Aortic Regurg confusion

[theTruth_97]

so I thought I knew all about Aortic Regurg but I think I have confused myself- in aortic regurg I know that there is increased pulse pressure due to the increase in systolic pressure and the decrease in diastolic (since each time blood flows back there is a decrease in diastolic and that means more volume now in the ventricle so there will be a greater stroke volume which will lead to increase in systolic)

But with a greater volume now being present in the LV wouldn't that lead to eventual dilation of the chamber and would that not lead to systolic dysfunction and a decrease in contractility?

There was a Uworld question [238] that tells about a guy with head bobbing and immediately I knew it was AR. Then it asked like what feature is true about the problem the patient has- and the answer was widening of pulse pressure, which I know is correct (and i dont know why i didnt pick it lol) but I had answered it as "impaired left ventricle contractility"- is that not correct as well? I always though AR leads to eventual LV dilation which would lead to systolic dysfunction and problems with LV contractility

This may be a very simply concept but for some reason I have really confused myself. Any help will be appreciated

---

Members don't see this ad.

 

[Transposony]

You have to understand the concept of concentric hypertrophy v/s eccentric hypertrophy.

Volume overload leads to eccentric hypertrophy causing systolic dysfunction due to increased compliance.
Pressure overload leads to concentric hypertrophy causing diastolic dysfunction due to reduced compliance.

It's very well described here: http://en.wikipedia.org/wiki/Ventricular_hypertrophy

Also, learning cardiac Pressure-volume loop diagram will be very helpful to understand this.
http://www.cvphysiology.com/Cardiac Function/CF024.htm

 

[syoung]

Do you mean to switch diastolic/systolic dysfunctions? CVS just mentioned that diastolic dysfunction -> decreased compliance ?

also one way to remember increased compliance -> less stiff ventricle and decreased compliance -> more stiff

diastolic dysfunction means the ventricles are unable to relax properly and be filled, so if a ventricle has decreased compliance/is more stiff, you can imagine it's unable to be filled properly
systolic dysfunction means the ventricles are unable to pump blood out effectively, so if a ventricle has a widened chamber from volume overload leading to increased compliance/is less stiff, then it's difficult to pump out all that extra blood

 

[dfib slim]

You have to understand the concept of concentric hypertrophy v/s eccentric hypertrophy.

Volume overload leads to eccentric hypertrophy causing systolic dysfunction due to increased compliance.
Pressure overload leads to concentric hypertrophy causing diastolic dysfunction due to reduced compliance.

It's very well described here: http://en.wikipedia.org/wiki/Ventricular_hypertrophy

Also, learning cardiac Pressure-volume loop diagram will be very helpful to understand this.
http://www.cvphysiology.com/Cardiac Function/CF024.htm

Aortic regurg leads to eccentric hypertrophy due to the volume overload from the back flow which can eventually lead to systolic dysfunction and impaired LV contractility. I think reason the correct answer is widening pulse pressure over impaired LV contractility is he has the head bobbing which is from the hyperdynamic circulation. If he had impaired LV contractility, there wouldn't be a wide pulse pressure and no resulting head bobbing.

 

[Transposony]

I always though AR leads to eventual LV dilation which would lead to systolic dysfunction and problems with LV contractility

You are right. However, "eventual" being the keyword here since before LV dysfunction sets in there is normal SV and a normal left ventricular EF as the dilation and eccentric hypertrophy of the LV allows it to eject a larger stroke volume without requiring any increase in the relative shortening of each myofibril (sarcomeres in-series).
But eventually, these compensatory measures fail as the LV function deteriorates, the end-diastolic volume rises and the SV and EF decrease.
Basically if the heart cannot pump enough to compensate for the regurg then there will be no head bobbing as dfib slim explained above.

 

[Instatewaiter]

LV dilation can be relatively quick (within a few weeks). The main compensatory mechanism for AI is dilation, not hypertrophy. Because the dilation takes some time, acute AI is devastating because the ventricle has not dilated yet.

The AI will cause LV dysfunction in the long run and this is an indication to replace the valve (NYHA II and EF < 50%)- but I'm assuming they gave you a vignette of acute AI and this is a late finding.