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The cardiac valves permit efficient forward blood flow while preventing backflow, in turn creating unidirectional forward cardiac output. Valve disease leads either to reduction in orifice area (stenosis), impeding forward flow, or to incompetence, permitting either regurgitant flow or a combination of these effects. Valve stenosis exerts a pressure overload on the ventricle behind the stenotic valve because that chamber must generate increased pressure to drive the bloodstream past the narrowed orifice. Valve incompetence exerts a volume overload on the affected ventricle, which must enlarge to compensate for the forward flow that is lost to regurgitation. The effects of these overloads on ventricular function and geometry are dealt with in subsequent chapters. This chapter focuses on the evaluation of valve lesion severity and the effects of valve disease on hemodynamics.
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Usually in early diastole, there is a small gradient across the mitral valve that initiates filling and then rapidly dissipates (Fig. 8-1A).1 Indeed, the normally opened mitral orifice is 4 to 5 cm2, which creates a functionally single chamber of left atrium and left ventricle (LV) during diastole; thus, pressures in both chambers are equal. Mitral stenosis, which is usually caused by rheumatic heart disease, reduces orifice area, in turn causing a gradient between left atrium and LV. Mitral stenosis eventually leads to pronounced hemodynamic effects, although little hemodynamic disturbance develops until orifice area is compromised to less than half its normal size. As stenosis worsens, the pressure gradient between left atrium and LV becomes larger and longer in duration (Fig. 8-1B). This gradient is added to normal left atrial pressure, causing left atrial hypertension, eventually leading to pulmonary congestion. As mitral stenosis worsens further, reduced valve aperture impairs LV filling, limiting cardiac output. Thus, despite usually normal LV muscle function, the hemodynamics are those of LV failure. Although left atrial contraction assists late atrial emptying, most transmitral flow occurs early in diastole, and much of the propellant force creating the pressure driving blood across the valve ultimately is derived from the right ventricle. Therefore, it is this chamber that is pressure overloaded by the disease. Still further stenosis of the mitral valve causes secondary pulmonary vasoconstriction, reinforcing and worsening pulmonary hypertension and right ventricular pressure overload.
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