Cardiac Arrhythmia

Arrhythmias or dysrhythmias are abnormal heart rhythms. They can cause the heart to pump less effectively.

Normally the heartbeat starts in the right atrium when a special group of cells sends an electrical signal. (These cells are called the sinoatrial or SA node, the sinus node or "pacemaker" of the heart.) This signal spreads throughout the atria and to the atrioventricular (A-V) node. The A-V node connects to a group of fibers in the ventricles that conduct the electric signal. The impulse travels down these specialized fibers (the His-Purkinje system) to all parts of the ventricles. This exact route must be followed for the heart to pump properly.

The heart contracts (beats) as the electrical impulse moves through it. This normally occurs 60 to 100 times a minute. The atria contract a split-second before the ventricles. This lets them empty their blood into the ventricles before the ventricles contract.

Under some conditions almost all heart tissue can start a heartbeat. In other words, another part of the heart can become the pacemaker. An arrhythmia occurs

These problems can produce a heartbeat that's either too slow or too fast. A heart rhythm that's too slow (bradycardia) can cause fatigue, dizziness, lightheadedness, fainting or near-fainting spells. These symptoms can be easily corrected by implanting an electronic pacemaker under the skin to speed up the heart rhythm

Rapid heart beating, called tachycardia or tachyarrhythmia , can produce symptoms of palpitations, rapid heart action, dizziness, lightheadedness, fainting or near fainting if the heart beats too fast to circulate blood effectively. Heartbeats may be either regular or irregular in rhythm.

When rapid heart beating arises in the ventricles - called ventricular tachycardia - a life-threatening situation can arrise. The most serious cardiac rhythm disturbance is ventricular fibrillation , where the lower chambers quiver and the heart can't pump any blood. Collapse and sudden death follows unless medical help is provided immediately.

If treated in time, ventricular tachycardia and ventricular fibrillation can be converted into normal rhythm with electrical shock. Rapid heart beating can be controlled with medications by identifying or destroying the focus of rhythm disturbances. Today one effective way of correcting these life-threatening rhythms is by using an electronic device called an implantable cardioverter / defibrillator .

Blood clots can form during atrial fibrillation , a disorder found in close to 2 million Americans. In atrial fibrillation the two small upper chambers of the heart, the atria, quiver instead of beating effectively. Blood isn't pumped completely out of them when the heart beats, allowing the blood to pool and clot. If a piece of the blood clot in the atria becomes lodged in an artery in the brain, a stroke results. About 15 percent of strokes occur in people with atrial fibrillation.

Cardiac Arrhythmia: Current Therapy

MICHAEL R. GOLD and MARK E. JOSEPHSON
University of Maryland and Harvard University

Rhythm disturbances can range from the harmless to the life-threatening, and treatment varies accordingly, from watchful waiting to emergency intervention. Traditional antiarrhythmic medications have largely been supplanted by newer agents; pharmacologic therapy is giving way to device-based treatment, including pacemakers, defibrillators, and catheter ablation.

Dr. Gold is Director, Cardiac Electrophysiology Service, and Associate Professor of Medicine, University of Maryland School of Medicine, Baltimore. Dr. Josephson is Professor of Medicine, Harvard Medical School, and Director, Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, Boston.

During the past few years, the treatment of many cardiac arrhythmias has tended to move away from drug therapy and toward device-based therapy. The latter may involve pacemakers, implantable defibrillators, or catheter ablation, depending on the type of arrhythmia. When drug therapy is the preferred route, the agents used are different from those selected several years ago. The treatment changes affect the management of the most common arrhythmias seen in primary care practice, including atrial fibrillation, atrial flutter, supraventricular tachycardia, and ventricular arrhythmia.

Atrial Fibrillation

The prevalence of atrial fibrillation increases with age; this arrhythmia is most often seen in patients older than 65 years. Atria9l fibrillation is typically associated with some form of cardiovascular disease, such as hypertension, coronary artery disease, or valvular heart disease, but it can also occur secondary to metabolic disorders such as thyrotoxicosis. In a minority of young patients, there is no obvious cause, a condition known as lone atrial fibrillation.

Anticoagulation. Since disruption of normal atrial blood flow with stasis can promote thrombus formation, leading to stroke or peripheral embolization, first-line therapy for patients with atrial fibrillation is anticoagulation. The drug of choice is warfarin, typically in conjunction with heparin until warfarin reaches therapeutic levels. Multiple studies have demonstrated that anticoagulation with warfarin prevents strokes much better than with any other therapy, including aspirin.

