ace inhibitor

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anes121508

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Conflicting data out there. JCVA published one recently that said it does not even cause hypotension.

Regardless of your pre-op recommendation to either hold for 24 hrs or to continue taking, anyone cancelling elective non-cardiac cases for those patients who take an ace/arb within 24hrs of surgery?

If so, what's reasoning?

If not, why not?

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No, because there are always more pressors.

My patients take them all the time, despite having been told not to.
 
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Saw that. Still hold it. I’ve dealt with it enough times to know it’s real. No downside to hold ARBs and ACE-I.
 
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Where I train, some attendings will cancel elective non-cardiac cases if a patient took their acei/arb but obv depends on the procedure, comorbidities, etc. Obviously we have ways to mitigate the hemodynamic issues, but some people don't feel the risk is justified on an elective basis.
 
If the patient's BP is uncontrolled at baseline I ask them to take it. If they are well controlled I ask them to hold. I agree there are more pressors usually and your private practice group will get rid of you for cancelling cases over patients taking an ACE-I. Really the cases I see cancelled for meds are vascular angios with patients not holding xarelto or eliquis or patients taking phentermine within past 1-2 weeks for an elective case
 
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Had handful cases of ACEI and ARB induced vasoplegia during residency. It's real. Uptodate cites multiple studies showing increase in perioperative hypotension with continuing ACEI though no change in mortality.

Attendings pretty much never cancelled cases over it. No consensus in the preop clinic, some would tell them to hold and others would say continue.
 
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It is a point in favor of cancelling. Standing alone I would never cancel for this reason.

But, How about a patient with CVD, PAD, renal insufficiency, BP in preop is 85/50, for a sitting shoulder with a slow surgeon?
 
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Oh goodness. You guys talk to your non cardiac elective patients preop? Why?
 
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It is a point in favor of cancelling. Standing alone I would never cancel for this reason.

But, How about a patient with CVD, PAD, renal insufficiency, BP in preop is 85/50, for a sitting shoulder with a slow surgeon?

Yeah for sure cancel, but I'd tell the surgeon it's due to unexplained hypotension needing work up not because the patient took an ACE-I. Agreed the hypotension is real but have you ever seen it refractory to vasopressin or norepi?

Would not want to do that case anyway sounds like a watershed infarct waiting to happen
 
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Had handful cases of ACEI and ARB induced vasoplegia during residency. It's real. Uptodate cites multiple studies showing increase in perioperative hypotension with continuing ACEI though no change in mortality.

Attendings pretty much never cancelled cases over it. No consensus in the preop clinic, some would tell them to hold and others would say continue.

I was taught it was real, never really questioned it. I don't have as many cases under my belt as you to have seen it first hand. Based on the article, made me start wondering if it's something we've been wrong about. Pretty conflicting stuff in literature out there and somewhat difficult to be sure of. Which study for or against seems to be the strongest?

In the studies that find ace/arb to lead to hypotension, how severe was it? Refractory to vaso?

I don't have access to uptodate at home. Do you mind sharing the citations?
 
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I was taught it was real, never really questioned it. I don't have as many cases under my belt as you to have seen it first hand. Based on the article, made me start wondering if it's something we've been wrong about. Pretty conflicting stuff in literature out there and somewhat difficult to be sure of. Which study for or against seems to be the strongest?

In the studies that find ace/arb to lead to hypotension, how severe was it? Refractory to vaso?

I don't have access to uptodate at home. Do you mind sharing the citations?


It’s very severe...bp 50s-60s systolic for no apparent reason. When I first encountered it I would bolus phenylephrine and vasopressin...often going through 2-3vials. Nowadays I start vaso and norepi infusions and pray for the gut. The thing is when you turn the anesthetic off they are fine and require nothing in PACU.
 
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I was taught it was real, never really questioned it. I don't have as many cases under my belt as you to have seen it first hand. Based on the article, made me start wondering if it's something we've been wrong about. Pretty conflicting stuff in literature out there and somewhat difficult to be sure of. Which study for or against seems to be the strongest?

In the studies that find ace/arb to lead to hypotension, how severe was it? Refractory to vaso?

I don't have access to uptodate at home. Do you mind sharing the citations?
My personal experience is that it can be very bad. The point is that you need to get prepared and treat it before the bp drops significantly. Sometimes I will give pt vasopressin (0.5-1 unit every few minutes).
 
