There seems to be discrepancy when it comes to MVP murmur intensity.
So my understanding is that MVP is a fundamental problem of "properly closing" the valves due to redundancy of glycosaminoglycans. In other words, there's too much of crap so you can't precisely get them to kiss each other upon closure.
In increased preload situtation (i.e. squatting), increased volume expands the ventricle, makes more room for the leaflets, which allows them to close properly. As the volume of the ventricle is reduced, the leaflets become "floppy" again which make them prolapse and produce the "click". The onset of click is later in the systole compared to decreased preload situation.
Now what happens to the intensity of the MVP murmur in high preload vs. low preload situation?
So my understanding is that MVP is a fundamental problem of "properly closing" the valves due to redundancy of glycosaminoglycans. In other words, there's too much of crap so you can't precisely get them to kiss each other upon closure.
In increased preload situtation (i.e. squatting), increased volume expands the ventricle, makes more room for the leaflets, which allows them to close properly. As the volume of the ventricle is reduced, the leaflets become "floppy" again which make them prolapse and produce the "click". The onset of click is later in the systole compared to decreased preload situation.
Now what happens to the intensity of the MVP murmur in high preload vs. low preload situation?