what do you make of this ekg?

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toughlife

toughlife

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toughlife said:
thoughts?
Click to expand...
Slow atrial fibrillation with remarkable low voltage in V1.
If low voltage is present in all precordial leads I would think of something preventing the electric current from reaching the surface: Pericardial effusion, severe emphysema....
If it's confined to certain leads it could be due to old MI.
The rest of the EKG leads would be helpful.
 
That pt is about to croak.
 
dig level a little too high???

hard to tell with it being so small
 
Image is definitely too small to make anything of value of it, but it kinda looks like a sinus exit block- you have a junctional bradycardia, and every now and then the sinus node perks up and fires off a p-wave, so you get an "irregular" sinus beat in the middle of the "regular" junctional rhythm.

It's really too faint to tell for sure though.

Agree with the low voltages in V1, and it would also obviously be nice to have the full 12 lead and to know how long these flipped Ts have been around.

May be time to scrounge up some pacer pads to keep handy...
 
This is too small. Looks like pt has afib with resultant severe bradycardia from treatment. Regardless, pt needs some sort of intervention asap.
 
UTSouthwestern said:
Are you implying that a junctional rhythm or complex is always or usually regular?
Click to expand...
When the AV junction becomes the pacemaker the rhythm is usually regular and varies in morphology according to the level at which it originates (high versus low junctional rhythm).
It is possible to have junctional premature beats that could cause pseudo irregular appearance.
The EKG in question appears irregularly irregular to me and the simplest explanation to that would be A fib.
Can not be certain though since the rest of the EKG is missing and the quality is very poor.
The low voltage in V1 is interesting though.
 
Planktonmd said:
When the AV junction becomes the pacemaker the rhythm is usually regular and varies in morphology according to the level at which it originates (high versus low junctional rhythm).
It is possible to have junctional premature beats that could cause pseudo irregular appearance.
The EKG in question appears irregularly irregular to me and the simplest explanation to that would be A fib.
Can not be certain though since the rest of the EKG is missing and the quality is very poor.
The low voltage in V1 is interesting though.
Click to expand...

Possible, but with what I see on this rhythm strip are areas of smooth tracing between some of the QRS complexes that could be VERY fine Afib with SVR or motion artifact, but there are bidirectional low voltage QRS complexes in V1, negative repolarization throughout, and what appears to be two P waves visible one in each strip in lead II. Junctional rhytm or escape complex with VERY slow SA node output.

Bottom line: Need intervention now and 12 lead for better analysis.
 
You guys are smoking crack.:laugh:

Its too small to call. We can make guesses, like you are doing, but its too small for me.

Get 12 lead and start treatment.
 
Noyac said:
You guys are smoking crack.:laugh:

Its too small to call. We can make guesses, like you are doing, but its too small for me.

Get 12 lead and start treatment.
Click to expand...

What if the dude jogged into pre-op for his trigger finger release and his vitals were:

hr: per ECG
BP: 133/87

rr: 25 (kind of up because of his jog in)

t: 99.0 (kind of up because of his jog in)
 
militarymd said:
What if the dude jogged into pre-op for his trigger finger release and his vitals were:

hr: per ECG
BP: 133/87

rr: 25 (kind of up because of his jog in)

t: 99.0 (kind of up because of his jog in)
Click to expand...

I'd still get a 12 lead.
 
UTSouthwestern said:
It's crank for the gentile, if you don't mind. Crack is so 80's.
Click to expand...

Yes your right!

Or maybe its LSD you guys are doing b/c you're all hallucinating.:laugh:

People still do LSD don't they?😎

And here in southwest Colorado we call crank just plain METH.
 
High degree AV block? Tiny, tiny, tiny. Got a larger image?

-copro
 
Arrival in PACU
Minute 00

ekg1.jpg


Minute 57

ekg2.jpg


Minute 60

ekg3.jpg


minute 75

ekg4.jpg


Isoprel 2mcg/min, pacing

EKG5.jpg
 
Ok I've posted the sequence of events above. No 12 lead ekg available. BP did continue to decrease to 60/30, isoproterenol and transcutaneous pacing initiated. Why would this happen in a pt with heart transplant after adrenalectomy for pheo resection?
 
