Cardiophile MD Archive » ventricular fibrillation

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.

Potential hazards of using MRI with Pacemakers

Johnson Francis — Sun, 16 Nov 2008 20:35:15 +0000

Magnetic resonance imaging (MRI) utilises a very strong magnetic field which could be deleterious to the implanted cardiac pacemaker in various ways. Mechanical forces on ferromagnetic components of the pacemaker could occur due to the strong electromagnetic fields. This could lead to unpredictable magnetic sensor activation. Usually magnetic sensor causes closure of a reed switch which makes the pacemaker insensitive to the cardiac signals leading to asynchronic pacing. Asynchronous pacing can lead on the cardiac arrhythmias including the lethal ventricular fibrillation. Heating of cardiac tissue adjacent to lead electrodes could occur due to the currents generated by alternating magnetic fields. Radiofrequency interactions with the device can cause over- and under-sensing due to the induced voltages on leads. If the pacemaker has been implanted recently it could also lead to physical movement of device within a loose pocket.

Variables affecting the magnitude of risks include the length/position of pacing leads, patient and device position within machine, duration of the MRI scan, blood flow at lead/tissue interface, strength of radiofrequency field and the design of the pacemaker and the lead.

Commotio Cordis – a cause for sudden death of athletes

Johnson Francis — Sat, 15 Nov 2008 16:27:19 +0000

Commotio cordis is the term given to sudden arrhythmic death due to blunt chest wall trauma. Death is almost instantaneous and the victims are in ventricular fibrillation. Usually there is no structural damage to the heart or thoracic structures. Impacts which occur in the vulnerable phase of ventricular repolarisation just before the peak of the electrocardiographic T wave result in ventricular fibrillation. Rapid rise in ventricular pressure due to the impact possibly causes activation of ion channels by mechano-electric coupling. This causes a ventricular ectopic beat which triggers ventricular fibrillation. Commotio cordis has to be differentiated from contusio cordis in which there is direct myocardial tissue damage and damage to overlying structues of the chest due to a high velocity projectile impact. United States Commotio Cordis Registry instituted in 1996 has collected over 180 cases. Generally commotio cordis is caused by impact by a ball with a dense solid core like base ball. Balls with non-solid core tend to collapse on contact and absorb most of the impact energy so that commotio cordis is quite rare with impact by an air filled soccer ball.

Commotio cordis is more likely to occur in younger individuals, possibly because of greater transmission of the impact energy by a compliant chest wall. Only 28% of cases in the United States Commotio Cordis Registry were over 18 years and the oldest victim was 44 years old. Resuscitation is often difficult in commotio cordis with overall survival of only 15%. An excellent review on the pathophysiology of commotio cordis by Christopher Madias and associates is available, free full text online [Indian Pacing Electrophysiol. J. 2007;7(4):235-245].

Catheter Ablation for Ventricular Fibrillation

Johnson Francis — Thu, 23 Oct 2008 17:18:12 +0000

Thejus et al has written an editorial on catheter ablation for prevention of recurrent ventriular fibrillation in the current issue of Indian Pacing and Electrophysiology Journal (Thejus J et al. Indian Pacing Electrophysiol J. 2008; 8:238-241]. The current recommendation for treatment of recurrent ventricular fibrillation is the implantation of an ICD (Implantable Cardioverter Defibrillator). ICDs are costly and have a finite battery life, requiring replacement when the end of battery life is reached. The tolerance of ICD shocks are also not very good among patients, often leading to psychological problems due to fear of an impending shock. To overcome this problem, Haissaguerre et al pioneered the radiofrequency ablation of ventricular fibrillation and it has been taken up by several other investigators. Ventricular fibrillation is triggered by an ectopic impulse falling in the vulnerable period of the ventricular repolarisation and is maintained by multiple wavelets of reentry. Radiofrequency catheter ablation aims at controlling this trigger. Most of the cases of ventricular fibrillation are precipitated by ventricular premature complexes arising from the Purkinje system. Origin of the ventricular ectopic beat from the Purkinje system is identified by a Purkinje potential occurring just before the ectopic beat. It is a sharp spike of less than 10 msec in duration. Radiofrequency catheter ablation at this site causes the cessation of ventricular ectopic beats which trigger the ventricular fibrillation. The recurrence rate after successful ablation was only 9% over a mean follow up period of 22 months in cases of idiopathic ventricular fibrillation.

In another article in the same issue of the journal, Thoppil et al describe the successful treatment of post myocardial infarction electrical storm by targeting the Purkine potentials [Thoppil PS et al. Indian Pacing Electrophysiol J. 2008; 8: 298-303].

Fragmented QRS – a new predictor of prognosis in Brugada Syndrome

Johnson Francis — Tue, 21 Oct 2008 01:54:33 +0000

Multiple spikes within the QRS is known as fragmented QRS (f-QRS). Morita et al, from Okayama, Japan has found an association between f-QRS and ventricular fibrillation in Brugada Syndrome (Circulation. 2008;118:1697-1704). 115 patients were evaluated – 13 resuscitated from ventricular fibrillation, 28 with syncope and 74 asymptomatic. 43% of them had f-QRS. The highest occurrence was in the group with ventricular fibrillation (85%) while the lowest was in the asymptomatic individuals (34%; P<0.01). Those with f-QRS were more likely to have SCN5A mutations (33% in those with f-QRS vs 5% in those without f-QRS). In the group with ventricular fibrillation or syncope, only 6% without f-QRS had VF during follow up while 58% with f-QRS had recurrent syncope due to ventricular fibrillation (P<0.01). The authors go on to recommend implantation of an ICD (implantable cardioverter defibrillator) in Brugada Syndrome patients who experienced syncope without detected ventricular fibrillation, but have f-QRS as they are at increased risk for a subsequent arrhythmic event. In those with prior ventricular ventricular fibrillation, f-QRS indicates a risk of recurrent ventricular fibrillation including arrhythmic storm.

Electrical Therapy in Ventricular Fibrillation

Johnson Francis — Fri, 03 Oct 2008 09:02:15 +0000

Electrical storm: Recurrent unstable VT / VF requiring more than three DC shocks per day

Beta blocker is the single most effective therapy for recurrent VT unless the person is in shock

There should be a low threshold for inserting IABP in those with electrical storm

Hypothermia has been shown to suppress electrical storms in animal models

The converse is that patients with fever may have worsening of electrical storms; so the control of fever may be useful

Monomorphic PVCs which trigger the VF should be targeted during ablation of VF. The best time to take them up for EP study is during a storm as the tachycardia may not be inducible at other times. Marking electrode positions while taking ECG will help pacemapping at EPS to get an exact match.

What are the phases of ventricular fibrillation (VF)?

Johnson Francis — Sun, 21 Sep 2008 11:01:23 +0000

Electrical phase: Initial 4 minutes of VF.

Hemodynamic phase: 4 minutes to 10 minutes after the onset of VF.

Metabolic phase: Beyond 10 minutes after the onset of VF.

If EMS (Emergency medical service) arrives within 4 min (electrical phase) – defibrillation first – It is likely to be coarse VF and responds better to defibrillation.

If after 4 min, but before 10 min, cardiopulmonary resuscitation (CPR) followed by defibrillation.

If beyond 10 min, limited success – induction of hypothermia is recommended.