Afterload and LVOT Obstruction in HCM

[IveGotTwins]

Can someone answer something for me? I'm reading about cardiomyopathies and cannot find an answer for why increasing afterload improves LVOT obstruction and decreasing afterload exacerbates it. I would think that an increased afterload would promote mitral regurgitation that accompanies HCM and decrease the overall CO.

I'm reading Anesthesia and Co-Existing Disease. Perhaps there is a better source for this question?

Thanks.

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[fakin' the funk]

I'm reading Anesthesia and Co-Existing Disease. Perhaps there is a better source for this question?

FWIW, Kaplan very much glosses over (de-emphasizes) MR in HOCM and instead emphasizes this thing aboout the LV-to-aorta pressure gradient.

It says that maintaining afterload/SVR high keeps this LV-to-aorta pressure gradient low, which minimizes the LVOT obstruction by minimizing the Venturi/SAM action.

Hope that helps.

 

[MD Dreams]

Keeping high svr (after load) keeps the left ventricular outflow tract open preventing the hypertrophic heart from collapsing in on itself and causing further obstruction. Think of a balloon filled with water. As long as you've got the end of it pinched (high after load, high svr) it will stay filled. As soon as you release the end of it, the balloon (heart) collapses. Not the most accurate analogy but may help get the point across.

 

[sevoflurane]

A couple of things to add to increased SVR.

Good preload (volume) and afterload (SVR/neo)
Avoid increased contractility to avoid dynamic obstruction (they should be on a beta blocker)
Avoid tachycardia (ephedrine, pain, hypovolemia)

 

[DrBeaker]

Dropping a TEE probe and actually seeing the obstruction followed by relief with increased preload/afterload, decreased heart rate is very awesome too. This is a dynamic process, meaning it can change at any moment, TEE is great for keeping an eye on it.