The value of long-term anticoagulation has been questioned only in the small group of patients with lone atrial fibrillation, who have a low risk of stroke. It is clear that even elderly patients with paroxysmal atrial fibrillation--in whom atrial fibrillation occurs for relatively short periods followed by a spontaneous return to sinus rhythm--have a high risk of stroke and should receive more than merely acute anticoagulation therapy.

The recommended duration of anticoagulation therapy is longer now than in the past. Previously, the rule was to anticoagulate for four weeks or so after cardioversion had restored sinus rhythm. It is now clear that many patients will revert to atrial fibrillation after that time and may present with a stroke if anticoagulation has been discontinued. Consequently, many physicians will continue anticoagulation indefinitely in patients at risk for atrial fibrillation. The consensus is to maintain anticoagulation until the patient has had at least six months of documented sinus rhythm. Even when the episode of atrial fibrillation is the patient's first and sinus rhythm is readily restored, long-term anticoagulation is recommended in those with risk factors for atrial fibrillation (e.g.,older than 65 years with hypertension or coronary artery disease). It is especially important to maintain anticoagulation in patients who are asymptomatic during episodes of atrial fibrillation since they may not seek medical attention. This new approach to anticoagulation therapy has, admittedly, been shaped more by experience than by data from controlled clinical trials.

Rate Control. In addition to anticoagulation, the acute management of atrial fibrillation includes rate control. This can be achieved with beta-blockers, calcium channel blockers, or digoxin. Traditionally, digoxin has been the first-line drug, but studies have shown it to be less effective over a 24-hour period than are drugs from the other two classes. While digoxin may be effective for controlling ventricular response when patients are at rest, it is relatively ineffective during activity or exercise.

Because calcium channel blockers and beta-blockers are about equally effective treatments for rate control, the choice between them often depends on other factors, such as side effects and concomitant clinical conditions. In patients with asthma or another contraindication to beta-blockade, we administer a calcium channel blocker. In those who have had a myocardial infarction, a beta-blocker would be the drug of choice, especially when the patient has left ventricular dysfunction.

Even if conversion to sinus rhythm is successful and fibrillation does not recur, we usually keep patients on a rate-control drug indefinitely. Beta-blockers are the preferred agents because they may help to prevent the recurrence of atrial fibrillation and also reduce the ventricular rate and symptoms if fibrillation does recur.

The only patients who do not require long-term drug therapy for rate control are those in whom atrial fibrillation develops after cardiac surgery. Their risk is limited to the first couple of weeks postoperatively. After that, they require no further treatment, provided that sinus rhythm has been restored.

Acute Rhythm Control. When patients present with persistent atrial fibrillation (>48 hours in duration), we attempt to restore sinus rhythm with an antiarrhythmic drug or electrical cardioversion. Before proceeding with either of those, however, it is necessary to minimize the risk of embolism that may be caused by terminating atrial fibrillation. One way to do that is to provide adequate anticoagulation therapy for at least three weeks--adequate is defined as a warfarin dosage sufficient to produce a prothrombin time with an international normalized ratio (INR) of greater than 2.0. If it is important to restore sinus rhythm sooner or anticoagulation therapy is contraindicated, a transesophageal echocardiogram can be performed to look for evidence of thrombus in the left atrial appendage. If anticoagulation is adequate or there is no evidence of thrombus, pharmacologic or electrical cardioversion can be performed safely (i.e., with extremely low risk). It should be noted that even if a transesophageal echocardiogram shows no thrombus in the left atrial appendage, the patient should receive heparin anticoagulation at the time of cardioversion because the procedure leads to atrial dysfunction and potential clot formation. In addition, oral anticoagulation with warfarin should be initiated after cardioversion when feasible.

Acutely, a number of intravenous drugs can be used to terminate atrial fibrillation. Amiodarone or procainamide have been the traditional choices. A newer drug, ibutilide, a type III antiarrhythmic that is available only in intravenous form, has been effective in terminating new-onset atrial fibrillation (and even more effective in terminating atrial flutter). However, the efficacy rates are still only about 30% for atrial fibrillation and 50% for atrial flutter.

