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free120/Block 1/Question#11 (24.6 difficulty score)
A 26-year-old man is brought to the emergency ...
Arterial baroreceptor firing rate: decreased;
Systemic vascular resistance: increased;
Pulmonary vascular resistance: increased;
Systemic capillary fluid transfer: absorption
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 +5 
submitted by benwhite_dotcom(465),
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tallerthanmymom  Another thing contributing to the increased SVR is increased SNS tone and decreased PNS tone. When BP is low --> Afferent BR firing decreased ---> Efferent SNS firing increases, and PNS decreases --> the inc in SNS tone stimulates a1 receptors ---> Inc SVR BUT, I don't understand what is causing the increase in the PVR because I always thought that inc SNS tone should be causing vasodilation in the lungs and that is why PCWP is decreased. +3  



 +3 
submitted by anu(4),
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ahtw about teh acsnerei in umarolypn aruacvls iessctrena ? tdeons WPPC llfa ni hmeghroacri oskhc

ibestalkinyo  I think this may have something to do with hypoxic vasoconstriction? +  
medguru2295  PCWP falls because there is less blood going into the Lungs and therefore, less blood coming out (decreased preload). However RESISTANCE is a measure of how difficult it is for blood to flow. That essentially means constriction. As stated above, it is likely hypoxic vasoconstriction as well as just global sympathetic attempt to maintain BP. If it said pressure in pulmonary arteries, it would likely be decreased as the vasoconstriction cannot full compensate the blood loss! +1  
medguru2295  PCWP falls because there is less blood going into the Lungs and therefore, less blood coming out (decreased preload). However RESISTANCE is a measure of how difficult it is for blood to flow. That essentially means constriction. As stated above, it is likely hypoxic vasoconstriction as well as just global sympathetic attempt to maintain BP. If it said pressure in pulmonary arteries, it would likely be decreased as the vasoconstriction cannot full compensate the blood loss! +  
sharpscontainer  Actually I don't think this is due to hypoxic vasoconstriction. The alveolar oxygen content of the lungs remains high, so there's still a good amount of oxygen getting into the pulmonary vessels, even if less of it can bind to Hb. I think instead it's that there's tons of sympathetic stimulation from hypovolemia, so alpha 1 in the pulmonary blood vessels is activated (which is separate from beta 2 bronchodilation which is a smooth muscle thing). https://www.ncbi.nlm.nih.gov/pubmed/10378571 +6  
avocadotoast  PVR = (PAP - PCWP) / CO. There is a decrease in cardiac output in hypovolemic shock. Given its inverse relationship with pulmonary vascular resistance, we should choose an increase in PVR for this question. +1