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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?
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?