VENTRICULAR RHYTHM DISTURBANCES



Premature ventricular complexes (PVC’s) are premature, bizarrely shaped QRS complexes of prolonged duration differing in contour from the dominant QRS complex. The T wave is large and oriented in the opposite direction from the major QRS deflection. The sinus node and atria are usu­ally not activated prematurely by retrograde con­duction from the PVC, and therefore a “compen­satory pause” results; that is, the pause after the PVC is sufficiently long that the interval between the two normally conducted QRS complexes flanking the PVC equals two sinus cycle lengths. A PVC that does not produce a pause is termed interpolated. Two successive premature PVC’s are termed a pair or couplet, while three or more suc­cessive PVC’s are arbitrarily termed ventricular tachycardia. If PVC’s have different contours, they are called multifocal, multiform, polymorphic, or pleomorphic. If PVC’s are not coupled to the pre­vious QRS, parasystole should be considered; however, many nonparasystolic PVC’s do not ex­hibit fixed coupling. The prevalence of PVC’s in­creases with age. They are often asymptomatic but can give rise to palpitations, or if present in long runs of bigeminy, may produce hypotension, since they are premature and relatively ineffective at ejecting blood. The number of PVC’s may in­crease during infection, ischemia, anesthesia, psychological stress, and excessive use of tobacco, caffeine, or alcohol. In the absence of underlying heart disease, the presence of PVC’s probably has no significance regarding longevity or limitation of activity, and antiarrhythmic therapy is not in­dicated. The presence of PVC’s identifies patients at an increased risk of cardiac death if they have coronary artery disease, hypertrophic cardiomy­opathy, or mitral valve prolapse; however, treat­ment of PVC’s has not been demonstrated to de­crease sudden death. If drug therapy is indicated fusuallv only in patients with symptoms), lido­caine can be used acutely and procainamide, quinidine, or disopyramide may be considered for chronic therapy.

Ventricular tachycardia occurs when three or more consecutive PVC’s occur with a rate ex­ceeding 100 per minute. The QRS complexes usu­ally have a prolonged duration and bizarre shape, with ST and T vectors opposite to the major QRS deflection. Atrial activity may be indepen­dent of ventricular activity (AV dissociation), or the atrium may be depolarized by the ventricles retrogradely (VA association). QRS contours may be unchanging (uniform) or may vary. The differ­entiation between sustained and nonsustained ventricular tachycardia is somewhat arbitrary but clinically useful; one guideline is that sustained ventricular tachycardia lasts at least 30 seconds or requires termination prior to 30 seconds be­cause of hemodynamic decompensation.
The electrocardiographic distinction between supraventricular tachycardia with abnormal in­traventricular conduction and ventricular tachy­cardia can be difficult. Supraventricular tachy­cardia may be associated with prolonged QRS complexes when pre-existing bundle branch block is present, functional aberration exists, or conduction over an accessory pathway is present. When fusion or capture QRS complexes occur during a wide-complex tachycardia (that is, early, narrow complexes that are either partially [fusion] or completely [capture] caused by activation from a supraventricular source), ventricular origin of the tachycardia can be assumed. The identifica­tion of AV dissociation, sometimes requiring esophageal or intracardiac recordings to deter­mine atrial activity, is much more characteristic of ventricular than supraventricular tachycardia. However, only about 50 per cent of ventricular tachycardias demonstrate complete AV dissocia­tion. In addition, the following characteristics favor a supraventricular origin: slowing or ter­mination of the tachycardia by increased vagal tone, onset after a premature P wave; RP interval ^100 msec, more atrial impulses than ventricular impulses (for example, 2:1 AV conduction), ini­tiation of wide complexes after a long/short cycle sequence; and rsR’ in Vj. With preceding normal QRS conduction, if left axis deviation or QRS du­ration of 140 msec or more is present during tachy­cardia, ventricular tachycardia is likely.

Ventricular tachycardia occurs in patients with ischemic heart disease, congestive and hyper­trophic cardiomyopathy, mitral valve prolapse, valvular heart disease, and primary electrical dis­ease (no identifiable structural heart disease). Even short runs of ventricular tachycardia may be important when detected in the late hospital phase of acute myocardial infarction, since the one-year mortality rate of this group appears to be much greater than for patients without tachycar­dia.

Deciding when to treat patients with ventricular tachycardia is sometimes difficult. Patients with chronic recurrent sustained ventricular tachycar­dia and those with symptomatic nonsustained ventricular tachycardia are treated. Treatment of patients with asymptomatic nonsustained ven­tricular tachycardia is controversial; we tend to treat those with structural heart disease, espe­cially left ventricular dysfunction, and not treat those with no structural heart disease. Acute ther­apy of ventricular tachycardia is achieved with intravenous lidocaine; if unsuccessful, intrave­nous procainamide or bretylium may be used. If hypotension, shock, angina, congestive heart fail­ure, or symptoms of cerebral hypoperfusion are present, the rhythm should be terminated promptly with DC cardioversion, beginning with very low energies (10 to 50 joules) synchronized with the QRS. DC cardioversion of digitalis-in­duced ventricular tachycardia may be hazardous but is sometimes necessary. If ventricular tachy­cardia is recurrent despite drug therapy, pacing may occasionally be useful for termination. Before embarking on chronic drug therapy, a search for reversible conditions contributing to the arrhyth­mia should be initiated; for example, metabolic abnormalities, hypoxia, digitalis excess, and congestive heart failure should be corrected. Ef­fective drugs for chronic therapy include quini­dine, procainamide, disopyramide, and tocainide. Phenytoin is usually not successful unless digi­talis toxicity is present, and propranolol is usually unsuccessful unless the ventricular tachycardia is related to ischemia or catecholamine stimulation. Amiodarone (investigational) is very effective in patients in whom conventional agents have failed. Combinations of drugs are sometimes necessary. Surgery or implantable electrical devices may be considered in patients with ventricular tachycar­dia refractory to drug therapy.

