Question about regurgitation/passive filling and end diastolic volumes

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Corporal_cavernosum

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I'm having trouble wrapping my mind around what seems like a straight-forward concept: but how does aortic regurgitation increase end diastolic volume? If the LV fills with a certain amount of blood based on the size of the chamber, how does regurgitation increase the amount of blood that can occupy it? Is the pressure of regurgitation enough to force more blood into the LV in excess of the amount of blood flowing in from the mitral valve during diastole? Why does aortic regurgitation increase EDV rather than simply filling the LV more quickly with no increase in EDV?

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After ventricular systole ends, there is ventricular relaxation without change in volume so that pressure drops lower than the pressure in the corresponding atria. After which opening of AV valves causes filling of blood in the LV based on "Pressure gradient" .
For simplicity sake, instead of imagining 80 ml from the atria and 30ml of regurgitant blood coming from the aorta, imagine 110ml flowing in directly from one source. Except, in each cycle the regurgitant blood adds to the volume flowing in ( increases above 110 ).
 
The LV getting blood both via the MV and the AV valve which increases end diastolic pressure --> to reduce pressure back to normal, the heart undergoes eccentric hypertrophy ie increased chamber size --> increased EDV.

If the heart only filled in faster rather than taking in extra volume, it would imply less blood entering from the LA. This blood pooling in the LA would increase LA pressure and be reflected to the pulmonary circulation --> RV --> RA. RA increasing its pressure would result in decreased venous return --> decreased CO --> heart must pump a greater amount of volume and to do so, the LV needs to take in more blood.

A more intuitive way to look at it is an inefficiency in the CO. Normally after ejection the AV closes and all the blood that the heart has ejected flows into the systemic circulation. With AR, some of the CO flows back into the LV, hence the actual CO is lower. The only way to compensate would be to pump out an initial, higher volume.
 
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If the LV fills with a certain amount of blood based on the size of the chamber
Is this correct?

I believe it's as simple as this; increased EDV means volume overload (increased preload) which in the long term will lead to the adding of new sarcomeres in series (i.e. dilation or eccentric hypertrophy).

Consequently, compliance increases because of dilation.
 
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