Aortic stenosis is the most common cardiac valve lesion in the United States. The underlying cause is progressive calcification and sclerosis of the aortic valve leaflets, due either to a congenital condition (Bicuspid Aortic Valve is found in 1-2% of the population), or as a natural part of the ageing process. The classic triad of symptoms is angina, syncope, and congestive heart failure. Chronically, the pressure gradient between the left ventricle and aorta results in LV hypertrophy. Decreased diastolic compliance makes atrial systole crucial to ventricular filling. Up to 40% of the total cardiac output may come from the “atrial kick” in patients with AS making normal sinus rhythm a primary goal in its management. For this reason, atrial fibrillation is clearly detrimental to patients with AS.
Atrial fibrillation is a narrow-complex tachyarrhythmia characterized by a rapid and irregular atrial focus (atrial rate of 350 to 500 beats/min and ventricular rate of 60 to 170 beats/min). The treatment of atrial fibrillation is similar to that of atrial flutter, and includes rate control, conversion to sinus rhythm, and/or anti-coagulation. Treatment also depends on whether the atrial fibrillation is acute or chronic, and if the patient is stable or unstable. Rate control can be obtained with either beta-blockers (e.g. esmolol) or calcium channel blockers (e.g. diltiazem). Beta blockers and CCBs are also effective in prevention of atrial fibrillation. Digoxin is more useful for chronic atrial fibrillation since it is difficult to achieve therapeutic levels quickly. In the stable patient, amiodarone, sotalol, or procainamide may be used to achieve conversion to sinus rhythm. Amiodarone may be a more suitable option in acute management because it causes less cardiac depression. Synchronized DC cardioversion can also be used for conversion to sinus rhythm, and is the preferred treatment for patients with hemodynamic instability. Caution is advised with conversion to sinus rhythm when atrial fibrillation has persisted over 48 to 72 hours due to the possibility of thromboembolism. In non-emergent cases, transesophageal echocardiographic examination can be used to rule out atrial thrombi or the patient should be adequately anticoagulated for 3 to 4 weeks.
- Up to 40% of total cardiac output from “atrial kick”
- Treatment goals: Sinus rhythm, Increased preload, Increased afterload
- Avoid: Hypotension, Tachycardia, Bradycardia
- Rate control: beta-blocker, calcium channel blocker
- Cardioversion: amiodarone, sotalol, procainamide, synchronized DC cardioversion (TEE to rule out clot or anti-coagulation)
- Unstable – synchronized DC cardioversion
- Miller, RD et al. Miller’s Anesthesia, 7th edition, Churchill Livingstone. 2009
- Kaplan, JA et al. Essentials of Cardiac Anesthesia, 1st edition, Saunders. 2008