Asystole during induction/Intubation

[toughlife]

While on call in SICU last night, had a 47 y/o male s/p open AAA repair,POD #2, hemodynamically stable, 280lbs, hx of OSA on bipap at home.

Pt had hx of HTN on 5 antihypertensives at home, with rebound hypertension post-op not amenable to scheduled lopressor and labelatol. Started him on a labelatol gtt. Pressures back to 120-130s systolic. Pt also on 0.1mg dilaudid IVPCA q6 min.

Post-op, pt brought intubated from OR, extubated on DOS, on cpap overnight then switched to bipap next day with FiO2 70%. Pt desatting to high 80%s while attempting to wean FiO2 to 60-65% overnight. ABGs looking OK. Work of breathing increasing early this am, now on 80% FiO2. Pt endorsing difficulty keeping up with breathing effort. CXR showing fluffly alveolar infiltrates bilaterally. Attending decides to intubate.
Glidescope, CA-2 and attending at bedside. Pt gets 20mg of etomidate, 200 of sux, CA-2 with some difficulty getting tube in. All of the sudden pt bradys down to 60s-->40s->20s-->asystole all within 15 seconds. Tube finally in.
Start chest compressions, 1mg atropine in, nothing, continues chest compressions for 15 secs, HR kicks in at 10s and increases to 80 over 1 minute. BP back to 120s systolic. pt stable.

Never seen this before. Any ideas?

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[InGasWeTrust]

high dose sux....

200 of sux?

 

[Conflicted]

Hmm

How would suxx cause asystole regardless of the dose?

 

[PGY2]

Patient may have been acidotic to begin with, then the 200mg of sux may have been just enough to push his potassium levels high enough to cause this.

Just my 2 cents

 

[ecCA1]

succ acts like ach. ach can slow down hr, right?

 

[Conflicted]

bradycardia due to suxx is usually transient and easily fixed. However, asystole is a whole other issue.

PGY2, thats a reasonable question. Suxx does not shift potassium fast enough to cause asystole so quickly. Moreoften this happens on duschannes MS kids who get suxx and it starts with Vtach/Vfib.

After reviewing big miller, i dont see any pharmacologic way that suxx alone could cause asystole. I use it on an almost daily basis and have never even seen bradycardia associated with it let alone asystole.

I suspect something else was happening.

 

[militarymd]

hypoxia

 

[Conflicted]

exactly

 

[rn29306]

I've seen a couple hyperkalemic arrests after anectine and trust me...the codes are MUCH longer and more involved than 15 seconds of CPR, one round of atropine, and oxygenation / ventilation.

True hyperkalemic arrests are a beoch.

 

[7by11thenout]

bradycardia due to suxx is usually transient and easily fixed. However, asystole is a whole other issue.

PGY2, thats a reasonable question. Suxx does not shift potassium fast enough to cause asystole so quickly. Moreoften this happens on duschannes MS kids who get suxx and it starts with Vtach/Vfib.

After reviewing big miller, i dont see any pharmacologic way that suxx alone could cause asystole. I use it on an almost daily basis and have never even seen bradycardia associated with it let alone asystole.

I suspect something else was happening.

di acetylcholine the byproduct of sux breakdown and overdosage. try looking that up. I have seen asystole with sux not just hyperkalemic arrest

 

[Noyac]

I've seen a couple hyperkalemic arrests after anectine and trust me...the codes are MUCH longer and more involved than 15 seconds of CPR, one round of atropine, and oxygenation / ventilation.

True hyperkalemic arrests are a beoch.

I have never seen one. I don't make it a habit giving sux to the wrong folks (not that you do) and neither do the guys I work with.
But you are right, they do not return in 15 sec. They rarely return at all.

This is, as Mil stated, hypoxia more than likely.

 

[Conflicted]

Nifty

Seems its rare but here are a couple articles:

Acta Anaesthesiol Scand. 1984 Apr;28(2):232-5. Links
Bradycardia and cardiac asystole following a single injection of suxamethonium.

