A thorough understanding of the cardiovascular hemodynamics of valvular heart disease is essential to the medical, interventional, and/or surgical management of patients with heart valve disease. Understanding the pathophysiology of valvular heart disease requires knowledge of normal cardiovascular hemodynamics, the dynamic nature of those hemodynamics, and how abnormalities of hemodynamics affect overall heart function. This chapter describes in detail the cardiovascular hemodynamics of valvular heart disease, enabling the reader to understand the pathophysiology of valvular heart disease.
PHYSIOLOGY OF VALVULAR HEART DISEASE
Valve stenosis describes a valve that does not open fully. The orifice is narrowed or “stenotic.” The resultant physiologic abnormality is a pressure phenomenon. Additional pressure is required to force blood across the stenotic valve, resulting in pressure elevation in the chamber in front of the valve and a pressure gradient across the valve. Chamber hypertrophy is a more likely response to pressure abnormalities than chamber dilatation. Both can occur, but dilatation is slightly more likely in the atria than ventricles. The degree of pressure increase (and thus the gradient) is an indicator of severity of stenosis.
Valve insufficiency describes a valve that does not close completely, thus resulting in “leaking” of that valve with regurgitant flow retrograde across the valve. This is the only situation where flow is “backward.” The physiologic abnormality of an insufficient valve is a volume phenomenon. The volume of blood crossing the valve retrograde is the determinant of severity of valve insufficiency. That volume is difficult to measure accurately and often can only be estimated. The size (degree of dilatation) of the receiving chamber is helpful in determining the severity of the valve insufficiency.
Combined stenosis and insufficiency describes a valve that neither opens fully nor closes completely. A stenotic valve may have a mild or moderate leak. An insufficient valve may have some leaflet thickening, leading to impaired opening of that valve. Alternatively, a valve can have a “fixed orifice,” indicating equal degrees of impaired opening and closing. Of note, a severely stenotic valve cannot leak severely—a valve cannot leak more than it can open. The worst it can be is a fixed orifice valve.
The above physiologic descriptions pertain to chronic valve disease. Both pressure phenomena and volume phenomena have been present long enough to result in upstream and downstream compensation and physiologic adjustments to the abnormalities. The hemodynamics of acute valvular heart disease are different because the heart has not had time to adjust to or compensate for sudden malfunction of a valve. Acute insufficiency of a valve is more common than acute stenosis, but either can occur.
Acute valve stenosis can occur with a prosthetic valve when a leaflet or poppet becomes “stuck.” Acute inflammatory disease (eg, rheumatic, vasculitis, lupus) can result in rapid valve swelling and narrowing. Acute endocarditis will occasionally result in valve narrowing. Thromboembolic events may occasionally result in ...