Refractory Hypotension in setting of ACE Inhibitor

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So studying for the Basic and, this has come up across before, but I was curious of what people think. I remember reading (or being told) that vasopressin is a a good agent to use, but the qbank I'm using suggest that norepinephrine should be first line.
 
0kazak1 said:
So studying for the Basic and, this has come up across before, but I was curious of what people think. I remember reading (or being told) that vasopressin is a a good agent to use, but the qbank I'm using suggest that norepinephrine should be first line.
Click to expand...

Saw that as well. Was vasopressin a choice? We are taught that vaso is first line since its a diff receptor all together
 
waterbottle10 said:
It seems like all the guidelines for everything hates vasopressin.
Click to expand...
Yes, because it produces vasoconstriction in almost all territories (the brain and lung are among the exceptions). One gets nice central numbers with piss-poor peripheral perfusion (including major organs). That's why the recommended doses in sepsis are only 0.03-0.04U/min.
 
waterbottle10 said:
It seems like all the guidelines for everything hates vasopressin.
Click to expand...
Weirdly, with all the guidelines, I couldn't find one for ACE-I induced hypotension. Plus, IRC the question explanation also seem to suggest that vasopressin doesn't work to increase blood pressure in that case. And of all the papers I could find (may be confirmation bias on my end), most of them seem to suggest vaso as first line as well.
 
FFP said:
Yes, because it produces vasoconstriction in almost all territories (the brain and lung are among the exceptions). One gets nice central numbers with piss-poor peripheral perfusion (including major organs). That's why the recommended doses in sepsis are only 0.03-0.04U/min.
Click to expand...

Isn't that a good thing. Not constricting lung and brain.
 
FFP said:
Yes, because it produces vasoconstriction in almost all territories (the brain and lung are among the exceptions). One gets nice central numbers with piss-poor peripheral perfusion (including major organs). That's why the recommended doses in sepsis are only 0.03-0.04U/min.
Click to expand...

Another way of rewriting the vasopressin dosage is 0.04U/min = 2.4U/Hr which in the grand scheme of things doesn't seem like that much doesn't it.

Noyac said:
How about methylene blue?
Click to expand...
How easy is it to get methylene blue vs vasopressin? And what about possible concerns of inaccurate pulse ox or serotonin syndrome?
 
Vasopressin or its synthetic analogues can restore the sympathetic response and may be useful pressors in cases of refractory hypotension during anaphylaxis 9 and septic shock 10 as well as in patients on RAS inhibitors, although norepinephrine has been reported to have a more favorable effect on splanchnic perfusion and oxygen delivery 11

Refractory hypotension during general anesthesia despite preoperative discontinuation of an angiotensin receptor blocker

Terlipressin versus norepinephrine to counteract anesthesia-induced hypotension in patients treated with renin-angiotensin system inhibitors: effec... - PubMed - NCBI
 
Have you ever used methylene blue? The effect on SpO2 monitoring is quite short lived. And certainly you'd avoid in patients on MAOI/SSRI's.

Vasopressin is currently quite pricey due to only one manufacturer that now holds a new patent for a new indication (post CPB vasoplegia) but in the setting of refractory vasoplegia (low SVR in the setting of adequate CO/CI) after failure of other pressor agents it is appropriate to attempt to correct with Vaso.
 
0kazak1 said:
Another way of rewriting the vasopressin dosage is 0.04U/min = 2.4U/Hr which in the grand scheme of things doesn't seem like that much doesn't it.


How easy is it to get methylene blue vs vasopressin? And what about possible concerns of inaccurate pulse ox or serotonin syndrome?
Click to expand...
Well, it's not easy to get any longer and it takes a large dose. I wouldn't be giving it to someone on an SSRI, so no real concerns there. Pulse on reading doesn't matter.
But think of this, what is vasopressin doing to perfusion? It may be improving it if you strictly look at BP but it is likely decreasing perfusion to a few vital organs.
 
