There are three basic components to the treatment for atrial tachycardia and flutter:
- Ventricular rate control
- Chemical or electrical cardioversion
- Maintenance of sinus rhythm
The basic treatment plan for patients with atrial flutter. In general, patients with focal atrial tachyardia – regardless of duration – do not require anticoagulation before undergoing chemical or electrical cardioversion. Consequently, treatment of focal atrial tachycardia is generally less complex than the treatment of atrial flutter (or atrial fibrillation).
VENTRICULAR RATE CONTROL
Patients who present to their physician or the emergency room with atrial flutter
usually do so because they are having symptoms related to rapid or irregular heart
activity. Symptoms may include palpitations, shortness of breath, and fatigue and
these symptoms are, in part, due to the rapid ventricular response associated with
new onset atrial fibrillation. Acute treatment to slow the ventricular response and
lessen the symptoms may include medications such as digoxin, beta-adrenergic blocking agents, or calcium channel blocking drugs. All of these agents can be administered orally as tablets or pills and some of these drugs can also be given intravenously in the emergency room. The table below summarizes the drugs used for ventricular rate control. These drugs exert their effect by slowing electrical impulse conduction within the AV node. The AV node is the critical structure that acts as a “toll booth” regulating electrical traffic flow between the upper and lower heart chambers.
Basic overview of treatment options for patients with atrial flutter. Patients with focal atrial tachycardia do not require antiocagulation before electrical or chemical cardioversion. Abbreviations: AFL, atrial flutter; SR, sinus rhythm.
Choice of Treatments Following Acute Ventricular Rate Control
After the initial acute therapy is administered to slow the ventricular rate, a decision must be made concerning further therapy for the atrial tachycardia or flutter. Long-term treatment options following ventricular rate control include:
- Chronic ventricular rate control and long-term anticoagulation (in the case of atrial flutter), or
- Termination of the atrial tachyarrhythmia and long-term maintenance of sinus rhythm
Which treatment pathway the patient chooses may depend upon a number of factors,
including the ventricular rate, the severity of symptoms caused by the arrhythmia,
and the willingness of the patient to undergo sequential treatments and tests (and
accept the associated small risks of these interventions) that may be required to
maintain sinus rhythm.
COMMON MEDICATIONS USED FOR TREATMENT OF ATRIAL FLUTTER
In most cases, focal atrial tachycardias will spontaneously self-terminate and are
often suppressed with medication or cured with catheter ablation. Therefore,
patients with fast or symptomatic focal atrial tachycardia generally benefit from
pursing treatment options to medically suppress or cure their atrial tachyarrhythmia. However, atrial flutter may be more difficult to prevent or cure and some patients with minimal or no symptoms may choose to remain in atrial flutter after considering the available alternative treatments. In addition, many (possibly all)patients with atrial flutter also have (or may develop) atrial fibrillation, further complicating therapy. In consultation with their physician, and after reviewing their options, patients with atrial flutter must decide whether to: 1) remain in atrial flutter and only receive treatment to slow ventricular rate (to prevent tachycardiainduced cardiomyopathy) and minimize the risk of stroke, or 2) pursue cardioversion of atrial flutter and maintenance of sinus rhythm.
Chronic Ventricular Rate Control and Long-Term Anticoagulation
A patient can choose the remain in atrial flutter as long as the risk of stroke is
treated with warfarin anticoagulation and the ventricular rate is controlled. If a
patient chooses to remain in atrial flutter over the long term (years), subsequent
atrial remodeling may eventually eliminate the possibility that sinus rhythm can ever again be restored and maintained. Also, if the ventricular rate is not adequately controlled, a tachycardia-induced cardiomyopathy may develop. In general, ventricular rate control implies average ventricular rates below 100 beats/min, and perferably less than 80 beats/min. There are two options for chronic ventricular rate control in thesepatients: drug therapy or catheter ablation therapy.
Drug Therapy for Long-Term Control of Ventricular Rate
The preferred drug treatment for ventricular rate control includes digoxin, beta-adrenergic blocking agents, or calcium channel blocking drugs (see table below). Occasionally, these medications may be used in combination. In rare patients with difficult-to-control, rapid ventricular rates the class III antiarrhythmic drug amiodarone may be used. However, the potential side effects of amiodarone treatment are more serious than the relatively minor side effects associated with digoxin, beta-adrenergic blocking agents, or calcium channel blocking drugs.
Radiofrequency Catheter Ablation for Control of Ventricular Rate
Catheter ablation to permanently control ventricular rate is generally restricted to
patients with permanent atrial flutter or tachycardia and one of the following limitations:
- all conventional medical therapies have proved unsuccessful
- curative catheter ablation has been tried, was unsuccessful, and is no longer an option
- long-term ventricular rate control with amiodarone is not considered an option
In general, catheter ablation is a “last resort” therapy. Only rarely is it used for
patients with paroxysmal atrial flutter. The primary catheter ablation treatment for
rate control involves totally destroying the AV node, thereby eliminating the electrical connection between the upper and lower heart chambers. This is normally a simple, quick, and safe procedure. Elimination of the AV nodal conduction pathway
means that there is no way for electrical activity in the atria to get to and activate the ventricles. Therefore, a pacemaker must be implanted before or immediately following this procedure to permanently stimulate the ventricles to pump at an adequate rate. Ablation of the AV node is not reversible – it is permanent. After this procedure the patient is “pacemaker dependent” and if the pacemaker were to malfunction (very rare) the patient may faint and could possibly even die.
