Clinical

[sevoflurane]

70 y/o male scheduled for Adrenalectomy 2/2 pheo.

PMHx:
DCM (EF 25%), CABGx5/MVR, COPD (smoker and barrel chested), PAs 70's/40's, IDDM, Sjogrens, hyperlipidemia.

Pre-op labs: nml except for erythrocytosis with a Hgb of 17.3

CT:

Pre-op EKG:

You induce anesthesia. As the surgeons get to the capsule of the adrenal mass, your rhythm converts to this:






What are your concerns?

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[GaseousClay]

Looks like Bigeminy on the screen. Vitals? Assuming stable hemodynamics i would draw a gas and check lytes. Does he have an ICD with DCM and low EF? What is our access do we have a-line, CVP? just a first couple thoughts.

 

[Per4mer8]

Looks like Bigeminy on the screen. Vitals? Assuming stable hemodynamics i would draw a gas and check lytes. Does he have an ICD with DCM and low EF? What is our access do we have a-line, CVP? just a first couple thoughts.

Did we happen to get a few slices of pericardial sac in that abdominal CT? I definitely want vitals, that bigeminy concerns me for apparent ventricular irritability, knowing this dude has DCM and pHTN and is likely fairly volume/preload dependent I want to rule out (or in) hemodynamically significant pericardial effusion/tamponade pretty quickly. His ischemic cardiac disease, diastolic dysfunction, pHTN, and incoming surge of catecholamines sounds like a horrible concoction to this beginner.


0

 

[fakin' the funk]

Why does he have electrical alternans on his pre-op EKG? Pre-op TTE?

THAT'S the adrenal mass? THAT presented as pheo, not as abd distention?

Let's assume that's true ventricular bigeminy and not V-paced beats...probably major badness like acute hypovolemia, acidosis, catechol surge, etc.

I assume you already had A-line and CVC in before...now it's TEE time.

 

[sevoflurane]

Looks like Bigeminy on the screen. Vitals?

Yep.

What does bigeminy mean in anesthesia land. What does it mean when the patient has a normal pre-op EKG?

100%, 154/90, 90, etCO2 45.

 

[sevoflurane]

I like the sat waveform. What's going on there?

 

[DrBeaker]

The normal beat produces a better SV while the ventricular beat does not have as big of a SV. This patient doesn't have a great EF. The atrial kick will help it fill. Are this guys PA pressures high from his MR sp MVR? What is the function of the valve currently?

 

[sevoflurane]

Yep. Good analysis of the pulse ox waveform. With progressive DCM, the old MV has started to leak and he now has moderate MR. His PA pressures are a combination of COPD/MR.

Anybody want to do anything about the new bigeminy? Why or why not? Is new onset bigeminy concerning in a typical patient? How about this one?

 

[bobow98]

One could argue in a pt with cabg x5 and low ef that ectopic beats decrease time in Diastole and every extra beat increases oxygen demand risking intra or post op mi. Wild guess is yes fix now or regret later. Especially with increased alpha stim from impending adrenal procedure.

Also, maybe start amiodarone for now to prevent further arrythmias?

 

[Idiopathic]

i dont think this is bigeminy, but rather sinus rhythm with intermittent LBBB. Im more concerned about that than i would be with simple ectopy, at least as far as it being a harbinger of myocardial ischemia. your LBBB beats will perfuse less well (at least in a less orderly fashion) and certainly wont help your MR. Would pause adrenal massage and place TEE or PAC in addition to lytes/abg. Im concerned about this

 

[sevoflurane]

Labs are drawn:





How do you guys want to treat this... or do you want to treat it? Someone mentioned amio.

What are the challenges of a pheo resection?

What is the anesthetic plan for this type of case?

 

[sevoflurane]

Not sure about intermittent LBBB idio. It was pretty consistent conduction once it started, which makes me think bigeminy.
I don't know if I've ever seen intermittent LBBB. I think it's pretty rare.
I agree that in a normal patient, bigeminy is not a big deal. I do think that if you can get coordinated conduction, the extra bit of SV you might be able to achieve in a patient with a low EF and DCM might be significant.

 

[Mapleson D]

I've certainly seen patients flip in and out of LBBB but have never seen or heard of doing so on a beat-to-beat basis. I also interpret it as bigeminy with PVCs.