I don't know to many people that use vasopressin as first line - even in the setting of someone on an ARB or ACE-I.

However, when sympathomimetics don't work (which surprisingly - happens sometimes on these patients), then V1 receptors need flogging.

For the OP in case it hasn't been clear -

We maintain blood pressure with three systems - Angiotensin/Renin system, sympathetic system, and V1 receptors. (there probably is many more systems and it is likely 100x more complicated then that, but we ******ed doctors think someone discovers a receptor, a paper is written, then somehow we KNOW exactly how things work now....so dumb).

Anyway, anesthesia drugs completely obliterate the sympathetic system. The patient has obliterated the Angiotensin system, and so Vasopressin works because that is what is left.

I don't really care about perfusion to many organs, other than spinal cord, heart, brain. Your kidney is SO good at regulating perfusion, not much we can do to influence that so I'm not really worried.
 
I'd add that patients on ACE inhibitors are also very commonly on beta blockers as well. Squeezing a patient until their eyes water while ignoring a HR in the 50's is dumb.
 
I bet over half the cases I do have patients on ACEs/ARBs. Very rarely do I see hypotension that ephedrine or phenylephrine can't fix.
 
Had a patient (380 pounder) bmi 46 reverse total shoulder. Usual mess Cad, dm, pvd,osa.

He took his ace inhibitor in am. Anyways. Blocked him. Put him to sleep. Refractory hypotension (bp in 60s/70s sys). Put a line and those were real Bp readings as well. Fought with Bp for 30 min after induction. Vasopressin did the trick. Got his Bp up quickly. Still he dipped down to the 70s after a few minutes . Ortho doc concerned. Didn't want to make incision for 2.5-3 hour case. We woke up the patient. And canceled case. Didn't want to run vasopressors through elective case.
 
I've had more than a dozen cases so far in my career requiring Inotropic support for patients who take ARBs/ACE inhibitors on a regular basis.

My last case (a few weeks ago) was supposed to have surgery under GA. Usual Blade type patient with multiple co-mobidities. He was canceled the day before because after induction the anesthesia team couldn't maintain his BP without vasopressin or Epi. So, I got him 24 hours later with the theory things would be better because patient had been off his ARBs. Well, the RN on the floor gave the patient his ARB that night so when I got him he had not been off it for 24 hours.

Plan:

1. Arterial line prior to induction
2. Low dose propofol with low dose ketamine for induction
3. Low dose Epi (4 ug/ml) and Vasopressin (1 unit per ml) ready to go in room
4. Nitrous oxide plus 0.5 MAC vapor as the anesthetic post induction

Yes, I had hypotension post induction but it was easily treated with vasopressin. I didn't need any "drips" but rather 10 units of vasopressin for the entire case. Mean BP was maintained above 80 for the entire case in the prone position. Patient did fine and went home the next day.

I've never cancelled a case in my entire career secondary to ARBs, ACE, Ca++ channel blockers etc but rather placed arterial lines and started inotropic support. Not one of these patients had a complication postop (that I'm aware of) after the anesthetic was discontinued at the end of the case. I don't have an issue with cancelling the case but I simply prefer doing the case if at all possible.

For beach chair position I would use cerebral oximetry and arterial line transducer at the level of the tragus while maintaining mean BP above 75-80 at all times.
 
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To add to the controversy, 3 large cohort studies that evaluated long-term outcomes in patients on AAB undergoing anesthesia arrived at remarkably conflicting conclusions. Railton et al11 found increased mortality in vascular surgery patients with the perioperative continuation of AAB. Toppin et al12reported decreased mortality with the continuation of these drugs in noncardiac surgical patients, whereas Turan et al13 found no difference in 30-day mortality in this population.

