MAP in valve dysfunction

[tomtom1287]

in Aortic stenosis, why MAP is not decreased as less volume is ejected, and why baroreceptor not stimulated and no reflex increase in contractility/hr

In Mitral Regurgitation, I would expect MAP to decrease as ejection fraction is decreased but it doesn’t change. here as well not much reflex increase in contractility/hr

Why is that?

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[zhopv10]

With aortic stenosis you get adaptations that allow it to maintain EF for quite awhile usually (leads to LV hypertrophy etc). So basically there is increased afterload so you compensate by making the heart work harder but maintain the SV/EF for the most part.

Mitral regurg you actually have an increased EF usually (remember it is defined as end diastolic-end systolic volumes. Since the open mitral valve represents a path of less resistance you you essentially decease afterload and eject more (albeit a good bit of that is going to the LA). So now again that increase in fluid in the LA leads to increase preload this then will help compensate for the loss to the LA and you will maintain MAP if the heart can compensate. After awhile you can get LV dilation and resulting failure leading to a decreased EF and start effecting things but as long as it's in a compensated state output will be maintained.


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[deleted763299]

Since you asked about MAP specifically, recall the equation for mean arterial pressure (MAP): MAP = CO x SVR

So MAP can be maintained by increasing systemic vascular resistance (SVR) even if cardiac output (CO) decreases.

 

[tomtom1287]

With aortic stenosis you get adaptations that allow it to maintain EF for quite awhile usually (leads to LV hypertrophy etc). So basically there is increased afterload so you compensate by making the heart work harder but maintain the SV/EF for the most part.

Mitral regurg you actually have an increased EF usually (remember it is defined as end diastolic-end systolic volumes. Since the open mitral valve represents a path of less resistance you you essentially decease afterload and eject more (albeit a good bit of that is going to the LA). So now again that increase in fluid in the LA leads to increase preload this then will help compensate for the loss to the LA and you will maintain MAP if the heart can compensate. After awhile you can get LV dilation and resulting failure leading to a decreased EF and start effecting things but as long as it's in a compensated state output will be maintained.


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thank you so much, so the increased ventricular systolic pressure in aortic stenosis is not due to increased contractility, but due to increased contraction to overcome the increased resistance?

 

[zhopv10]

Ya so you have to generate more force to get the valve open so this increases pressure, it's as if the pressure in the aorta were to be increased, you would have to produce more pressure in the LV to get the leaflets open. So it acts similar to HTN in a sense (and you see LV hypertrophy in both). I suggest checking out a pressure volume loop of aortic stenosis and walking through it, it will help reinforce the concept.


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