 

[Idiopathic]

the hallmark of a pvc is an early ventricular beat with a subsequent prolonged repolarization these R-R intervals look the same to me, suggesting underlying sinus rhythm. i dont know, its probably nothing but it caught my eye. maybe im analyzing it too much but this seems different to me - these ventricular beats are early which is what you see in bigeminy, but the ones in the above ECG look sinus in nature, suggesting intermittent intraventricular conduction delay/LBBB. im almost certainly overreading it.

 

[Idiopathic]

although there is this vignette

 

[itwasalladream]

The QRS axis changes with each beat, making me think more PVC than LBBB.

Think I would stop surgery, try to improve alpha then beta blockade (pre-op EKG not that slow). TEE a good idea, but if stable BP, not sure what I would get out of it. Even if function appears normal, in CABGx5 and huge pheo with new bigeminy right after adrenal manipulation, I would not take the chance by continuing. Preop EKG looks more like significant respiratory variation in QRS height than classic beat to beat alternating heights you might see with an effusion, but I could be wrong.

Bigeminy with unifocal PVCs may signify irritation (ischemia?) of a specific area of myocardium, which would generally be more concerning than multifocal ectopy.

 

[deleted9493]

Sevo's initial strip makes me think fusion beats. The best example is in the 6th complex. There you can see a p wave with a subsequent wide complex QRS...making me think it's not pure bigeminy. Because the sinus and ventricular rhythms occur concomitantly, you don't see the repolarization pause that Idio pointed out would be there in true bigeminy.

My bet would be that induction slowed the patient's sinus rhythm enough (from preop EKG of ~100bpm) to allow an irritable ventricular focus to begin pacing in the context of a high catechol state.

I would do the same, confirm that it was not electrolyte-related and if pressures are adequate, let it ride. I'm guessing that the very catechol release that is causing the ectopy is also giving robust hemodynamics, in spite of the cardiomyopathy. In another context, if a patient with atrioventricular dyssynchrony like this was hemodynamically unstable, I'd titrate atropine to bring up the atrial rate a bit and try to overdrive pace out of it.

Esophageal pacing lead? It'd be fun to play with here.

 

[Planktonmd]

If we agree that this is bigemini the first thing I would do is hyperventilate a little to decrease the ETCO2 from the above mentioned 45.
Hypercarbia is not good for the PA pressure or for ventricular irritability.

 

[sevoflurane]

If we agree that this is bigemini the first thing I would do is hyperventilate a little to decrease the ETCO2 from the above mentioned 45.
Hypercarbia is not good for the PA pressure or for ventricular irritability.

Yep, yep. Glad somebody picked this up.

So, common causes for new onset bigeminy under GA:

1) Electrolyte abnormalities. Hypokalemia is probably the MCC (this guy had a k+ of 4.4)
2) Hypercarbia
3) Inadequate analgesia
4) Retractors
5) Old age
6) Cardiac irritability

So what to do about it if it persists once you drop your ETCO2?

I like this chart:

 

[sevoflurane]

Just caught the very end. 100mg of lido.
If we improve his SV by 20ml/beat by converting him to NSR, how much extra forward flow per minute do we get at a HR of 71 BPM?

The real question is how long does this effect last?

 

[Laryngophed]

Just caught the very end. 100mg of lido.
If we improve his SV by 20ml/beat by converting him to NSR, how much extra forward flow per minute do we get at a HR of 71 BPM?

delta20ml/beat * 71beat/min = 1420ml/min of additional CO.

The real question is how long does this effect last?

This answer gets tricky. It depends on the etiology. If it is because somebody was diddlin' the pheo, it'll likely last as long as it is being handled and has a systemic vascular connection. If that is going to be a while, you could give some more phentolamine and esmolol or labetolol to help blunt the catecholamine burden. (The vitals in a post above suggest this patient could tolerate more sympathetic blockade.) If the 'lytes are fine, you've breathed 'em down to ETCO2 of 30-35, and you're left with lido you are looking at about 2 hours of half-life for lidocaine in low EF states.

Sound good?

 

[Mman]

I like how the algorithm suggests titrating in 0.5-1 mg/kg of lidocaine over 2 minutes. I usually just shove 100 mg in as fast as it will go. I mean what's the downside? I'm not trying to academically figure out the exact dose it takes to break it.

 

[Idiopathic]

Just caught the very end. 100mg of lido.
If we improve his SV by 20ml/beat by converting him to NSR, how much extra forward flow per minute do we get at a HR of 71 BPM?

