Mitral Valve Prolapse (MVP) is a common condition where the two flaps of the mitral valve do not close smoothly, instead bulging backward into the upper left chamber of the heart during contraction. This structural change produces an abnormal heart sound, or murmur, often detected during a routine physical examination. The Valsalva maneuver, a specific breathing technique involving forced exhalation against a closed airway, is frequently used to diagnose and characterize heart murmurs. This diagnostic tool is particularly useful for MVP because it causes a unique response: the characteristic heart murmur becomes noticeably louder. Understanding this intensification requires examining the valve’s structure and the maneuver’s effect on blood flow.
The Mechanics of Mitral Valve Prolapse
The mitral valve is positioned between the left atrium (the heart’s upper collecting chamber) and the left ventricle (the main pumping chamber). Its primary function is to ensure blood flows only from the atrium into the ventricle, preventing backward leakage during contraction. The valve apparatus consists of two leaflets, anchored to the ventricular muscle wall by thin, fibrous cords called chordae tendineae.
Mitral Valve Prolapse occurs when one or both leaflets are abnormally thickened or redundant, often due to myxomatous degeneration. Instead of closing tightly, the excess tissue causes the leaflets to “billow” or prolapse into the left atrium during the heart’s systolic phase (contraction). This backward displacement defines the disorder.
When the leaflets prolapse, their edges may not meet perfectly, creating a gap that allows blood to leak back into the left atrium. This backward flow is termed mitral regurgitation, and the turbulent movement of blood generates the heart murmur. The characteristic sound of MVP is typically a mid-systolic click, caused by the sudden tensing of the chordae tendineae as the valve reaches its maximum backward excursion.
Following the click, the regurgitation produces a late-systolic murmur. The intensity and duration of this murmur depend on the severity of the prolapse. Since the underlying structure of the valve is fixed, any change in the volume or pressure within the left ventricle can alter the mechanics of the prolapse and thus the sound of the murmur.
Hemodynamic Changes During Valsalva
The Valsalva maneuver is performed by asking a person to exhale forcefully for about 10 to 15 seconds while keeping the mouth and nose closed. This forced expiration significantly increases the pressure within the chest cavity (intrathoracic pressure).
This rise in pressure mechanically compresses the large veins, impeding the flow of blood returning to the heart. This reduction in venous return causes a sharp drop in the volume of blood filling the ventricles. This phase of sustained straining is referred to as Phase II of the maneuver.
The volume of blood filling the ventricles at the end of the heart’s resting phase is known as preload. By impeding venous return, the Valsalva maneuver dramatically reduces this preload. A reduced preload means the left ventricle starts its contraction cycle with a smaller volume of blood than normal, leading to a temporary decrease in cardiac output.
The reduced volume effectively makes the left ventricular cavity smaller. This smaller ventricular size is the crucial link that explains the change in the MVP murmur. The altered hemodynamics create a low-volume state that directly influences the mechanics of the abnormal mitral valve.
Why Preload Reduction Intensifies the Murmur
The reduction in left ventricular volume caused by the Valsalva maneuver directly affects the geometry of the mitral valve apparatus. When the ventricle is less full, its internal physical dimensions shrink. This reduction in cavity size shortens the distance between the papillary muscles and the mitral annulus, where the leaflets are anchored.
Because the chordae tendineae have a fixed length, the shrinking ventricular size creates relative slack in the cords earlier in the contraction cycle. This slack allows the already “floppy” mitral valve leaflets to prolapse into the left atrium sooner than under normal filling conditions. This earlier and more forceful displacement increases the severity of the prolapse.
The mechanical consequence is two-fold. First, the mid-systolic click, which signals the chordae becoming taut, occurs earlier in the systolic cycle. Second, the subsequent mitral regurgitation begins sooner and lasts for a longer duration of the systolic period.
This longer duration of blood turbulence is perceived clinically as an intensification and prolongation of the late-systolic murmur. This distinctive response, along with the earlier click, helps physicians differentiate MVP from nearly all other heart murmurs, which typically decrease in loudness when preload is reduced.