USMLE afterload in Mitral Regurgitation

[Northerncardinal]

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Why does the afterload increase in chronic MR (with decompensated heart failure)?

I understand it decreases in acute MR adn may become normal in compensated chronic MR.

 

[Phloston]

Why does the afterload increase in chronic MR (with decompensated heart failure)?

I understand it decreases in acute MR adn may become normal in compensated chronic MR.

The question you're asking is open-ended but I'll try to keep it short and focused. Left atrial afterload will increase as the LV stiffens over time from needing to handle increased preload secondary to the regurgitant volume that will be added back during diastole. Preload is volume; afterload is more from muscular resistance. So the LA can experience the afterload only if LVH ensues chronically. The LV won't experience an afterload augmentation unless there's a pathological development at the semilunar valve or distal. USMLE likes that pulmonary edema is characteristic of acute MR because the LA hasn't had a chance to dilate and adapt; in chronic MR it has, so pulmonary symptoms are less salient. I've seen questions of the latter comparison in graph form, with two different lines, so attempt to visualize that, where PCWP increases more sharply per change in volume in the acute scenario.

 

[Saxappeal1]

So what you're saying is that with acute MR you'll have a more severely increased wedge pressure because the left atrium hasn't compensated for change that results from the MR, but with the chronic MR there is some adaptation of the left atrium to make the blood flow more fluid in the pulmonary artery resulting in a less sharply decreased wedge pressure?

 

[DrPicard]

Yes with acute MR the left heart gets overloaded with volume which increases pressure massively. This gets reflected backwards --> increased hydrostatic pressure in pulmonary capillaries --> pulmonary edema. With MR that develops slowly, the left heart adapts by dilating. Increased chamber size allows it to accommodate the larger volume without an increase in pressure.

This is why papillary muscle rupture post MI can lead to acute pulmonary edema, whereas MR resulting from something like RHD can remain asymptomatic for long periods of time.

 

[Saxappeal1]

Thanks DrPicard!