Well, I'm not seeing any good P waves. Looks like it progressed to an idioventricular rhythm, but the QRS is narrow too. Maybe a-fib with slow ventric response.

I would imagine that in an orthotopic transplant, your loss of cardiac accelerators probably contributed to this.

Just my (somewhat educated) guess.

-copro
 
I'd call it a junctional escape rhythm. Pharmacologically manipulate it so its OK or resembles a rhythm that you can use an ACLS protocol on. Regards, ---Zip
 
Clear P waves, lengthening PR interval, then dropped beat with recovery. No PVC's that I can see (and I would know cause I have em and the friggen suck).
 
VentdependenT said:
Wait, I'm wrong. I dunno WTF that is.
Click to expand...

That's a Mobitz I you're describing, aka Wenckebach (2nd degree block). But, I still don't see P waves. And, I don't think that's what it is.

-copro
 
toughlife said:
Ok I've posted the sequence of events above. No 12 lead ekg available. BP did continue to decrease to 60/30, isoproterenol and transcutaneous pacing initiated. Why would this happen in a pt with heart transplant after adrenalectomy for pheo resection?
Click to expand...
Now it looks more like sinus brady-arrhythmia with irregular junctional or atrial escape beats.
Sudden withdrawal of cathecolamine chronotropic efects on the transplanted heart after pheo resection is the likely cause.
 
coprolalia said:
Well, I'm not seeing any good P waves. Looks like it progressed to an idioventricular rhythm, but the QRS is narrow too. Maybe a-fib with slow ventric response.

I would imagine that in an orthotopic transplant, your loss of cardiac accelerators probably contributed to this.

Just my (somewhat educated) guess.

-copro
Click to expand...

Yeah loss of cardiac accelerator fibers likely contributed to this, but the other issue is that tranplanted hearts are dependent on circulating catecholamines for sympathetic stimulation. After resection of the pheo, it was surmised that levels of these were low. However, when checked they were still about 200% of normal and only decreased to 150% of normal after two weeks post resection.
 
Planktonmd said:
Now it looks more like sinus brady-arrhythmia with irregular junctional or atrial escape beats.
Sudden withdrawal of cathecolamine chronotropic efects on the transplanted heart after pheo resection is the likely cause.
Click to expand...

Levels were checked post op and were still high.
 
toughlife said:
Levels were checked post op and were still high.
Click to expand...
Maybe not high enough though because this is a heart that was accustomed to high concentrations of catecholamines and the beta receptors are less sensitive.
Beta blockers given pre or intra op could be to blame as well.
The low voltage in V1 I guess could be explained by abnormal axis of the transplanted heart but needs to be clarified.
 
toughlife said:
Yeah loss of cardiac accelerator fibers likely contributed to this, but the other issue is that tranplanted hearts are dependent on circulating catecholamines for sympathetic stimulation. After resection of the pheo, it was surmised that levels of these were low. However, when checked they were still about 200% of normal and only decreased to 150% of normal after two weeks post resection.
Click to expand...

Well, that's interesting. It's interesting because now you're getting into dysregulation of adrenergic receptors within the respective nodes.

Did you, by any chance, try a little epi (like 30-40mcg bolus) to see if you could break the patient out of this? What might have happened is that the beta receptors were so down regulated because of the overabundance of catecholamine from the pheo that even with the high level in the background, you still didn't have enough post-resection to provide adequate stimulation.

Interesting case, toughlife, thanks for sharing. Let us know what else you tried.

-copro
 
Planktonmd said:
Maybe not high enough though because this is a heart that was accustomed to high concentrations of catecholamines and the beta receptors are less sensitive.
Beta blockers given pre or intra op could be to blame as well.
The low voltage in V1 I guess could be explained by abnormal axis of the transplanted heart but needs to be clarified.
Click to expand...

