This patient is presenting with with STEMI (FA2019 p301), thus the entire vessel must be occluded. Coronary vasospasm via a1 stimulation (increased smooth muscle contraction) would lead to these findings.
As far as the nitro aspect, I think this could be referring to pt history of ischemic heart disease, and the scenario of coronary steal, however I don't think you would need that to answer this question (and I could be going down an unnecessary rabbit hole of misery).
Other helpful pages are FA2019 p238, a1 sympathetic stimulation results in increased vascular smooth muscle contraction.
Last, big ups to the brother for setting arguments aside and still taking his hermano to the emergency department. Perhaps they were arguing at who responded to COVID-19 and medical education worse: USMLE or Prometric.
chaosawaitsWho else got a little distracted by the tragic story of watching your brother have a heart attack because of an argument you were having with him and then had to refocus to get this question?+
an1wouldn't coronary vasospasm refer to prinzmetal angina? can someone go over the other options?+
neurotic999The way I approached it was, since they specifically asked about the role that the argument played in developing the symptoms, it seemed as though they were pointing in the direction of vasospasm rather than an occlusive cause like atheroemboli, ruptured plaque, etc. So I looked at the options with that in mind.
Some of the options were blatantly wrong:
-vasospasm d/t beta (beta is vasodilatory)
-increased afterload d/t beta (beta 2 would cause vasodilation, decreasing afterload. beta 1 would increase hr but I don't think it alone is enough to increase afterload)
-negative chronotropy d/t alpha (that would be a beta blocker)
-positive inotropy d/t b2 (that would be beta 1, not 2)
The one I wasn't sure about was decreased perload d/t alpha1 stimulation. I was thinking decreased preload, hence decreased blood in the coronary circulation. But it didn't seem convincing enough to cause an MI. Plus not sure if alpha stimulation decreases preload to begin with. +
neurotic999If the ST elevation part of it throws you off, FA2019 301 says prinzmetal angina has transient ST elevation.+1
submitted by โpeteandplop(42)
This patient is presenting with with STEMI (FA2019 p301), thus the entire vessel must be occluded. Coronary vasospasm via a1 stimulation (increased smooth muscle contraction) would lead to these findings.
As far as the nitro aspect, I think this could be referring to pt history of ischemic heart disease, and the scenario of coronary steal, however I don't think you would need that to answer this question (and I could be going down an unnecessary rabbit hole of misery).
Other helpful pages are FA2019 p238, a1 sympathetic stimulation results in increased vascular smooth muscle contraction.
Last, big ups to the brother for setting arguments aside and still taking his hermano to the emergency department. Perhaps they were arguing at who responded to COVID-19 and medical education worse: USMLE or Prometric.