The real question is how long does this effect last?

i still think that is a sinus beat with LBBB not PVC. if lidocaine worked there it was purely coincidental

 

[sevoflurane]

delta20ml/beat * 71beat/min = 1420ml/min of additional CO.



This answer gets tricky. It depends on the etiology. If it is because somebody was diddlin' the pheo, it'll likely last as long as it is being handled and has a systemic vascular connection. If that is going to be a while, you could give some more phentolamine and esmolol or labetolol to help blunt the catecholamine burden. (The vitals in a post above suggest this patient could tolerate more sympathetic blockade.) If the 'lytes are fine, you've breathed 'em down to ETCO2 of 30-35, and you're left with lido you are looking at about 2 hours of half-life for lidocaine in low EF states.

Sound good?

Excellent.

i still think that is a sinus beat with LBBB not PVC. if lidocaine worked there it was purely coincidental

This was bigeminy. No coincidence. 100mg IVP, w/in 15 seconds the PVCs started to drop out. @ 30 seconds they were completely gone.

I like how the algorithm suggests titrating in 0.5-1 mg/kg of lidocaine over 2 minutes. I usually just shove 100 mg in as fast as it will go. I mean what's the downside? I'm not trying to academically figure out the exact dose it takes to break it.

I'm 95% with you. I think the algorithm is being cautious as to the "awake" elderly patient getting 100mg IVP. I've witnessed 2 seizures secondary to colleagues giving 5ccs of 2% lido pre-induction to 70+ year olds. Both were treated by induction of GA. I'm not quite sure how long they persist once you render them under the effects of prop/volatiles/etc since neither had EEGs. If bigeminy occurs intra-op and they are already under GA, there is probably little risk to give it as IVP- I personally would divide it up if it's a 90 y/o getting a TFN or something of that nature. I would likely also stick to 1mg/kg vs 100mg in the 60kg 90 y/o's. Outside of this population group, 100mg IVP all the way.

 

[sevoflurane]

How long does this effect last?

Well in short, I think most on this board would agree that it is patient dependent. Some patients will have a very short duration of action before they revert into recurrent PVCs, i.e., 5-10 minutes. Others, as in this patient, the effect will last hours. By the time we got back to pacu, he started developing very few, but present PVC's. He was back into bigeminy before discharge to ICU. He received a second dose once in ICU, and again, they went away.

So is it worth it to treat?

I think it depends on your patient. This one certainly benefited from it intra-op as the extra stroke volume did help out during a dicey operation.

Young and healthy? Check lytes, analgesia, ventilation, etc , and let it ride if you want. No worries. No need to treat, unless you want to.

 

[sevoflurane]

Anybody care to comment on this? What is the diagnosis and why am I posting it with regards to this patient?

 

[sevoflurane]

What is the natural course of the above diagnosis?

 

[deleted162650]

Looks like Takotsubo CM from prolonged high catechol state

 

[urge]

i still think that is a sinus beat with LBBB not PVC. if lidocaine worked there it was purely coincidental

The PR intervals are different |shorter on the wide complexes. They are PVCs. I don't think it was
coincidental. The preop ekg had a faster rate of 100 with no problems.

 

[sevoflurane]

Yup.

Broken heart syndrome.

The heart looks like an Octopus trap.

Big association with pheochromocytoma.

http://www.ncbi.nlm.nih.gov/pubmed/21029177

http://www.ncbi.nlm.nih.gov/pubmed/19797977

http://circ.ahajournals.org/content/113/17/e738.full#F1

http://www.ncbi.nlm.nih.gov/pubmed/19491077

http://www.innovationsincrm.com/car...-multiple-monomorphic-ventricular-tachycardia


Most of these patients recover their ventricular function once the Pheo comes out.

Reverse Tokotsobo's or "squid syndrome" also exists. It describes basal ballooning versus apical ballooning of the LV. It is also associated with a pheo.

 

[sevoflurane]

So knowing all the above, how would you guys do this case?

Pre-op: workup, etc.

Intra-op: Monitors, vasoactives, etc. What part is associated with the biggest flux of catecholamines?

Post-op: What happens to these patients immediately post-op?