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I was taught it was real, never really questioned it. I don't have as many cases under my belt as you to have seen it first hand. Based on the article, made me start wondering if it's something we've been wrong about. Pretty conflicting stuff in literature out there and somewhat difficult to be sure of. Which study for or against seems to be the strongest?

In the studies that find ace/arb to lead to hypotension, how severe was it? Refractory to vaso?

I don't have access to uptodate at home. Do you mind sharing the citations?

It’s definitely real and can be very bad in my anecdotal experience (maybe get 2-3 cases per year that are severe enough to be memorable). Barely responds at all to multiple sticks of phenylephrine or ephedrine. Vaso 1-2u or norepinephrine 16-32 mcgs usually perks them right up, although I did have a carotid in resident who didn’t respond to anything and we canceled the case after induction but before incision and he was perfectly fine without anything after the anesthesia wore off.

Vasoplegic Syndrome and Renin-Angiotensin System Antagonists - Anesthesia Patient Safety Foundation
 
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The post-op rebound hypertension that can occur in patients that you don't want it to (ie CEA's) has been problematic for us in pts that have these meds held. Folks will show up for emergencies without having held them all the time and they're just managed.

Pressor without meaningful volume and raising the HR doesn't go too far for too long.
 
Wow. It's only hypotension if you measure it. Set the BP to q5mins and let the R1 smash the airway for a while. Be grand
 
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I don't cancel for ACE-I, but have vasopressin ready just in case. In an ideal world, would prefer my pt not take them pre-op.

But for any article to tell me that ACE-I induced hypotension under anesthesia isn't real is just laughable. I've seen it a handful of times where the BP is resistant to Ephedrine and Phenylephrine at big doses but responds to .5 or 1U vaso and then that's it. It's DEFINITELY a thing.
 
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Conflicting data out there. JCVA published one recently that said it does not even cause hypotension.

Regardless of your pre-op recommendation to either hold for 24 hrs or to continue taking, anyone cancelling elective non-cardiac cases for those patients who take an ace/arb within 24hrs of surgery?

If so, what's reasoning?

If not, why not?

That JVCA article was retrospective and the endpoint was a difference in blood pressure between groups (taking ACE-I/ARB, and not taking) at 15min post induction. I don’t think that “study” should change practice.
 
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cancel? depends, but most of the time no. i've seen very resistant hypotension during sitting shoulder surgeries in particular so i would have pressors handy to titrate if necessary.
 
No M and M but has some hypotension (poor definitions):
Take It or Leave It: A Meta-analysis of Perioperative ACE Inhibitors and ARBs
Nathan, Naveen MD

Author Information
Anesthesia & Analgesia: September 2018 - Volume 127 - Issue 3 - p 589
That JVCA article was retrospective and the endpoint was a difference in blood pressure between groups (taking ACE-I/ARB, and not taking) at 15min post induction. I don’t think that “study” should change practice.

This is the type of response I was hoping for. Evaluation of the quality of this study in comparison to those before it. With this study however, I'm not asking if I am going to change my practice, I am asking if all these supposed cases of vasoplegia are truly ace inhibitor or something missed. I mean this is literally saying that all you guys are wrong and you overlooked something else and blamed the ace inhibitor.

In the most recent 2018 meta analysis regarding ace inhibitors, they conclude that ace inhibitors are associated with hypotension. If you look at the analysis you find that one study specifically (pasted below) is where most of this data came from. If you then go to that study and look at what their definition for hypotension was....something along the lines of SBP <90 at any point in the case and required some intervention. By the nature of this study, there was a ton of stuff they couldn't control for and look at.

Maybe it's real, maybe it's not. In anesthesia we have many tales and dogma type practices. What if this thing turns out to be the boogie man?

Withholding versus Continuing Angiotensin-converting Enzyme Inhibitors or Angiotensin II Receptor Blockers before Noncardiac Surgery. An Analysis of the Vascular events In noncardiac Surgery patIents cOhort evaluatioN Prospective Cohort

Anesthesiology 2017
 
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No M and M but has some hypotension (poor definitions):
Take It or Leave It: A Meta-analysis of Perioperative ACE Inhibitors and ARBs
Nathan, Naveen MD

Author Information
Anesthesia & Analgesia: September 2018 - Volume 127 - Issue 3 - p 589


This is the type of response I was hoping for. Evaluation of the quality of this study in comparison to those before it. With this study however, I'm not asking if I am going to change my practice, I am asking if all these supposed cases of vasoplegia are truly ace inhibitor or something missed. I mean this is literally saying that all you guys are wrong and you overlooked something else and blamed the ace inhibitor.