* Sorensen M,
* Engbaek J,
* Viby-Mogensen J,
* Guldager H,
* Molke Jensen F.

Twenty cases of severe bradycardia, including 12 cases of cardiac asystole, following administration of a single dose of suxamethonium to 17 adult patients are presented. Treatment consisted of i.v. atropine in 16 cases, and in four cases external cardiac massage or a precordial thump was also given. Remission was complete in all cases. The mechanism is not known, but it is suggested that i.v. administration of fentanyl at induction may enhance the tendency to bradycardia following suxamethonium. Absence of preoperative atropine may also be of importance.

: Acta Anaesthesiol Scand. 1986 Oct;30(7):571-3. Links
Asystole and bradycardia in adult patients after a single dose of suxamethonium.

* Inoue K,
* Reichelt W.

Two cases of cardiac asystole and one case of severe bradycardia were seen following a single injection of suxamethonium in a series of 46 adult patients in whom anaesthesia was induced with fentanyl and etomidate. It is suggested that the vagomimetic effects of fentanyl and, possibly also of etomidate, may contribute to the enhancement of the bradycardic effects of suxamethonium.

 

[Antibiotix2006]

Its definitely hypoxia.

Someone requiring that high FiO2s will desaturate immediately, esp if you knock off their spontaneous efforts.
Sometimes its hard to maintain saturation even while mask ventilating these guys after giving a relaxant.

I've seen it happen within 10-15 seconds of giving a relaxant... and it has nothing to do with the relaxant.

 

[EV-Stentor]

While on call in SICU last night, had a 47 y/o male s/p open AAA repair,POD #2, hemodynamically stable, 280lbs, hx of OSA on bipap at home.

Pt had hx of HTN on 5 antihypertensives at home, with rebound hypertension post-op not amenable to scheduled lopressor and labelatol. Started him on a labelatol gtt. Pressures back to 120-130s systolic. Pt also on 0.1mg dilaudid IVPCA q6 min.

Post-op, pt brought intubated from OR, extubated on DOS, on cpap overnight then switched to bipap next day with FiO2 70%. Pt desatting to high 80%s while attempting to wean FiO2 to 60-65% overnight. ABGs looking OK. Work of breathing increasing early this am, now on 80% FiO2. Pt endorsing difficulty keeping up with breathing effort. CXR showing fluffly alveolar infiltrates bilaterally. Attending decides to intubate.
Glidescope, CA-2 and attending at bedside. Pt gets 20mg of etomidate, 200 of sux, CA-2 with some difficulty getting tube in. All of the sudden pt bradys down to 60s-->40s->20s-->asystole all within 15 seconds. Tube finally in.
Start chest compressions, 1mg atropine in, nothing, continues chest compressions for 15 secs, HR kicks in at 10s and increases to 80 over 1 minute. BP back to 120s systolic. pt stable.

Never seen this before. Any ideas?

Hey this may very well be secondary to severe hypoxia but why 200mg of sux? Could it be that the asystole was preceded by VFib induced by hyperkalemia that no one noticed? Also just curious why the Glidescope? Was he a documented or suspected difficult intubation? Sometimes that glidescope thingy takes too long and hence the probable hypoxia. Me personally I would stick in a Mac 4 in this obese dude and get done with it
Good job with the CPR though and remember always go on the lower dose with sux...i never give more than 100mg and on the floors during a emergent intubation my regimen is 20mg ONLY if needed. Peace out!

 

[militarymd]

Hey this may very well be secondary to severe hypoxia but why 200mg of sux? Could it be that the asystole was preceded by VFib induced by hyperkalemia that no one noticed? Also just curious why the Glidescope? Was he a documented or suspected difficult intubation? Sometimes that glidescope thingy takes too long and hence the probable hypoxia. Me personally I would stick in a Mac 4 in this obese dude and get done with it
Good job with the CPR though and remember always go on the lower dose with sux...i never give more than 100mg and on the floors during a emergent intubation my regimen is 20mg ONLY if needed. Peace out!

