NBME 23 Answers : Block 4 : #45 = A 32-year-old man has a diastolic blood pressure ...

NBME 23 Answers

nbme23/Block 4/Question#45

A 32-year-old man has a diastolic blood pressure ...

Precapillary resistance

+19 upvote downvote
submitted by ferrero(19),

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.

seagull The question clearly lead us to think about Osmotic pressure by talking about protein and urine. I wonder how many people used that line of reasoning (like myself)? +11

mousie Great explanation, I chose lymphatic drainage for the same reasoning (similar Q on different bank) +1

sympathetikey My reasoning was much more simplistic (maybe too simple) but in my mind, systolic BP is determined by Cardiac Output and diastolic BP is determined by arterioles. Therefore, what comes before the capillary and regulates resistance? Arterioles. That's why I said that pre-capillary resistance. +14

cr the main difference between the 2 cases is that in this case the patient has high BP +

link981 So in kindergarten language the question is essentially asking how high pressure in the arterial system is NOT transmitted to the venous system (which is where EDEMA develops). But you know they have to add all this info to try confuse a basic principle and make you second guess yourself. (Got it wrong by the way) because of what @ferrero said of Qbank questions. +

hello @ferrero what are you talking about? lymphatic drainage is the wrong answer... +

hello ok never mind. i got it. hard to understand b/c it was a big block of text. +

asteroides I think they may be talking about the myogenic compensatory mechanism: https://www.ncbi.nlm.nih.gov/books/NBK53445/figure/fig4.1/?report=objectonly "Increased arterial or venous pressure also induces myogenic constriction of arterioles and precapillary sphincters, which raises arteriolar resistance (thereby minimizing the increase in capillary pressure) and reduces the microvascular surface area available for fluid exchange. For example, because vascular smooth muscle in arterial and arteriolar walls contracts when exposed to elevated intravascular pressures, this myogenic response increases precapillary resistance and protects capillaries from a concomitant rise in their intravascular pressure." +

+2 upvote downvote
submitted by notadoctor(66),

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

+0 upvote downvote
submitted by ferrero(19),

+0 upvote downvote
submitted by sanup400(0),

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.

+0 upvote downvote
submitted by divya(2),

i don't think you need to think all that much. look at all the options and think of what happens when they increase. A, B, C, D and F all can cause interstitial edema. But increasing precapillary resistance definitely doesn't.

+0 upvote downvote
submitted by hello(83),

why is plasma oncotic pressure wrong?

+0 upvote downvote
submitted by chagas14(0),

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

+0 upvote downvote
submitted by staph_aureusxx(0),

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.

+0 upvote downvote
submitted by usmleuser007(135),

Aortic Diastolic Pressure

High TPR = high DP
High HR = high DP
High SV = high DP

Aortic Systolic Pressure

High Contractility = high SP
High SV = high SP
Low Compliance = high SP

-1 upvote downvote
submitted by usmleuser007(135),

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

yex https://cvphysiology.com/Microcirculation/M012 This helps somehow, the first part about capillary pressure. +

usmlelol that's the exp part:: The average capillary hydrostatic pressure is determined by arterial and venous pressures (PA and PV), and by the ratio of post-to-precapillary resistances (RV/RA). An increase in either arterial or venous pressure will increase capillary pressure; however, a given change in PA is only about one-fifth as effective in changing PC as the same absolute change in PV. Because venous resistance is relatively low, changes in PV are readily transmitted back to the capillary, and conversely, because arterial resistance is relatively high, changes in PA are poorly transmitted downstream to the capillary. +