In the most recent 2018 meta analysis regarding ace inhibitors, they conclude that ace inhibitors are associated with hypotension. If you look at the analysis you find that one study specifically (pasted below) is where most of this data came from. If you then go to that study and look at what their definition for hypotension was....something along the lines of SBP <90 at any point in the case and required some intervention. By the nature of this study, there was a ton of stuff they couldn't control for and look at.

Maybe it's real, maybe it's not. In anesthesia we have many tales and dogma type practices. What if this thing turns out to be the boogie man?

Withholding versus Continuing Angiotensin-converting Enzyme Inhibitors or Angiotensin II Receptor Blockers before Noncardiac Surgery. An Analysis of the Vascular events In noncardiac Surgery patIents cOhort evaluatioN Prospective Cohort

Anesthesiology 2017


What point are you trying to make? And why?

Most patients who continue their ARBs and ACE inhibitors do not get profound, refractory hypotension but some do. The degree of hypotension and the response to the usual pressors are not normal in these patients. I’m talking healthy ASA2 knee scope. Not a single patient I have taken care of has had morbidity from it. Still, given a choice, I’d rather not deal with it. It’s more work and stress for me intraop and I like to keep my life as easy as possible.
 
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It’s definitely real and can be very bad in my anecdotal experience (maybe get 2-3 cases per year that are severe enough to be memorable). Barely responds at all to multiple sticks of phenylephrine or ephedrine. Vaso 1-2u or norepinephrine 16-32 mcgs usually perks them right up, although I did have a carotid in resident who didn’t respond to anything and we canceled the case after induction but before incision and he was perfectly fine without anything after the anesthesia wore off.

Vasoplegic Syndrome and Renin-Angiotensin System Antagonists - Anesthesia Patient Safety Foundation

Going down the rabbit hole of the citations from the article you shared. Appreciate it.

Influence of chronic angiotensin-converting enzyme inhibition on anesthetic induction. Anesthesiology 1994;81:299-307.

1583113339796.png
 
What point are you trying to make? And why?

Most patients who continue their ARBs and ACE inhibitors do not get profound, refractory hypotension but some do. The degree of hypotension and the response to the usual pressors are not normal in these patients. I’m talking healthy ASA2 knee scope. Not a single patient I have taken care of has had morbidity from it. Still, given a choice, I’d rather not deal with it. It’s more work and stress for me intraop and I like to keep my life as easy as possible.

Fair question.

1. I think we have much dogma in anesthesia. This article in JCVA made me stop and think because it challenges a common concept. Unless I'm crazy (probably true) it's not challenging the fact that ace inhibitors cause refractory hypotension, it's saying they don't do sh**. Every now and then we should re-examine our beliefs and practices. Probably important to understand where that practice and belief came from and the quality of evidence behind it.

2. Do ace inhibitors truly increase risk of severe refractory hypotension? "This one time....so I blamed the ace-I".

3. Outside of this forum, I've been told that some people are cancelling cases for patients taking ace-inhibitors within 24 hrs of surgery. Telling people to withhold medication based on some data that says they might cause some hypotension is one thing, but cancelling!?!?! So I wanted to poll the audience.
 
Fair question.

1. I think we have much dogma in anesthesia. This article in JCVA made me stop and think because it challenges a common concept. Unless I'm crazy (probably true) it's not challenging the fact that ace inhibitors cause refractory hypotension, it's saying they don't do sh**. Every now and then we should re-examine our beliefs and practices. Probably important to understand where that practice and belief came from and the quality of evidence behind it.

2. Do ace inhibitors truly increase risk of severe refractory hypotension? "This one time....so I blamed the ace-I".

3. Outside of this forum, I've been told that some people are cancelling cases for patients taking ace-inhibitors within 24 hrs of surgery. Telling people to withhold medication based on some data that says they might cause some hypotension is one thing, but cancelling!?!?! So I wanted to poll the audience.


It wasn’t a thing until it started happening to a bunch of us multiple times and across the country.
 
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What point are you trying to make? And why?

