Interesting case

[Hork Bajir]

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Had an interesting thing happen in the cardiac OR yesterday:

50 year old man, severe MR w/ P2 prolapse, scheduled for MV repair. Otherwise pretty healthy and well compensated, had albuterol on his med list but didn't carry a formal diagnosis of asthma and denied using his inhaler in years.

At the end of the bypass run, cross clamp comes off, start to pace, did a little recruitment then started trying to ventilate but was getting very high airway pressures. In the surgical field, the lungs looked VERY hyper-inflated- pooching out into the midline from both sides. I disconnected the ETT, and the lungs didn't really come down at all. Surgeon tells me that the lungs actually seemed like they were kind of inflated for the bypass run. I pass a suction catheter down the ETT, get nothing back. Call for a bronchoscope, do a quick look, ETT is in perfect position and the proximal airways look totally normal. At this point I'm a bit at a loss, and surgeon is getting impatient. I give more paralytic, ask the perfusionist to increase the iso, no change. At this point I'm figuring it must be bronchospasm, so I give 15mcg of epi and 50mg of ketamine... over the next few minutes, lungs gradually deflate. I'm able to start ventilating and the airway pressures normalize. Come off pump and everything is fine. Minimal obstructive changes to the capnographic waveform, though really not dramatic- gave some albuterol since we were moving air at this point. Next day I see the patient in the ICU- extubated, doing great, no respiratory issues.

I feel like it must have been bronchospasm, since I don't know how else to explain what happened... Anaphylaxis or generalized histamine release feels less likely, since the hemodynamics were fine the whole time and there were no other signs/symptoms. No medications had been given while we were on pump other than heparin. Maybe it was bronchospasm from heparin? But we saw no issues with the initial dose for cannulation.

Anyway, I thought it was interesting and had never encountered anything quite like that before. Curious if anyone has any thoughts, or has seen a similar situation

 

[narcotics999]

If anaphylaxis on pump, will you see significant hemodynamic changes?

 

[vector2]

Had an interesting thing happen in the cardiac OR yesterday:

50 year old man, severe MR w/ P2 prolapse, scheduled for MV repair. Otherwise pretty healthy and well compensated, had albuterol on his med list but didn't carry a formal diagnosis of asthma and denied using his inhaler in years.

At the end of the bypass run, cross clamp comes off, start to pace, did a little recruitment then started trying to ventilate but was getting very high airway pressures. In the surgical field, the lungs looked VERY hyper-inflated- pooching out into the midline from both sides. I disconnected the ETT, and the lungs didn't really come down at all. Surgeon tells me that the lungs actually seemed like they were kind of inflated for the bypass run. I pass a suction catheter down the ETT, get nothing back. Call for a bronchoscope, do a quick look, ETT is in perfect position and the proximal airways look totally normal. At this point I'm a bit at a loss, and surgeon is getting impatient. I give more paralytic, ask the perfusionist to increase the iso, no change. At this point I'm figuring it must be bronchospasm, so I give 15mcg of epi and 50mg of ketamine... over the next few minutes, lungs gradually deflate. I'm able to start ventilating and the airway pressures normalize. Come off pump and everything is fine. Minimal obstructive changes to the capnographic waveform, though really not dramatic- gave some albuterol since we were moving air at this point. Next day I see the patient in the ICU- extubated, doing great, no respiratory issues.

I feel like it must have been bronchospasm, since I don't know how else to explain what happened... Anaphylaxis or generalized histamine release feels less likely, since the hemodynamics were fine the whole time and there were no other signs/symptoms. No medications had been given while we were on pump other than heparin. Maybe it was bronchospasm from heparin? But we saw no issues with the initial dose for cannulation.

Anyway, I thought it was interesting and had never encountered anything quite like that before. Curious if anyone has any thoughts, or has seen a similar situation

What were the lung mechanics like after intubation and before bypass? How the baseline capnography look? What was the CO2 and P:F on the baseline blood gas?

 

[Hoya11]

Had an interesting thing happen in the cardiac OR yesterday:

50 year old man, severe MR w/ P2 prolapse, scheduled for MV repair. Otherwise pretty healthy and well compensated, had albuterol on his med list but didn't carry a formal diagnosis of asthma and denied using his inhaler in years.

