Common Arrhythmias
Paroxysmal atrial (supraventricular) tachycardia is characterized by sudden onset (perceived almost always as a pounding of the heart) and abrupt, spontaneous termination. It can last from minutes to several days. It often affects young, healthy persons: in some, attacks may recur only at long intervals; other may remain susceptible to frequent attacks, which can produce periodic disability. Many tachycardias respond to various maneuvers applied by a physician or even by patients themselves. These include applying pressure to the carotid artery in the neck, holding one's breath, or straining to force respiration, any of which may terminate an attack. Intravenous administration of certain drugs is more reliable in restoring normal heart rhythm. In rare instances, particularly when the rapid rate is poorly tolerated by the patient and unresponsive to drug therapy, it may be necessary to administer direct-current electric shock (cardioversion). As a general rule, no treatment of paroxysmal atrial tachycardia is needed between attacks; but if attacks recur frequently, preventive drugs can be prescribed.
Atrial flutter and atrial fibrillation are the most serious disruptions
of atrial rhythm. These two arrhythmias are related and may occur in the same patient. Both may develop in healthy persons but are more frequent in patients with various cardiac disorders. Atrial flutter and atrial fibrillation can be paroxysmal, that is, terminate within hours or days, or permanent, in which case normal rhythm usually should be restored by various interventions.
As mentioned, in atrial flutter the rhythm is regular and the heart rate (rate of ventricular contractions) is about 150 beats a minute since the ventricles respond to alternate atrial impulses. Drugs can partially block the pathways to every third impulse, reducing the rate to 100 beats a minute, or to every fourth impulse, lowering the rate to 75 beats a minute, thereby abolishing the tachycardia. Atrial flutter can in most cases be terminated by one of three methods: drugs, electric shock, or pacemaker stimulation of the right atrium (see chap. 4).
Atrial fibrillation is a much more common arrhythmia than atrial flutter; in fact, it is one of the most frequently encountered arrhythmias, particularly in patients over 60 years of age. Before the start of treatment the ventricular rate is usually within the range of 150 to 180 beats a minute, and the rhythm is irregular. Atrial fibrillation may develop as a complication of many cardiac disorders but most often results from mitral stenosis. The rapid rate of untreated atrial fibrillation, its major deleterious effect, is often poorly tolerated and may induce heart failure. Even in otherwise healthy persons atrial fibrillation may produce considerable discomfort, although it is unlikely to affect cardiac function. The rapid heart rate can be promptly and predictably reduced by drugs to a rate comparable to that of a normal, though irregular, rhythm, thereby alleviating the discomfort and other consequences. With a heart rate adequately controlled by a program of drug therapy, a patient may remain in atrial fibrillation for years and lead an active life. Thus atrial fibrillation is not a life-threatening arrhythmia. However, it does introduce a serious risk: the noncontracting atria can facilitate the development of blood clots attached to their walls, which can break loose and travel within the arterial system, producing emboli (clots occluding important vessels) and leading in some cases to stroke.
The approach to the treatment of atrial fibrillation involves two options: restoring normal rhythm or slowing the heart rate in patients remaining in atrial fibrillation. Normal rhythm can almost
always be restored either by drugs or by cardioversion. Restoration of normal rhythm is obviously the more advantageous option. But in patients prone to atrial fibrillation the arrhythmia may recur despite a course of preventive drugs. Patients who remain in atrial fibrillation are often given anticoagulants, drugs that inhibit clot formation, as protection against stroke. The choice of restoration of normal rhythm or control of the ventricular rate is usually made after estimating the probability of the arrhythmia recurring, which in turn may depend on the underlying cardiac disease.
Ventricular arrhythmias present one of the most difficult problems in cardiology. On the one hand, ventricular arrhythmias are ubiquitous in healthy adults; on the other hand, they can eventually result in fatal ventricular fibrillation. Consequently, a great deal of attention is given to recognizing and classifying them. Furthermore, ventricular arrhythmias are often closely linked to serious diseases of the myocardium, as evidence of electrical instability (the tendency to develop serious arrhythmias), and then require aggressive intervention.
Whereas the clinical importance of ventricular arrhythmias primarily depends on the underlying condition of the heart muscle, their appearance in the electrocardiogram often provides clues as to their prognostic significance. The simplest ventricular arrhythmia is the ventricular premature (ectopic) beat. However, its shape and timing in relation to the preceding normal beat may be telling. Ventricular ectopic beats that are alike and fixed in their timing are the least significant, except when they occur before the T wave of the preceding beat is completed. Ectopic beats varying in shape and timing may be evidence of electrical instability. Ectopic beats appearing in pairs or in groups of three are also considered potentially more serious. Ventricular ectopic beats appearing in runs of more than three beats are called ventricular tachycardia. All varieties of ventricular arrhythmia, including short runs of ventricular tachycardia, may be present in healthy persons; however, the more precarious the type of arrhythmia, the higher the probability of an underlying heart problem. Simpler ventricular arrhythmias do not affect heart function or cause discomfort.
Ventricular tachycardia plays a pivotal role in the evaluation of arrhythmias and in decisions regarding management, for under certain circumstances it can degenerate into fatal ventricular fibrillation.
