Two questions regarding blood pressure that have been REALLY confusing me...

[SDQW22]

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1. FA 2017 p. 235 says Norepi increases pulse pressure. If PP = SBP - DBP, how is this possible if norepi causes a reflex bradycardia? I thought SBP was a determinant of cardiac output. In which case, I would expect PP to be decreased.

2. Same page, it says Epi increases MAP. Is this because of the B1 effect on heart in conjunction with the a1 effect on the vasculature despite b2 activity in the vasculature?


Thanks!

 

[woolsocks90]

1. SBP is a component of CO as well as TPR. NE has greater effect on alpha-1 vasoconstriction than on Beta-1 contractility. Therefore your SBP is increasing more than the DBP so PP is increased.

2. Yes. Epinephrine has more effect on B1 receptors than B2 receptors. So even though there may be a slight decrease in DBP due to vasodilation (though minimal) there is a greater increase in cardiac contractility which means increased SBP. If our SBP is increased to a greater extent than the decrease in DBP, it means our MAP is increased.

 

[SDQW22]

1. SBP is a component of CO as well as TPR. NE has greater effect on alpha-1 vasoconstriction than on Beta-1 contractility. Therefore your SBP is increasing more than the DBP so PP is increased.

2. Yes. Epinephrine has more effect on B1 receptors than B2 receptors. So even though there may be a slight decrease in DBP due to vasodilation (though minimal) there is a greater increase in cardiac contractility which means increased SBP. If our SBP is increased to a greater extent than the decrease in DBP, it means our MAP is increased.

thanks for the response! just had a few more clarifying Qs regarding this--

perhaps ive been understanding it incorrectly, but i thought TPR was moreso reflective of diastolic BP? is it reflective of both systolic/diastolic pressure?

also, re PP, lets say an individual was given an a-1 agonist like phenylephrine, is it that his BP would be elevated throughout systole and diastole thus causing an increased PP despite reflex brady ?

in this thread there was a uworld question about the same concept which said there would be a DECREASE in PP due to decreased CO. making me extra confused, because i would expect an a-agonist like norepi to have similar effects

Phenylephrine's effects on pulse pressure First Aid 237 page 237

 

[ASM student]

HR and SBP doesn't necessarily correlates, the pressure generated in the aorta depends on two factors; it's compliance and the volume of blood ejected into it (SV) according to this equation( C = ∆V / ∆P so ∆P = ∆V / C ) so bradycardia wouldn't necessarily means low SBP and tachycardia wouldn't necessarily means increased SBP, on the other hand cases in which you would have increased venous return with maintained ejection fraction or increased ejection fraction ( thyrotoxicosis, fever, hypervolumia in pregnancy ) you would have increased PP

- it's not correct to compare phenylephrine ( PURE alpha agonist) with norepi which has limited effect on beta receptors which at least can limit reflex vagal activity on the heart.

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