Accelerated idioventricular rhythm refers to impulse formation originating in the ventricle with a rate of approximately 60 to 110 per minute. It often competes with the sinus node for control of the heart, and fusion and capture complexes occur commonly. The onset of the arrhythmia is often gradual (nonparoxysmal), and enhanced au-tomaticity is presumed to be the mechanism. Pre­cipitation of more rapid ventricular arrhythmias is not common. The arrhythmia usually occurs in patients with acute myocardial infarction or dig­italis toxicity, and suppressive therapy is usually not necessary. If symptoms occur or if more ma­lignant tachyarrhythmias result, therapy as noted above is indicated. Often simply increasing the sinus rate with atropine or atrial pacing sup­presses the accelerated idioventricular rhythm.

The term torsades de pointes refers to a ven­tricular tachyarrhythmia characterized by QRS complexes of changing amplitude that appear to twist around the isoelectric line, occurring in the setting of a prolonged QT interval. Episodes of torsades de pointes often terminate sponta­neously, but ventricular fibrillation may super­vene. The syndrome may be either congenital or acquired. Acquired forms may be caused by any antiarrhythmic drug that prolongs the QT interval (for example, quinidine, procainamide, or diso­pyramide) or by psychoactive drugs such as phenothiazines and tricyclic antidepressants. In addition, potassium depletion, liquid protein diet, and other metabolic abnormalities may be asso­ciated with the long QT syndrome. Acute therapy involves withdrawing the offending drug and cor­recting metabolic abnormalities. Antiarrhythmic agents that prolong the QT interval may worsen the arrhythmia. Temporary ventricular or atrial pacing is the most effective therapy for suppress­ing the bursts of polymorphic tachycardia. Iso­proterenol has been reported to be effective until pacing is instituted. Magnesium or bretylium therapy may be useful. If a polymorphic ventric­ular tachycardia resembling torsades de pointes is present but the QT interval is normal, standard antiarrhythmic drugs may be given.

Patients with congenital prolonged QT syn­drome who are at increased risk for sudden death include those who have family members who died suddenly at an early age and those who have ex­perienced syncope or torsades de pointes. Elec­trocardiograms should be obtained from all family members when a patient presents with suspected congenital long QT syndrome. Auditory stimuli, psychological stress, and exercise may provoke an arrhythmia in susceptible patients. For patients who have idiopathic long QT syndrome but no syncope, complex ventricular arrhythmias, or family history of sudden cardiac death, no therapy is recommended. In asymptomatic patients with long QT syndrome who have complex ventricular arrhythmias or a family history of premature sud­den cardiac death, beta blockers at maximally tol­erated doses are recommended. In patients with syncope, beta blockers at maximally tolerated doses, combined with phenytoin or phenobarbital if necessary, are suggested. For patients who con­tinue to have syncope despite drug therapy, left-sided cervicothoracic sympathetic ganglionec-tomy has been effective, since sympathetic im­balance appears to be important in the pathogen­esis of this syndrome.

Ventricular fibrillation generates little or no blood flow and is usually fatal within three to five minutes unless terminated. Ventricular fibrilla­tion is recognized by the presence of irregular un­dulations of varying contour and amplitude with­out distinct QRS complexes, ST segments, or T waves. Ventricular flutter appears as a sine wave with regular, large oscillations occurring at a rate of 150 to 300 per minute. Ventricular fibrillation occurs in a variety of situations, including coro­nary artery disease, antiarrhythmic drug admin­istration, hypoxia, ischemia, atrial fibrillation with rapid ventricular rates in the pre-excitation syndromes, accidental electrical shock, and poorly timed cardioversion. Most patients resus­citated from out-of-hospital cardiac arrest have ventricular fibrillation as their arrhythmia, often without acute myocardial infarction. Treatment is an immediate nonsynchronized DC shock using 200 to 400 joules. If ventricular fibrillation has been present for more than a few minutes, cor­rection of metabolic abnormalities may aid in electrically converting the rhythm, although DC shock should not be delayed to await correction of hypoxia or acidosis. Once ventricular fibrilla tion has been terminated, medications to prevent recurrence of ventricular fibrillation should be in­itiated (e.g., lidocaine). Ventricular fibrillation rarely, if ever, terminates on its own and is lethal unless DC shock is applied.