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Chapter: Medicine and surgery: Cardiovascular system

Ventricular tachycardia - Ventricular arrhythmias

Tachycardia of ventricular origin at a rate of 120–220 bpm.- Definition, Incidence, Aetiology, Pathophysiology, Clinical features, Complications, Investigations, Management, Prognosis.

Ventricular tachycardia




Tachycardia of ventricular origin at a rate of 120–220 bpm.




Ventricular tachycardia is normally associated with underlying coronary, ischaemic or hypertensive heart disease, or cardiomyopathies.




The underlying mechanism is thought to be enhanced automaticity, leading to re-entry circuit as in other tachycardias. In ventricular tachycardia there is a small (or sometimes large) group of ischaemic or electrically non-homogeneous cells, typically resulting from an acute myocardial infarction.


Clinical features


The condition is episodic with attacks usually lasting minutes. Patients may experience palpitations, shortness of breath, chest pain and if there is a resultant compromise of cardiac output overt cardiac failure or loss of consciousness may occur. The presenting picture is dependent on the rapidity of the tachycardia and the function of the left ventricle, as well as general condition of the patient (e.g. hypovolaemia, anaemia, ischaemic heart disease, etc). On examination during an acute episode the rapid regular pulse is felt and as the atria are dissociated from the ventricles they may contract against a closed AV valve resulting in cannon ‘a’ waves in the JVP. Carotid sinus massage may help to distinguish ventricular tachycardia, which does not respond, from supraventricular tachycardia with bundle branch block, which may respond.




The ECG shows a broad complex tachycardia, AV dissociation (independent P wave activity). Low serum potassium or magnesium may predispose to arrhythmias, so levels should be checked.




Cardiac arrest due to pulseless ventricular tachycardia or ventricular fibrillation. Pulmonary oedema or syncope may also occur.




Any underlying electrolyte disturbance should be identified and managed.


If the patient has low cardiac output and is hypotensive, intravenous amiodarone or emergency synchronised DC cardioversion is used.


Anti-arrhythmic drugs such as amiodarone and β-blockers often in combination with other drugs are used to prevent further episodes. Implantable cardioverter defibrillators, which automatically detect VT and VF and terminate the arrhythmia with overdrive pacing or DC shock, may be used.


Patients require treatment of any underlying condition such as ischaemic heart disease.


Pulseless VT is treated as per cardiac arrest with basic and advanced life support. Early defibrillation is needed to restore sinus rhythm.




Recurrent VT has a worse prognosis, particularly in the context of myocardial infarction.

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