At the end of the bypass run, cross clamp comes off, start to pace, did a little recruitment then started trying to ventilate but was getting very high airway pressures. In the surgical field, the lungs looked VERY hyper-inflated- pooching out into the midline from both sides. I disconnected the ETT, and the lungs didn't really come down at all. Surgeon tells me that the lungs actually seemed like they were kind of inflated for the bypass run. I pass a suction catheter down the ETT, get nothing back. Call for a bronchoscope, do a quick look, ETT is in perfect position and the proximal airways look totally normal. At this point I'm a bit at a loss, and surgeon is getting impatient. I give more paralytic, ask the perfusionist to increase the iso, no change. At this point I'm figuring it must be bronchospasm, so I give 15mcg of epi and 50mg of ketamine... over the next few minutes, lungs gradually deflate. I'm able to start ventilating and the airway pressures normalize. Come off pump and everything is fine. Minimal obstructive changes to the capnographic waveform, though really not dramatic- gave some albuterol since we were moving air at this point. Next day I see the patient in the ICU- extubated, doing great, no respiratory issues.

I feel like it must have been bronchospasm, since I don't know how else to explain what happened... Anaphylaxis or generalized histamine release feels less likely, since the hemodynamics were fine the whole time and there were no other signs/symptoms. No medications had been given while we were on pump other than heparin. Maybe it was bronchospasm from heparin? But we saw no issues with the initial dose for cannulation.

Anyway, I thought it was interesting and had never encountered anything quite like that before. Curious if anyone has any thoughts, or has seen a similar situation

hard for me to believe that bronchospasm would lead to both lungs being severely overinflated even with the ETT disconnected
maybe there was a foreign body like mucus or a piece of plastic in the ETT acting like a one way valve, and when you passed the catheter and scope you broke it up, but it took a while for the lungs to completely come down and so you attributed it to the drugs - which 15mcg of epi and whatever ketamine unlikely to do anything if its a severe bronchospasm..

 

[DrOwnage]

If anaphylaxis on pump, will you see significant hemodynamic changes?

I mean yes, especially if the perfusionist has to keep going up on the flow or pressor requirements.

 

[Hork Bajir]

@vector2 Baseline lung mechanics, capnography, blood gas, P:F, etc. were all stone cold normal prior to that point in the case.

@Hoya11 I agree that 15mxg of epi and 50 of ketamine isn’t a huge dose for bad bronchospasm; I didn’t give more epi at first because the MAP was already like 80 and I didn’t want to be too hypertensive… Speaking of, @narcotics999 I would expect that anaphylaxis while on pump would still manifest with hypotension as a result of vasodilation, assuming a normal pump flow. In this case we were flowing a 2.4 index, not really on any phenylephrine during the bypass run.

Lastly, @Hoya11 I don’t believe that the suctioning or bronch accomplished anything therapeutic- there were no secretions whatsoever, and the tube was in textbook perfect position. If there had been some sort of obstruction that was so dramatic that both lungs were entirely hyper-inflated, almost surely would’ve gotten SOMETHING back when suctioning, or seen something with the bronch…

I appreciate everyone’s thoughts. I posted the case here because it was a little bit strange, certainly not a slam dunk for bronchospasm for reasons that have already been pointed out, but curious to hear any others’ ideas

 

[Arch Guillotti]

I am having a hard time understanding the ketamine. Was albuterol given?

 

[Hork Bajir]

Gave it as a bronchodilator, and to deepen anesthesia (though primarily as a bronchodilator). Didn't give albuterol right away because I didn't want to (or couldn't) really ventilate at that point, seeing as the lungs were so hyper-inflated. I gave albuterol as soon as the lungs deflated enough that we were able to re-establish ventilation.

 

[nimbus]

Sounds like some kind of one way ball valve air trapping phenomenon but mechanistically I couldn’t explain it. You ruled out an endobronchial tumor with FOB. It would have been interesting to see what happened if the surgeon gave a gentle squeeze to the hyperinflated lungs. How did the initial alveolar recruitment feel?

Good strange case.

 

[Arch Guillotti]

Had an interesting thing happen in the cardiac OR yesterday:

50 year old man, severe MR w/ P2 prolapse, scheduled for MV repair. Otherwise pretty healthy and well compensated, had albuterol on his med list but didn't carry a formal diagnosis of asthma and denied using his inhaler in years.

