First dose hypotension with ACE-I

Discussion in 'Step I' started by Diggidy, 05.21.14.

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  1. Diggidy

    Diggidy 7+ Year Member

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    Question # 693 for those who'd like to follow along.

    I have a serious issue with the logic of this question and I would like for someone to explain how on earth this question only has one answer.

    For those who can't see the question, it basically asks about a certain phenomenon that can occur with the first dose of an ACE-I (hypotension), and which concurrent medications you should ask your patient about taking beforehand, to prevent a compounded issue of this.

    The correct answer to this was a Thiazide diuretic, their logic being that someone on this medication could already be volume depleted/hypotensive and you could drop their BP even more with the first dose of an ACE-I. Completely understandable and I guess I agree.

    However, another answer choice, the one I ended up picking, was a Beta-1 selective antagonist. If you were to experience a first done hypotension from the ACE-I, presumably in someone with an intact SNS, your heart would be able to compensate by increasing HR and thus CO -- the classic compensatory tachycardia that occurs with almost all vasodilators. Now logically I believe that if you were to become hypotensive, and your Beta-1 system was blocked due to medication, you could not get this compensatory tachycardia to maintain your CO and could become profoundly hypotensive.

    Where is the fault in this reasoning? This wasn't even a "most likely" question, where it's correct but not most correct -- UWorld just flat out says it's incorrect.
     
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  3. k-bourne

    k-bourne 2+ Year Member

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    My simple understanding ..
    Is that first dose effect of ACEI is classic with a diuretic .. thus Thiazide is truly is the best answer .. also if a loop diuretic is one of the answer chices ..it would be the best answer coz it is more powerful as a diuretic.

    As for B1 reflexes in hypotension they are truly less efficient than alpha mediated
    effects of vasoconstriction .. thus hypotension or potentiation of hypotensive effect of ACEI is not significant clinicaly for B1 blockers that is justified for UW to consider it wrong.
    Hope that helps..
     
  4. Diggidy

    Diggidy 7+ Year Member

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    Then what is reflex tachycardia the result of? It's certainly not alpha-1 stimulation...
     
  5. Apoplexy__

    Apoplexy__ Blood-and-thunder appearance Bronze Donor 2+ Year Member

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    You definitely have a good point. B1-blockers shouldn't be an option. I'd write feedback about it -- I've done that for a couple questions with a similar situation.

    The only thing I can think of is that UWorld's explanation is saying that hyponatremia + hypovolemia predispose to the ACE-I hypotension; something a thiazide would do and not a B-blocker. Still, that's a pretty obscure/unfair fact for the "best answer" to hinge on.
     
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  6. periaqueductal

    periaqueductal

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    I completely agree. I answered the same thing and scratched my head at the answer explanation. I was thinking the reflex tachycardia response blocking would cause the hypotension. I think the physiology is correct, they are just trying to make a point that thiazides augment first dose hypotension. Bad overall question but still taught me something I suppose.
     
  7. Diggidy

    Diggidy 7+ Year Member

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    Does anybody know if UWorld actually uses the feedback given? I've written in for a few questions now but I've never heard anything back from them.

    Also, thanks for the confirmation that I am indeed correct. I thought my reasoning was pretty bullet-proof -- as there are UWorld questions that have tested the theory of reflex tachycardia/bradycardia that I used to answer this. The lack of consistency is quite frustrating.
     
  8. k-bourne

    k-bourne 2+ Year Member

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    U misinterpreted my words
    I didn't say there is no reflex tachycardia (B mediated) .. I said it is less important than vasoconstrictive effet of alpha ( remember that alpha blockers are more associated with hypotension than beta blockers).

    As for ur reasoning with the question is quite correct .. but I think this question is more of knowledge question.. u know the ACEI and diuretic interaction or u don't.

    Bottom line:
    Very legit question. . Move on bro
     
  9. Ionian

    Ionian 2+ Year Member

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    Where is this classic association though?
    Is their a review source or even a book I can find it in?
    Not FA/Pathoma/RapidReview/Robbins? Surely must be a one liner in some dedicated pharm book? Sounds low yield.

    Like many of the questions I got wrong in uworld, I just say meh, w/e and move on.

    I felt 10% of Uworld questions honestly hold no value, in terms of learning, reviewing, or becoming a better test taker.
    And this was one of those.
     
  10. k-bourne

    k-bourne 2+ Year Member

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    Actually Ionian..
    I am a fresh grad IMG with 9 months clinical
    Experience ..
    So .. I know these kinda assocassociations from clinical rotations not from reading a particular book ..

    When u get to medicine rotations .. physicians will go on and on ..about these kinda associations .. as for step 1 .. I think question banks will prepare for what u need to know.. that what I heard.
     
  11. Cyal

    Cyal 2+ Year Member

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    I did choose thiazide for this question because I considered volume depletion and hyponatremia to be more significant issues compared to B1 blockade. I also anticipated that reflex sympathetic outflow could help constrict alpha1 receptors, hence the effect of a diuretic would require more caution. What I found puzzling was their introduction of some Jarisch reflex which would INCREASE vagal output and further cause hypotension--made no sense to me, except it's some paradoxical reflex.
     

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