Additionally, there has been inconsistency regarding the association between perioperative AAB and the development of end-organ damage. The incidence of acute kidney injury (AKI) in patients on perioperative AAB undergoing vascular surgery,14 thoracic surgery,15 and orthopedic surgery16 has been shown to be increased. However, the incidence of AKI in the same population following cardiac surgery has been shown in certain studies to be increased,17-19unchanged,20 and even decreased.21,22

Likewise, there has been a discrepancy in the reported perioperative mortality of patients on AAB. In different studies, mortality has been shown to be increased,18,20,22 not different,13 or even decreased.23 Similarly, the development of atrial fibrillation in post–cardiopulmonary bypass (CPB) patients on perioperative AAB has been shown to be increased.20,24 However, the evidence for these associated complications, overall, is weak and based primarily on observational data.

http://www.anesthesiologynews.com/R...gs-In-the-Perioperative-Period/35357/ses=ogst


Medscape: Medscape Access (the evidence now strongly suggests to discontinue ARBS/ACE 24 hours prior to surgey)
 
bigdan said:
aneftp - not a surprised vaso worked; shocked that the ortho doc cared.
Click to expand...
You see. It depends on the employment model.

This happened last year when I was in still in private practice. But ortho doc who was new 1 year out and still in a partnership Buy in.

The 2 senior ortho partners give him the junk high risk patients while they take most of the healthier (and skinner) patients (read Asa 1 and 2).

Anyways a lot of factors into the cancellation after induction Medicine doc had "cleared" patient. But no true cardiac workup. You know those "intermediate risk surgery" in higher risk patient with supposed no symptoms. Proceed with surgery the note says.

I followed him up post procedure. He had ischemic ekg changes in pacu. No MI fortunately. My old hospital has immediate cardiology and cardiac surgeon availability. So he was cath that afternoon and 2 stents put in.

We get away with these cases all the time with hypotension throughout the case and nothing happens. But this particular patient was too high risk for me (and the surgeon). He's getting paid a salary by his bosses anyways till the real money comes in. So no big incentive for him proceeding.

You been in the business long enough. Trust your instincts. I rather be wrong and cancel the case. But if you have intraop death in elective outpatient coming in for surgery. It's a big deal.
 
 
F1.medium.gif



Within the group of patients with myocardial injury, the first elevated troponin I level was found on the first postoperative day in 162 patients (51.4%; Figure 1). Stratification of the patients into decades of age showed that the incidence of postoperative myocardial injury increased with age

Myocardial Injury After Noncardiac Surgery and its Association With Short-Term MortalityClinical Perspective | Circulation
 
Noyac said:
But think of this, what is vasopressin doing to perfusion? It may be improving it if you strictly look at BP but it is likely decreasing perfusion to a few vital organs.
Click to expand...

True, but how much perfusion are those organs really getting when the SBP is in the 60s-70s? Obviously, pressing to an SVRI in the 4000s is probably less than ideal, but using a little vaso to bring the resistance back near their normal is likely less damaging than allowing the severe hypotension/hypoperfusion to continue.
 
BLADEMDA said:
Yes, I had hypotension post induction but it was easily treated with vasopressin. I didn't need any "drips" but rather 10 units of vasopressin for the entire case. Mean BP was maintained above 80 for the entire case in the prone position. Patient did fine and went home the next day.
Click to expand...

What did you do post-op/pacu?

Had this same case. R TSA. Interscalene block, clean low dose anesthetic (.5 mac/30 mg ketamine/mag/antiemetics).
Refractory to phenylephrine and fluids. Vaso worked and maintained BPs. IM ephedrine at the end of the case.
Patient woke up AAOx3, no pain.
Low BPs in pacu.
Started a vaso infusion, ran some labs, called the hospitalist and sent tot he icu for 24 hrs.
Did fine, but took about 10 hrs to wean her off the vaso gtt.
 
Anectotally, was I was recenlty called to a partners room to place a TEE for refractory hypotension after induction.
TEE was completely normal.
No ACE inhibitors or ARBs on board but sure was acting vasoplegic.

Any guesses as to cause?
 
