Like the chaos of a hailstorm on a tin roof comes the electrical storm of atrial fibrillation. During AF, the atria are quivering (fibrillating) and firing hundreds of impulses from different locations at the same time. It’s as if the electrical circuits have gone haywire.

AF is a major health, social, and economic problem affecting more than 2 million U.S. adults. It’s becoming increasingly common as the population ages, with nearly 10% of people over the age of 80 affected. By the middle of this century, it’s estimated that over 5.5 million people will have AF, with more than 50% of them over 80.¹ The economic and social burden will be significant, putting a strain on already limited health care resources.

Nurses should be able to recognize this dysrhythmia, understand the etiologies and pathogenesis, and educate patients about treatment options so that they may make sound, evidence-based decisions about their treatment.^2-4

Clinical conditions associated with AF include COPD; primary pulmonary hypertension; rheumatic heart disease, resulting in valvular disorders; coronary artery disease; hyperthyroidism; and pulmonary embolism. AF may also occur with chronic alcohol ingestion and increased sympathetic activity. Occasionally, it’s familial. Some patients with AF, fewer than 10%, have “lone” AF — AF with no clinical electrocardiographic or echocardiographic evidence of structural heart disease and none of the clinical conditions cited above.¹

Whatever its cause, during AF the atria depolarize erratically. The quivering atria contract inefficiently, resulting in a reduced output of blood into the ventricle. The atrioventricular (AV) node, usually a “gatekeeper” or “filter” of electrical impulses it receives from the sinoatrial (SA) node, is bombarded with impulses and cannot depolarize fast enough to let all the impulses through. When one of the impulses does get through, it is propagated normally, producing normal-appearing QRS complexes on the ECG. This rhythm may be sustained or intermittent.

The ventricular rate will depend on the degree of blockade (of impulses) at the AV node. Nomenclature often reflects rate-related severity. For example, AF with a controlled ventricular response implies that the ventricular rate is normal: between 60 and 100 bpm. If the ventricular rate (number of QRS complexes) is greater than 150 bpm, the ventricular rate is said to be “uncontrolled”; a ventricular rate greater than 100 bpm is called “rapid atrial fibrillation.” AF with a ventricular rate of less than 60 bpm is called “slow atrial fibrillation.” Atrial rates can be as high as 350 to 700 bpm. Uncontrolled or rapid ventricular rates associated with AF can lead to tachycardia-mediated cardiomyopathy.⁵ This condition involves heart chamber dilation and wall thickening and may lead to heart failure. In this case, the heart failure results from the rapid ventricular rate.

Two criteria aid in the diagnosis of AF: The ventricular rate is irregularly irregular, and a P wave is not discernable. On an ECG, atrial contraction (signaled as P waves) is nondetectable because of the quivering of the atria. In place of P waves, fibrillatory waves are present, which may look like an undulating baseline on the ECG between complexes. Since there are no discrete P waves, there is no PR interval. The QRS complex is of normal duration as the impulse passes down the usual and normal electrical pathway in the ventricle.

Two serious hemodynamic problems may arise with AF. First, it causes a drop in cardiac output because of the loss of effective atrial contraction (also called atrial kick). Atrial contraction contributes 15% to 30% to overall cardiac output.⁶ Loss of atrial kick may result in dizziness, lightheadedness, fatigue, or syncope because of a subsequent drop in cardiac output and then blood pressure.

A second hemodynamic problem is an increased threat of blood clots as the blood in the atria is allowed to pool when the atria fibrillate rather than contract completely and effectively. Pooled blood may ultimately form clots and precipitate MI, strokes, or pulmonary emboli. As a result, most, if not all, patients with the diagnosis of AF are anticoagulated, generally with warfarin (Coumadin). Patients with AF not receiving anticoagulant therapy may have up to a fivefold increased risk of stroke.⁵

Heart ‘palpitations’

Some patients with AF are asymptomatic, with the diagnosis made on a regular annual examination or as an incidental finding. Other patients report sensations that reflect the irregularity of the rhythm, which they often describe as “palpitations” or “the heart pounding.” As a result of decreased cardiac output secondary to loss of atrial kick, patients may present with symptoms of fatigue, shortness of breath at rest or activity, decreased exercise capacity, or chest pain. Severe symptoms and physical examination findings of heart failure occasionally are found in patients with new onset AF with a rapid or uncontrolled ventricular response.¹

Is it really AF?

