rhythm → ↓ blood flow into the ventricle during diastoleCO

Clinical features

References:[6][7]

Subtypes and variants

Torsades de pointes

References:[6][8]

Diagnostics

ECG

  • 3 or more consecutive premature ventricular beats (i.e., widened QRS)
  • Heart rate > 120 bpm
  • Duration
    • Nonsustained: < 30 s
    • Sustained: > 30 s
  • Morphology
  • Other possible ECG findings
    • AV-dissociation: no relationship between P waves and QRS complexes (in VT, ventricular rhythm is often faster than atrial rhythm)
    • Fusion complex: atrial and ventricular impulses occur simultaneously
    • Capture beats: Occasionally, a supraventricular impulse may reach AV node and produce a subsequent ventricular beat (similar to a beat in sinus rhythm).

Other diagnostic tests

  • Holter monitor: useful for diagnosing intermittent VT which may not be present on a single ECG
  • Patient-activated (manual) event recorder
  • Echocardiography: provides information about possible etiologies of VT (e.g. structural heart disease, prior MI) and is thus a useful tool for evaluation of VT

References:[9][10][8]

Differential diagnoses

Confirming the diagnosis of VT can be challenging and, in some cases, impossible. However, VT accounts for nearly 80% of wide-complex tachycardias.

  • Supraventricular tachycardia with aberrancy (RBBB, LBBB, Wolff-Parkinson-White)
    • It is important to make the distinction between SVT with aberrancy and VT because treatment of the two conditions differs and sometimes the wrong treatment can lead to hemodynamic instability (e.g., using AV-nodal blocking drugs in patient with VT).
    • Signs and symptoms that suggest VT rather than SVT are:
      • Age > 35 (high PPV)
      • History of structural heart defects or past MI
      • AV dissociation, fusion beats, and capture beats
    • Signs and symptoms that suggest SVT with aberrancy rather than VT are:
  • If there is any doubt regarding the diagnosis, assume VT rhythm and treat accordingly.

References:[7][11]

The differential diagnoses listed here are not exhaustive.

Treatment

  • Initial therapy
    • If patient is hemodynamically unstable (hypotension, loss of consciousness):
    • If patient is hemodynamically stable:
    • In all patients, look for and address possible causes of VT such as:
      • Electrolyte abnormalities (e.g., hypokalemia) → correct any electrolyte imbalances
      • Medication-induced QT prolongationremove any offending medication, digoxin immune fab (fragment antigen-binding) for digoxin toxicity
  • Long-term therapy
    • Intracardiac devices (ICD); (most effective treatment for reducing mortality): indicated in case of VT that does not respond to therapy
    • Catheter ablation
    • Antiarrhythmics (usually class I or III)

References:[6][7][9][12][13]