BLADEMDA said:
Conclusion: Intraoperative hypotension, but not hypertension, is associated with increased 30-day operative mortality.

Association between Intraoperative Hypotension and Hypertension and 30-day Postoperative Mortality in Noncardiac Surgery | Anesthesiology | ASA Publications
Click to expand...

This one of those studies that I feel I need to really dissect. Yeah, there are a myriad of very morbid conditions like heart failure, sepsis, myocardial infarction, etc. that lead to hypotension and mortalities. Is this study just saying these conditions are associated with increased mortality? It's like saying not having a pulse or readable blood pressure can lead to death.

Need to look at it.
 
sevoflurane said:
Anectotally, was I was recenlty called to a partners room to place a TEE for refractory hypotension after induction.
TEE was completely normal.
No ACE inhibitors or ARBs on board but sure was acting vasoplegic.

Any guesses as to cause?
Click to expand...

What was the case?
 
Ignatius J said:
What was the case?
Click to expand...

It was going to be a post. lumbar fusion. Case was cancelled before it began (very rare... but I was there watching my partner give boluses of epi for hypotension with minimal/short lasting effects). I am the anti-case canceller (sp?) of the universe... but I concurred with my partner to sit this one out.
 
sevoflurane said:
Anectotally, was I was recenlty called to a partners room to place a TEE for refractory hypotension after induction.
TEE was completely normal.
No ACE inhibitors or ARBs on board but sure was acting vasoplegic.

Any guesses as to cause?
Click to expand...

Boards would say hypovolemia, anaphylaxis, acidosis, hypocalcemia, sepsis, and insert case or pt specific zebra here.
 
sevoflurane said:
Anectotally, was I was recenlty called to a partners room to place a TEE for refractory hypotension after induction.
TEE was completely normal.
No ACE inhibitors or ARBs on board but sure was acting vasoplegic.

Any guesses as to cause?
Click to expand...
A hamfisted 400 mg propofol induction? 🙂 Sevo dial at 5%? Helpful cardiologist started him on a beta blocker or calcium channel blocker to "optimize" him a few days before surgery?
 
sevoflurane said:
Anectotally, was I was recenlty called to a partners room to place a TEE for refractory hypotension after induction.
TEE was completely normal.
No ACE inhibitors or ARBs on board but sure was acting vasoplegic.

Any guesses as to cause?
Click to expand...

Shouldnt you be seeing some abnormal end-systolic areas if vasoplegia/low SVR (enough to cause profound hypotension) is the diagnosis here?
 
Great differential here guys. 👍

There is one more out there that I know all your smart guys have in the back of your head that we are missing.

GA def. unmasked this disease process.
 
Heading out for my 10th day in a row of biking before having to go back to work... will give y'all the answer after the climb and before the decent.
 
If my patients have taken their ace inhibitor that day I usually tank them up with 250-500cc bolus of crystaloids prior to induction. Its my suspicion that bolusing an awake patient the fluid distributes more intravascularly versus after induction. A good measure is when the patient last used the restroom. If in the last 15 minutes your good on induction.
 
BLADEMDA said:
I've had more than a dozen cases so far in my career requiring Inotropic support for patients who take ARBs/ACE inhibitors on a regular basis.

My last case (a few weeks ago) was supposed to have surgery under GA. Usual Blade type patient with multiple co-mobidities. He was canceled the day before because after induction the anesthesia team couldn't maintain his BP without vasopressin or Epi. So, I got him 24 hours later with the theory things would be better because patient had been off his ARBs. Well, the RN on the floor gave the patient his ARB that night so when I got him he had not been off it for 24 hours.

Plan:

1. Arterial line prior to induction
2. Low dose propofol with low dose ketamine for induction
3. Low dose Epi (4 ug/ml) and Vasopressin (1 unit per ml) ready to go in room
4. Nitrous oxide plus 0.5 MAC vapor as the anesthetic post induction

Yes, I had hypotension post induction but it was easily treated with vasopressin. I didn't need any "drips" but rather 10 units of vasopressin for the entire case. Mean BP was maintained above 80 for the entire case in the prone position. Patient did fine and went home the next day.

