NBME 20 Increased total peripheral resistance and decreased cardiac output (NBME Answers)

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nbme20/Block 4/Question#25 (reveal difficulty score)
A 52-year-old man is brought to the emergency ...
Increased total peripheral resistance and decreased cardiac output 🔍 / 📺 / 🌳 / 📖
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submitted by ∗strugglebus(189)

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Propanolol is a non-selective Beta blocker. So your HR will decrease (B1), which will cause a compensatory increase in TPR.

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home_run_ball ^ Above is partially right: Propranolol is non-selective Beta blocker: Beta1 stimulation causes inc HR, therefore blocking it will dec HR and dec Cardiac output Beta 2 stimulation causes vasodilation, therefore blocking it will CAUSE UNOPPOSED alpha1 activation --> therefore increasing total peripheral resistance. +47

amarousis so why tf do we give beta blockers for hypertension -.- +7

dr_jan_itor I would also add that the patient was previously on an a2 inhibitor (clonidine), which he ran out of. So he is rebounding on that with upregulated a1 receptor activity. Adding labetalol would cause a greater degree of unopposed alpha, increasing tpr +1

llamastep1 @amarousis They are used for hypertension because the hypotensive effect of the reduced CO is greater than that of the effect of the increase of TPR. Cheers. +11

hungrybox @dr_jan_itor Adding labetalol would not cause unopposed α1 because labetalol and carvedilol are α1 blockers in addition to being nonspecific β blockers (great name btw, I love scrubs haha) +5

mw126 Beta 1 blockade in the kidney (JG cells) would also decrease renin release, which would also help with HTN. FA2019 pg 245 +

rockodude @dr_jan_itor clonidine is an a2 agonist not an a2 inhibitor +1

feanor I believe that in addition to the compensatory increase in TPR due to the decreased CO; Beta blockers such as propanol which are nonselective Beta Antagonists also have an effect on the B2 receptors to a certain degree, which would explain the increase in the sudden TPR. +

feanor sudden increase** P.S. Ignore my OCD(egodystonic), Thanks! +

bfinard1 Just to pipe in here, I guess the decreased renin activity from the B1 blockade is being overrun by the vasodilation inhibition of the B2 blockade? +

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submitted by ∗hungrybox(1277)

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So... theoretically an isolated decrease in HR would increase CO due to inc. preload, right?

But CO decreases in this case b/c the effect of inc. TPR is more powerful?

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kernicterusthefrog @hungrybox: No. Isolating HR, you would look at CO like this: CO=HR*SV so if HR or stroke volume go down, CO goes down. The change in preload wouldn't affect the CO as much as the change in rate of flow. So, the decrease in CO is solely due to the beta1 blocking effect on the AV node to decrease HR. +

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submitted by ∗maxillarythirdmolar(45)

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Where does the role of B1 stimulation of RAAS come into this? Wouldn't the B1 action cause decrease RAAS? That being said, I can also understand if that's a long term thing and this is a question about the immediate effects...?

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