Most patients who continue their ARBs and ACE inhibitors do not get profound, refractory hypotension but some do. The degree of hypotension and the response to the usual pressors are not normal in these patients. I’m talking healthy ASA2 knee scope. Not a single patient I have taken care of has had morbidity from it. Still, given a choice, I’d rather not deal with it. It’s more work and stress for me intraop and I like to keep my life as easy as possible.

The first case i had that made me a believer was a knee scope in a semi pro soccer player with HTN. After the case, he told me he never used to take his BP meds. Said he figured “since he had to have surgery he should be a good patient and follow the rules” so he started taking them the week before and day of surgery. Maps in the 30s and 40s, systolics in the 50s, for a morning case with LMA in a guy with competitive soccer functional capacity.
 
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i don’t even ask if they took it. I’m not gonna cancel and there is always pressors....
 
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Where I train, some attendings will cancel elective non-cardiac cases if a patient took their acei/arb but obv depends on the procedure, comorbidities, etc. Obviously we have ways to mitigate the hemodynamic issues, but some people don't feel the risk is justified on an elective basis.

Thats absurd and just shows how unrealistic academic medicine can be. Go to private practice and try to cancel a case because a patient took an ARB/ACE-i. I see way too many new grads trying to be way too cerebral rather than just doing the dang case.
 
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Refractory hypotension from ACEi is very real but doesn't happen commonly. It's a concern if your patient has CAD or cerebral vascular disease. I've had people with SBP in the 60s after sticks of phenylephrine and units of vaso. I don't cancel cases for it but I make sure to know if they've taken it. I've had to give methylene blue before which immediately reversed it
 
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Refractory hypotension from ACEi is very real but doesn't happen commonly. It's a concern if your patient has CAD or isn. I've had people with SBP in the 60s after sticks of phenylephrine and units of vaso. I don't cancel cases for it but I make sure to know if they've taken it. I've had to give methylene blue before which immediately reversed it

If all you do is pound away with pressor (i.e. you don't raise the HR and give volume as well) you'll see this problem.
 
Refractory hypotension from ACEi is very real but doesn't happen commonly. It's a concern if your patient has CAD or isn. I've had people with SBP in the 60s after sticks of phenylephrine and units of vaso. I don't cancel cases for it but I make sure to know if they've taken it. I've had to give methylene blue before which immediately reversed it
What is isn?
 
If all you do is pound away with pressor (i.e. you don't raise the HR and give volume as well) you'll see this problem.

Yes give volume and titrate ephedrine, small dose epi or glyco. Besides just phenlyephrine/vaso I've given 10-20mcg of epi until their heart rate is in the 90s, BP only budged up into the 80/90s. The hypotension isn't a pump (cardiac) problem, it's a pipes (peripheral vasodilation) problem, likely from nitric oxide dysregulation given that methylene blue helps.

@Arch Guillotti isn is a typo
 
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Yes give volume and titrate ephedrine, small dose epi or glyco. Besides just phenlyephrine/vaso I've given 10-20mcg of epi until their heart rate is in the 90s, BP only budged up into the 80/90s. The hypotension isn't a pump (cardiac) problem, it's a pipes (peripheral vasodilation) problem, likely from nitric oxide dysregulation given that methylene blue helps.

Ah...but it frequently isn't just a "pipes" problem. How many patients do you see on an acei that are not also on a beta blocker and maybe a diuretic too? These agents contribute to the problem and make it all the more difficult to manage if not addressed directly, which it looks like you did.
 
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ACe-I induced severe refractory hypotension isn’t real. It’s a rash of confirmation bias. Patients differ in their blood pressure response to anesthesia and inflammatory insults . That’s it. We never hold cardiac meds for cases on cardiopulmonary bypass and there is no correlation in my experience between vasoplegic episodes and ace inhibitors.
 
ACe-I induced severe refractory hypotension isn’t real. It’s a rash of confirmation bias. Patients differ in their blood pressure response to anesthesia and inflammatory insults . That’s it. We never hold cardiac meds for cases on cardiopulmonary bypass and there is no correlation in my experience between vasoplegic episodes and ace inhibitors.

A sample size of 108 was able to show a significant difference in refractory hypotension with ACEi. Whether or not your institution chooses to hold ACEi and whether or not you personally notice, is not evidence that refractory hypotension with ACEi doesn’t exist. Happy to hear out your counter argument.



