in Aortic Regurgitation there is a pooling of blood from both aorta and right atrium into right ventricle, so blood volume in right ventricle increases and it should generate a huge pressure over the tricuspid valve so there should be a LOUD S1 but rather we find a SOFT S1 ? Any Explanation For SOFT S1 ?
explained it as due to premature closure of AV valve in Aortic regurgitation.
What I understood, may b wrong, was like for loud S1 we need to close AV valve with higher force. Now in AR at end diastole the vol of blood in ventricle(EDV) is more than normal. Now as AV is open, the gradient between atrium and ventricle will be less than normal as EDV is more. And as the grad is less the AV valve leaflets are less open than normal as more will be grad more open will b the valve. If we take the valve orifice-valve leaflet angle to be theta. Then the angle theta is less in AR.
Now as soon as the sustole starts valve has to slam through that angle theta. So angular displacement is theta And the angular velocity will be omega, and that will be proportional to theta. This omega will be less in AR. And at end of slamming the kinetic energy=1/2× moment of inetria× square of angular velocity, will also be less for AR.
Now when the valve closes, this kinetic energy changes into sound energy. This sound energy generated will be less in AR. So I think that may b the explanation of soft s1
What I understood in S1 gen was like.
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At first we need widely opened AV valve before systole starts(this is decresed in AR ans increased in Short PR)
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Then we need adequate change rate of ventricular cavity size or in other words inotropy(which decreses in myocarditis, ischemia etc etc)
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Then we need adequate rate of pressure generation due to this vol change(which is jeopardized in MR)
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And then finally we need adequate coaptation of AV valve (which is jeopardized in calcific degeneration of AV valve)
Due to inc. LV pressure in AR, there is premature closure of AV valve so soft S1