Aortic Stenosis


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Aortic Stenosis

Rheumatic heart disease and calcification deposits due to age (senile calcific aortic stenosis) are the most common pathologic conditions associated with aortic stenosis.  Congenital malformations such as a bicuspid aortic valve with a small annulus, or unicuspid valve usually develop symptoms at an early age but occasionally surface in later years.  Calcification of the valve eventually develops in all stenotic aortic lesions including congenital defects.66  The normal valve diameter is 2-3 cm2 and essentially no change in cardiac output develops until the lesion narrows to 1 cm2 or less.


Patients with aortic stenosis usually present at middle age with angina, syncope, and congestive heart failure.  Aortic valve replacement or repair is indicated for patient survival as a result of ventricular non-compliance, increase in left ventricular end-diastolic pressure, and narrowing of the aortic valve.  This outflow tract obstruction leads to left ventricular pressure overload, and an essentially fixed cardiac output.
Left ventricular hypertrophy compensates for aortic stenosis by maintaining cardiac output.  Concentric development reduces wall stress but decreases compliance resulting in an increase in filling pressures, increased ventricular work load and increased myocardial oxygen demand.  Ventricular dilation occurs when myocardial contractility is depressed.  Subendocardial ischemia due to wall thickening can occur even in the presence of normal coronary circulation.  Wall and fiber stretching may lead to arrhythmias, and malposition of the structures supporting the aortic valve.


Anesthetic management should anticipate the loss of sinus rhythm associated with diminished atrial contraction.  If cardioversion becomes necessary, it should be cautioned that closed chest massage (CPR) and defibrillation may prove ineffective because external compression may impede subendocardial and midcardial blood flow already compromised from a thickened ventricle.10  Attempts should be forwarded to maintain systemic pressures close to the patient’s pre-induction baseline, maintain volume in the heart, and to avoid inotropic stimulation.  Tachycardia must be avoided to ensure that the valve gradient is not increased and that oxygen demand is not heightened.

Air embolus in patients undergoing aortic valve replacement is a consideration once separated from cardiopulmonary bypass.  Dislodgement and migration of entrapped air to the right coronary artery can lead to sudden heart block, right ventricular depression, and ischemic changes in leads II, III, and aVF.  The right coronary artery is most susceptible to entraining air emboli due to it’s uppermost position while the patient is supine.  Cerebral embolism is at risk when the patient’s head is elevated.      Prior to closure of the left ventricle the patient should be placed in trendelenberg position, the ventricle should be filled by the perfusionist, the heart should be vigorously massaged, and the anesthesia team may be asked to provide positive intrathoracic pressure by ventilation, to ensure removal of air from the ventricle.  Transesophageal echocardiogram is essential for documentation and assessment of air extracted from the ventricle.

Conduction disturbances during the postoperative period are particularly significant for patients undergoing aortic valve replacement and may manifest as new arrhythmias or develop into complex ventricular ectopy possibly leading to ventricular tachycardia.  Utilization of a temporary pacemaker becomes an essential clinical tool under these circumstances.

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Lewis KP. Early intervention of inotropic support in facilitating weaning from cardiopulmonary bypass: The New England Deaconess Hospital experience.     Journal of Cardiothoracic and Vascular Anesthesia. 1993;7(Suppl 2):40-45.

Tse J, Cimini C, Kedem J, Rodriguez E, Gonzalez M, Weiss HR. Role of ischemia-reperfusion on myocardial cyclic AMP and cyclic AMP phosphodiesterase: Effects of amrinone on regional myocardial force and shortening. Journal of     Cardiothoracic and Vascular Anesthesia. 1993;7:566-572.

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