What drip would you choose in this patient post-arrest?

  • Dopamine

    Votes: 11 44.0%
  • Phenylephrine

    Votes: 3 12.0%
  • Norepinephrine

    Votes: 3 12.0%
  • Dobutamine

    Votes: 5 20.0%
  • Dobutamine + Norepinephrine

    Votes: 1 4.0%
  • Other

    Votes: 2 8.0%

  • Total voters
    25

waterski232002

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Here's an interesting case I had in the ER today.

86 yo F w/ hx of HTN, CVA, presented to the ER after 4 hrs of AMS and new L sided hemiplegia in a non-verbal state, but airway intact. Her BP was 205/100, HR 130-170 in paroxysmal A-fib w/ RVR and going in and out of sinus tach. Multiple repeat BP's were over 200 systolic. It was obvious she was stroking out, and we suspected an ICH. I gave her 20mg of labetalol and her HR slowed down into the 90-100 range w/ BP in the 170-200 range, which I was satisfied with. About 3 minutes later she seized and was given 2 mg ativan. Immediately after the ativan, her O2 sat and HR began dropping steadily from the 90's to 80's to 70's.... to the 30's when she lost a pulse and we initiated CPR (all within a matter of 40 seconds) and intubated her. We regained a pulse after 1 round of epi and atropine. Her post-arrest BP was 97/40 and HR in the low 90's. Then I called for a drip....

So... what would you guys choose and why? Three different drips were thrown in the air before we settled on one (attending's decision, but not my choice... I got trumped).

I'll give an update on the outcome later....
 

southerndoc

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waterski232002 said:
Here's an interesting case I had in the ER today.

86 yo F w/ hx of HTN, CVA, presented to the ER after 4 hrs of AMS and new L sided hemiplegia in a non-verbal state, but airway intact. Her BP was 205/100, HR 130-170 in paroxysmal A-fib w/ RVR and going in and out of sinus tach. Multiple repeat BP's were over 200 systolic. It was obvious she was stroking out, and we suspected an ICH. I gave her 20mg of labetalol and her HR slowed down into the 90-100 range w/ BP in the 170-200 range, which I was satisfied with. About 3 minutes later she seized and was given 2 mg ativan. Immediately after the ativan, her O2 sat and HR began dropping steadily from the 90's to 80's to 70's.... to the 30's when she lost a pulse and we initiated CPR (all within a matter of 40 seconds) and intubated her. We regained a pulse after 1 round of epi and atropine. Her post-arrest BP was 97/40 and HR in the low 90's. Then I called for a drip....

So... what would you guys choose and why? Three different drips were thrown in the air before we settled on one (attending's decision, but not my choice... I got trumped).

I'll give an update on the outcome later....
Ugh, did you try an IV fluid bolus first??????

If you didn't, then this is a moot point. If you did, then I would go with an alpha agonist.

It is unlikely that a beta agonist will overcome the beta blockade of labetalol unless you use high doses. These high doses would approach alpha agonistic doses. Alpha agonism will work because labetalol has a 7:1 beta-to-alpha antagonism when given intravenously (3:1 when given orally).

So out of this, it would be either norepinephrine, phenylephrine, or high-dose dopamine.
 
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waterski232002

waterski232002

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southerndoc said:
Ugh, did you try an IV fluid bolus first??????

If you didn't, then this is a moot point. If you did, then I would go with an alpha agonist.

It is unlikely that a beta agonist will overcome the beta blockade of labetalol unless you use high doses. These high doses would approach alpha agonistic doses. Alpha agonism will work because labetalol has a 7:1 beta-to-alpha antagonism when given intravenously (3:1 when given orally).

So out of this, it would be either norepinephrine, phenylephrine, or high-dose dopamine.
The patient was getting IVF the entire time. Slow drip at first sinced she was already hypertensive, then wide open when the code started. However, the etiology of the arrest was likely secondary to herniation vs apneic induced cardiac arrest. Neither one likely to respond to IVF alone.
 
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NinerNiner999

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Of those choices, I chose NE due to the catecholamine load that is needed to maintain CCP and attempt to maintain an elevated blood pressure in this already presumed hypertensive stroke patient. Also, I'd bolus some phenytoin...
 

beyond all hope

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Try to reverse the labetolol with glucagon. She was bradying down and you had her on a beta blocker. Then I would have considered used an agent that I normally hate that causes significant tachycardia (dopamine)

Of course, the problem with reversing the beta blockage is unopposed alpha blockade. Hence Vasopressin - a vasopressor with significant peripheral effects that doesn't act on the catecholamine system.

IVF always comes first. They say in cerebrovascular accidents you want to maintain euvolemia, but when you haven't got a BP that's number one priority.

P.S. All of the BS about which pressor is better hasn't bourne out any fruit in the research. Some would suggest they're all about the same and all make very little difference in outcome, unlike the River's protocol for sepsis, ASA in MI, etc.
 

Seaglass

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Umm . . . this lady is dead. By starting any drip you are doing her a disservice. That said I would start Epi. Good beta, good alpha.
 

NinerNiner999

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Not so sure she's dead - one round of epi/atropine and she is perfusing within 2 minutes. Assuming the stroke didn't do too much damage, her brain should still be ok. It sounds like the ativan dropped her pressure too low...
 

beyond all hope

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Just because someone crashes doesn't mean that they are dead. Yes, probably at least 80% mortality at this point, but that leaves a good strong 20%. The probability of survival neurologically intact is probably close to 5%. (note these numbers are entirely speculation and based on no evidence whatsoever)

I agree that in a system with limited resources, critical care time should be rationed out to those it stands to benefit the most. But in the system that we work in we are expected to shoot 90% of our effort at the 10% that are least likely to benefit and that's not going to change any time soon.