I've never cancelled a case in my entire career secondary to ARBs, ACE, Ca++ channel blockers etc but rather placed arterial lines and started inotropic support. Not one of these patients had a complication postop (that I'm aware of) after the anesthetic was discontinued at the end of the case. I don't have an issue with cancelling the case but I simply prefer doing the case if at all possible.

For beach chair position I would use cerebral oximetry and arterial line transducer at the level of the tragus while maintaining mean BP above 75-80 at all times.
Click to expand...

I don't disagree with anything you said, except for not needing any drips. Unless the case was longer than 4-8 hours, you gave as much or more vaso than if you had run an infusion at 0.02 or 0.04u/min, and probably with worse hemodynamic variability.
 
Looked just like vasoplegia.
50 mcgs of epi would bring up his pressure to 110-120 systolic and then he'd just drift back down.
Cancelled the case and we found out the next day that this guys adrenals were completely shut down.

Just a heads up for you guys out there.
Was scratching my head on this one until labs came back.
 
WholeLottaGame7 said:
I don't disagree with anything you said, except for not needing any drips. Unless the case was longer than 4-8 hours, you gave as much or more vaso than if you had run an infusion at 0.02 or 0.04u/min, and probably with worse hemodynamic variability.
Click to expand...

Actually the majority of vasopressin was given in the first 10 minutes post induction (6 units). The remaining 4 units were given over the next 90 minutes. Everyone's a critic on SDN but I have no plans on running any drips now or in the future when I can push some meds via a syringe. I only use drips when absolutely necessary because I keep it KISS.
 
drmwvr said:
I'd add that patients on ACE inhibitors are also very commonly on beta blockers as well. Squeezing a patient until their eyes water while ignoring a HR in the 50's is dumb.
Click to expand...
 
Yes. Speed them up and squeeze a little. Ephedrine and glyco combo usually works well in a non emergent situation.
 
aneftp said:
You see. It depends on the employment model.

This happened last year when I was in still in private practice. But ortho doc who was new 1 year out and still in a partnership Buy in.

The 2 senior ortho partners give him the junk high risk patients while they take most of the healthier (and skinner) patients (read Asa 1 and 2).

Anyways a lot of factors into the cancellation after induction Medicine doc had "cleared" patient. But no true cardiac workup. You know those "intermediate risk surgery" in higher risk patient with supposed no symptoms. Proceed with surgery the note says.

I followed him up post procedure. He had ischemic ekg changes in pacu. No MI fortunately. My old hospital has immediate cardiology and cardiac surgeon availability. So he was cath that afternoon and 2 stents put in.

We get away with these cases all the time with hypotension throughout the case and nothing happens. But this particular patient was too high risk for me (and the surgeon). He's getting paid a salary by his bosses anyways till the real money comes in. So no big incentive for him proceeding.

You been in the business long enough. Trust your instincts. I rather be wrong and cancel the case. But if you have intraop death in elective outpatient coming in for surgery. It's a big deal.
Click to expand...
LMA or ETT?
I ask because I think it makes a difference. Respiratory efforts are indicative of good or bad things happening in the Mellon.
 
sevoflurane said:
Looked just like vasoplegia.
50 mcgs of epi would bring up his pressure to 110-120 systolic and then he'd just drift back down.
Cancelled the case and we found out the next day that this guys adrenals were completely shut down.

Just a heads up for you guys out there.
Was scratching my head on this one until labs came back.
Click to expand...
What was induction agent?
 
A general thought on all of this.
When a pt takes an ACE/ARB and requires BP support I just consider it similar to the thoracic epidural situation where we have removed the pts physiological mechanisms of BP Support. I have no problem giving the pt whatever it takes to get the BP where I want it. Same with these drugs. I would just rather not have to do this.
 
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