ECT Case

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SurferBoyMD

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Wanted to run an ECT case by you all.

74yo M hx CAD s/p CABG x 4 in the 90s, HTN, HLD, coming in for ECT first time in a year after going into a major depressive episode no suicidal ideation as far as we know.

The nurse in preop calls me and states his heart rate is in the 30s-40s, and wanted me to evaluate.

Pt denies any anginal symptoms and heart failure symptoms. Functionally able to walk around the house and climb stairs. The patient is on metop, and his wife gave him his metoprolol this morning.

He has a normal BP, mentating well, HR 30s. EKG done shown to be sinus bradycardia w/ first degree AV block. No ST changes. Previous 1 year old EKG shows AV block, sinus in 70s-80s.

What would you do? Do the case with risk of parasympathetic response potentiating bradycardia? Give some glyco and proceed? Let the metop metabolize and then do the case? Cancel for workup? Admit w/ cards consult?

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Cancel, cardiology consult, guy needs a pacemaker. Or at least hold metoprolol.
 
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Agree with above. I've coded someone after the shock, I think d/t combo of vagal sux and para activation.

Besides, "Nobody ever died of depression..."

Do you put a magnet on the AICD they newly implanted?
 
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Agree with above. I've coded someone after the shock, I think d/t combo of vagal sux and para activation.

Yep. ECT leads to profound bradycardia in an awful lot of pts, so it's not the kind of case you want to do with someone who starts out in the 30s. If the psychiatrist argues that he's Really Really Depressed, as in thinking of hurting himself, suggest the inpatient treatment he would need anyway in that case.

As for Cards workup, the operative question for me is whether he was on beta blockade when the previous EKG was done. If his heart rate is half what it was a year ago on unchanged therapy, then yeah, he probably deserves a visit to the local EP guy. On the other hand, if he's gone from 70s to 30s by starting metoprolol, maybe he's just getting too much metoprolol and I'd try holding it for a day or two first.
 
Is it possible his wife just accidentally gave him too much metoprolol?
 
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From the 2011
Practice Advisory for the Perioperative Management of Patients with Cardiac Implantable Electronic Devices: Pacemakers and Implantable Cardioverter-Defibrillators
An Updated Report by the American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Implantable Electronic Devices

pg 253:
Advisory for Managing EMI from Electroconvulsive Therapy:
Although transient or long-term myocardial and nervous system effects may be associated with ECT, the Task Force believes that such therapies may be administered to CIED patients without significant damage to a disabled CIED. If ECT must be performed, consult with the ordering physician and the patient’s cardiologist to plan for the first and subsequent ECT’s. All CIEDs should undergo a comprehensive interrogation before the procedure(s). ICD functions should be disabled for shock therapy during ECT; however, be prepared to treat ventricular arrhythmias that occur secondary to the hemodynamic effects of ECT. CIED-dependent patients may require a temporary pacing system to preserve cardiac rate and rhythm during shock therapy. Also, the CIED may require programming to asynchronous activity to avoid myopotential inhibition of the device in pacemaker-dependent patients.
 
Why not slap pads on him, shock the brain, pace transcutaneously if needed?
 
Wanted to run an ECT case by you all.

74yo M hx CAD s/p CABG x 4 in the 90s, HTN, HLD, coming in for ECT first time in a year after going into a major depressive episode no suicidal ideation as far as we know.

The nurse in preop calls me and states his heart rate is in the 30s-40s, and wanted me to evaluate.

Pt denies any anginal symptoms and heart failure symptoms. Functionally able to walk around the house and climb stairs. The patient is on metop, and his wife gave him his metoprolol this morning.

He has a normal BP, mentating well, HR 30s. EKG done shown to be sinus bradycardia w/ first degree AV block. No ST changes. Previous 1 year old EKG shows AV block, sinus in 70s-80s.

What would you do? Do the case with risk of parasympathetic response potentiating bradycardia? Give some glyco and proceed? Let the metop metabolize and then do the case? Cancel for workup? Admit w/ cards consult?
Cancel the case. Call whomever prescribed him the metoprolol to ask if they want him admitted or not. I don't think you can send him home like that. I would send him to the ER if I cannot get a hold of anyone.
 
I ended up cancelling the case, tried calling his cardiologist, left a message, and referred him to our in house cardiology service who'll evaluate him.

I wanted to know if there was anyone out there who might have proceeded with the case.
 
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Then what? Discharge home with HR=30?

So you would cancel/delay any case with a heart rate in the 30s if the patient was otherwise asymptomatic?
 
Actually that bradycardia and the betablockade is optimal for an ECT, it will likely minimize the need for controlling the blood pressure and the tachycardia triggered by the ECT.
I would proceed without hesitation.
 
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I wanted to know if there was anyone out there who might have proceeded with the case.

Actually that bradycardia and the betablockade is optimal for an ECT, it will likely minimize the need for controlling the blood pressure and the tachycardia triggered by the ECT.
I would proceed without hesitation.

 
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So you would cancel/delay any case with a heart rate in the 30s if the patient was otherwise asymptomatic?