Risk factors for post-cardiopulmonary bypass vasoplegia in patients with preserved left ventricular function.
Mekontso-Dessap A, et al. Ann Thorac Surg. 2001.
Show full citation
Abstract
BACKGROUND: Although vasodilatory shock (VS) is one of the main complications of cardiopulmonary bypass (CPB), its pathophysiologic basis remains unclear. The aim of this study was to identify predisposing factors for the development of VS after CPB independent of ventricular function.
METHODS: Thirty-six patients undergoing coronary artery bypass grafting who developed VS were compared with 72 control patients without post-CPB cardiogenic or vasoplegic shock, in a 2:1 case control study. Patients and controls underwent the same anesthetic protocol and were matched by age, sex, operation date, and left ventricle ejection fraction.
RESULTS: Preoperative and intraoperative patient characteristics were not significantly different between the two groups. Preoperative use of angiotensin-converting enzyme inhibitors and intravenous heparin were independent predictors for post-CPB VS by multivariate analysis (relative risk of 2.26 and 2.78, respectively). Intensive care unit stay and hospital stay were significantly longer in VS cases than controls, without any difference in early postoperative mortality.
CONCLUSIONS: The only independent risk factors for postoperative VS identified were preoperative use of angiotensin-converting enzyme inhibitors and intravenous heparin. These risk factors were independent of age, gender, anesthetic protocol, and left ventricle ejection fraction.
 
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A sample size of 108 was able to show a significant difference in refractory hypotension with ACEi. Whether or not your institution chooses to hold ACEi and whether or not you personally notice, is not evidence that refractory hypotension with ACEi doesn’t exist. Happy to hear out your counter argument.



Risk factors for post-cardiopulmonary bypass vasoplegia in patients with preserved left ventricular function.
Mekontso-Dessap A, et al. Ann Thorac Surg. 2001.
Show full citation
Abstract
BACKGROUND: Although vasodilatory shock (VS) is one of the main complications of cardiopulmonary bypass (CPB), its pathophysiologic basis remains unclear. The aim of this study was to identify predisposing factors for the development of VS after CPB independent of ventricular function.
METHODS: Thirty-six patients undergoing coronary artery bypass grafting who developed VS were compared with 72 control patients without post-CPB cardiogenic or vasoplegic shock, in a 2:1 case control study. Patients and controls underwent the same anesthetic protocol and were matched by age, sex, operation date, and left ventricle ejection fraction.
RESULTS: Preoperative and intraoperative patient characteristics were not significantly different between the two groups. Preoperative use of angiotensin-converting enzyme inhibitors and intravenous heparin were independent predictors for post-CPB VS by multivariate analysis (relative risk of 2.26 and 2.78, respectively). Intensive care unit stay and hospital stay were significantly longer in VS cases than controls, without any difference in early postoperative mortality.
CONCLUSIONS: The only independent risk factors for postoperative VS identified were preoperative use of angiotensin-converting enzyme inhibitors and intravenous heparin. These risk factors were independent of age, gender, anesthetic protocol, and left ventricle ejection fraction.

I dont care either way for whatevers going on in here in this thread but thats post pump vasoplegia. Hardly the same as hypotension in elective non cardiac surgery?

Would you cancel a case cause they had an acei in the AM?
What about someone who takes their meds at 10pm and they're first on the list at 7.30am?
Isnt perindoprils half life something ridiculous like 30 hours?
 
I’m not going to read that study but it’s interesting that the conclusion doesn’t mention Time on pump or complexity of the operation or if there was endocarditis, or circulatory arrest episodes or all the other things that ACTUALLY cause vasodilation

Lol
 
I’m not going to read that study but it’s interesting that the conclusion doesn’t mention Time on pump or complexity of the operation or if there was endocarditis, or circulatory arrest episodes or all the other things that ACTUALLY cause vasodilation

Lol

They mention time on pump in their discussion. Noones arguing that. As for endocarditis, the study was on normal to moderately reduced EF CABGs. Both groups had similar pump times. I mean i realize it’s a case control study but seems like reasonable evidence that ACEi are linked with vasoplegia. Point was just that i do think ACEi refractory hypotension is a real thing.

As for cancelling cases, no i wouldn’t cancel but i would prefer patients not be on them for 24 hours prior to most surgeries.

*accidentally posted the wrong link
 
Having a patient population (like mine), the vast majority of whom is taking a combination of things like beta blockers, CCB's and ACEI/ARB's, diruetics, has a way of conditioning me to expect very specific responses to what I do to them such that when I encounter that outlier "healthy" patient not on these cocktails, I see a "normal" response that I have become unaccustomed to and therefore caught off guard....it happens...