The ONE AND ONLY hyperkalemic arrest from succinylcholine that I attended had a sinusoidal ECG.....patient never fibrillated.

 

[jetproppilot]

on the floors during a emergent intubation my regimen is 20mg ONLY if needed. Peace out!

I agree.

I give 40mg but same concept.

 

[Conflicted]

JPP and EV

Why do you fellows use such a low dose? In emergent intubations im using 2 mg / kg which is typically in the 120-160 range.

 

[jetproppilot]

JPP and EV

Why do you fellows use such a low dose? In emergent intubations im using 2 mg / kg which is typically in the 120-160 range.

If youre on the floor you probably have no backup.

A small dose doesnt take that much longer to hit...and you can mask in the meantime....40 mg will give you a minute or so of paralysis...just enough for the intubation...and will redistribute quickly in case things go awry.

In essence its all you need for a floor intubation.

Same for laryngospasm in the OR....usually you just need 20-40 mg sux to break it (adults)....saves you 5-10 minutes of sitting in the room waiting for the big dose of sux to wear off.

 

[Conflicted]

JPP

thanks, ill keep that in mind!

 

[toughlife]

Hey this may very well be secondary to severe hypoxia but why 200mg of sux? Could it be that the asystole was preceded by VFib induced by hyperkalemia that no one noticed? Also just curious why the Glidescope? Was he a documented or suspected difficult intubation? Sometimes that glidescope thingy takes too long and hence the probable hypoxia. Me personally I would stick in a Mac 4 in this obese dude and get done with it
Good job with the CPR though and remember always go on the lower dose with sux...i never give more than 100mg and on the floors during a emergent intubation my regimen is 20mg ONLY if needed. Peace out!

I agree 200mg was way much since usually 1-1.5mg/ks is the appropriate dose. On reviewing pt's anesthesia record I noticed it said fiberoptic was used but also said Grade I view, mac 4 blade. Then I realized the pt had a DLT placed and a fiberoptic was used to likely check placement of the DLT.

The glidescope was used in case the pt had a difficult airway and since the FOB comment was there the attending didn't want to take chances.

The guy was hypoxic and I was the first to notice when his sats went from low 90s to 80 to 70s and on. I was only the intern caring for the patient in the ICU so I was not able to dictate what he got in terms of drugs since the attending and CA-2 were present. Good learning experience though

 

[EV-Stentor]

JPP and EV

Why do you fellows use such a low dose? In emergent intubations im using 2 mg / kg which is typically in the 120-160 range.

I use small doses on the floor for the reasons Jet mentioned...you really only need a brief relaxation in such emergent conditions and furthermore on the floors the patients are generally bedbound for weeks sometime especially in the ICUs.... this inactivity can theoretically cause unregulation of extra-junctional nAch receptors which will increase the risk of massive hyperkalemia from sux...not much different from a burn patient only maybe to a lesser degree of severity.

Also in the OR lean towards the 1- 1.5 mg/kg dose and not the full 2mg/kg you mention. Peace bro and keep the gas flowing

 

[EV-Stentor]

I agree 200mg was way much since usually 1-1.5mg/ks is the appropriate dose. On reviewing pt's anesthesia record I noticed it said fiberoptic was used but also said Grade I view, mac 4 blade. Then I realized the pt had a DLT placed and a fiberoptic was used to likely check placement of the DLT.

The glidescope was used in case the pt had a difficult airway and since the FOB comment was there the attending didn't want to take chances.

