Chapter 7: Mitral Valve Disease

Whereas the aortic valve serves as the gateway to the systemic circulation, the mitral valve (MV) is the doorway to the left ventricle (LV). Should the valve be too tight as in mitral stenosis (MS), the LV is under loaded reducing the stroke volume (SV) (Video 7–1A, Video 7–1B, Video 7–1C). Moreover, the narrowed MV prevents adequate drainage of the left atrium (LA) and the pulmonary circulation. With time, the LA dilates and pulmonary arterial (PA) pressures increase, leading to atrial fibrillation, pulmonary edema, and right ventricular failure. Consequently, these conditions make the anesthetic management of the MS patient for MV replacement most challenging.

When the MV becomes incompetent, it no longer functions to ensure the one-way, forward flow of blood during each cardiac cycle. As the LV contracts during systole, blood can be ejected forward through the aortic valve (AV) into the systemic circulation, or the blood can flow backward into the LA via the leaky MV. Like aortic regurgitation (AR), mitral regurgitation (MR) can develop both acutely or exist chronically. Patients with chronic MR develop compensatory mechanisms, which permit them to eject a sufficient SV into the systemic circulation to maintain circulatory function. Conversely, the patient with acute MR lacks adequate compensatory mechanisms. Acute MR frequently presents secondary to papillary muscle dysfunction or rupture following myocardial infarction or due to the destruction of the valve by mechanical trauma or infectious processes. As such, the acute MR patient usually presents in cardiogenic shock as the SV ejected into the systemic circulation is inadequate to meet the patient’s metabolic demands. Additionally, acutely increased pulmonary artery pressures contribute to the development of pulmonary edema in the MR patient.