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regurgitant fraction =
Volume of MR Total LV stroke volume
oratio rises when the resistance to aortic outflow is increased
Extent to which LA pressure rises in response to regurgitated volume is determined by LA compliance.
Acute MR: ex: caused by sudden rupture of chordae tendineae
LA compliance undergoes little change, so have a stiff chamber that causes great inc in LA pressure along with the inc in LA volume. Inc pressure helps prevent further regurgitation, but it is also transmitted to the pulmonary circulation…resulting in rapid pulmonary congestion and edema.
Measure LA pressure in acute MR and see a prominent “v” wave, which shows the increased LA filling during systole…
Chronic MR: gradual development allows for LA to undergo compensatory changes to lessen the effects of regurgitation on the pulmonary circulation. oLA dilate to accommodate larger volumes without inc in pressure. oGet inadequate forward cardiac output because the LA becomes a low pressure sink for LV ejection compared to the high pressure aorta.
oMain symptoms of chronic MR are those of decreased forward CO – fatigue and weakness oLA enlargement predisposes to atrial fibrillation oLV undergoes gradual compensatory dilatation (eccentric hypertrophy – hypertrophy of wall with dilatation of
cavity) in response to volume load oForward output preserved to near-normal through Frank-Starling mechanism (maintaining high SV). oOver time, chronic volume overload results in poor LV systolic function and poor forward CO Æ symptoms of
pulmonary venous pressure
low forward cardiac output
Summary Table for Acute vs. Chronic MR:
To the right is a Frank-Starling diagram highlighting the relationship between increased venous filling (inc volume and pressure) and stroke volume. This is how the forward CO is preserved in Chronic MR in spite of the enlarging LV.