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NBME 20 Answers

nbme20/Block 4/Question#25

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(69),

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

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. +9  
amarousis  so why tf do we give beta blockers for hypertension -.- +2  
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 +  




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submitted by hungrybox(226),

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?

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(1),

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...?