At the end of the bypass run, cross clamp comes off, start to pace, did a little recruitment then started trying to ventilate but was getting very high airway pressures. In the surgical field, the lungs looked VERY hyper-inflated- pooching out into the midline from both sides. I disconnected the ETT, and the lungs didn't really come down at all. Surgeon tells me that the lungs actually seemed like they were kind of inflated for the bypass run. I pass a suction catheter down the ETT, get nothing back. Call for a bronchoscope, do a quick look, ETT is in perfect position and the proximal airways look totally normal. At this point I'm a bit at a loss, and surgeon is getting impatient. I give more paralytic, ask the perfusionist to increase the iso, no change. At this point I'm figuring it must be bronchospasm, so I give 15mcg of epi and 50mg of ketamine... over the next few minutes, lungs gradually deflate. I'm able to start ventilating and the airway pressures normalize. Come off pump and everything is fine. Minimal obstructive changes to the capnographic waveform, though really not dramatic- gave some albuterol since we were moving air at this point. Next day I see the patient in the ICU- extubated, doing great, no respiratory issues.

I feel like it must have been bronchospasm, since I don't know how else to explain what happened... Anaphylaxis or generalized histamine release feels less likely, since the hemodynamics were fine the whole time and there were no other signs/symptoms. No medications had been given while we were on pump other than heparin. Maybe it was bronchospasm from heparin? But we saw no issues with the initial dose for cannulation.

Anyway, I thought it was interesting and had never encountered anything quite like that before. Curious if anyone has any thoughts, or has seen a similar situation

So the surgeon is looking directly at the lungs - can he not tamp them down?

 

[vector2]

Only things I can think of are bronchospasm related to subclinical anaphylaxis, hypothermia (like cold induced asthma), or maybe his bronchioles were really sensitive to a beta blocker given that day?

 

[vector2]

So the surgeon is looking directly at the lungs - can he not tamp them down?

Smashing down hyperinflated lungs secondary to expiratory obstruction while fully heparinized wouldn't be my first choice. With obstruction that bad you're more likely to rupture alveoli than actually de-gas the lung.

 

[Hoya11]

@vector2 Baseline lung mechanics, capnography, blood gas, P:F, etc. were all stone cold normal prior to that point in the case.

@Hoya11 I agree that 15mxg of epi and 50 of ketamine isn’t a huge dose for bad bronchospasm; I didn’t give more epi at first because the MAP was already like 80 and I didn’t want to be too hypertensive… Speaking of, @narcotics999 I would expect that anaphylaxis while on pump would still manifest with hypotension as a result of vasodilation, assuming a normal pump flow. In this case we were flowing a 2.4 index, not really on any phenylephrine during the bypass run.

Lastly, @Hoya11 I don’t believe that the suctioning or bronch accomplished anything therapeutic- there were no secretions whatsoever, and the tube was in textbook perfect position. If there had been some sort of obstruction that was so dramatic that both lungs were entirely hyper-inflated, almost surely would’ve gotten SOMETHING back when suctioning, or seen something with the bronch…

I appreciate everyone’s thoughts. I posted the case here because it was a little bit strange, certainly not a slam dunk for bronchospasm for reasons that have already been pointed out, but curious to hear any others’ ideas

you never know maybe it was something subtle clogging the tube or creating a one way valve.

you did all the right things and it got better - good job!!

 

[sevoflurane]

def. sounds like ow valvevitis

 

[Arch Guillotti]

Smashing down hyperinflated lungs secondary to expiratory obstruction while fully heparinized wouldn't be my first choice. With obstruction that bad you're more likely to rupture alveoli than actually de-gas the lung.

ok so I haven't done hearts since residency > 10 yrs ago but I think there is a distinction between pressing the lung down firmly to see what happens vs "smashing" it down.

 

[Hork Bajir]

ok so I haven't done hearts since residency > 10 yrs ago but I think there is a distinction between pressing the lung down firmly to see what happens vs "smashing" it down.

While you are correct, I’m not sure I would trust this surgeon to make that distinction 😆

 

[Hork Bajir]

For what it’s worth, also, the right pleural space wasn’t open- so I could see the tongue of the left lung popping out into the midline sternotomy, but could only see the medial bulging of the right pleura into the mediastinal space. This was enough visualization to diagnose the problem, but would have been hard to apply any sort of gentle yet effective manual compression to the lungs without opening the right pleural space and doing some additional dissection

 

[vector2]

ok so I haven't done hearts since residency > 10 yrs ago but I think there is a distinction between pressing the lung down firmly to see what happens vs "smashing" it down.

The situation Hork is describing where the circuit is disconnected but yet the lungs are maximally inflated is analogous to one of those bronchospasm scenarios where the lungs are just rocks, e.g. like post-induction and the tube is definitely in but you’re not getting any tidal volume or etco2 even with the popoff closed all the way.