The ECG confirms AF and determines the ventricular rate (uncontrolled, fast, slow, or controlled). Definite attempts should be made to determine the underlying etiology once the patient has been stabilized and rate control and rhythm conversion have been addressed. Many cardiovascular and systemic conditions may be associated with AF.

Based on potential conditions/causes associated with AF, several diagnostic tests are commonly recommended, including continuous ECG monitoring (Holter or transtelephonic event), thyroid function and electrolyte blood tests, echocardiography, and functional stress testing.⁷

The Holter monitor is a simple ECG monitoring device worn for 24 to 48 hours. During that time, the patient keeps a diary of any symptoms. Once the recording is complete, the rhythms are analyzed and identified. Symptoms are correlated with any abnormal ECG findings.

Transtelephonic event monitors transmit recordings by telephone to a central location. A patient may wear the device to record data for up to 30 days. Unlike a Holter monitor, a transtelephonic event monitor transmits data only when the patient activates the device based on symptoms such as dizziness, syncope, or palpitations.

Laboratory testing should be performed to evaluate thyroid status and screen for electrolyte abnormalities. Hyperthyroidism, hypokalemia, and hypomagnesemia may contribute to the electrical instability of the heart and, thus, the development of AF, and they should be ruled out.

Echocardiography allows visualization of cardiac anatomy. It may reveal valvular problems or chamber enlargements that could contribute to the development of AF. Echocardiography may be used to evaluate pulmonary artery pressures and ventricular ejection fraction (the fraction of blood pumped out of the ventricle with each heartbeat). The nature and severity of structural heart disease, if present, determine the therapeutic options for managing AF.⁷

The patient may undergo exercise or pharmacologic stress testing to identify an ischemic etiology for AF. If the test is abnormal, suggesting decreased myocardial perfusion, coronary angiography is indicated to rule out coronary artery disease as a contributing or single factor for the dysrhythmia.

Gaining control

AF treatment generally involves three goals: anticoagulation, ventricular rate control, and rhythm conversion, depending on a patient’s symptoms.

Anticoagulation: Unless the risks outweigh the benefits, all patients with a diagnosis of AF should be anticoagulated. Warfarin is the medication used most often to reduce the risk of stroke or other thromboembolic complications.⁷ Aspirin may be used in people up to age 75 who don’t have any risks for thromboembolism. Before patients start anticoagulation, clinicians must consider their risk of bleeding and ability to comply with treatment, weighing the risks and benefits. If the patient is at high risk for falls, which may result in an intracranial hemorrhage, he or she shouldn’t receive warfarin anticoagulation therapy. If the patient’s cognitive state would preclude frequent dosage titration and compliance with testing regimens, anticoagulation with warfarin may be contraindicated, and aspirin will be used alone.

The nurse has an important role in educating patients and families about the purpose of warfarin therapy, required laboratory tests, signs and symptoms of excess anticoagulation, and possible food, drug, and nutritional supplement interactions. Anticoagulation therapy is complex and requires many lifestyle adjustments. Therefore, patients need reinforcement of this information during the initial treatment and in later health care visits.

Close monitoring of blood clotting is necessary when initiating and maintaining anticoagulation. The international normalized ratio (INR) is the most widely used test to monitor effective coagulation. The goal of therapy for the patient with AF is an INR of 2.5; range: 2-3.⁷

Ventricular rate control: Patients with AF generally receive pharmacologic therapy to slow the ventricular response to a normal heart rate and improve symptoms and hemodynamic parameters. If the ventricular rate is rapid (greater than 100 bpm), cardiac output may be further reduced secondary to decreased diastolic filling time in the ventricles. Patients commonly receive calcium channel blockers, beta blockers, and digitalis to reduce ventricular rate by increasing block at the AV node.² The choice of drug depends on whether heart failure or decreased ejection fraction exists.

Rhythm conversion: Conversion of AF to sinus rhythm may occur spontaneously or pharmacologically or with electrical cardioversion. Deliberate attempts are made to convert the rhythm to preserve AV synchrony, optimize cardiac output, reduce symptoms, and decrease risk of thromboembolism.