Ventricular tachycardia is usually similar to supraventricular tachycardia in its effect on the circulation and in discomfort to the patient, but its prognostic implications are different. It is customary to classify ventricular tachycardia into two types, nonsustained and sustained . The former is characterized by spontaneous resumption of normal rhythm; the latter persists until terminated by intervention. Nonsustained tachycardia may not compromise health; sustained tachycardia is always considered serious. Ventricular flutter and ventricular fibrillation are the commonest causes of cardiac arrest. As a rule, ventricular fibrillation is fatal unless treated immediately. Occasionally, however, ventricular flutter and fibrillation appear in nonsustained form, and normal rhythm spontaneously resumes in less than four minutes, in which case they result in cardiac syncope (see chap. 7).
Evaluation of ventricular arrhythmias requires two steps: recognition of the type and frequency of arrhythmia and diagnosis of its cause, including any underlying heart disease. An ordinary electrocardiogram is inadequate for diagnosing the extent of the arrhythmia. For that purpose it is necessary to record a continuous electrocardiographic tracing by means of a Holter monitor, which can display every heartbeat over a 24-hour period. An alternate method is continuous electrocardiographic monitoring of patients in an appropriate unit in a hospital; important arrhythmias observed on the video display are then printed out for further examination.
In evaluating the background of the arrhythmia, the physician considers the state of the heart, especially the presence of heart disease, and the possible specific causes of arrhythmias, such as acute myocardial infarction, myocardial ischemia, the toxic effect of a drug, abnormalities of electrolytes or acid-base balance, and certain abnormalities of renal or hepatic function. If the ventricular arrhythmia is of a serious variety and none of the reversible causes can be identified, except for the presence of myocardial disease, further tests may be indicated, including an electrophysiological study. Here the patient is taken into a cardiac catheterization laboratory, where a pacing wire is introduced into a cardiac ventricle. The heart can then be stimulated through the wire by an electronic pacemaker outside the body to determine whether an appropriate stimulus can initiate a nonsustained or sustained ventricular tachycardia. Such pacing studies can also be used for testing responses to
antiarrhythmic drugs. In patients in whom the pacing stimulus induces a ventricular tachycardia, stimulation is repeated after a drug is administered: if tachycardia can no longer be induced, the drug may be considered efficacious in preventing naturally occurring attacks. However, there is still some controversy as to whether suppression of artificially induced tachycardia translates into reliable prevention of future attacks.
Treatment of ventricular arrhythmias includes both prophylactic and remedial therapy. The latter is rather limited, involving emergency treatment of ventricular tachycardia and ventricular fibrillation, termination of tachycardias, and the elimination of frequent premature beats that may produce discomfort or disability. Prophylactic therapy is the principal goal of antiarrhythmic treatment and includes a wide range of approaches. The most important caution in initiating prophylactic therapy of ventricular arrhythmia is that antiarrhythmic drugs carry a definite risk to the patient. Some have undesirable side effects that may unfavorably affect quality of life; furthermore, drugs may compromise the function of vital organs such as the blood, liver, and kidneys. And in about 10 percent of patients arrhythmias could be made worse by such drugs, owing to a paradoxical action. Thus the physician has to balance the risk of antiarrhythmic therapy against the risk of serious arrhythmias developing in the future. Short-range antiarrhythmic therapy, such as may be indicated in acute myocardial infarction, presents no problem; but the persistence of ominous arrhythmias may require lifelong antiarrhythmic therapy, which—particularly in patients who have no symptoms—poses a serious dilemma as to whether and when treatment is indicated. In the minority of cases successful treatment may be accomplished if a clear cause of ventricular arrhythmias can be identified and eliminated.
In general, certain priorities are assigned in initiating antiarrhythmic therapy. The first priority is given to patients who have been resuscitated from cardiac arrest. Second, aggressive therapy is usually needed for patients with recurrent sustained ventricular tachycardia. Last, patients with less-serious ventricular arrhythmias are often grouped according to the precariousness of the observed arrhythmias and the severity of underlying heart disease. Those with no evidence of organic heart disease usually require no treatment; those with myocardial disease are treated aggressively,
particularly if myocardial function is seriously impaired. During the 1980s a large number of new antiarrhythmic drugs were introduced and approved by the Food and Drug Administration, and others are still being tested. So far no drug has been produced that is highly effective yet devoid of undesirable effects.
In patients with demonstrated life-threatening arrhythmias, more-drastic interventions are available, such as surgery. The principle behind a surgical approach to the treatment of ventricular arrhythmias is the hypothesis that most serious arrhythmias involve the reentry phenomenon: if the pathway of reentry could be identified and interrupted, further arrhythmias could be prevented. Surgical incision of areas of the endocardium (the inner layer of the heart) determined by electrophysiological studies as likely reentry pathways has eliminated serious arrhythmias in some cases. However, such operations (requiring open-heart surgery) have not been uniformly successful. The possibility that similar results could be obtained by the simpler method of introducing a cardiac catheter into the heart and producing damage (either by burning or freezing) to a critical area of abnormal conduction is now being tested.
Patients who have been resuscitated from cardiac arrest caused by documented ventricular fibrillation can now be treated by automatic defibrillators, which can recognize ventricular fibrillation and immediately apply an electric shock capable of terminating the arrhythmia. This treatment requires surgical introduction of a wire into the surface of the heart. Initial experience with automatic defibrillators has been satisfactory, though they have not proven to be without risk.