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NBME 24 Answers

nbme24/Block 3/Question#31 (46.9 difficulty score)
A 65-year-old man is brought to the emergency ...
Systemic vascular resistance: increased;
Pulmonary vascular resistance: decreased;
Pulmonary capillary wedge pressure: increased
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 +8  upvote downvote
submitted by yb_26(191),
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susyars  The question says “ST elevation in the anterior leads“ so, in some way I was thinking of the most anterior part of the heart which is the right ventricle, and not the left one. +1  
makinallkindzofgainz  Anterior STEMI = ST elevations in V3, V4 which is supplied mostly by the LAD. RV is mostly supplied by the RCA, which would show up on an EKG with ischemic changes in II, III, and avF +4  
qiss  Btw increased PCWP indicates increased blood in the left atrium, not necessarily increased blood in the pulmonary vasculature see here. +  



 +6  upvote downvote
submitted by keycompany(268),
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pathogen7  Just to add, CHRONIC heart failure is a cause of pulmonary hypertension. So in the acute setting, pulmonary edema leads to decreased PVR, while in the chronic setting, it can lead to increased PVR, I think? +  
hungrybox  This doesn't make sense. Activating the sympathetic nervous system would cause bronchodilation (via β2) but it's unclear to me whether it would constrict the blood vessels (via α-1) or dilate them (via β2). +  



 +6  upvote downvote
submitted by hungrybox(791),

I really didn’t understand this question even after reading all the answers here so I emailed Dr. Klabunde (the expert)!

Here’s what he said:

This is a case of acute heart failure following an acute ischemic event (ST elevation in anterior leads). SVR increases because of neurohumoral activation, which helps to maintain BP. PCWP increases because acute HF causes blood to back up into the pulmonary circulation. Increased pulmonary blood volume causes all the pulmonary pressures to increase. PVR DECREASES because the pulmonary vasculature has a very high compliance, and therefore passively distends in response to increase volume. This passive dissension decreases the PVR.




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sheska  yes, in boards and beyond he explain this. extralveolar vessels= arteries and veins, intraalveolar vessels=capillaries. capillaries will increase resistance because will have more blood from backup of the left atrium and will get smudged => increase PCWP arteries and veins with more blood will open more and thus decrease pulmonary vascular resistance. +  



I was confused because UW 19280 says pulmonary artery systolic pressure will be increased to maintain forward movement of blood. How does this not lead to pulmonary vascular resistance being increased?

boostcap23  Pressure doesn't necessarily equal increased vascular resistance. Pulmonary resistance regulation mainly increases in areas of hypoxia, and decreases in well-oxygenated area's to send blood to well ventilated areas, nothing to do with an acute MI. In fact in MI there is vasodilation of apical capillaries and the V/Q ratio will approach 1 to accommodate the extra blood. In this patient, you can see his systemic blood pressure is low yet his systemic vascular resistance is high (due to sympathetic constriction of vessels in response to low CO). I just thought of it like how in normal resting state ventilation is wasted at the apex so in a volume overloaded state that extra blood could go up to the apex. +1  



 +1  upvote downvote
submitted by keycompany(268),
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sajaqua1  I believe that keycompany's answer comes the closest. In an MI, consider it as cardiogenic shock. The heart is a pump, and it is failing to move blood out of the heart and into vasculature. This is why PCWP increases. Because of insufficient output, the body has a sympathetic response. The catecholamines then cause vasoconstriction in peripheral vasculature to keep blood pressure up and continue flow, leading to increased SVR. Meanwhile, the sympathetic response causes vasodilation in the lungs; this would be an appropriate autoregulatory response, because the body is trying to keep up the flow of oxygen throughout the system. This decreases PVR. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5715548/ Is a pretty good article on this. Of course the binding of catetcholamines changes depending on saturation and the response is not perfectly understood. +10  
usmleuser007  My understanding is that the pulmonary circulation changes very little in terms of an acute MI. It is b/c pulmonary circulation has a lot more room to fill with blood much like the spleen in terms of blood accumulation. With higher volume of blood in pulmonary circulation, more blood vessels are able to be recruited specially the apex. With more recruited blood vessels = reduced pressure d/t circulation in parallel. +1  



 +1  upvote downvote
submitted by mousie(171),
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ug123  My take on this----His respirations are high-22/min--that will cause c02 washout---so actually lung has high oxygen---pulmonary vasodilation. Dont know if its right. +5  
usmleuser007  My understanding is that the pulmonary circulation changes very little in terms of an acute MI. It is b/c pulmonary circulation has a lot more room to fill with blood much like the spleen in terms of blood accumulation. With higher volume of blood in pulmonary circulation, more blood vessels are able to be recruited specially the apex. With more recruited blood vessels = reduced pressure d/t circulation in parallel +  



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