No beta blockers given. Only meds pt was on preoperatively were cardura and norvasc for htn control.
 
tough, do you know what the catecholamine levels were presurgery (i.e. were they greater than 200% normal)? It is possible that persistent supranormal levels of catecholamines (i.e. much greater than 200% normal) were present and that downregulation of beta adrenergic receptors has occurred in this transplant heart. In that event, which I have seen before with heart transplant patients, what you experienced with this patient is not altogether unusual or unexpected.

I had a patient with a heart transplant and a pheo producing 5 times the normal amount of catecholamines go aystolic 2 hours after the removal of the pheo, brought back on Isuprel gtt, then had to be weaned off Isuprel over the next three weeks, but it worked.

Alternatively, you have to work up the heart for ischemic events as well. Epinephrine and norepinephrine increase coronary blood flow as well as lead to a favorable redistribution of flow to the flow sensitive endocardial regions. A heart that has been accustomed to high levels of catecholamines could be adversely affected by even a small decrease in circulating levels.
 
So to end, the pt went to SICU, cards consulted and they agreed it was receptor downregulation 2/2 to high levels of cathecholamines. Patient was weaned off isoproterenol on POD #2 and did well.

A renal attending said hypotension and bradycardia can happen in OHT patients but looking at the whole picture, the downregulation theory makes more sense.

Interestingly, in heart transplant patients, you actually see resting tachy since the parasympathetic innervation to the SA node has been nixed. If you ever come across this kinda situation, it's good to remember that using drugs that mediate their actions through the ANS are ineffective in altering HR and contractility. Drugs that act directly on the heart (dopa, iso, norepi, etc) are your best bet.
 
UTSouthwestern said:
tough, do you know what the catecholamine levels were presurgery (i.e. were they greater than 200% normal)? It is possible that persistent supranormal levels of catecholamines (i.e. much greater than 200% normal) were present and that downregulation of beta adrenergic receptors has occurred in this transplant heart. In that event, which I have seen before with heart transplant patients, what you experienced with this patient is not altogether unusual or unexpected.

I had a patient with a heart transplant and a pheo producing 5 times the normal amount of catecholamines go aystolic 2 hours after the removal of the pheo, brought back on Isuprel gtt, then had to be weaned off Isuprel over the next three weeks, but it worked.

Alternatively, you have to work up the heart for ischemic events as well. Epinephrine and norepinephrine increase coronary blood flow as well as lead to a favorable redistribution of flow to the flow sensitive endocardial regions. A heart that has been accustomed to high levels of catecholamines could be adversely affected by even a small decrease in circulating levels.
Click to expand...

Good points. In review of her labs, 5 months prior to admission, her levels were 5 times of normal and a week before 3 times of normal.
 
toughlife said:
Good points. In review of her labs, 5 months prior to admission, her levels were 5 times of normal and a week before 3 times of normal.
Click to expand...

Something I read: "Anticholinesterases normally act indirectly on the myocardium, and should have no HR effects on the denervated heart. According to recent data, however, neostigmine can induce bradycardia via a direct activation of cholinergic receptors on cardiac ganglionic cells, causing release of acetylcholine from their nerve terminals."
 
toughlife said:
Something I read: "Anticholinesterases normally act indirectly on the myocardium, and should have no HR effects on the denervated heart. According to recent data, however, neostigmine can induce bradycardia via a direct activation of cholinergic receptors on cardiac ganglionic cells, causing release of acetylcholine from their nerve terminals."
Click to expand...

This is why I am such a big fan of Nimbex. Let it break down itself. Until Sugamedex is out, I prefer to use something I know will be gone on its own.
 
Utsouthwester,
I don't really understand your logic. You like nimbex because it breaks down itself. But what is the benefit of that in a pt with a heart transplant and normal working kidneys and liver? It's not like nimbex will be shorter than rocuronium in this scenario. Probably you will end up reversing both if the pt still has some fade. I understand nimbex in the setting of liver kidney failure, but not as a drug to avoid reversal.
 
it looks like a classic sick sinus syndrome tracing (irregularly irregular bradycardia is one of common presentations, but it may present as a variety of brady/tachy arrythmias). CCB could be the cause, although hyperkalemia,hypoxia, dig, beta-blockers, and a million other things could be responsible.
 
urge said:
Utsouthwester,
I don't really understand your logic. You like nimbex because it breaks down itself. But what is the benefit of that in a pt with a heart transplant and normal working kidneys and liver? It's not like nimbex will be shorter than rocuronium in this scenario. Probably you will end up reversing both if the pt still has some fade. I understand nimbex in the setting of liver kidney failure, but not as a drug to avoid reversal.
Click to expand...