In this kind of air trapping situation where the small airways can’t even get the air out to the big airways under atmospheric pressure (15 psi = 1000 cm H20….which is so high it typically causes deflation and immediate ptx in normal lungs in a closed chest), think about how much external pressure the surgeon would need to put. It’s either gonna be insufficient to the point of not doing anything or strong enough that you’re still getting acute lung injury even you’re lucky enough to not pop some alveoli.

 

[dchz]

I actually have seen this before in fellowship.

The bronchospasm happened after i started to ventilate the lungs during the same time period that happened to OP.

I was freaking out as well like wtf? did something go down and plug the sub segmental bronchus? Nothing suctioned out with ETT suction, didn't have bronchoscope but i called for it. The CT surgeon apparently have seen this and he told me to calm down and just give it a few minutes, and the lungs eventually went back to the same compliance while we just hung out on bypass. Weaned bypass after the lungs functioned normally. Uneventful rest of the case.

The only thing I would have done differently is to give endotracheal Epi. I'd give 10 ccs at 10mcg/cc and then mannually inflate lungs and rinse and repeat until lungs came back to normal. Fwiw I'm not sure whether or nor albuterol would get there if you can't ventilate much, but i know for a fact it won't hurt. So i would have given it as well down the ETT.

 

[Hork Bajir]

@dchz Interesting to hear you've seen something similar. I can't say I've ever actually given tracheal epi- I'm not sure how effective it would have been in this case (nor albuterol for that matter), but it's an interesting idea. The lungs looked like they were about to pop, I really didn't feel like I could give a breath for the sake of getting either medication beyond the carina.

But educate me- you would give 100mcg of epi down the ETT? The MAP was already on the high side- wouldn't you expect significant systemic HTN from that much epi, even given via the trachea?

 

[dchz]

@dchz Interesting to hear you've seen something similar. I can't say I've ever actually given tracheal epi- I'm not sure how effective it would have been in this case (nor albuterol for that matter), but it's an interesting idea. The lungs looked like they were about to pop, I really didn't feel like I could give a breath for the sake of getting either medication beyond the carina.

But educate me- you would give 100mcg of epi down the ETT? The MAP was already on the high side- wouldn't you expect significant systemic HTN from that much epi, even given via the trachea?

Great questions. Disclaimer: I do not have any good medical evidence to back what i'm saying, as i'm not aware of any prospective RCTs involving ETT epi. everything is purely anecdotal/theoretical.

Bottom line: systemic absorption is low and it's really a secondary concern.

Recall that Epi is an ACLS drug that can be given through the ETT. It's on the PALS algorithm and the rule of thumb evident by their algorithm is ETT dose should be 10x the IV dose. So in my mind, giving 100mcg in 10ccs is really akin to giving 10mcg IV. That has been consistent with my experiences when i've given ETT Epi for high suspicion of bronchospasm - the MAP change is barely noticeable.

I think the benefit comes from the volume rather than the amount of epi - giving 100mcgs with 10ccs is way better than giving 100mcgs in 1 cc. The goal is topical Beta 2 agonism. taking from my experience while giving fluids during a bronch, 10ccs down the ETT allows a good amount of fluids to go down to each lung and the manual bagging after helps it to be mixed/pushed down to the distal lung segments. I disagree it won't get past the carina as the mere squirt from the syringe will get the fluids well into more distal segments, I can confirm this as I have bronched many times after I squirt epi and the 10ccs are not visible in the proximal segments.

Regarding the hypertension in your scenario: that is on the bottom of the list of concerns. You're still on CPB, you can't come off anyways without working lungs. The priority is fixing the lungs at all cost and then dealing with the consequences, which is fairly easy on CPB - if you see the BP go high and there is increased cardiac output, just take volume out of the heart and wait it out.

Gave it as a bronchodilator, and to deepen anesthesia (though primarily as a bronchodilator). Didn't give albuterol right away because I didn't want to (or couldn't) really ventilate at that point, seeing as the lungs were so hyper-inflated. I gave albuterol as soon as the lungs deflated enough that we were able to re-establish ventilation.

I also question ketamine as bronchodilator under GA. Yes, ketamine is a bronchodilator because epi is a broncho dilator and the epi is released 2/2 hallucinations while awake.

I do not believe the same effect is had under GA as there is no epi release during GA. I give about 200 mg of ketamine for > 90% of my CPB cases and I don't believe I have noticed any bronchodilatory effects.