Depends on type of case, urgency, and postop disposition. I would cancel this one or any elective outpatient case. I wouldn't cancel an emergency cabg with ischemic heart block or a perf'd viscous.

Fortunately in my 20 year career, the only patients I have encountered presenting with a HR in the 30s have been for cardiac procedures.

Seriously you would do this case? How about a hernia or a knee scope? I would cancel every one. And I'm considered a cowboy where I work.
 
I ended up cancelling the case, tried calling his cardiologist, left a message, and referred him to our in house cardiology service who'll evaluate him.

I wanted to know if there was anyone out there who might have proceeded with the case.
I don't do ECTs, but I do retina with retrobulbar blocks (or just plain old GA cases). In a situation like this, I want to know whether it's the drugs (e.g. beta-blocker) or the patient (i.e. conduction disease). The way I determine it is by pumping the patient full of glycopyrrolate pre-induction (some colleagues even argue for epi to counteract the beta-blockade). If, after titrating up to 0.6 mg of glyco, I cannot budge the heart rate to at least 60-ish, case postponed (extremely rare). If I can fix the bradycardia, the case proceeds; no complications to date. Usually, once they get normocardic, they stay there for the rest of the procedure.
 
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I don't do ECTs, but I do retina with retrobulbar blocks (or just plain old GA cases). In a situation like this, I want to know whether it's the drugs (e.g. beta-blocker) or the patient (i.e. conduction disease). The way I determine it is by pumping the patient full of glycopyrrolate pre-induction (some colleagues even argue for epi to counteract the beta-blockade). If, after titrating up to 0.6 mg of glyco, I cannot budge the heart rate to at least 60-ish, case postponed (extremely rare). If I can fix the bradycardia, the case proceeds; no complications to date. Usually, once they get normocardic, they stay there for the rest of the procedure.
This.
 
Very funny... how many ECTs have you witnessed or your attendings allowed to prticipate in may I ask?
I would say over 200, doubtful 300.

Why do you ask? Is yours bigger than mine?
 
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Would anyone consider atropine? Or do most feel that glyco would be more gentle?
 
Would anyone consider atropine? Or do most feel that glyco would be more gentle?

74yo M hx CAD s/p CABG x 4 in the 90s

These patients don't often appreciate tachycardia. A slug of atropine probably wouldn't kick his HR up to 100, but it might. I'd use glyco.
 
Geez, all my partners are men and I have to deal, almost daily, with the d*ck measuring contests.... Not Sdn too! without beta blockade this would freak me out. Assuming patient is asymptomatic I'd give some glyco and see what happens. If he speeds right up, get ekg - if NSR then over beta blockade and proceed. Changes with ECT are so transient I found they almost never need to be treated. but maybe this is my private practice mentality where surgeons throw an absolute fit if you cancel.... Now that I'm off to academics maybe my thought processes will change. What's it like in academics? Surgeons freak if you cancel?
 
Geez, all my partners are men and I have to deal, almost daily, with the d*ck measuring contests.... Not Sdn too! without beta blockade this would freak me out. Assuming patient is asymptomatic I'd give some glyco and see what happens. If he speeds right up, get ekg - if NSR then over beta blockade and proceed. Changes with ECT are so transient I found they almost never need to be treated. but maybe this is my private practice mentality where surgeons throw an absolute fit if you cancel.... Now that I'm off to academics maybe my thought processes will change. What's it like in academics? Surgeons freak if you cancel?

I'm in PP and my surgeons never freak out. At least not out loud. Most of the time we come to the decision together. They understand it hurts me as much as them to cancel a case.
 
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I ended up cancelling the case, tried calling his cardiologist, left a message, and referred him to our in house cardiology service who'll evaluate him.

I wanted to know if there was anyone out there who might have proceeded with the case.

So what's the verdict from the cardiologist?
 
If he is asymptomatic Id just go forward after getting his rate up with Glyco. I really don't see the need for any urgent admission / cards consult in the setting of a beta blocked patient with asymptomatic sinus bradycardia. I'm surprised so many would cancel. And I don't have a problem sending someone home in sinus rhythm in the 30s-40s of asymptomatic.
 
If he is asymptomatic Id just go forward after getting his rate up with Glyco. I really don't see the need for any urgent admission / cards consult in the setting of a beta blocked patient with asymptomatic sinus bradycardia. I'm surprised so many would cancel. And I don't have a problem sending someone home in sinus rhythm in the 30s-40s of asymptomatic.

I do. I have never discharged a patient with heart rate in the 30s. I would only consider it if his name was Bjorn Borg and it was 1980.
 
To the people sending him home as if he were a well baby: are you giving him any instructions like stop taking beta blocker, and go see your doctor?
 
If he is asymptomatic Id just go forward after getting his rate up with Glyco. I really don't see the need for any urgent admission / cards consult in the setting of a beta blocked patient with asymptomatic sinus bradycardia. I'm surprised so many would cancel. And I don't have a problem sending someone home in sinus rhythm in the 30s-40s of asymptomatic.

