Chronic atrial fibrillation

Chronic atrial fibrillation (A fib) has an incidence of 0.4% in the general population (approximately 10% of those more than 60 years of age) and many of these patients are admitted to intensive or intermediate care units for reasons unrelated to this diagnosis.

Chronic atrial fibrillation needs to be clearly differentiated from new-onset atrial fibrillation since the treatment and management strategies will differ.

Since Chronic atrial fibrillation or paroxysmal atrial fibrillation has a very low likelihood of converting to sinus rhythm and remaining in sinus, the primary strategy is rate control with agents that slow conduction through the atrioventricular (AV) node so that the patient does not experience a rapid ventricular response that may severely compromise cardiac output.

Patients with Chronic atrial fibrillation already have lost approximately 20% of their diastolic filling secondary to the loss of coordinated atrial kick at end diastole. A rapid heart rate that compromises diastolic filling time further can thus compromise cardiac output to the point of shock.

This may especially be true with patients who have diastolic dysfunction secondary to aortic stenosis and chronic hypertension. Commonly used agents include beta-blockers or calcium channel blockers. Digoxin was a mainstay of treatment in the past but is much less commonly used currently.

Pharmacological rhythm control, that is, converting atrial fibrillation to sinus rhythm, is not desirable in Chronic atrial fibrillation. Patients with Chronic atrial fibrillation may develop clot in the fibrillating atria, particularly in the atrial appendage.

Sudden conversion to sinus may lead to an embolus that can result in a stroke, myocardial infarction, gut ischemia, or limb infarction.

For this reason, patients with chronic atrial fibrillation, especially if it is paroxysmal in nature, are usually on anticoagulation therapy to reduce the risk of developing atrial clot. Agents that promote conversion to sinus rhythm such as amiodarone and procainamide are not used to acutely treat Chronic atrial fibrillation.

Treatment and management of new-onset atrial fibrillation falls into two primary approaches and practitioners vary as to which they subscribe to. The first, like Chronic atrial fibrillation, is rate control and the second is rhythm control.

So long as the patient has not been in atrial fibrillation for an extended period of time (generally more than 48 hours), the risk of having developed clot is judged to be low and conversion may be desirable.

This may be achieved electrically with synchronized cardioversion or pharmacologically with amiodarone or other agents. However, the natural history of new-onset atrial fibrillation is such that most patients (80%) will spontaneously convert on their own, usually within 2 weeks.

Several factors contribute to this, most notably the reasons most patients develop new-onset atrial fibrillation. Postcardiac surgical patients have some of the highest rates of new-onset atrial fibrillation (reportedly as high as 60%), presumably secondary to tissue damage associated with cannulation of the atrium during surgery.

General surgical patients also have a high incidence of this condition (as high as 40% in noncardiac thoracic patients) secondary to a variety of factors including atrial stretch induced by hypervolemia and circulating catecholamines.

Once these perturbations have resolved, so mostly does the Chronic atrial fibrillation. Because of this, many advocate that rate control is perfectly adequate in new-onset atrial fibrillation since it is usually a self-limiting phenomenon. Amiodarone, betablockers, and calcium channel blockers are good choices.

Rate control may be the goal (amiodarone will slow the rate) but conversion, whether spontaneous or pharmacological, is likely to be sustained at which time the drug may be weaned off.

For the unusual patient who remains in Chronic atrial fibrillation, one must then determine whether to switch to chronic rate control with long-term anticoagulation or consider electrophysiological studies and possibly ablation therapy.

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