Ventricular arrhythmias

Ventricular arrhythmias

Ventricular arrhythmias are caused by ectopic ventricular foci. They have a wide QRS due slow conduction through the ventricle outside the specialised conduction system, with QRS width > 120 msec. P waves are either absent or dissociated from the QRS. The mechanisms of ventricular arrhythmias could be reentrant circuits, automatic foci or triggered activity. Ventricular rhythms will have 30% lesser cardiac output for that particular rate, due to lack of AV synchrony as well as less effective contraction due to the abnormal sequence of activation. Faster rhythm will have less cardiac output due reduction in the time available for diastolic filling. Up to about a heart rate of about 120/min, diastole shortens more with increasing heart rate, while above that rate the duration of systole also decreases. The various ventricular arrhythmias are premature ventricular contractions {PVC, VPC (Ventricular Premature Complex), VPB (Ventricular Premature Beat)}, idioventricular rhythm (including accelerated idioventricular rhythm), ventricular tachycardia, torsades de pointes (polymorphic ventricular tachycardia with QT interval prolongation), ventricular flutter, ventricular fibrillation and finally, asystole.

Premature ventricular complexes are characterised by a wide QRS and discordance between QRS and ST segment / T wave. This means that the polarity of the ST segment and T wave are opposite to that of the dominant QRS. In leads in which the QRS is positive, there will be ST segment depression and T wave inversion and vice versa. If two VPCs occur without an intervening sinus beat, it is called a couplet. A sequence of three VPCs is called a salvo and also as a short run of nonsustained ventricular tachycardia (NSVT). If the ventricular ectopic falls on the T wave of the preceding beat, it is called R on T phenomenon, which could be the forerunner of more severe ventricular arrhythmias like ventricular tachycardia or fibrillation. If ventricular ectopics arise from a single focus, they usually have same morphology and coupling interval. Coupling interval is the interval between the onset of the ectopic QRS and the preceding one. Varying coupling intervals can occur in either multifocal ectopics or in parasystole, an ectopic focus which is protected from the dominant activation. Varying morphology of QRS usually indicates multifocal origin. The inter ectopic intervals in a parasystolic rhythm has a common denominator. Fixed rate pacing is a simple example of an artificial parasystolic rhythm. VPCs occuring in an individual with a normal heart needs no treatment if asymptomatic. If symptoms interfere with daily activities, beta blockers are the first of line therapy. Antiarrhythmic drugs are rarely indicated if at all. VPC in an abnormal heart also seldom need suppression as the effect on mortality is little. Underlying left ventricular dysfunction has to be looked for and managed as it is the more important factor determining prognosis. While treating VPCs, watch out for pro-arrhythmia, a worsening of the arrhythmia or the occurrence of more complex arrhythmia due to the therapeutic regimen itself. Cardiac ion channelopathies like long QT syndrome as the initiating factor should also be thought of.

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