Valvular Regurgitation Flashcards
Regurgitant fraction/volume
severity of valvular regurg expressed as volume overload due to addition of regurg volume
What kind of hypertrophy occurs in adaptation to regurg?
eccentric hypertrophy minimizes increase in wall stress associated w/increase in diastolic volume and pressure via laplace –> increase wall thickness, increase mass, no change in relative wall thickness
How do the papillary muscles close valve leaflets?
they don’t –> they simply prevent the leaflets from going into the atria by holding them at tension against ventricular pressure (which actually closes them)
3 functional etiologies of regurg a la carpentier
- normal leaflet motion (annular dilation, perforation)
- increased leaflet motion (myxomatous, flail)
- decreased leaflet motion (rheumatic disease)
Etiology of myxomatous mitral valve disease
increased leaflet motion due to mitral prolapse or flail leaflet (chords ruptured)
*associated w/Marfan’s, eccentric mitral regurg (away from leaflet that prolapses)
Etiology of ischemic mitral regurg
- posteromedial papillary muscle more vulnerable to ischemia (single blood supply)
- MI causes thinning and dilatation of the wall –> asymmetric distortion of valve
What factors determine absolute volume of mitral regurg
- pressure gradient between LV/LA
- size of orifice area
- LV systolic ejection time and time orifice is regurgitant
*if parallel emptying into Ao and A, then possibility of lowering SVR might increase flow into systemic circulation (mostly when acute) –> but doesn’t really work b/c systemic pressure is so much higher than atrial pressure
What happens to LA pressure during acute MR?
increase
What happens to afterload during acute MR?
lower –> increases TSV
What happens to preload during acute MR?
increase due to return of RV (regurgitant volume), increased SV, increased LVEDP
What happens to ejection fraction during acute MR?
higher
What happens to forward stroke volume during acute MR?
lower
What happens to RF during acute MR?
increase –> regurgitant fraction should normally be zero
Compensatory changes in chronic MR
initial LV dilation increases EDV and total stroke volume –> eccentric hypertrophy serves to normalize wall stress
*the story is that in MR you get better contractility and contraction of the ventricle but you still have a reduced CO because a bunch of the blood is ending up in the LA instead of the Ao
Why are sarcomeres more stretched out in acute vs chronic MR?
chronic can remodel and add more in series to cause eccentric hypertrophy