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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.
+9
ibestalkinyo
I think this may have something to do with hypoxic vasoconstriction?
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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!
+2
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
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
+11
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.
+4
topgunber
in hypovolemic/hemorrhagic shock there is a decrease in systemic blood pressure , there is an Increase in TPR (it's a compensation) to maintain flow. I think it's safe to apply the same logic to the pulmonary circulation where there is decreased blood pressure there will be an increase in TPR to maintain flow. (due to the sympathetic activation from the baroreceptor reflex). As someone said, the PCWP will fall, the increase in TPR is a compensation just like in systemic circulation. There will be absorption - we wouldn't want to lose more intravascular volume when you've lost blood. I'm not 100% if its due to hemoconcentration or a severe decrease in hydrostatic pressure in the capillaries, though
+1
submitted by โbwdc(697)
The baroreceptors are stretch receptors (the more fluid in the vessel, the more they fire). So a patient with hemorrhagic shock will see a decrease in the baroreceptor firing rate. Activation of RAAS will result in increased vascular resistance (vasoconstriction) in order to maintain blood pressure. And capillaries, such as those in the kidney, will be primed for resorption and not filtration (no one wants to pee out good dilute urine when theyโre dehydrated). Likewise, systemic capillaries will prefer to hold onto plasma and not let it leak into the interstitium (third-spacing).