CARDIOVERSION OF ATRIAL TACHYCARDIA AND FLUTTER TO SINUS RHYTHM
If resumption and maintenance of sinus rhythm is the goal, then the first step
toward that goal is cardioversion of the atrial tachyarrhythmia to sinus rhythm.
Cardioversion means termination of the tachyarrhythmia allowing resumption of
sinus rhythm. In many cases, atrial flutter and atrial tachycardia will spontaneously convert to sinus rhythm. Many patients have paroxysmal atrial flutter or tachycardia in which the arrhythmia repeatedly starts and stops spontaneously.
Each episode may sustain for seconds, minutes, hours, or days in duration. If a
patient has a previous history of recurrent episodes of atrial flutter or tachycardia,there is little benefit to simply terminating the paroxysmal atrial tachyarrhythmia with, for example, an electrical cardioversion, without instituting in advance a drug therapy designed to provide long-term suppression of the atrial arrhythmia. The atrial tachyarrhythmia will likely recur unless suppressive drug therapy is also administered.
While focal atrial tachycardia can be terminated at any time, regardless of its duration, conversion of atrial flutter to sinus rhythm should not be attempted because of the risk of stroke unless the atrial flutter is clearly of recent onset. In general, “recent onset” means continuous atrial flutter duration of less than 48 hours. For patients at the highest risk for stroke (i.e., those with significant structural heart disease such as dilated or hypertrophic cardiomyopathy), many physicians do not perform cardioversion even if the atrial flutter duration has been only 24-hours. In addition, many patients may not be able to accurately determine the exact moment of onset of their atrial flutter, making a precise assessment of atrial flutter duration unreliable. If there is any doubt about the duration of the atrial flutter it is generally best to treat the patient with at least four weeks of anticoagulation before attempting cardioversion. During this period of time, ventricular rate control drugs should be administered if needed, but antiarrhythmic drugs or electrical therapies designed to terminate the atrial flutter should be avoided unless absolutely necessary.
There are two main methods for cardioversion: chemical (pharmacologic) cardioversion
and electrical cardioversion. Electrical cardioversion is significantly
more effective than chemical cardioversion. Electrical cardioversion involves delivering an electrical shock through two patches placed on opposite sides of the
patient’s chest after rendering the patient briefly unconscious using a short-acting
drug. The electrical current travels from one skin patch, through the heart, to the
other skin patch. The electrical shock “resets” the cardiac electrical activity allowing the normal sinus node pacemaker to resume control of the heartbeat.
Chemical cardioversion involves administration of a medicine (intravenously or
orally) that has been shown to be effective at terminating atrial flutter or tachycardia (see table). Two commonly used intravenous medications include ibutilide and procainamide. Even if an intravenous medication is used initially in the hospital or emergency room for cardioversion, long-term drug therapy usually involves a pill or tablet that can be taken at convenient times. There are many oral medications available. The class IA, class IC, and class III (see table) are the most commonly used agents and have proven to be the most effective.
Although electrical cardioversion is the most effective means to terminate atrial flutter, chemical cardioversion is often attempted before electrical cardioversion. There are two reasons for this. First, while electrical cardioversion is a very safe procedure, it is an in-hospital procedure that involves anesthesia with some associated small risk. Second, by its nature atrial flutter or focal atrial tachycardia have a high rate of recurrence (i.e., they are often paroxysmal). Therefore, merely converting the arrhythmia to sinus rhythm does not prevent it from recurring minutes, days, months, or years latter. Commonly, therefore, patients are administered a medication that is designed to prevent a recurrence of the atrial arrhythmia. Ideally, this is a medication that the patient can take long-term without causing intolerable side effects. Consequently, it is optimal to initiate therapy with a medication, achieve a stable dosage regimen, and then proceed to electrical cardioversion if the medication alone fails to terminate the arrhythmia. If the medicine therapy is administered only after the electrical cardioversion, the atrial tachyarrhythmia may recur before the medical therapy can be initiated or before a therapeutic level is achieved. In this case a second electrical cardioversion may have to be performed. If medical therapy had been started first, a second cardioversion procedure could potentially be avoided.
MAINTENANCE OF SINUS RHYTHM
Maintenance of sinus rhythm in patients with a history of atrial flutter or focal atrial tachycardia may not always be possible. While complete elimination of the tachycardia may be achieved in many patients, some patients may have to accept a lesser goal of incomplete suppression of the arrhythmia but in association with a significant improvement in their quality of life. Along the way, patients must constantly reevaluate whether their quality of life improvement exceeds the small risks, discomfort, and potential side effects that may be associated with the treatment regimen. Treatment options for suppression of atrial flutter and focal atrial tachycardia are divided into drug therapy and catheter ablation therapy.
