In atrial fibrillation, the two atria quiver instead of contracting rhythmically. Quivering of the atria impairs filling of the ventricles and results in a reduction in cardiac output of approximately 15%. During atrial fibrillation, numerous small electrical impulses from the atria appear on the electrocardiogram as irregular fibrillatory waves. Some of these fibrillatory waves pass through the AV node and cause the two ventricles to contract rapidly and irregularly.
Atrial fibrillation can be identified from heart rhythm recordings based on the presence of fibrillatory waves, which may be fine or coarse and the irregular intervals between QRS complexes resulting from irregular contraction of the ventricles. During an initial episode of atrial fibrillation, patients frequently experience palpitations and a rapid irregular tachycardia. They may experience minor chest discomfort and transient shortness of breath. Often they note easy fatigue and reduced endurance during exertion, resulting from the 15% reduction in cardiac output caused by atrial fibrillation. Thin-chested individuals are more likely to experience symptoms during new onset atrial fibrillation; overweight individuals with large chests may experience no symptoms and are often unaware of atrial fibrillation. Atrial fibrillation is much more common in older individuals and can be associated with any type of heart disease. It is common in patients with congestive heart failure, prior myocardial infarction, congestive cardiomyopathy, hypertensive heart disease, and valvular heart disease.
Furthermore, patients with completely normal hearts may occasionally experience atrial fibrillation. The exact causes of atrial fibrillation are not completely understood, but it is known that atrial fibrillation is more common when the right or left atriums are dilated by high-filling pressures. Thus failure of either the right or left ventricles to pump normally may cause blood to back up in either atrium, stretching the atrium and triggering atrial fibrillation. Clinically, atrial fibrillation is also more common in individuals who are sleep-deprived and/or consume large quantities of alcoholic beverages. Patients with thyrotoxicosis due to elevated thyroid hormone levels also are more likely to develop atrial fibrillation. Commonly elderly patients will develop atrial fibrillation during an acute stressful illness, such as pneumonia or urosepsis. Initial episodes of atrial fibrillation are often transient and brief, often lasting a few seconds or a few minutes.
Patients commonly experience these episodes as a fluttering sensation, which are initially infrequent, often occurring at intervals of weeks or months. Later, the episodes of atrial fibrillation tend to occur more frequently and are more prolonged. This pattern of transient episodes of atrial fibrillation is referred to as paroxysmal atrial fibrillation.
Atrial fibrillation is much more common in elderly patients by may occur at any age. Some patients have atrial fibrillation continuously for years, occasionally for thirty or more years. Although atrial fibrillation does not appear to harm the ventricles, several studies have shown that patients with atrial fibrillation for long periods are more likely to develop congestive heart failure.
The most devastating consequence of atrial fibrillation is thromboembolic stroke. Because blood flow through the atriae is sluggish when the atriae are fibrillating rather than contracting, blood clots or thrombi occasionally develop in the atriea during atrial fibrillation. Clots in the left atrium are particularly dangerous because they can break lose from the atrial wall and embolize in seconds to the brain causing massive strokes. These thromboemboli strokes are infrequent but are often very disabling and may result in paralysis of the arm and leg on one side (hemiparesis), inability to speak (aphasia), and difficulty swallowing (dysphasia). The incidence of thromboembolic stroke in patients with atrial fibrillation who are not treated with anticoagulants is approximately 3 to 4% per year. Clots in the left atrium resulting from atrial fibrillation can also embolize to any other part of the body, blocking blood flow and resulting in permanent damage. For example, left atrial clots occasionally embolize to the legs, causing a painful, pulseless, cold leg. Removal of the occlusive clot by surgical embolectomy is required to restore blood flow and save the leg.
The likelihood of thromboembolism in patients with atrial fibrillation is closely associated with the extent of structural heart disease. Thus, thromboembolic stroke is much more common in patients with mitral valve disease, left atrial enlargement, or congestive heart failure; in patients with structurally normal hearts, thromboembolic stroke is much less frequent.
The risk of thromboembolic stroke can be reduced considerably with warfarin anticoagulation. Warfarin, first introduced in 1949, has been taken by millions of Americans with atrial fibrillation for protection from stroke. Warfarin induces deficiency of vitamin K, which is necessary for production of clotting proteins by the liver. Normal blood coagulates in approximately 10 to 12 seconds. In patients taking warfarin, blood coagulation is prolonged as determined by the prothrombin test (PT). Individual patients require wide variations in warfarin doses, and the optimal warfarin dose often varies over time. Therefore, frequent PT determinations are necessary initially to select the warfarin dose that anticoagulants the patient’s blood appropriately. Monthly PT determinations are necessary to adjust Coumadin doses because multiple factors, including changes in diet and medications, can alter warfarin doses over time.
The efficacy of warfarin anticoagulation for preventing strokes in patients with atrial fibrillation is well established. Furthermore, patients can take warfarin daily for years without any long-term adverse effects. However, warfarin anticoagulation always is associated with some risk of bleeding complications. The risk of serious bleeding is low, but warfarin should only be taken when necessary. Thus, after a patient has been in normal sinus rhythm for several weeks, warfarin should be stopped to eliminate risk of bleeding. By recording their heart rhythm on a daily or weekly basis, patients with atrial fibrillation can determine when their rhythm has converted to normal sinus rhythm. They can then discontinue warfarin with their physician’s approval, to reduce risk of bleeding from warfarin. Warfarin is prescribed for several other cardiovascular disorders besides atrial fibrillation, and it is therefore essential that patients confer with their physician before stopping warfarin.