The guy was hypoxic and I was the first to notice when his sats went from low 90s to 80 to 70s and on. I was only the intern caring for the patient in the ICU so I was not able to dictate what he got in terms of drugs since the attending and CA-2 were present. Good learning experience though

Oops didn't see your response before my above post but its all good. Keep up the good work.
I know exactly what you mean with those silly anesth records...you place the DLT with simple laryngoscopy but have to check the FOB box for tube placement check..it may at first glance appear to be a straight FOB for difficult airway...merde

 

[amar_ml]

was the patient adequately preoxygenated?
hypoxiai is the most commonest thing. a patient with 280 lbs can easily deplete his oxygen stores
is the time to intubate prolonged?
mask ventlation must be done inbetween attempts in such cases
hyperkalemia?
a possibility
sux?
the dose used is high. might have produced a transient hyperkalemia, or the increased dose of sux could have produced increased levels of succinyl monocholine, resulting in bradycardia

the way the event occured is strongly in favour of hypoxia....hyperkalemic arrests are not so simple to resuctitate in most cases.

 

[lotsapain]

Wow.. this is an old thread but interesting discussion I am a CA-3 and though I wa sick as a dog on call last night... induced on the floor with 20 of etmodate plus 80 of sux ona somewhat hypotensive paitnet... my CA-1 meddled with intubation a bit... the guy bradyied down to 30s I called for the code cart started CPR... etc. I don't think this was sux, I think it was hypoxia which was left untreatd too long causing ischemia...I very rarely use sux on the floor..... but even when I do I have never seen brady...

 

[Planktonmd]

Wow.. this is an old thread but interesting discussion I am a CA-3 and though I wa sick as a dog on call last night... induced on the floor with 20 of etmodate plus 80 of sux ona somewhat hypotensive paitnet... my CA-1 meddled with intubation a bit... the guy bradyied down to 30s I called for the code cart started CPR... etc. I don't think this was sux, I think it was hypoxia which was left untreatd too long causing ischemia...I very rarely use sux on the floor..... but even when I do I have never seen brady...

Use it more and you will.
By the way the bradycardia seen with hypoxia is caused by a vagal response rather than ischemia and it can be delayed by anticholinergics.

 

[Pooh & Annie]

Wow.. this is an old thread but interesting discussion I am a CA-3 and though I wa sick as a dog on call last night... induced on the floor with 20 of etmodate plus 80 of sux ona somewhat hypotensive paitnet... my CA-1 meddled with intubation a bit... the guy bradyied down to 30s I called for the code cart started CPR... etc. I don't think this was sux, I think it was hypoxia which was left untreatd too long causing ischemia...I very rarely use sux on the floor..... but even when I do I have never seen brady...

I always wonder about when to use sux or not on the floor. Obvoiusly avoid it with the major contrainications, but otherwise it seems like absolutely every person has their own reasons for using or not using it. We had a MICU intubation last night on what looked like a tough intubation and likely a tough mask. Would you guys use it to make the DL easier (assuming no FOB immediately available), or would you try with just induction agent first? Would you be more likely to use it if you're expecting sats to drop fast? We rarely used relaxants on kids, and the DL didn't seem any more difficult. Is it usually way more dfficult with adults?

 

[Arch Guillotti]

I always wonder about when to use sux or not on the floor. Obvoiusly avoid it with the major contrainications, but otherwise it seems like absolutely every person has their own reasons for using or not using it. We had a MICU intubation last night on what looked like a tough intubation and likely a tough mask. Would you guys use it to make the DL easier (assuming no FOB immediately available), or would you try with just induction agent first? Would you be more likely to use it if you're expecting sats to drop fast? We rarely used relaxants on kids, and the DL didn't seem any more difficult. Is it usually way more dfficult with adults?

There was a good thread on this very subject a wjile back, it's the old burning bridges theory. I personally hardly ever use sux but wished I had after a few etomidate only inductions. I think a very low dose of sux is a good choice in a lot of situations.

 

[Jeff05]

SUCC stimulates autonomic ganglia - causing parasympathetic overdrive, brady and asystole. hypoxia may also be a contributing or primary factor. additionally, prolonged laryngoscopy (even with glide) can elicit a strong vagal response.