Pharmacological therapies include calcium channel blocking agents, beta-adrenergic
blocking agents along with the class IA, class IC, and class III antiarrhythmic drugs (see table). Class IC drugs exert their antiarrhythmic effect primarily by slowing electrical conduction in the heart by blocking sodium-dependent electrical currents in cardiac cells. Class III drugs exert their therapeutic effects primarily by blocking cellular potassium currents. Blocking potassium currents prolongs the time after a heart beat before the heart tissue can again be reactivated. Class IA drugs exert their antiarrhythmic effect by blocking both sodium and potassium currents. Amiodarone is an unusual drug in that it can block sodium, potassium, and even calcium currents, although it exerts its primary effect on potassium currents. Calcium channel blocking agents appear to provide little benefit at suppressing or preventing atrial flutter. beta-adrenergic blocking agents may have some efficacy at preventing atrial tachyarrhythmias, especially in patients whose atrial arrhythmia may be triggered by high adrenaline states, such as stress, anger, anxiety, etc.
Many patients will require treatment with antiarrhythmic drugs for termination
and suppression of atrial flutter or tachycardia. The class IC and class III drugs usually are most effective. Drug efficacy, however, is highly individualized, with some patients responding very well to these medications, while other patients may find these medications completely ineffective. It is rare that a medication is either 100% effective or 100% ineffective, with most providing partial improvement in the frequency, severity, and duration of arrhythmia episodes. In addition, drug therapy of these arrhythmias is a “trial and error” proposition; it is not possible to determine ahead of time which medication will work best in a particular patient. The critical feature of drug therapy is that it does not cure the tachycardia; at best it only can suppress the atrial arrhyhtmia if the medication is taken on a regular basis.
Basic components of an electrophysiology (EP) laboratory.
Radiofrequency Catheter Ablation
The general principle of any catheter ablation procedure is to destroy (“ablate”)
one or more areas of heart tissue that is/are critical to the development or maintenance of an arrhythmia. Catheter ablation using radiofrequency energy has been
successfully employed since the late 1980s to eliminate a wide variety of cardiac
arrhythmias. The radiofrequency catheter ablation technique is similar to the electrocautery device used during surgery to cut tissue. However, the particular type of radiofrequency energy employed during the catheter ablation procedures heats the tissue enough the destroy heart cell function without cutting the tissue.
Ablation of atrial flutter or focal atrial tachycardia is usually an outpatient procedure (no overnight stay in the hospital is required). The procedure is performed in a special procedure room called an electrophysiology (EP) laboratory. The EP laboratory houses a table and an x-ray (fluoroscopy) machine that is suspended over the table. In addition, there is a large number of special electronic and computer equipment in the laboratory that is used during the electrophysiology study to determine the target tissue in the heart for the ablation of the procedure. The patient is heavily sedated during the procedure using short acting intravenous drugs. The procedure generally takes 2-4 hours, sometime longer.
Special “wires” called electrode catheters are inserted into the heart through veins
in the right and possibly left upper leg (groin) region and sometimes through a vein
in the right neck region. Catheters must be inserted into various regions of the
heart, including the coronary sinus and right atrium, and sometimes the left atrium.
If the tachycardia involves the left atrium, a special procedure called trans-septal
left heart catheterization must be performed to gain access to the left atrium.
During this procedure a small hole is created in the wall between the right and left
atrium in order to pass catheters into the left atrium. The goal of the ablation procedure is to find the precise location of the triggering arrhythmia focus, or the critical portion of the reentrant circuit, inside the right or left atrium. Once localized, the electrode at the tip of the ablation catheter is positioned at that target site and radiofrequency (heat) energy is delivered to destroy the culprit tissue. Destroying the critical spot in the heart responsible for the atrial tachyarrhythmia may eliminate the arrhythmia. For ablation of the typical clockwise of counterclockwise forms of atrial flutter, the ablation procedure requires creating a line of conduction block (destroy a linear patch of tissue) in the isthmus between the inferior vena cava and tricuspid valve annulus in the right atrium. For ablation of focal atrial tachycardia, a small patch of tissue – generally 0.5 - 1.0 centimeter – must be destroyed at the precise location of the origin of the atrial tachycardia focus.
The risks of the radiofrequency catheter ablation procedure are small; however, as
with any invasive procedure it is not a risk-free procedure. The most serious
reported complications in the medical literature include death, stroke, heart attack, cardiac perforation requiring emergency surgery, heart valve damage, injury to a large vein or artery, blood clots, infection, and complete heart block requiring implantation of a permanent pacemaker. While the risk is low for any of these complications, the risk of the procedure is not zero. The success rate for radiofrequency ablation procedure varies depending upon the location of the arrhythmia. In genral, for the typical clockwise of counterclockwise forms of atrial flutter, or the right atrial forms of focal atrial tachycardia, the success rate is approximately 80-90%. Some patients may require repeat procedures – if the arrhythmia recurs – and/or postablation treatment with medication to achieve a durable long-lasting cure.