When AF is confirmed, the clinician must determine the patient’s hemodynamic status. If the status is compromised, the patient may require immediate or urgent cardioversion (electrical or pharmacologic). Indicators of hemodynamic compromise include symptomatic hypotension, decreased level of consciousness, chest pain, or pulmonary edema. These indicators are all evidence that AF is compromising cardiac output, and cardioversion to sinus rhythm is needed to improve hemodynamic status.² Nursing care at this stage includes monitoring the patient’s heart rate and rhythm, blood pressure, and respiratory status; assessing for adverse effects of medication therapy; and controlling symptoms. Therapeutic interventions to reduce anxiety may help offset potential increases in heart rate, which could provoke continuation of symptoms or further symptoms.

During conversion from AF to sinus rhythm, the patient is at high risk for embolization and stroke. Before immediate or urgent cardioversion, anticoagulation with IV heparin is indicated, and a transesophageal echocardiogram (TEE) — a test to demonstrate cardiac anatomy via endoscopic approach — is necessary to rule out an atrial thrombus. If the dysrhythmia has been present for less than 48 hours, immediate cardioversion may also be considered in stable patients without concomitant anticoagulation. If the time of onset of AF is unknown or uncertain and the patient is stable, cardioversion is delayed. The patient should be anticoagulated to an INR of 2-3 for at least three weeks before the procedure to avoid the risk of an embolic stroke.²

In some cases, the patient may be allowed to remain in AF if attempts at conversion have been unsuccessful. Among these patients, rate control is the primary objective and may be established with rate-controlling drugs and therapeutic anticoagulation. Adequate rate control is considered 90 bpm or less at rest and less than 110 bpm with moderated activity.⁵ Studies show that for patients older than 65, acceptance of AF with rate control is not inferior to restoring and maintaining sinus rhythm with drug therapy.⁸

Drug selection should be based on guidelines from the American College of Cardiology, American Heart Association, and European Society of Cardiology, whose recommendations depend on a patient’s previous medical history and risk factors.⁴

Nonpharmacologic therapies for rhythm conversion include interventional elimination or ablation of the AV node with electronic pacing for rate control (i.e., “ablate and pace”); surgery; and radiofrequency catheter ablation (also called “pulmonary vein isolation”).⁹

Ablation of the AV junction with permanent pacemaker implantation should be considered in patients who are refractory to aggressive attempts at medical therapy or who develop adverse effects from medications.⁹ Most patients are pacemaker-dependent after AV junction ablation; therefore, it may not be an appropriate choice for a relatively young patient. The procedure is palliative; the patient persists in AF, and life-long anticoagulation is necessary.

One surgical approach for AF is the maze procedure, requiring open-heart surgery. In this procedure, the surgeon makes small incisions in the atria to interrupt re-entrant atrial dysrhythmias, thus providing one pathway from the sinus node to the AV node.¹ After the procedure, patients usually continue to receive anticoagulation therapy. The procedure may be complicated by the need for permanent pacing. The maze procedure is usually reserved for patients undergoing planned cardiac surgical procedures for other reasons (coronary or valvular heart disease).

Radiofrequency catheter ablation is yet another approach.¹⁰ In this procedure, abnormal electrical impulses (ectopic foci) are isolated via electrical mapping in the atria. These ectopic foci usually exist around the pulmonary veins in the left atrium. During this procedure, a catheter is inserted into the blood vessels of the atrium, and energy is delivered to the area of the atria that connects to the pulmonary vein. The energy (ablation) produces a circular scar that blocks any impulses firing from within the pulmonary vein, thereby “disconnecting” the pathway of the abnormal impulses and preventing atrial fibrillation. This procedure may cure AF, eliminating the need for antiarrhythmic drugs and anticoagulation in many patients.¹⁰ Ablation may also be performed in other parts of the heart that demonstrate ectopic focal activity contributing to the continuation of the dysrhythmia. Because it is an invasive procedure with risks including stroke and pulmonary vein stenosis,¹⁰ ablative therapy is usually considered only after drugs have failed to control the AF.

The incidence of AF is increasing, making it a major public health concern. As the elderly population grows and more people survive with cardiovascular conditions, AF is expected to affect thousands more in future decades.⁵ But AF also occurs among younger people:

13-time all-star hockey player Mario Lemieux of the Pittsburgh Penguins recently had to retire from the game at age 40 in part because of AF.¹¹

Much more remains to be learned about the causes of AF, and the ideal treatment approach remains elusive. However, evidence-based guidelines are available (see, for example, references 2-5), supporting strategies for reducing complications and improving function and quality of life.