Dr. Jamal Dabbas Interventional cardiologist &

internist

Ventricular tachycardia

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 Cardiac scars (usually due to infarction; also iatrogenic, e.g., postoperative) Conduction disorders Drugs (e.g., digitalis, antiarrhythmics) • Long-QT syndrome

• Congenital long-QT syndrome • Acquired long-QT syndrome

• Drugs • Antiarrhythmics

• Class Ia (e.g., quinidine, disopyramide) • Class III (e.g., sotalol, amiodarone)

• Antibiotics (e.g., macrolides, fluoroquinolones)

• Antidepressants (most tricyclic and tetracyclic antidepressants, lithium)

• Antipsychotics (e.g., haloperidol) • Anticonvulsants (fosphenytoin, felbamate)

• Electrolyte imbalances (hypokalemia, hypomagnesemia, hypocalcemia)

• Ischemic stroke or intracranial hemorrhage • Endocrine disorders (e.g., hypothyroidism) • Nutritional disorders (e.g., anorexia nervosa)

• In rare cases, VT can occur in healthy individuals.

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 diastole → ↓ CO

→ hemodynamic compromise → symptoms of syncope, MI, angina

Clinical features Often asymptomatic, especially if nonsustained Common symptoms of sustained VT include:

• Palpitations • Hypotension • Syncope

In more severe cases: • Chest pain/pressure (often in conjunction with MI) • Cardiogenic shock • Loss of consciousness • Progression to ventricular fibrillation • Sudden cardiac death

Subtypes and variants Torsades de pointes Polymorphic ventricular tachycardia with QRS complexes that appear to twist around the isoelectric line Most severe complication: progression to life-threatening ventricular arrhythmia Cause: prolonged QT interval caused by congenital disease, electrolyte abnormalities , and drugs Treatment

If hemodynamically unstable → defibrillation If hemodynamically stable → IV magnesium sulfate

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 Monomorphic: all QRS complexes look similar (identical origin) Polymorphic: QRS complexes are different (multiple origins)

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

Differential diagnoses Confirming the diagnosis of VT can be challenging and, in some cases, impossible. However, VT accounts for nearly 80% of wide-complextachycardias. 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: Bundle branch block on prior ECG History of SVT Evidence of WPW (e.g., delta wave)

If there is any doubt regarding the diagnosis, assume VT rhythm and treat accordingly. The differential diagnoses listed here are not exhaustive.

Treatment Initial therapy

If patient is hemodynamically unstable (hypotension, loss of consciousness):

VT with pulse → cardioversion VT without pulse → defibrillation See “Advanced cardiac life support”

If patient is hemodynamically stable: Antiarrhythmics (typically lidocaine, procainamide, amiodarone) Cardioversion if medical therapy fails

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 prolongation → remove 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)