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For some reason, I had two answers that I felt like both made absolute sense to me. As explained above, that totally came to my mind and I knew this was the case. When I thought about Metoprolol blocking B1 receptors in a patient with an ejection fraction of only 30%, I was thinking this could as well be a contraindication, not sure if it's an absolute one or relative. Now, am I right if I said that Beta-blockers are only contraindicated in acute decompensated HF? and can be used unless otherwise? Someone, please help me clarify this, so then this distinction can come clean in my thoughts. Thanks
I thought the same thing as you, I think we're just overthinking the most important thing - never give antihypertensive with Viagra lmfao. I totally thought too deep into it.
sildenafil does make sense, especially since hes on 2 vasodilators. I picked diltiazem because the pt has systolic heart failure. thought it was contra indicated to give CCB to systolic heart failure because you could further decrease contractility. Either way never give NTG and viagra
Yeah @topgunber I also picked diltiazem.... I guess they were looking for "COMBINATION" rather than a specific contraindication
@lee280 you are right in saying that beta blockers are only contraindicated in acute decompensated heart failure. this is because beta blockers, which would normally prevent the deleterious effects of neurohormones like norepinephrine on cardiac remodeling that occurs in HFrEF, will further impair cardiac output in decompensation. hope this helps :)
The answer to all your queries lies in the fact that a combination of Metoprolol and vasodilators would actually be beneficial in dampening the REFLEX TACHYCARDIC effect of nitrates, hydralazines etc. Hence, decreasing the work load on the heart.
submitted by ∗cassdawg(1778)
Sildenafil is a PDE5 inhibitor that runs the risk of causing hypotension in patients on nitrates due to the synergy of the mechanisms of action. [FA2020 p246]
Nitrates, like nitroglycerin, work by increasing NO production which in turn acts to increase cGMP in smooth muscle causing vasodilation. PDE5 inhibitors act by decreasing the breakdown of cGMP in smooth muscle, enhancing the action of NO to cause vasodilation. Thus, when combined there can be systemic vasodilation that leads to dangerous hypotension.