The adequate management of atrial fibrillation has resisted the major advances in cardiology that have been made in the past 40 years. This stubborn and bothersome arrhythmia has increased to epidemic proportions over the past 20 years, particularly because of an aging population and beneficial treatments for many other heart disease processes that are complicated by atrial fibrillation. The only test available for the diagnosis of atrial fibrillation is the simple, an inexpensive ECG, a clinical test that has remained virtually unchanged since its inception in the 1940s.
Figure 1 shows the electrical system of the heart, the conduction system that transports the current of energy initiated in the sinus node which is then delivered to the ventricular structures to initiate the heartbeat. The ECG picks up the heart’s electrical impulses transmitted through the skin of the chest. The normal physiologic process should be understood in order to recognize the clinical features and electrocardiographic findings observed in atrial fibrillation.
The sinoatrial (SA) node is unique and has no steady resting potential. After repolarization, slow spontaneous depolarization occurs. Thus, this unique pacemaker provides individuals with an automatic, infinitesimal current that sets the electrical activity and contraction of the heart. The SA discharge rate, usually 50–100 per minute, is under autonomic, chemical, and hormonal influence.

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• I. EPIDEMIOLOGY
  Atrial fibrillation is a common arrhythmia found in greater than 1% of persons older than 60 years. This rate rises to above 5% in people older than 69, and increases to more than 10% in people older than 79. Prevalence of this disorder increases dramatically with age, but it is also becoming more prevalent with time, even after adjustment for age and underlying structural heart disease. More than 85% of patients with atrial fibrillation are older than 65. In the elderly this disorder causes substantial morbidity including stroke, heart failure, and hospitalization. Patients require an anticoagulant to prevent stroke; this therapy occasionally causes cerebral hemorrhage and requires bothersome laboratory testing every 2 weeks.
• II. DIAGNOSIS
  Diagnosis of atrial fibrillation is based on history, clinical examination, and confirmation with an ECG. The patient may experience rapid and irregular heartbeats usually from one to several hours. Associated symptoms include mild shortness of breath that can become severe if serious underlying heart disease is present. During atrial fibrilla¬tion the atrium does not contract normally and blood is therefore not delivered rapidly into the left ventricle. Poor filling of the ventricle and the fast ventricular rate may cause a fall in blood pressure resulting in lightheadedness and dizziness. Because the atrium is fibrillating and notcontracting, there is stasis of blood in the atrial appendage. Stasis predisposes the patient to clot formation and these thrombi may be dislodged and fly into the circulation and travel to other organs (embolize). The embolus can block an artery in the brain and cause a stroke.
• III. CAUSES AND RESEARCH IMPLICATIONS
  Diseases or disorders that cause atrial fibrillation are shown in Fig. 2. Due to the vast number of both serious diseases and disorders that cause atrial fibrillation, it is not sur¬prising that a definitive cure is rarely possible. This has become most frustrating for cardiologists and technologists who strive to provide advances in technologic equipment and strategies for the management of atrial fibrillation.The prevention of atrial fibrillation is therefore of para¬mount importance. There has been little focus in the past 20 years on the prevention of this abnormality.
• IV. PATHOPHYSIOLOGY
  During the past 50 years different theories have been proposed to explain the mechanism underlying atrial fibrillation, but many controversies surrounded these mechanisms. In the past decade it seems well accepted that both focal and reentrant mechanisms are involved, playing a different role in the initiation and perpetuation of the arrhythmia. Several recent human multielectrode mapping systems and other studies indicate that in atrial fibrillation the dominant mechanism incorporates multiple meandering wavelets, both in the acute and chronic form of this condition. Multiple wavelengths of excitation propagate around the atrial myocardium and the arrhyth¬mia is perpetuated because of an abnormal atrial tissue substrate, particularly in patients with structural heart disease and permanent atrial fibrillation. Patients with paroxysmal atrial fibrillation with no evidence of structural heart disease appear to have a trigger-predominant mechanism, but the two basic mechanisms reflect a large overlap. After very long periods of permanent atrial fibrillation, if sinus rhythm is restored, reverse remodeling usually fails to occur. This may explain why in patients with persistent atrial fibrillation for more than 12 months it is difficult to maintain sinus rhythm following cardioversion.
• V. CLASSIFICATION AND MANAGEMENT A. Acute Atrial Fibrillation
  An episode of atrial fibrillation observed within 48 h of its onset is described as acute. If the ventricular rate is greater than 160 beats per minute and results in acute cardio¬vascular decompensation manifested by hypotension, shortness of breath, chest pain, confusion, or heart failure, the rhythm should be converted to normal sinus rhythm. DC cardioversion is usually the initial treatment of choice.
• VI. ANTICOAGULANTS A. Warfarin
  Patients with atrial fibrillation considered high risk for stroke require anticoagulation with warfarin to maintain an INR of 2–3 to prevent stroke. An INR of 1.4–1.9 has been shown to be associated with a stroke or mortality rate similar to that for an INR of less than 1.5. The loss of atrial contraction leads to stasis of blood in the atrium and is more marked in the left atrial appendage, the most common site for clot formation. Stasis is accompanied by hypercoagulability and there is increased concentrations of fibrinogen and fibrin D-dimer and increased concentra¬tions of von Willebrand factor. These derangements all contribute to the development of a prothrombotic state and embolization. Five randomized clinical trials indicate that warfarin anticoagulation reduces the risk of stroke by 68% and lowers mortality by 33%. The risk of hemorrhagic complications, particularly cerebral hemor¬rhage, rises greatly when the INR exceeds 3.9. Patients on oral anticoagulants should have blood tests every 2–3 weeks to maintain an INR of 2–3 in order to prevent serious hemorrhagic events. In patients over 80 years of age and in those with small risk of bleeding, the INR is maintained at 1.8–2.8. Patients at high risk for bleeding are not given anticoagulants.
• VII. ELECTRONIC PACING
  It is known that conversion of atrial fibrillation to sinus rhythm does not improve survival. The reason for trying to maintain sinus rhythm is mainly to control symptoms. Neither antiarrhythmic drugs nor atrial pacing alone have been successful in suppressing atrial fibrillation.