Aortic Stenosis

Aortic Stenosis

1. The etiology is usually progressive calcification and narrowing of a tricuspid or bicuspid valve. A valve area less than 1.0 cm² or mean gradient greater than 40 mm Hg defines severe stenosis. Mild stenosis is defined as a valve area of greater than 1.5 cm² or mean gradient of less than 25 mm Hg. Moderate stenosis is defined as a valve area between 1.0 and 1.5 cm² or a gradient between 25 and 40 mm Hg.
2. Symptoms of angina, syncope, or heart failure develop late in the disease process. In the absence of surgical intervention, the average survival is 2 to 3 years following the onset of symptoms.
3. PathophysiologyThe ventricle becomes hypertrophied and stiff in response to the increased pressure load. Coordinated atrial contraction becomes critical to maintaining adequate ventricular filling and stroke volume. The ventricle is susceptible to ischemia due to increased muscle mass and decreased coronary perfusion in the setting of increased intraventricular pressure.
4. Anesthetic considerations. Aortic stenosis is the only valvular lesion associated with an increased risk of perioperative ischemia, MI, and death.
   1. Normal sinus rhythm and adequate volume status should be maintained.
   2. Avoid systemic hypotension. Hypotension should be treated immediately and aggressively with an α-agonist such as phenylephrine to maintain adequate coronary perfusion pressure.
   3. Avoid tachycardia. Tachycardia results in increased oxygen demand along with a shorter period of diastole leading to decreased coronary perfusion and reduced cardiac output. Severe bradycardia can lead to reduced cardiac output and should be avoided as well. Cardiac pacing capabilities should be considered to treat severe bradycardia. Supraventricular tachydysrhythmias should be treated aggressively with direct current cardioversion.
   4. Nitrates and peripheral vasodilators should be administered with extreme caution.
   5. The treatment of ischemia in these patients is directed at increasing oxygen delivery by raising coronary perfusion pressure and decreasing oxygen consumption (by increasing blood pressure and lowering heart rate).