The ideal way of establishing a causal relationship between a symptom and a rhythm disturbance is to demonstrate the presence of the rhythm during the symptom. Unfortunately, this is not always easy because symptoms are usually sporadic.
Patients with aborted sudden death and recent or recurrent syncope are often monitored in the hospital. Those with less ominous symptoms may be monitored as outpatients. When episodes are infrequent, use of an event recorder is preferable to 24-hour continuous monitoring. Exercise testing may be helpful when the symptoms are associated with exertion or stress. If symptomatic bradyarrhythmias or supraventricular tachyarrhythmias are detected, therapy can usually be initiated without additional diagnostic studies. Further electrophysiologic studies may be useful in evaluating ventricular tachyarrhythmias.
Caution is required before attributing a patient’s symptom to rhythm or conduction abnormalities observed during monitoring without concomitant symptoms. In many cases, the symptoms are due to a different arrhythmia or to noncardiac causes. For instance, dizziness or syncope in older patients may be unrelated to concomitantly observed bradycardia, sinus node abnormalities, or ventricular ectopy. Ambulatory monitoring is frequently used to quantify ventricular ectopy and detect asymptomatic ventricular tachycardia in post-myocardial infarction or heart failure patients. Unfortunately, while asymptomatic ventricular arrhythmias have concerning prognostic implications, there are few data to support specific therapeutic intervention. Thus, monitoring in asymptomatic individuals is usually not indicated.
Crawford MH et al: ACC/AHA Guidelines for Ambulatory Electrocardiography. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the Guidelines for Ambulatory Electrocardiography). Developed in collaboration with the North American Society for Pacing and Electrophysiology. J Am Coll Cardiol 1999;34:912.
Heart Rate Variability
Although it has long been appreciated that there are periodical fluctuations in heart rate even under basal conditions, considerable recent interest has been focused on measurements of heart rate variability. These measurements can be made under controlled conditions in the electrocardiography laboratory or from recordings obtained during ambulatory monitoring. Greater fluctuations in heart rate correspond to greater parasympathetic activity, and several studies have indicated that greater heart rate variability is associated with a better prognosis and fewer life-threatening arrhythmias in a variety of cardiac conditions. More recently, analyses have employed frequency transformation of RR cycle length variability to provide indices of the relative balance between parasympathetic and sympathetic activity, with the greater contribution of the parasympathetic system being considered to confer a better prognosis. In studies of postinfarction patients and patients with symptomatic arrhythmias, these indices have had some prognostic value. However, adequate data are not yet available to support routine use of this technique in clinical practice.
Pumprla J et al: Functional assessment of heart rate variability: physiological basis and practical applications. Int J Cardiol 2002;84:1.
Another technique is the signal-averaged ECG. Most commonly, an orthogonal three-lead system is employed to record 300 consecutive beats during basal conditions. Using appropriate electrical filtering and computer averaging of the signal, very low frequency signals called “late potentials” can be identified in the period following the QRS complex. Abnormal late potentials are considered markers for potential ventricular arrhythmias. Adequate data are not yet available to define the role of this technique with confidence, but it may be useful in detecting groups of patients at increased risk for arrhythmic events after myocardial infarction. Approximately one-third of post-myocardial infarction patients will have abnormal late potentials, and these individuals are at higher risk for arrhythmic events, though the positive predictive value of this finding is relatively low (10-15%). More importantly, the absence of late potentials identifies a group of patients at low risk for arrhythmic events, so post-myocardial infarction patients found to have frequent ventricular ectopy or nonsustained ventricular tachycardia in the absence of late potentials may not require further investigation or treatment. The prognostic value of late potentials in patients with chronic ischemic heart disease who are more than 6-12 months removed from myocardial infarction and in patients with other forms of heart disease is not yet known.
Gomes JA et al: Prediction of long-term outcomes by signal- averaged electrocardiography in patients with unsustained ventricular tachycardia, coronary artery disease and left ventricular dysfunction. Circulation 2001;104:436.
Electrophysiologic testing employing intracardiac electrocardiographic recordings and programmed atrial or ventricular (or both) stimulation is useful in the diagnosis and management of complex arrhythmias. The primary indications for electrophysiologic testing are (1) evaluation of recurrent syncope of possible cardiac origin when the ambulatory ECG has not provided the diagnosis, (2) differentiation of supraventricular from ventricular arrhythmias, (3) evaluation of therapy in patients with accessory atrioventricular pathways, (4) evaluation of the efficacy of pharmacotherapy in survivors of aborted sudden death or other patients with symptomatic or life-threatening ventricular tachycardia, and (5) evaluation of patients for catheter ablation procedures or antitachycardia devices.
