Why no preload reducers/vasodilators with RV MI?

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engineeredout

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I guess I'm having trouble conceptually wrapping my mind around this. We've been continuously told that we are to not use preload reducers or vasodilators such as nitro or morphine on pts with suspected RV infarct, but I'm not fully sure why.

I would figure that more preload = more work demand on infarcted RV. Is it because less preload on already strained RV would lead to decreased RV output and all sorts of respiratory badness?
 
Your thought process is mostly correct. Reducing preload in the setting of an acutely dysfunctional RV can lead to decreased left ventricular filling, decreased cardiac output, and circ collapse. Bad times.

Essentially in right-sided MI you want to preserve CO while not burning excess muscle. That's why you avoid RV afterload increase, so as to keep the RV pumping as needed but not making it strain any more than needed.
 
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