Cardiovascular Physiology Concepts
                                    Richard E. Klabunde, Ph.D.

Valvular Insufficiency (Regurgitation)

Valvular insufficiency results from the valve leaflets not completely sealing when the valve is closed so that regurgitation of blood occurs (backward flow of blood) into the proximal chamber. 

Aortic regurgitation occurs when the aortic valve fails to close completely and blood flows back into the left ventricle after ejection into the aorta is complete (after S₂). Normally, there is a brief period of time after the aortic valve closes when the ventricle relaxes isovolumetrically (the mitral valve is also closed during this phase). But when the aortic valve is leaky, the ventricle begins to fill from the aorta after the incomplete closure of the aortic valve. This leads to an increase in ventricular volume prior to the opening of the mitral valve and normal ventricular filling. Because blood is leaving the aorta in two directions (back into the heart as well as down the arterial network), the aortic diastolic pressure falls more rapidly thereby leading to a decrease in arterial diastolic pressure.  Because the ventricle fills from both the aorta and the left atrium, there is a large increase in left ventricular volume and pressure (increased preload), which is best depicted by pressure-volume loops for this condition. The increased preload causes the left ventricle to contract more forcefully (Frank-Starling mechanism), thereby increasing ventricular (and aortic) systolic pressure and increasing stroke volume to help compensate for the regurgitation. The increase in ventricular end-diastolic pressure, however, also leads to an increase in left atrial pressure, which can result in pulmonary congestion and edema. Regurgitation, coupled with enhanced left ventricular stroke volume, results in a characteristic widening of the aortic pulse pressure. The backward flow of blood into the ventricular chamber during diastole results in a diastolic murmur between S₂ and S₁.

Early in the course of regurgitant aortic valve disease, there is a large increase in left ventricular end-diastolic pressure and left atrial pressure. The ventricle and atria function on a stiffer portion of their compliance curves so that the increased volume results in a large rise in pressure.  With long-standing regurgitation, the ventricles and atria dilate so that the increased volume does not result in an exceptionally large increase in pressure. In other words, remodeling of the chambers results in increased compliance and more normal filling pressures.

Pulmonary valve regurgitation has a similar hemodynamic basis as aortic regurgitation except that the changes in pressures and volumes are noted on the right side of the heart (pulmonary artery, right ventricle, and right atrium).

Mitral valve regurgitation occurs when the mitral valve fails to close completely, which causes blood to flow back (regurgitate) into the left atrium during ventricular systole (between S₁ and S₂). The backward flow results in a holosystolic murmur. Because the left atrium now receives blood from the ventricle as well as from the pulmonary veins, there is a large increase in the v-wave as the left atrium fills. The regurgitation reduces the net stroke volume of the ventricle into the aorta, although total ventricular stroke volume defined as the end-diastolic minus the end-systolic volume increases. Changes in ventricular pressures and volume are best depicted using pressure-volume loops. Increased blood volume in the left atrium enlarges the atrial chamber and increases the atrial pressure.  The left atrium compensates by increasing its force of contraction through the Frank-Starling mechanism in order to enhance ventricular filling. However, the increased atrial pressure can lead to pulmonary congestion and edema.

In in the course of chronic mitral regurgitation (or after sudden regurgitation caused by rupture of the chordae tendineae or papillary muscle dysfunction), the atrial pressure can become very elevated.  In long-standing mitral regurgitation, the left atrium adapts to the larger volume by dilating, which increases its compliance. This remodeling can help to normalize the left atrial pressure.

Tricuspid valve regurgitation has a similar hemodynamic basis as mitral regurgitation except that the changes in pressures and volumes are noted on the right side of the heart (pulmonary artery, right ventricle, and right atrium).

RK Revised 04/05/07

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.

© 1999-2007 Richard E. Klabunde, all rights reserved.