Angiotensin 2 blockers and hypotension

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catcolalex

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Has anyone besides me noticed an increased incidence of severe hypotension resistant to most pressors after induction with pts who took their arb's the day of surgery. I had to cx a case yesterday because of this.

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Has anyone besides me noticed an increased incidence of severe hypotension resistant to most pressors after induction with pts who took their arb's the day of surgery. I had to cx a case yesterday because of this.


Yeah.. it can happen with ace inh. also. If your pressors don't work... a wiff of vasopressin usually solves the problem.
 
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What?

Explain please.

2-6 mg/kg Q 6 hours, infusion (can do 1-3 mg/kg in 20 minutes, regimens are widely variant). It's my desperation tactic and your pulse ox can go to hell in a handbasket (too much MB --> significant methemoglobinemia --> impaired arterial oxygen delivery --> bad). It inhibits guanylate cyclase and thus reduces cGMP levels that cause vascular smooth muscle relaxation.

All you younger guys out there, please don't start asking for methylene blue infusions from the pharmacy for every episode of hypotension.

If nothing else is working or you are doing an autopsy under anesthesia (i.e. dead guy trying to be kept alive by the surgeons), by all means.

There are five or six articles on methylene blue and vasoplegic syndrome, refractory ACE/ARB hypotension, and/or CPB.
 
2-6 mg/kg Q 6 hours, infusion (can do 1-3 mg/kg in 20 minutes, regimens are widely variant). It's my desperation tactic and your pulse ox can go to hell in a handbasket (too much MB --> significant methemoglobinemia --> impaired arterial oxygen delivery --> bad). It inhibits guanylate cyclase and thus reduces cGMP levels that cause vascular smooth muscle relaxation.

All you younger guys out there, please don't start asking for methylene blue infusions from the pharmacy for every episode of hypotension.

If nothing else is working or you are doing an autopsy under anesthesia (i.e. dead guy trying to be kept alive by the surgeons), by all means.

There are five or six articles on methylene blue and vasoplegic syndrome, refractory ACE/ARB hypotension, and/or CPB.

oohhhh...that's a very high dose.

I just give 25 mg....then maybe another 25 mg...and that's it.

The descriptions of its use in the vasplegic syndrome...the treatment groups actually had better outcome, but I think the treatment group only got 1 mg/kg one time?

Nitric oxide scavenger....
 
oohhhh...that's a very high dose.

I just give 25 mg....then maybe another 25 mg...and that's it.

The descriptions of its use in the vasplegic syndrome...the treatment groups actually had better outcome, but I think the treatment group only got 1 mg/kg one time?

Nitric oxide scavenger....

There are two studies I have seen. Both had totals in the 3-5 mg/kg range as an infusion titrated to effect or starting at 0.1 mcg/kg/min to a max of 5 mg/kg.

Are you bolusing that 25 mg? I have found that even a low infusion rate produces good clinical effect even coming off long bypass runs. Unfortunately, even with the low infusion rates, I have seen the oximeter read 70% O2 sats on a high FiO2 and with higher infusion rates the ABG's pO2 reading shows a much lower than expected value. Maybe I should lower the infusion rate even more if I have to use it again. One patient that I used it on developed renal insufficiency on pump when the perfusionist allowed the pressure to drop to low for more than 30 minutes. That may have accounted for his adverse reaction, including severe hypoxia and cyanosis, when I used what I thought was a small dose after his CPB run.

It has been reported that this is a factitious hypoxia/cyanosis but with all the readings indicating severely decreased oxygen content, it would be difficult to just overlook this event as factitious.

Hence it is my med of last resort.
 
You're right about the data....I was commenting that it seems like very high doses.

I have no experience with it in the vasoplegic syndrome......I have only used in patients with overwhelming sepsis with hypotension that is intractable to EVERYTHING else.

And the doses that I have used were just 25 mg bolus ....which had a clinical effect...so I figure I would not give any more that what it took to raise the BP (also a surrogate endpoint).

