This is defined as three or more ventricular beats occurring at a rate of 120 b.p.m. or more. Often the patient will be hypotensive and ill but some ventricular tachycardias are well tolerated.
Examination reveals a pulse rate of 120-220 b.p.m. Usually there are clinical signs of atrioventricular dissociation, i.e. intermittent cannon a waves and variable intensity of the first heart sound. The ECG shows a rapid ventricular rhythm with broad (often 0.14 s or more), abnormal QRS complexes. Dissociated P wave activity may be seen. Supraventricular tachycardia with bundle branch block (aberration) may resemble ventricular tachycardia on the ECG; the diagnostic features are indicated in Table 11.16. In all cases of doubt, a ventricular tachycardia should be diagnosed.
Treatment may be urgent depending on the haernodynamic situation . If the cardiac output and the blood pressure are very depressed, emergency DCcardioversion must be considered. On the other hand, if the blood pressure and cardiac output are well maintained, intravenous therapy with class I drugs is usually advised. First-line drug treatment consists of lignocain (50-100 mg i.v. over 5 min) followed by a lignocaine infusion (2-4 mg min ” i.v.). DC-cardioversion may be necessary if medical therapy is unsuccessful. The administration of multiple antiarrhythmic drugs should be avoided.
Prophylaxis against relapse is extremely important. If possible, the likely success of therapy should be judged by Holter monitoring, exercise testing or other provocative techniques. Initial therapy is usually with a l3-blocker if exercise induces the arrhythmia, or a class I drug if exercise is not responsible. If these drugs fail, a class III drug such as amiodarone or sotalol is tried. When severe left ventricular dysfunction is present, most antiarrhythmic drugs cannot be used because they cause further depression of myocardial function (negative inotropic effect). In such cases amiodarone or mexiletine may be the agent of choice.
This is very rapid and irregular ventricular activation with no mechanical effect. The patient is pulseless and becomes rapidly unconscious, and respiration ceases. The ECG shows shapeless, rapid oscillations and there is no hint of organized complexes . It is usually provoked by a ventricular ectopic beat (especially in acute myocardial infarction), ventricular tachycardia or torsades de pointes. Ventricular fibrillation rarely reversesspontaneously. The only effective treatment is electrical defibrill ation or, on rare occasions, intravenous bretylium 5-10 mg kg-lover 5 min. Basic and advanced cardiac life support is needed.
Drugs that modify the rhythm and conduction of the heart are used to prevent cardiac arrhythmias. All such drugs may aggravate or produce arrhythmias and they may also depress ventricular contractility and must therefore be used with caution. There are more than 30 antiarrhythmic drugs. They are classified according to their effect on the action potential (Vaughan Williams’ classification;)
Class I drugs
These are membrane-depressant drugs that reduce the rate of entry of sodium into the cell. They may slow conduction, delay recovery or reduce the spontaneous discharge rate of myocardial cells. Class Ia drugs (e.g. disopyramide) lengthen the action potential, Class Ib drugs (e.g. lignocaine) shorten the action potential, and Class Ie (flecainide, propafenone) do not affect the duration of the action potential.
In one postinfarction study in the USA (cardiac arrhythmia suppression trial-CAST), mortality in the patient group receiving flecainide was twice that of the control group. In view of this, flecainide should be reserved for life-threatening ventricular arrhythmias or supraventricular arrhythmias causing disabling symptoms in patients who do not have significant left ventricular dysfunction or a previous myocardial infarction.
class II drugs
These antisympathetic drugs prevent the effects of catecholamines on the action potential. Most are f3- adrenergic antagonists. Cardioselective f3-blockers (f3,) include metoprolol, atenolol and acebutalol.
Class III drugs
These prolong the action potential and do not affect sodium transport through the membrane. There are two major drugs in this class: amiodarone and sotalol. Sotalol is also a f3-blocker.
Class IV drugs
The non-dihydropyridine calcium antagonists that reduce the plateau phase of the action potential are particularly effective at slowing conduction in nodal tissue. Verapamil and diltiazem are the most important drugs in this group. Another clinical classification is based on the part of the heart that is affected by the antiarrhythmic drug .
The features of the major antiarrhythmic drugs are given.