Several factors determine the choice between pharmacologic and electrical cardioversion. If the patient already has been hospitalized, we often treat with an antiarrhythmic drug. We also tend to use pharmacologic cardioversion in patients who probably will require chronic treatment with an antiarrhythmic agent. In general, however, we favor electrical cardioversion, since it is a simple outpatient procedure and faster and more effective than pharmacologic cardioversion.

Chronic Rhythm Control. Once sinus rhythm has been restored, physicians must decide whether to attempt to maintain sinus rhythm with antiarrhythmic drug therapy. The use of antiarrhythmic drugs for atrial fibrillation has fallen somewhat out of favor recently because of consistently disappointing study results and a high incidence of adverse effects. Regardless of the drug selected, at least 50% of patients revert to atrial fibrillation within about six months.

The National Institutes of Health is conducting the Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) trial, comparing rate control to rhythm control in more than 4,000 patients with atrial fibrillation. The goal of the AFFIRM trial is to determine whether maintaining sinus rhythm with antiarrhythmic drugs improves survival and quality of life.

Results of the trial will not be available for several years. In the meantime, it is our practice to attempt to restore and maintain sinus rhythm in nearly every patient with atrial fibrillation. Patients first are cardioverted. If atrial fibrillation recurs, subsequent therapy depends on the patient's status. We aggressively treat with antiarrhythmic drugs if the patient has symptoms or if we believe that the arrhythmia may be deleterious over the long term, either because the patient is not a good candidate for prolonged anticoagulation (e.g., a history of peptic ulcer disease) or has active angina or congestive heart failure. Occasionally, we will leave patients in atrial fibrillation, provided that they are asymptomatic, demonstrate good rate control, and have no complicating cardiac disorders.

At present, the most successful drugs for maintaining sinus rhythm appear to be the type III antiarrhythmics, particularly amiodarone and sotalol. Despite amiodarone's potential for toxicity, we have found that if patients are monitored closely and the drug is used in low doses, treatment is safe and effective. Among cardiologists, and certainly amongelectrophysiologists, amiodaroneis rapidly becoming the most frequently used antiarrhythmic agent.

Traditionally, type IA antiarrhythmic drugs were employed for preventing atrial fibrillation. However, quinidine, the one most commonly used, has a high risk for provoking ventricular arrhythmia and is less efficacious than the type III drugs. In patients who do not have coronary artery disease, type IC drugs flecainide and propafenone can be useful to prevent atrial fibrillation. It is mandatory to use rate control drugs in conjunction with these agents because type IC drugs can convert atrial fibrillation to atrial flutter with a very rapid ventricular response.

AV Node Ablation and Pacemakers. A small subset of patients with chronic or paroxysmal atrial fibrillation have poorly controlled rates, despite treatment with multiple rate-slowing drugs. In these cases, we often recommend ablation of the AV node (thereby severing the connection between the atria and ventricles) and implantation of a permanent pacemaker. Although it is generally considered a therapy of last resort, AV node ablation effectively reduces symptoms, improves cardiac function, and improves quality of life. It is an especially useful technique in patients with obstructive lung disease or severe congestive heart failure and in them, it should be considered earlier than usual. In addition, in some patients, AV node ablation is preferred to chronic multiple-drug therapy.

Patients with atrial fibrillation and sick sinus syndrome, who tend to have bradycardia or long pauses while in sinus rhythm, usually need a pacemaker to help prevent bradyarrhythmia. A dual chamber pacemaker alone can sometimes prevent atrial fibrillation; in other cases it must be combined with antiarrhythmic drugs.

Atrial Flutter

Atrial flutter occurs in the same patient population as does atrial fibrillation. Atrial flutter is a much more regular, organized rhythm than is atrial fibrillation. The flutter typically produces an atrial rate of 300 bpm and has a sawtooth ECG pattern, seen best in lead II (Figure 1). There are also atypical forms of atrial flutter that have different ECG morphologies.

Cardiac Arrhythmia: Current Therapy

MICHAEL R. GOLD and MARK E. JOSEPHSON
University of Maryland and Harvard University

Atrial Fibrillation

Atrial Flutter

Cardiac Arrhythmia: Current Therapy

MICHAEL R. GOLD and MARK E. JOSEPHSON
University of Maryland and Harvard University

Atrial Fibrillation

Atrial Flutter

Cardiac Arrhythmia: Current Therapy

MICHAEL R. GOLD and MARK E. JOSEPHSON
University of Maryland and Harvard University