Autonomic Testing (Tilt-Table Testing)
In many patients with recurrent syncope or near syncope, arrhythmias are not the cause. This is particularly true when the patient has no evidence of associated heart disease by history, examination, standard ECG, or noninvasive testing. Syncope may be neurocardiogenic in origin, mediated by excessive vagal stimulation, or an imbalance between sympathetic and parasympathetic autonomic activity. With assumption of upright posture, there is venous pooling in the lower limbs. However, instead of the normal response, which consists of an increase in heart rate and vasoconstriction, a sympathetically mediated increase in myocardial contractility activates mechanoreceptors that trigger reflex bradycardia and vasodilation. Autonomic testing is an important component of the evaluation in these individuals and should usually precede invasive electrophysiologic procedures. Carotid sinus massage in patients who do not have carotid bruits or a history of cerebral vascular disease can precipitate sinus node arrest or atrioventricular block in patients with carotid sinus hypersensitivity. Head-up tilt-table testing can identify patients whose syncope may be on a vasovagal basis. Although different testing protocols are employed, passive tilting to at least 70 degrees for 10-40 minutes-in conjunction with isoproterenol infusion, if necessary-is typical. Syncope due to bradycardia, hypotension, or both will occur in approximately one-third of patients with recurrent syncope. Some recent studies have suggested that, at least with some of the more extreme protocols, false-positive responses may occur.
Fitzpatrick AP et al: Tilt methodology in reflex syncope: emerging evidence. J Am Coll Cardiol 2000;36:179.
Antiarrhythmic Drugs (Table 10-5)
Antiarrhythmic drugs have limited efficacy and produce frequent side effects. They are often divided into four classes based upon their electropharmacologic actions. Some have multiple actions.
Class I agents block membrane sodium channels. Three subclasses are further defined by the effect of agents on the Purkinje fiber action potential. Class Ia drugs slow the rate of rise of the action potential (Vmax) and prolong its duration, thus slowing conduction and increasing refractoriness. Class Ib agents shorten action potential duration; they do not affect conduction or refractoriness. Class Ic agents prolong Vmax and slow repolarization, thus slowing conduction and prolonging refractoriness, but more so than class Ia drugs.
Class II agents are the beta-blockers, which decrease automaticity, prolong atrioventricular conduction, and prolong refractoriness.
Class III agents block potassium channels and prolong repolarization, widening the QRS and prolonging the QT interval. They decrease automaticity and conduction and prolong refractoriness.
Class IV agents are the calcium channel blockers, which decrease automaticity and atrioventricular conduction.
Although the in vitro electrophysiologic effects of most of these agents have been defined, their use remains largely empirical. All can exacerbate arrhythmias (proarrhythmic effect), and most depress left ventricular function.
The risk of antiarrhythmic agents has been highlighted by the Cardiac Arrhythmia Suppression Trial (CAST), in which two class Ic agents (flecainide, encainide) and a class Ia agent (moricizine) increased mortality rates in patients with asymptomatic ventricular ectopy after myocardial infarction. A similar result has been reported with D-sotalol, a class III agent without the beta-blocking activity of D,L-sotalol, the currently marketed formulation. Therefore, these agents (and perhaps any antiarrhythmic drug) should not be used except for life-threatening ventricular arrhythmias and symptomatic supraventricular tachyarrhythmias.
The use of antiarrhythmic agents for specific arrhythmias is discussed below.
Goldschlager N et al: Practical guidelines for clinicians who treat patients with amiodarone. Arch Intern Med 2000; 160: 1741.
Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: advanced cardiovascular life support: section 5: pharmacology I: agents for arrhythmias. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 2000;102(8 Suppl):I112.
Kowey PR et al: Classification and pharmacology of antiarrhythmic drugs. Am Heart J 2000;140:12.
Roden DM: Antiarrhythmic drugs: from mechanisms to clinical practice. Heart 2000;84:339.
Radiofrequency Ablation for Cardiac Arrhythmias
Catheter ablation techniques have become the primary modality for treatment of many arrhythmias. This growing trend reflects the increasing ability to localize the origin or conduction pathways of many arrhythmias, the improved technology for delivering radiofrequency energy, and growing dissatisfaction with the efficacy and safety of pharmacologic therapy. Ablation has become the primary modality of therapy for many symptomatic supraventricular arrhythmias, including atrioventricular nodal reentry tachycardia, reentry tachycardias involving accessory pathways, paroxysmal atrial tachycardia, inappropriate sinus tachycardia, and automatic junctional tachycardia. Many laboratories have achieved reasonable success rates in preventing atrial flutter with radiofrequency techniques. Ablation of atrial fibrillation is more complex and involves electrical isolation of the pulmonary veins, which are often the site of initiation of atrial fibrillation, or placing linear lesions within the atria to prevent spread of the rhythm. Catheter ablation of ventricular arrhythmias has proved more difficult. Three specific forms of ventricular tachycardia, however, have proved to be amenable to radiofrequency ablation. These include bundle-branch reentry, tachycardia originating in the right ventricular outflow tract, and some tachycardias originating in the left side of the interventricular septum. Other forms of ventricular tachycardia, particularly in patients with coronary artery disease, may be amenable to ablation, but experience thus far is limited.
These procedures are generally safe, though there is a low incidence of perforation of the atria or right ventricle that results in pericardial tamponade and sufficient damage to the atrioventricular node to require permanent cardiac pacing in less than 5% of patients. In addition, some procedures involve transseptal or retrograde left ventricular catheterization, with the attendant potential complications of aortic perforation, damage to the heart valves, or left-sided emboli.
Calkins H: Catheter ablation for cardiac arrhythmias. Med Clin North Am 2001;85:473.
Revision date: June 22, 2011
Last revised: by Andrew G. Epstein, M.D.