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Ventricular arrhythmias

Created: 28/8/2006
Updated: 10/8/2006

Premature ventricular complexes (PVCs)

A premature ventricular contraction is an impulse that originates prematurely in the ventricles and perturbs the prevailing rhythm. The mechanism of PVCs may be either increased automaticity of ventricular foci or reentry.

ECG shows a premature wide, slurred, bizarre QRS complex followed by a T wave, usually in the opposite direction to the main QRS deflection. PVCs are usually followed by full compensatory pauses.

Unifocal premature ventricular complexes

Multifocal premature ventricular Complexes

The events following a PVC are of interest. Usually, a PVC is followed by a complete compensatory pause because the sinus node timing is not interrupted; a sinus P wave is unable to reach the ventricles because they are still refractory from the PVC; the following sinus impulse occurs on time, the time course being dependent on the sinus rate. By contrast, PACs are usually followed by an incomplete pause because the PAC usually enters the sinus node and resets its timing; this enables the following sinus P wave to appear earlier than expected. These concepts are illustrated below.

Ventricular bigeminy
is said to occur when PVCs alternate with the normal beat.  Causes may include electrolyte abnormalities, stimulants and digoxin toxicity.

Multifocal PVCs are characterised by at least two abnormal QRS complexes of different configurations. Certain types of PVCs are potentially dangerous because they may deteriorate into a ventricular tachycardia. This is particularly true when PVCs occur in couplets or triplets, are multi-focal or there is an "R-on-T phenomenon" (when the R wave of the PVC falls on the T wave of the previous beat). 

Triplet premature ventricular complexes

R-on-T phenomenon

Ventricular tachycardia

This is defined as episodes of four or more consecutive PVCs. It arises in the specialised conduction system distal to the bundle of His bifurcation, the mechanism of VT being abnormal automaticity or reentry.

The ECG in VT shows a uniform series of widened QRS complexes, usually regular with a rate ranging from 70-250 bpm. The hallmark of VT is AV dissociation.

Click here for a larger image

It is important to distinguish VT from a supraventricular tachycardia (SVT) with aberrant conduction. VT is diagnosed by the presence of fusion and capture beats, AV dissociation, left axis deviation and compensatory pauses. 

By contrast, an SVT with aberrant conduction is characterised by the presence of P waves preceding the QRS complexes, the onset of the dysrhythmia with a premature P wave, an RSR’ pattern in V1 and slowing/termination of the dysrhythmia by vagal stimulation.

Synchronous cardioversion is often required to treat VT failing, which may deteriorate into VF.

Torsade de pointes

This is VT with a varying axis and is caused by anything that prolongs the QT. Treatment is with magnesium sulphate 8mmol (4ml of 50%), or overdrive pacing.

Ventricular fibrillation (VF)

Ventricular fibrillation is an irregular rhythm resulting from a rapid discharge of impulses from one or more foci in the ventricles. The ventricular contractions are erratic and seen on the ECG as bizarre patterns of various sizes and configurations. No P waves are seen.

Some causes of VF include myocardial ischaemia, hypoxia, hypothermia, electrocution, electrolyte and acid-base imbalance, and drug effects.

Due to the absence of any effective cardiac output, life must be sustained by artificial means - i.e. external cardiac massage and defibrillation is "the" treatment.

Ventricular fibrillation

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