My point is that if timed right, I can minimize or avoid reversal altogether, especially in the transplanted heart patient. Neostigmine's effects are effects that I would rather my patients not have to experience.

All of the steroidal NMB's can have a residual effect hours after the last dose is given in even healthy young patients.

I use Nimbex because it is self-limiting and if timed right requires little or no reversal.

Case(s) in point today: 3 gastric bands and one bypass. Bands got 8 mg Nimbex up front, bypass got 12 mg. End of the case (1 hour for the bands, 1.5 for the bypass), no reversal needed. Two 400 pounders, a 370 pounder, and a 278 pounder all with OSA, two with asthma, one with mild AS and history of one episode of CHF, all awoke perfectly and without hypersalivation from the neostigmine, tachycardia and hypertension from the glycopyrrolate, etc. These effects can be controlled (esmolol, labetalol, etc.), but I didn't have to use 2 reversal agents plus a beta blocker on these patients. Just let them wake up with the Nimbex gone or in the last stages of breaking down.

For all of my hearts, regardless of their liver or kidney function, I use Nimbex up front and possibly before CPB if it is a slow surgeon (have seen two patients shiver on CPB), then let it ride to the end. Since most of my hearts are fasttracked, it is great to not have to fight a sudden spike in HR/BP, etc. and have the patient still wake up smoothly and with intact muscle strength.
 
UTSouthwestern said:
My point is that if timed right, I can minimize or avoid reversal altogether, especially in the transplanted heart patient. Neostigmine's effects are effects that I would rather my patients not have to experience.

All of the steroidal NMB's can have a residual effect hours after the last dose is given in even healthy young patients.

I use Nimbex because it is self-limiting and if timed right requires little or no reversal.

Case(s) in point today: 3 gastric bands and one bypass. Bands got 8 mg Nimbex up front, bypass got 12 mg. End of the case (1 hour for the bands, 1.5 for the bypass), no reversal needed. Two 400 pounders, a 370 pounder, and a 278 pounder all with OSA, two with asthma, one with mild AS and history of one episode of CHF, all awoke perfectly and without hypersalivation from the neostigmine, tachycardia and hypertension from the glycopyrrolate, etc. These effects can be controlled (esmolol, labetalol, etc.), but I didn't have to use 2 reversal agents plus a beta blocker on these patients. Just let them wake up with the Nimbex gone or in the last stages of breaking down.

For all of my hearts, regardless of their liver or kidney function, I use Nimbex up front and possibly before CPB if it is a slow surgeon (have seen two patients shiver on CPB), then let it ride to the end. Since most of my hearts are fasttracked, it is great to not have to fight a sudden spike in HR/BP, etc. and have the patient still wake up smoothly and with intact muscle strength.
Click to expand...

How you intubating these folks UT?
 
VentdependenT said:
How you intubating these folks UT?
Click to expand...

Are you talking about the obese pts? You intubate them just like everyone else. Topicalize in the pre-op, sedate slightly, start precedex, bring to OR, position on large ramp or in the semi recumbent position, start fiber optic procedure, have security come in to help hold one large pt down while saying "it's OK, it's OK, take a breath, take a breath, please stop hitting me" blah blah blah.

Or you could do like I do and put them to sleep, DL with MAC 4, next.


😍
 
now this was a good conversation ---

i am sure if this was posted on the cards forum they'd be scratching their head

i am sure if this was posted in the surgery forum they'd be surprised because they have no clue what we do

i am sure if this was posted in the CRNA forum - they would say that they see this all the time, and that they would have done a fine job without us
 
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