I've been searching for my source for this but can't seem to find it. However, the way I thought about it was that edema happens via the capillaries. If there is increased resistance via the precapillary sphincters as much blood wouldn't be able to get into the capillaries. The blood would instead get shunted via anastomoses to the veins. This article from cvphysiology.com explains it a little better: CV Physiology: Tissue Edema and General Principles of Transcapillary Fluid Exchange
A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.
This is how I interpreted it. The patient has diastolic hypertension. This leads to activation of RAAS System. Activation of RAAS will increase Aldosterone. Increase in Aldosterone result in increase in sodium reabsorption but the question is telling he is unlikely to get peripheral edema directing towards the " Aldosterone escape" mechanism. The mechanism is due to release of ANP/BNP.
ANP/BNP acts mainly by dilating the precapillary arterioles resulting in natriuresis and "Aldosterone escape" mechanism.
Maybe the question is dealing with the concept of myogenic arteriolar vasoconstriction which is a another anti-edema mechanism. The pre capillary sphincter contract in response to a raise in BP. I got the Q wrong because I picked lymphatic flow. They love to go for the "what else" element of any topic. I cannot find any reason why the lymphatic option could be wrong :/
https://www.ncbi.nlm.nih.gov/books/NBK53445/?report=classic Check the figure 4.1 The Margin of Safety Against Edema Formation – Edema Safety Factors
precapillary resistance = describing the arterioles. he's got minimal protein in the urine; and no albumin. the key was paying attention to the blood pressure. Pressure is regulated by the resistance vessels as boards calls it which is the arterioles aka precapillary resistance.
Aortic Diastolic Pressure
Aortic Systolic Pressure
1. Aortic Diastolic Pressure
1. High TPR = high DP
2. High HR = high DP
3. High SV = high DP
2. Aortic Systolic Pressure
1. High Contractility = high SP
2. High SV = high SP
3. Low Compliance = high SP
submitted by ferrero(19), 2019-05-30T22:14:59Z
A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.