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  • While the aortic valve serves as the gateway to the systemic circulation, the mitral valve is a one-way door to the left ventricle (LV). When intact, the mitral valve makes sure that a stroke volume's (SV) worth of blood is delivered to the LV. Should the valve be too tight as in mitral stenosis (MS), the LV is underloaded reducing the SV (Video 7–1A, 7–1B, 7–1C). Moreover, the narrowed mitral valve 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 the development of atrial fibrillation, pulmonary edema, and right ventricular failure. Consequently, these conditions make the anesthetic management of the MS patient for mitral valve (MV) replacement most challenging.
  • When the mitral valve 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 retrograde 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 infraction or due to the destruction of the valve during mechanical trauma or by 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.

Mitral Stenosis

The normal area of the MV is 4 to 6 cm2. Isolated narrowing of the MV is frequently associated with rheumatic heart disease.1 MS is more likely to occur in female compared to male patients by a ratio of 2:1. Calcification of the MV independent of rheumatic heart disease occurs infrequently. However, MV calcification can occur in dialysis-dependent chronic renal failure patients. As the rheumatic process progresses the valve area declines leading to an increased pressure gradient between the LA and the LV during diastole. This increased gradient drives diastolic filling of the LV as blood is pushed forcefully through the stenotic MV orifice.

As the gradient progressively increases and mitral valve area falls below 1.5 cm2, patients become increasingly symptomatic. Pressure gradients between the LA and LV can become greater than 25 mm Hg. Patients frequently become dyspneic as the high LA pressure is transmitted to the pulmonary ...

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