The converse may be true of those that don't see a lot of patients on these "cocktails" and interpret their responses as out of the ordinary and thus attribute what they see to a single cause when in fact there are many...
 
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Dont really care if they take or hold, unlses their pressure is out of wack.

does anyone cancel if they dont hold metformin for major surgeries? :)
 
Having a patient population (like mine), the vast majority of whom is taking a combination of things like beta blockers, CCB's and ACEI/ARB's, diruetics, has a way of conditioning me to expect very specific responses to what I do to them such that when I encounter that outlier "healthy" patient not on these cocktails, I see a "normal" response that I have become unaccustomed to and therefore caught off guard....it happens...

The converse may be true of those that don't see a lot of patients on these "cocktails" and interpret their responses as out of the ordinary and thus attribute what they see to a single cause when in fact there are many...

Exactly. It’s confirmation bias. Nearly all of my patients are cardiovascular cripples and vasculopaths. some take RAA axis drugs and some don’t, the vast majority will be prone to hypotension either way , more so than the infrequent ASC patient I see.

Data can be manipulated to support any conclusion you want. There is no correlation, and I don’t care about study data.
 
It is a point in favor of cancelling. Standing alone I would never cancel for this reason.

But, How about a patient with CVD, PAD, renal insufficiency, BP in preop is 85/50, for a sitting shoulder with a slow surgeon?
Is this a real or hypothetical patient? Cuz it doesn’t add up. Why is their nephrologist or cardiologist accepting those numbers?
 
The first case i had that made me a believer was a knee scope in a semi pro soccer player with HTN. After the case, he told me he never used to take his BP meds. Said he figured “since he had to have surgery he should be a good patient and follow the rules” so he started taking them the week before and day of surgery. Maps in the 30s and 40s, systolics in the 50s, for a morning case with LMA in a guy with competitive soccer functional capacity.

A semi pro soccer player with hypertension?? How old? If theyre young, Alarm bells should be going off for some sort of secondary hypertension that was missed by his / her careless primary care doc. Probably one of the hypovolemic , tight vessel forms of secondary hypertension , and that’s why the floor fell out on his blood pressure when you gave him a full dose of gas like the rest of your ASC patients.
 
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A semi pro soccer player with hypertension?? How old? If theyre young, Alarm bells should be going off for some sort of secondary hypertension that was missed by his / her careless primary care doc. Probably one of the hypovolemic , tight vessel forms of secondary hypertension , and that’s why the floor fell out on his blood pressure when you gave him a full dose of gas like the rest of your ASC patients.

Sure maybe that or maybe cocaine or meth use or extreme dehydration from playing soccer. Who knows but run of the mill hypertension is common, even in athletes. AAFP guidelines suggest routine screening for secondary causes of hypertension is not indicated. Could he have had something underlying we didn’t know about, sure.

Condescendingly throwing out another vague possibility for the sake of defending your hunch that ACEi refractory hypotension isn’t real isn’t a convincing argument. Until someone can produce data and a viable pathophysiologic explanation of why it shouldn’t exist, i am going to continue to keep it on my radar.

So in your practice, when you run into something like this, do you request follow up screening for secondary causes of HTN? I mean maybe your right and that’s something to consider but i don’t. Some people just need a little pressor.
 
So you agree that there are multiple possibilities besides the ace inhibitor which mysteriously causes insane hypotension in only a small fraction of anesthetics.

Have you ever canceled a case for blood pressure lability and found it to be a real undiagnosed issue? I’ve canceled a cardiac case for extremely high and refractory hypertension early in the case and kept the patient admitted to be worked up and it turned out to be a Pheo. My opinion of PCPs is they are too dismissive of new hypertension and don’t work it up. Hypertension in a young thin endurance athlete raises my eyebrow a little .
 
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So you agree that there are multiple possibilities besides the ace inhibitor which mysteriously causes insane hypotension in only a small fraction of anesthetics.

Have you ever canceled a case for blood pressure lability and found it to be a real undiagnosed issue? I’ve canceled a cardiac case for extremely high and refractory hypertension early in the case and kept the patient admitted to be worked up and it turned out to be a Pheo. My opinion of PCPs is they are too dismissive of new hypertension and don’t work it up. Hypertension in a young thin endurance athlete raises my eyebrow a little .
Mine too.
 
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