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Ventricular Tachycardia – Causes, Diagnosis And Treatment

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Ventricular Tachycardia

Ventricular tachycardia is a sequence of four or more depolarizations, with ventricular origin, meaning that this depolarizations are arising from an outbreak that is located below the bifurcation of His fascicle, and have a frequency of 100 beats / minute. Onset and end of ventricular tachycardia crisis are sudden, realizing short-term (paroxysmal) form or long-term form of ventricular tachycardia.


  • Ischemic heart disease: myocardial infarction in the acute phase (monomorphic or polymorphic ventricular tachycardia,with the risk of transforming into ventricular fibrillation) or in chronic phase (monomorphic ventricular tachycardia);
  • Cardiomyopathy: primitive (dilated, hypertrophic) or secondary (hypertension, mitral regurgitation, aortic regurgitation, aortic strenosis, mitral stenosis);
  • Arrhythmogenic right ventricular dysplasia;
  • Long QT syndrome;
  • Iatrogenic: digoxin toxicity after high-dose of  anti-arrhythmic drugs or after surgery (especially after aorto-coronary bypass).
Ventricular Tachycardia

Ventricular Tachycardia

Classification of ventricular tachycardia, is made after:

  1. Length: sustained ventricular tachycardia (lasting over 30 seconds) and unsustained ventricular tachycardia (duration less than 30 seconds).
  2. After QRS complex morphology: monomorphic (constant aspect of QRS complexes in all derivations), polymorphic (aspect of QRS complexes is polymorphic ) and bidirectional (QRS complexes, although from the same source, change their morphology, either alternatively either regularly – in digoxin toxicity).
  3. After origin: ventricular tachycardia of the right ventricle or ventricular tachycardia of the left ventricle.
Ventricular Tachycardia

Ventricular Tachycardia


The diagnosis of ventricular tachycardia is based on the symptoms, on physical examination and on ECG interpretation.

Symptoms may differ, depending on the type of ventricular tachycardia. In unsustained forms of ventricular tachycardia, symptoms are minimal, as palpitations or may be absent, and in sustained forms of ventricular tachycardia may appear palpitations, crisis of angina pectoris, paroxysmal dyspnea, syncope.

Physical examination shows the following: peripheral pulse is regular, fast, sometimes is slow and retrieval. Heart sounds are regular and tachycardic. Ventricular tachycardia can sometimes have the appearance of acute pulmonary edema or cardiogenic shock.

ECG in ventricular tachycardia has four important aspects:

  1. QRS complexes with abnormal morphology, with increased length, have the aspect of right bundle branch block, if the ventricular tachycardia has the origin from the left ventricle or left bundle branch block aspect if ventricular tachycardia has the origin on the right ventricle. Heart rate is 140-250 beats / minute, the rhythm can be regular or slightly irregular.
  2. Atrio-ventricular dissociation: in general the atrial and ventricular electrical activity are independent of each other.
  3. Ventricular capture: from time to time may appear thin QRS complexes, which are preceded by P waves, meaning ventricular  “capture” by the supraventricular stimulus.
  4. Fusion beats: QRS complex has a morphology intermediate between complexes of ventricular origin and those of supraventricular origin.
Ventricular Tachycardia ECG

Ventricular Tachycardia ECG


The objective of therapy in ventricular tachycardia is rapid conversion to sinus rhythm.

Sustained ventricular tachycardia and well tolerated hemodynamically, is treated with antiarrhythmics from class IA (procainamide), class III (amiodarone) or lidocaine, all administered intravenously. In case of failure of drug therapy is switched to electric conversion.

In the case of sustained ventricular tachycardia with low hemodynamic tolerance but with evolution to acute pulmonary edema or to cardiogenic shock, are made the following maneuvers : oxygen therapy on the mask or on the nasal tube and electric conversion, initially with 50 joules, then with 100 joules, 200 joules, up to 360 joules.

In the case of ventricular tachycardia with very sever hemodynamic deterioration is done electric conversion starting with 200 joules, up to 360 joules.

Prevention of recurrence of ventricular tachycardia is done by taking beta blockers, amiodarone, class IC antiarrhythmic agents, implantable defibrillator or ablation by radiofrequency current (is done only in some forms of ventricular tachycardia).

Ventricular Tachycardia Treatment algorithm

Ventricular Tachycardia Treatment algorithm

Special types of ventricular tachycardia:

Torsades de pointes is an atypical form of ventricular tachycardia, initiated only in the presence of long QT interval. Production of the latter is favored by the presence of major chronic bradycardia (grade III atrioventricular block), myocardial infarction, mitral valve prolapse, certain antiarrhythmic drugs (quinidine, procainamide), electrolyte disorders (hypokalemia, hypomagnesaemia), intracranial pathological processes.

On ECG are recorded the following aspects:

  • Started with a ventricular extrasystole, with phenomena R / T (which appears in a terminal period of large and extended T wave) in the presence of an elongated QT interval.
  • The succession of ventricular complexes, with frequency between 240-300 beats / minute with unequal amplitude, with spindle aspect, consisting of a rapid phase with a sharp point and a slow phase, of opposite direction, with rounded tip.
  • Progressive reduction of amplitude of QRS complexes, with sens reversal, a phenomenon that occurs cyclically, creating the appearance of oscillations around the isoelectric line.
  • Presence of atrioventricular dissociation.

The treatment of torsades de pointes is achieved by intravenous administration of magnesium sulfate or by atrial or ventricular electrical stimulation.

Torsades de points

Torsades de points

Accelerated idioventricular rhythm starts generally gradually, ventricular rate is lower, between 60 and 120 beats / minute, appears in accesses, usually short, but repetitive. Occurs trough the increase automatism of an outbreak which is located in the intraventricular conduction system, which compete with the stimuli that are coming from the sinus node.

The main causes are: myocardial infarction, digoxin toxicity, grade III atrioventricular block, cardiomyopathy or rheumatic fever.

On ECG are recorded the following aspects:

  • Enlarged and deformed QRS complexes, with frequencies between 60 and 120 beats / min, each QRS complex can be followed by a negative P wave, due to retrograde conduction.
  • May be present ventricular captures and ventricular fusion beats.

Accelerated idioventricular rhythm treatment should first treat the cause that triggered the arrhythmia and to increase the heart rate by intravenous administration of atropine or by electrical stimulation.