Same here.
 
maybe this is my private practice mentality where surgeons throw an absolute fit if you cancel

I never cancel cases, only the anesthesia for cases.

If it is a preop cancel, I present a cogent reason to the patient and the surgeon. This is very rare and usually the surgeon cancels.
 
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This week, 88 year-old patient on Atenolol for CAD, with distal unstentable lesion on recent cath, comes in with HR of 44 (was cleared by his cardiologist at HR of 47) for retina surgery with retrobulbar block. After 0.2 mg of glyco, still 44 (after a stint at 41). After another 0.1+0.1, 49. After a third vial of 0.1+0.1 mg, 55. Eye drops, proceed to OR. I give another 0.1, HR of 62. Easiest case of the day. :)

Btw, this was all done by the admitting nurse in the preop area, during one hour, while I was doing another case. She picked up on the bradycardia, came in the OR and asked me for guidance, I told her what to do and kept communicating with her over the phone, and by the time I got to the PACU the patient was ready to go.
 
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This week, 88 year-old patient on Atenolol for CAD, with distal unstentable lesion on recent cath, comes in with HR of 44 (was cleared by his cardiologist at HR of 47) for retina surgery with retrobulbar block. After 0.2 mg of glyco, still 44 (after a stint at 41). After another 0.1+0.1, 49. After a third vial of 0.1+0.1 mg, 55. Eye drops, proceed to OR. I give another 0.1, HR of 62. Easiest case of the day. :)

Btw, this was all done by the admitting nurse in the preop area, during one hour, while I was doing another case. She picked up on the bradycardia, came in the OR and asked me for guidance, I told her what to do and kept communicating with her over the phone, and by the time I got to the PACU the patient was ready to go.

has anybody seen paradoxical bradycardia with low dose glyco?
 
Isn't that something you see with atropine? Not glyco. I can't remember the details but I do remember to never give low dose atropine in a crisis.

Oops, sorry FFP. I didn't see your post. You win.
 
Isn't that something you see with atropine? Not glyco. I can't remember the details but I do remember to never give low dose atropine in a crisis.

Oops, sorry FFP. I didn't see your post. You win.

I had heard about the low dose atropine, but was just wondering since glyco is related if it was possible to do the same thing ....I can only find atropine reports via dr google
 
This week, 88 year-old patient on Atenolol for CAD, with distal unstentable lesion on recent cath, comes in with HR of 44
88 y/o vasculopath probably has a certain degree of renal dysfunction, atenolol is the only bblocker eliminated by the kidney: poor choice. Although i wouldn't care too much about a rate at 45
 
88 y/o vasculopath probably has a certain degree of renal dysfunction, atenolol is the only bblocker eliminated by the kidney: poor choice. Although i wouldn't care too much about a rate at 45
In old people, with crappy cardiac electrical systems and vagal predominance, I have seen cases where just inserting the needle for a retrobulbar block dropped the heart rate to 30-40, in one case from 70 to 20 (intermittent sino-atrial exit block, confirmed later by cardiology).
 
Not a myth, I've seen it.

The Myth of a Minimum Dose for Atropine
Pediatrics. 2011 Apr;127(4):783-4. Epub 2011 Mar 7.
1. Keith J. Barrington, MB, ChB

The highlight:

In the latest edition of PALS, the reference is a 1971 article written by Dauchot and Gravenstein.5 This interesting physiologic study demonstrated that very low doses of atropine, dosed on a per-kilogram basis, of 0.0036 mg/kg (3.6 μg/kg) or less may cause a mild slowing of heart rate. It should be noted that there were no premature infants included in the study; the youngest studied infants were between 6 weeks and 3 months of age, and in these infants the cardiac slowing effect was not statistically significant. The most markedly affected children were the 7- to 12-year-olds who had an average decrease in heart rate from 79 to 70 beats per minute; above this dosage, heart rate was increased by atropine. This effect was later demonstrated to be a result of blockade of M1 muscarinic receptors, whereas the familiar tachycardic response is a result of blockade of the M2 and M3 receptors.6

snip

It seems that the strict, universal, often-repeated, minimum absolute dose of atropine is derived from an unsupported and irrational statement in the discussion of the aforementioned article in which the authors stated, "we therefore give a minimum dose of 0.1 mg of atropine to our patients." This minimum total dose is completely out of keeping with the results of the careful physiologic investigation that they performed but has developed a scriptural correctness.

The myth of a minimum dose of Atropine is just that, a myth.
I give 20 mcg/kg, practically limited to 40 mcg/dose. If it doesn't give me the desired effect, I double the dose.
For micro preemies, I mix some custom unit doses of atropine and epi, etc. in case the stool hits the fan.
There was just an article in the April 11 issue of Pediatrics about this topic. The science behind this dosing is ancient and weak.
Hugely overdosing neonates is a crime and the fact that a minimum dose of 100 mcg is in PALS and every other reference chart in the world is even worse. Some very smart people still teach this today at big name Children's Hospitals. I wonder if they would try to testify against me in court citing this weak, dated evidence and a fantasy guesstimated minimum dosing?
 
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