1. Interventional cardiologist & internist
Ventricular tachycardia 
Dr. Jamal Dabbas
Interventional cardiologist & internist

2. 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.

3. 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)

4. 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.

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 diastole → ↓ CO
→ hemodynamic compromise → symptoms of syncope, MI, angina

6. 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

7. 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

10. 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

11. 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

15. 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.

16. 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

17. 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)