Aortic Regurgitation : 101
Rheumatic fever, syphilis, arthritic diseases, or connective tissue disorders (Marfans syndrome), are the common causes for the development of aortic insufficiency (regurgitation).
Aortic insufficiency results in greater than normal forward stroke volumes as a result of normal antegrade flow, combined with additional regurgitant filling due to valve incompetence. This increase in forward volume contributes to a higher systolic component. Regurgitation occurs during diastole, contributing to low systemic diastolic pressures and higher left ventricular end-diastolic pressures. In conjunction with a reduced coronary perfusion gradient, diastasis can occur in cases of prolonged diastole. The equilibration of decreasing aortic diastolic pressure and increasing left ventricular end-diastolic pressures can lead to a zero or negative net flow.
Initial compensation for volume overload in the left ventricle is increased myocardial fiber length. This allows for increased left ventricular volume which helps to maintain the ejection fraction. The corresponding increase in ejection velocity and rapid decrease in myocardial wall tension results in lowered myocardial oxygen consumption.
Long term compensation manifests as increased wall tension. This leads to left ventricular thickening (hypertrophy) and ultimately results in decreased compliance and contractility. Higher end-diastolic pressures are transferred to the left atrium, yielding an overall reduction in stroke volume.
The degree of valvular incompetence, length of diastole, and pressure differences between the aorta and left ventricle during diastole, dictate the magnitude of backward filling. Cardiac output measurements utilizing thermodilution should be considered valid because the site of flow measurement in the right ventricle must equal the net flow from the left ventricle.
Anesthetic considerations may include the use of systemic arterial dilators to decrease peripheral vascular resistance, and promote forward flow, while in most cases leaving coronary perfusion unimpaired. Increasing the heart rate will diminish regurgitant flow, whereas hypertension will exacerbate the condition and manifest with an increase in pulmonary artery pressures. Efforts should be made to avoid bradycardia as lower diastolic pressures will result in decreased coronary blood flow, while allowing increased ventricular filling and higher end-diastolic pressures.
Ross AF, Gomez MN, Tinker JH. Anesthesia for adult cardiac procedures. In: Rogers MC, Tinker JH, Covino BG, Longnecker DE, eds. Principles and Practice of Anesthesiology. St. Louis, MO. Mosby Year Book; 1993;2:1649-1679.
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.