nbmeanswers.com will be going offline for ~hour for some updates! we’ll be right back! --the webmaster (2:17am) ❤️

NBME 24 Answers

nbme24/Block 3/Question#31

A 65-year-old man is brought to the emergency ...

Systemic vascular resistance: increased;
Pulmonary vascular resistance: decreased;
Pulmonary capillary wedge pressure: increased


Login to comment/vote.

 +3  upvote downvote
submitted by keycompany(103),

Answered my own question. Increased stress from a STEMI will activate the sympathetic nervous system -- Pulmonary vasodilation.


 +0  upvote downvote
submitted by louisville(6),

Answer: SVR increased; PVR decreased; PCWP increased.


 +0  upvote downvote
submitted by keycompany(103),

Can somebody who understand why PVR decreases with a Left-Sided infarct please enlighten me. I would also appreciate it if you could relate it to right sided heart failure too (i.e. how would it change).

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. +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. +  

 +0  upvote downvote
submitted by mousie(74),

if your CO falls ... wouldn't that cause vasoconstriction in the lung vasculature? hypoxia induced vasoconstriction?

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. +3  
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 +  

 +0  upvote downvote
submitted by usmleuser007(84),

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


 +0  upvote downvote
submitted by yb_26(28),

My simple understanding is that pt's heart contractility is decreased due to MI => heart can't pump a lot of blood => increased backup flow into pulmonary vasculature => increased PCWP.

More blood in pulmonary vasculature => they will dilate in order to just keep all these blood => decreased pulmonary vascular resistance

Decreased cardiac output => peripheral vasoconstriction => increased systemic vascular resistance