 

[vector2]

Just want to add that ketamine has multiple postulated mechanisms in the treatment of bronchospasm:

Mechanism of action of ketamine as a bronchodilator​

The major pathophysiology in asthma comprises of airway hyper reactivity, increased vascular permeability, smooth muscle spasm, and release of inflammatory mediators. In many experimental studies, ketamine has been found to alter respiratory mechanics and produce airway relaxation by acting on various receptors and inflammatory cascades, which mediate bronchospasm. Several mechanisms of action have been proposed to explain this effect.[10,11,12,13,14,15,16,17,18]

Ketamine as an imunomodulator​

It has been demonstrated that the activation of NMDA (N-methyl-D-aspartic acid) receptors in the lung and airway triggers acute lung injury characterized by pulmonary edema and airway constriction. Ketamine blocks NMDA receptor-induced bronchoconstriction.[10]
It has been demonstrated that increased nitric oxide levels mediate bronchospasm. Ketamine reduces nitric oxide levels by downregulating inducible nitric oxide synthetase enzyme activity. It inhibits overexpression of mRNA and protein of induced nitric oxide synthetase and reduces the production of nitric oxide in pulmonary tissues.[11]
Release of inflammatory mediators form the central component of inflammatory changes and airway hyper-reactivity in acute asthma. It has been proved that a clinically significant concentration of ketamine can suppress macrophage function, oxidative ability, and inflammatory cytokine production via reduction of mitochondrial membrane potential. Ketamine interferes with the recruitment of macrophages and cytokine production and thus is a potent anti-inflammatory agent useful in acute asthma.[12] It also reduces Interleukin-4 (IL-4) concentration as shown in rat asthma models.[13] Ketamine has also been found to reverse histamine-induced bronchoconstriction and enhance adrenaline-induced bronchodilatation.[14]

Effect of ketamine on catecholamines​

One hypothesis is that ketamine increases synaptic catecholamine levels by blocking the re-uptake of norepinephrine into presynaptic sympathetic neurons. These endogenous catecholamines act on β2 receptors and lead to bronchodilation. It has been shown that increase in free norepinephrine parallels the peak bronchodilatory effect of ketamine, and this effect can be diminished by β-adrenergic blockade.[15]

Effect of ketamine on airway smooth muscles​

Ketamine exerts an anti-cholinergic effect on bronchial smooth muscles by inhibiting vagal outflow.[16] It decreases calcium influx in smooth muscles by inhibiting L-type calcium channels, and resultant decrease in intracellular calcium relaxes airway smooth muscle.[17]

Effect of ketamine on vagal nerve​

It has been studied that not only inflammatory cells but also neural mechanisms, by which tachykinins are released from vagal afferent C-fiber, contribute to asthma. Ketamine and its isomers have spasmolytic effects on airway smooth muscles precontracted with tachykinins, thus causing airway relaxation.[18]
These postulated mechanisms collectively indicate that ketamine attenuates many of the central components of inflammatory changes and airway hyper-responsiveness in asthma and can act as a suitable therapeutic intervention in status asthmaticus.

 

[Mman]

I also question ketamine as bronchodilator under GA

I have definitely seen ketamine bronchodilate under GA and routinely use it in small doses prophylactically in people I am worried about bronchospasm with.

 

[GassYous]

Sorta related but if you put a vial of phenylephrine in the nose with some lido for vasoconstriction, it doesn't increase the pressure like what you would see if you gave it IV.

 

[Hork Bajir]

@dchz and @vector2 i appreciate the discussion. I was of the impression that the bronchodilatory effects of ketamine were related to mechanisms beyond just increased catechol release, as Vector pointed out, but who really knows. At the end of the day I feel like it may have helped, and almost certainly didn’t hurt. Will consider ETT epi next time

 

[dchz]

Just want to add that ketamine has multiple postulated mechanisms in the treatment of bronchospasm:

Mechanism of action of ketamine as a bronchodilator​

The major pathophysiology in asthma comprises of airway hyper reactivity, increased vascular permeability, smooth muscle spasm, and release of inflammatory mediators. In many experimental studies, ketamine has been found to alter respiratory mechanics and produce airway relaxation by acting on various receptors and inflammatory cascades, which mediate bronchospasm. Several mechanisms of action have been proposed to explain this effect.[10,11,12,13,14,15,16,17,18]