As a resident it's common to get very cynical about patient outcomes. That being said, you'll lose a lot of these patients, but the first time that you rescue someone from certain death and they walk out of the hospital neurologically intact you'll be happy you put in the effort.
 

southerndoc

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beyond all hope said:
Of course, the problem with reversing the beta blockage is unopposed alpha blockade. Hence Vasopressin - a vasopressor with significant peripheral effects that doesn't act on the catecholamine system.
Glucagon doesn't reverse beta blockade. It increases inotropy and chronotropy through an independent G-protein stimulated pathway. In other words, it does the same thing as beta-stimulation, but through a different receptor. So you wouldn't have unopposed alpha blockade.

Glucagon is a good thought though, but I would try to avoid as much as possible. It would induce hyperglycemia, which we all know doesn't do so well in the setting of brain injuries.
 

Seaglass

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Hmm AMS (suspect ICH) -> sz -> progressive bradycardia -> asystolic arrest = very dead. Sure you can get the heart to beat again with enough epi but her chances of neurological survival approach 0.
 
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It doesn't make a difference how "dead" you think she is, or how poor her prognosis is... you still need to follow standard of care in the absence of a DNR/DNI order or a family memeber who agrees to withdrawl support. This means coding the patient, and starting a drip when she has ROSC.

I know you're not advocating letting this patient die b/c you feel like NOT starting a drip or doing CPR??? :rolleyes:
 

augmel

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Unless you left out that she was already adequately anticoagulated, I think an embolic stroke from her a-fib is much more likely. (or maybe you know the CT results now) If that is the case, then neurologists advocate letting the SBP ride to 220. I would have done dig first for her HR so as to let her autoregulate her BP to keep perfusing that penumbra. MIght not have seized that way. I'm not sure what to do about a SBP of 97 then. I have no idea what BP range to be shooting for in a recent stroke.
 
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waterski232002

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augmel said:
Unless you left out that she was already adequately anticoagulated, I think an embolic stroke from her a-fib is much more likely. (or maybe you know the CT results now) If that is the case, then neurologists advocate letting the SBP ride to 220. I would have done dig first for her HR so as to let her autoregulate her BP to keep perfusing that penumbra. MIght not have seized that way. I'm not sure what to do about a SBP of 97 then. I have no idea what BP range to be shooting for in a recent stroke.
The patient had no history of A-Fib and she never made it to CT. It was presumed that the patient had an ICH secondary to severe hypertension. In that case, decreasing the BP 20-30% is reasonable. Even if we suspected embolic stroke as the primary diagnosis, there wouldn't be anything to do except supportive care b/c tPA was out of the question (4 hrs out and BP >200).
 
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Case Follow up:

So... I wanted a dopamine gtt, but my attending wanted a phenylepherine gtt. I felt that tachycardia wasn't a concern anymore since the patient just suffered a bradycardic arrest, and dopamine is generally the gtt of choice post-arrest according to ACLS guidelines. The reasoning behind phenylephrine was that it was pure alpha and would not precipitate any further tachycardia/tachyarrhythmias. To me... it's hard to imagine that a pure alpha agonist drip is going to maintain cardiac contractility after just suffering a bradycardic arrest. I think she needed some Ionotropy.

Before we could start either drip the patient bradyed down to the 30's again and lost her pulse. CPR was restarted. We coded her for another 15 minutes and went through 3 more rounds or epi, threw in a little calcium and bicarb and called it a day.
 

augmel

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waterski232002 said:
The patient had no history of A-Fib and she never made it to CT. It was presumed that the patient had an ICH secondary to severe hypertension. In that case, decreasing the BP 20-30% is reasonable. Even if we suspected embolic stroke as the primary diagnosis, there wouldn't be anything to do except supportive care b/c tPA was out of the question (4 hrs out and BP >200).
I agree that if this was a hypertensive ICH that decreasing the BP 20-30% is reasonable, though the data is still not clear on whether this is truly the best thing or not. The point I was making is that severe hypertension is often the result of an embolic stroke as the brain tries to perfuse itself in the setting of disrupted autoregulation. Therefore, with new a-fib, I would still be more worried about embolic stroke. While TPA would not have been a consideration here, as you mentioned, not treating the hypertension would have been the preferred management strategy if embolic stroke was the presumed dx.
 

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waterski232002 said:
Case Follow up:
I agree with your reasoning, but after 30 years of doing this, I have to agree with Seaglass's contention that futile care should not be delivered. At most it prolongs the agony and increases the cost to family.

We can argue over whether this case was futile till the cows are in bed, and I'm not interested in doing that. I don't know what I would have done in the room. But through the retrospectroscope when a patient goes from presumed ICH with severe hypertension and tachycardia to hypotension and severe bradycardia, they've herniated and they're done.
 
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waterski232002

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Thanks for all the input guys.... I appreciate the feedback.
 

southerndoc

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waterski232002 said:
Before we could start either drip the patient bradyed down to the 30's again and lost her pulse. CPR was restarted. We coded her for another 15 minutes and went through 3 more rounds or epi, threw in a little calcium and bicarb and called it a day.
Epi wore off, eh?
 
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