Cardiophile MD Archive » VF

Ventricular flutter and fibrillation

Johnson Francis — Fri, 11 Sep 2009 12:57:15 +0000

Ventricular flutter is an extremely uncommon arrhythmia which is seldom recognized. It is a sine wave like pattern and associated with severe hemodynamic compromise. It rapidly degenerates into ventricular fibrillation.

Ventricular fibrillation (VF) is a disorganized ventricular rhythm which is immediately fatal unless treated promptly. Ventricular fibrillation can be either coarse fibrillation or fine fibrillation. Coarse ventricular fibrillation is more easily cardioverted than fine VF. Coarse VF degenerates into fine VF if defibrillation is delayed. It is worth remembering that VF also has an electrical axis so that a monitoring lead which is perpendicular to the axis of the VF can record it as ‘asystole’. This is the main rationale behind giving a couple of direct current shocks even if the monitor shows asystole. Asystole is a very difficult rhythm to resuscitate from and is most often fatal, while a primary VF has good prognosis if cardioverted promptly.

Ventricular arrhythmias

Johnson Francis — Fri, 11 Sep 2009 00:56:07 +0000

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 re-entrant 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, VPB), 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 non sustained 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 fore runner 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.

Congenital short QT syndrome

Johnson Francis — Mon, 26 Jan 2009 16:25:10 +0000

Congenital short QT syndrome is new inherited clinical syndrome which was described by Gussak et al in 2000. (Cardiology. 2000;94:99-102). A gene mutation causing short QT syndrome was first demonstrated by Brugada et al in January 2004. This mutation in HERG (KCNH2) gene was later called as SQT1 and was due to gain in function of Iks, the slow component of the delayed rectifier potassium current. Later on in the same year, SQT2 was described by Bellocq et al as a mutation in KCNQ1 (KvLQT1) which caused a gain in function of Ikr, the rapid component of delayed rectifier potassium current. SQT3 was identified by Priori et al as a mutation in KCNJ2 gene which causes a gain in function of Ik1 potassium current.

Short QT syndrome is characterized by consistently short QT intervals, usually below 300 msec, which does not lengthen with bradycardia. There is a propensity for sudden cardiac death and atrial fibrillation. Family history of sudden death may be forthcoming. Electrophysiologically short QT syndrome is characterized by short refractory periods and inducible VF (ventricular fibrillation) at EP (electrophysiological) study.

Shortening of QT interval can occur in tachycardia, hyperthermia and hypercalcemia. Digoxin can also shorten the QT interval. These should be excluded before considering a diagnosis of short QT syndrome.

Treatment options for short QT syndrome are limited. Some have reported lengthening of QT interval with quinidine. Most patients with short QT syndrome and a risk of sudden cardiac death get an ICD (implantable cardioverter defibrillator) implanted.