Ketamine as an imunomodulator​

It has been demonstrated that the activation of NMDA (N-methyl-D-aspartic acid) receptors in the lung and airway triggers acute lung injury characterized by pulmonary edema and airway constriction. Ketamine blocks NMDA receptor-induced bronchoconstriction.[10]
It has been demonstrated that increased nitric oxide levels mediate bronchospasm. Ketamine reduces nitric oxide levels by downregulating inducible nitric oxide synthetase enzyme activity. It inhibits overexpression of mRNA and protein of induced nitric oxide synthetase and reduces the production of nitric oxide in pulmonary tissues.[11]
Release of inflammatory mediators form the central component of inflammatory changes and airway hyper-reactivity in acute asthma. It has been proved that a clinically significant concentration of ketamine can suppress macrophage function, oxidative ability, and inflammatory cytokine production via reduction of mitochondrial membrane potential. Ketamine interferes with the recruitment of macrophages and cytokine production and thus is a potent anti-inflammatory agent useful in acute asthma.[12] It also reduces Interleukin-4 (IL-4) concentration as shown in rat asthma models.[13] Ketamine has also been found to reverse histamine-induced bronchoconstriction and enhance adrenaline-induced bronchodilatation.[14]

Effect of ketamine on catecholamines​

One hypothesis is that ketamine increases synaptic catecholamine levels by blocking the re-uptake of norepinephrine into presynaptic sympathetic neurons. These endogenous catecholamines act on β2 receptors and lead to bronchodilation. It has been shown that increase in free norepinephrine parallels the peak bronchodilatory effect of ketamine, and this effect can be diminished by β-adrenergic blockade.[15]

Effect of ketamine on airway smooth muscles​

Ketamine exerts an anti-cholinergic effect on bronchial smooth muscles by inhibiting vagal outflow.[16] It decreases calcium influx in smooth muscles by inhibiting L-type calcium channels, and resultant decrease in intracellular calcium relaxes airway smooth muscle.[17]

Effect of ketamine on vagal nerve​

It has been studied that not only inflammatory cells but also neural mechanisms, by which tachykinins are released from vagal afferent C-fiber, contribute to asthma. Ketamine and its isomers have spasmolytic effects on airway smooth muscles precontracted with tachykinins, thus causing airway relaxation.[18]
These postulated mechanisms collectively indicate that ketamine attenuates many of the central components of inflammatory changes and airway hyper-responsiveness in asthma and can act as a suitable therapeutic intervention in status asthmaticus.

I have definitely seen ketamine bronchodilate under GA and routinely use it in small doses prophylactically in people I am worried about bronchospasm with.

well i stand corrected.

However, my last 3 bronchospasms all got 200 mg of ketamine. I'm struggling with that.

 

[MirrorTodd]

well i stand corrected.

However, my last 3 bronchospasms all got 200 mg of ketamine. I'm struggling with that.

But they didn't get two hundred and ONE!

 

[vector2]

well i stand corrected.

However, my last 3 bronchospasms all got 200 mg of ketamine. I'm struggling with that.

I've never seen nor personally administered just ketamine in isolation for a bronchsopasm. I've always given it as a synergistic treatment after I've given albuterol, volatile, propofol, epi, mag etc. Despite its multiple mechanisms, I don't think it's particularly potent by itself compared to the mainstay treatments.

Also do you guys have routine access to terbutaline in the OR? I find 25-100 mcg IV q2ish min prn to be a nice alternative to IV epi when you're worried about hemodynamics.

 

[Arch Guillotti]

Also do you guys have routine access to terbutaline in the OR? I find 25-100 mcg IV q2ish min prn to be a nice alternative to IV epi when you're worried about hemodynamics.

I have only ever worked with one guy who used it and he swore by it.

 

[Hork Bajir]

Never seen terb in the OR

Mag also would have been a good idea in this case, since we were a bit hypertensive- don’t have it in the room, but probably could have gotten it faster than terbutaline

 

[Beeftenderloin]

Never seen terb in the OR

Mag also would have been a good idea in this case, since we were a bit hypertensive- don’t have it in the room, but probably could have gotten it faster than terbutaline

Ask perfusion if they’ve got any Mg. Ours routinely dump 2-4g in the reservoir in patients we have to shock more than a couple times coming off.

 

[dchz]

Also do you guys have routine access to terbutaline in the OR? I find 25-100 mcg IV q2ish min prn to be a nice alternative to IV epi when you're worried about hemodynamics.

Don't have it in my current practice.

I did give it during a horrible bronchospasm in fellowship. But I also gave Epi ETT and IV, albuterol, and recruitment. So who knows which one worked. Never gave terbutaline in isolation because it's not readily available.

 

[deleted875186]

Did he get the Covid vaccine …. If so you’ll have to write up the case report