AF is a chaotic atrial rhythm in which discrete atrial activity has been replaced by an irregular undulating atrial activity and a variable R-R interval. While the P wave vector is best appreciated in the inferior limb leads (II,AVF), fibrillatory waves are usually seen best in V1 and V2. Arial Fibrillation increases in prevalence with age and it's appearance is associated with a doubling of the mortality compared to those without it; the prognosis of "lone" AF is controversial but it appears to be better than when there is obvious cardiac pathology. Symptoms can include palpitations, fatigue, dyspnea, dizziness, and decreased stamina. The etiology or diseases associated with atrial fibrillation include: rheumatic valvular disease (mitral stenosis), valvular heart disease, hypertension, coronary artery disease, hyperthyroidism, pericarditis, myocarditis, cardiomyopathy (dilated/hypertrophic), alcohol (holiday heart syndrome), Hemachromatosis, post-coronary bypass surgery, Sick sinus syndrome, post-VVI permanent pacer placement, and pulmonary embolism.

Atrial fibrillation is usually easily distinguished from the only other irregularly-irregular SVT multi-focal atrial tachycardia. This condition has P waves of varying morphology and is associated with theophylline toxicity.

The underlying cause and chronicity of atrial fibrillation determine treatment. Infection, fever, hyperthyroidism, metabolic or electrolyte abnormalities, cardiomyopathy, myocardial infarction and valvular heart disease are all possibilities, although "lone AF" is possible. Usually a medical history and physical exam along with appropriate lab studies including thyroid function are indicated. An echocardiogram including a Doppler study and measurement of chamber size (including the left atrium) is especially indicated. If the patient is at high risk for thrombi (i.e., previous emboli), a transesophageal echo (TEE) may be advisable and thrombi should be searched for during the echocardiographic study. Anticoagulation to reach an INR of 2-3 is indicated for 2-3 weeks prior to attempting cardioversion unless there is convincing data to support the acuteness of the AF or if there is hemodynamic compromise. Rate control can be accomplished by digoxin, Diltiazem and/or a beta blocker. Diltiazem is preferred over a beta blocker since it preserves exercise capacity. Chemical cardioversion is usually attempted first using Ibutilide, quinidine, pronestyl (procainamide) or sotalol. Pronestyl (IV) is the drug of choice if the conduction is over an accessory pathway (with WPW). Patients with a history of CHF or documented structural heart disease should be admitted to the hospital for drug therapy because of the danger of proarrhythmia's. If this fails, the patient is admitted for direct electrical cardioversion (EC). An experienced cardiologist working with an anesthesiologist best carries out EC. The defibrillator should be synchronized on the QRS complex so that it does not induce ventricular fibrillation. Back to front paddles should be used starting at 100 joules and progressing to 300 joules.

The three therapeutic goals for patients with atrial fibrillation are:

1. Rate control - do not give Quinidine prior to slowing the rate with Digoxin since Quinidine and similar agents can speed A-V conduction. Diltiazem is preferable to a beta blocker since exercise capacity is improved except if the patient is hyperthyroid, then a beta blocker is preferred.
2. Cardioversion and maintenance of Sinus rhythm - About 50% of patients presenting with new onset AF will spontaneously convert within 2 days. Chemical cardioversion is usually 50% successful using Quinidine, propafenone, flecainide, sotalol or amiodarone. Usually two thirds of treated patients stay in sinus rhythm for one year. Patients with a history or findings of CHF should be hospitalized for chemical cardioversion because of the dangers of arrhythmia caused by the medications. Unless the atrial fibrillation can be documented as less than 48 hours duration the patient should be anti-coagulated for 3 weeks prior and 4 weeks after cardioversion.
3. Prevention of thromboembolism - The risk for thromboembolic stroke is about 1% per year for low risk patients and greater than 5% per year for high risk patients. Aspirin is sufficient for low risk patients while coumadin is needed for all others who do not have a contraindication. Usually a quarter or more of the patients with AF are at high risk. Markers of High risk are:
   • History of Hypertension
   • Prior stroke or TIA
   • Diabetes
   • History of CHF
   • Age greater than 65