I'm waiting for more data...but the data available would suggest that it is a good thing inl CPB (improved survival, improved markers of perfusion, etc.) despite bad numbers on the monitors.
 
You're right about the data....I was commenting that it seems like very high doses.

I have no experience with it in the vasoplegic syndrome......I have only used in patients with overwhelming sepsis with hypotension that is intractable to EVERYTHING else.

And the doses that I have used were just 25 mg bolus ....which had a clinical effect...so I figure I would not give any more that what it took to raise the BP (also a surrogate endpoint).

I'm waiting for more data...but the data available would suggest that it is a good thing inl CPB (improved survival, improved markers of perfusion, etc.) despite bad numbers on the monitors.

The situation that I use it most frequently in is an emergent ascending aortic dissection that will be repaired with circ arrest, especially if I know the surgeon is going to be very slow and methodical. I run it in after circ arrest to avoid any adverse effects that stasis would have in terms of prolonged organ exposure to static levels of MB.

I have used it with refractory hypotension associated with sepsis, but in one out of the seven cases I used it in in the ICU, the patient's SVR dropped even more with multiple urticarial lesions appearing on his face, torso, and legs (i.e. anaphylaxis).

Medication of last resort, but a good one to have in the armamentarium.
 
Merry Christmas!

I'm big on vasopressin, 1-2 units. Some of these hypotension effects on ARB/high-dose ACEi have been significantly refractory to neo, even epi. Amazing about the vasopressin.

Lit search reveals that supposedly norepi has a better recovery profile with regards to visceral perfusion. My rationale is if one high-dose alpha agent isn't working, and the BP is that low, I'm not so keen on playing around; just move on to vasopressin because I know it works (so far).
 
2-6 mg/kg Q 6 hours, infusion (can do 1-3 mg/kg in 20 minutes, regimens are widely variant). It's my desperation tactic and your pulse ox can go to hell in a handbasket (too much MB --> significant methemoglobinemia -->

I thought methylene blue was a treatment for methemoglobinemia.
 
by the way its not ans2 inhibs but instead ace inhibitors that can give you resistant hypotension during induction:eek:
 
it is a treatment and also a potential cause.

I think you are confusing Methemoglobinemia with the decreased pulse-oximetry that is simply caused by the interferance of the blue dye with infra red absorption (not real desaturation).
Methylene blue does not cause Methemoglobinemia, it treats it.
I think that it's hemodynamic effects are mostly placebo effects on the side of the treating physician.
 
I think you are confusing Methemoglobinemia with the decreased pulse-oximetry that is simply caused by the interferance of the blue dye with infra red absorption (not real desaturation).
Methylene blue does not cause Methemoglobinemia, it treats it.
I think that it's hemodynamic effects are mostly placebo effects on the side of the treating physician.


Incorrect. At high doses (greater than 5 mg/kg although the limit varies with the text you read), MB can induce methemoglobinemia.
 
I think you are confusing Methemoglobinemia with the decreased pulse-oximetry that is simply caused by the interferance of the blue dye with infra red absorption (not real desaturation).
Methylene blue does not cause Methemoglobinemia, it treats it.
I think that it's hemodynamic effects are mostly placebo effects on the side of the treating physician.


do a quick lit search using the phrase "methylene blue" and "sepsis"
 
do a quick lit search using the phrase "methylene blue" and "sepsis"

Mil,
I am aware of the data about sepsis and the use of Methylin blue, but don't you agree that these studies are pretty weak and the numbers can not be conclusive?
If I remember correctly one of them included only 14 patients.
Add to this the fact that if you use MB in a patient in such a critical situation you are going to lose a very valuable monitor (SPO2) for a while.
That's why I think we need more evidence before starting to advocate this treatment.
 
I guess I'm not sure what you mean when you say that the "hemodynamic effects" are a "placebo".

MB clearly raises the blood pressure in hypotensive patients.....no 2 ways around it....it does....you give it...watch the a-line tracing...and the bp goes up...

As for the hemodynamic effects leading to improved outcome.....well...I will be the first to say that BP is only an OK surrogate marker for perfusion.
 
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