Mitral Valve Prolapse

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aspiringmd1015

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you a get a softer midsystolic click with squatting because of increased systemic resistance--> increased afterload--> decreased LV empyting, so more volume of blood regurgitates back into the Left atrium, wouldnt a higher volume of blood make the intensity of the murmur louder?
 
you a get a softer midsystolic click with squatting because of increased systemic resistance--> increased afterload--> decreased LV empyting, so more volume of blood regurgitates back into the Left atrium, wouldnt a higher volume of blood make the intensity of the murmur louder?

Only in MR. In MVP the valves are big and floppy. When you increase preload you increase the stretch on the LV. Increasing the LV stretch results in the MV being pulled apart more. When the MV is pulled apart more, the huge leaflets you see in MVP are stretched out more and therefore will prolapse less, effectively making the valves function more like "normal" non-MVP valves --> less regurge.
 
okay and in MR, the increased EDV makes the murmur louder because increased turbulent blood flowing across the distorted valve causes a louder sound?
 
here's what I found:
http://www.blaufuss.org/HSM/TEXT/MVPMAN_txt.html

http://www.med.ucla.edu/wilkes/MVPmain.htm

remember that in mitral valve prolapse, the sub-mitral apparatus (chordae & papillary muscle) can't maintain the valve in a competent position --> hence, the prolapse. The prolapse occurs during Systole: when the left ventricle contracts to push blood out, the mitral valve should be closed shut, but in Mitral valve prolapse it's not - hence, blood goes into the left atrium, again: during systole.

It seems as though squatting increases the LV end-diastolic volume (preload) due to increased venous return--> this seems to strengthen the chordae thus preventing the prolapse from occurring.

From UCLA med:
" those maneuvers that increase venous return and diastolic filling (squatting) and thereby enhance the ventricular volume, help to maintain tension along the chordae and to keep the valve shut."

I'm not sure if my understanding is correct, so hopefully someone else can let us know if they have a better explanation.

Squatting mainly increases afterload. That's especially important in DiGeorge syndrome, where increased afterload decreases the R-->L shunt due to increased L-sided pressure.
 
you a get a softer midsystolic click with squatting because of increased systemic resistance--> increased afterload--> decreased LV empyting, so more volume of blood regurgitates back into the Left atrium, wouldnt a higher volume of blood make the intensity of the murmur louder?

We could first posit that more pressure is directed at the aortic valve over the mitral valve, since the shape of the LV is obviously designed to push blood through the former (i.e., we're not dealing with a uniform sphere). Therefore my guess would be that the expansile effects on the LV function such that increased volume corresponds to greater intrachamber pressure exerted at the aortic over the mitral valve, where decreasing volume increases the mitral/aortic "receptive pressure" ratio. This would result in a more salient MVP murmur when chamber volume is lesser.

However the reason this wouldn't apply to MVR is because the valve is already leaky so no threshold pressure (i.e., for the valve to pop back) is needed to cause the murmur, unlike MVP; in MVP, the threshold for murmur would be reached more quickly since the mitral/aortic receptive pressure ratio would be greater at lesser volume. In HOCM, which follows the same LV volume finding as MVP, I'd guess it would be a similar situation, where lesser volume means reaching the threshold more quickly for which the mitral valve obstructs the LV outflow tract.

I could be completely wrong, but those are my rationales.
 
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