NBME 20 Answers ↦
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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2019-06-08T20:13:13Z
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.
+37
2019-05-30T00:13:36Z
amarousis
so why tf do we give beta blockers for hypertension -.-
+5
2019-06-30T19:40:06Z
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
2019-07-30T13:05:54Z
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.
+4
2019-12-01T04:37:06Z
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)
+2
2020-01-11T14:18:55Z
mw126
Beta 1 blockade in the kidney (JG cells) would also decrease renin release, which would also help with HTN. FA2019 pg 245
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2020-03-24T19:23:00Z
rockodude
@dr_jan_itor clonidine is an a2 agonist not an a2 inhibitor
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2020-05-08T21:26:32Z
submitted by hungrybox(831), 2019-06-06T23:50:39Z
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tBu OC sseeaecdr ni htis seca /cb eth efftec of n.ic RPT is erom wr?opfuel