 

[Idiopathic]

or it blunted the sym

The PR intervals are different |shorter on the wide complexes. They are PVCs. I don't think it was
coincidental. The preop ekg had a faster rate of 100 with no problems.

if you have PR intervals then you dont have PVCs, those are sinus beats

it seems like a silly point to argue, but dont overlook LBBB, even when it is intermittent, as a worrisome sign, moreso than PVCs

 

[urge]

or it blunted the sym


if you have PR intervals then you dont have PVCs, those are sinus beats

it seems like a silly point to argue, but dont overlook LBBB, even when it is intermittent, as a worrisome sign, moreso than PVCs

There is a p on the qrs in the last beat. The pvcs are coming a little before the expected qrs. I would believe the ilbbb if all the pr had the same duration. But they don't.

Since you seem to be fixated with the ilbb, let's just agree to disagree.

 

[sevoflurane]

Closing the loop on this thread.

Lot's of good info for ITE and Board review on pheo. I'd encourage all residents to look through the complete workup of a pheo. (Echo, renal function, metanephrines etc.)

Couple of comments:

• Caution with beta blockers as it can leave unopposed alpha stim and precipitate a crisis. Alpha block them for a couple of weeks prior to the OR.
• Monitors: a-line, central line (sometimes a cordis... I lost 1.5 liters over a 2 hour case) + epidural. I don't think a TEE is necessary, but don't hesitate to drop one in on the sickos.
• These patients are usually dry pre-op (from high catechol state).
• Manipulation of the ADRENAL vein (not renal) during ligation can cause large fluctuations of catecholamines... so be prepared to reduce preload and afterload (Nitroglycerin, Nitroprusside).
• Positioning is dependent on the tumor. Our massive tumor was taken out in the SUPINE position (not lateral with the table flexed as you would with a nephrectomy).
• DON'T DOSE UP YOUR EPIDURAL INTRA-OP... or at least be very careful. These patients very frequently become hypotensive once you remove their catecholamine producing tumor. So have some pressors up and ready to go. I prefer Levophed. Likely have to use it post-op and in ICU for sometime afterwards. Titrate the epidural towards the end of the case.

I'm missing some additional topics, but I think this thread gives a basic view of how these cases go.

Over and out.

 

[sevoflurane]

Fun cases.

 

[Idiopathic]

Ill add some points to the excellent ones described above

Preoperatively, I feel much better if my pheos for adrenalectomy are orthostatic. That implies a good level of alpha blockade. Also, sevo mentioned them being dry, and this is true - these patients actually should be encouraged to hydrate well in the days and weeks leading up to this surgery. I get very concerned when i see a pheo patient whos HCT is >40 because I know they are not hydrated enough. Id like them at 30-35, SBP 100-120, just a little dizzy when they sit up too fast. Thats perfect for me.

These cases are being done more frequently in the prone jackknife position (although probably not for a mass the size of the one described above). you wont be able to rely on stat TEE in that setting, nor could you easily place a CVL/PAC. The upside is that the procedure is very quick and confined to that RP space.

With long standing catecholamine secretion and subsequent blockade, your patient may be extremely resistant to exogenous catecholamine therapy after adrenal vein ligation. So while volume administration is typically the first response to hypotension in this setting, you may also need vasopressin or an analogue to treat this hypotension. Ive also had more than one patient who was so well alpha-blocked that I had to give vasopressin after induction...actually needed a little tumor manipulation to maintain BP/continue the case

 

[pgg]

Great thread, always a couple of board questions on pheos.

I'm missing some additional topics, but I think this thread gives a basic view of how these cases go.

One recurring board question concerns preoperative optimization. Between AKTs, ITEs, and the real thing I think I saw preop alpha blockade questions 3 or 4 times. This one is from the 1995 exam

Each of the following statements concerning pheochromocytoma is true EXCEPT:
(A) Preoperative administration of alpha-adrenergic inhibitors will usually reverse ECG changes due to catecholamine myocarditis
(B) Preoperative administration of alpha-adrenergic inhibitors decreases operative mortality
(C) Beta-adrenergic inhibitors should be administered preoperatively only in conjunction with alpha-adrenergic inhibitors
(D) Vasopressor therapy may be necessary postoperatively for treatment of hypotension
(E) Nasal congestion is a sign of inadequate alpha-adrenergic block

Highlight the area below to see the answer and my notes from residency: E
Appropriate dosing of preoperative alpha blockade (usually prazosin or phenoxybenzamine, sometimes doxazosin or terazosin) is determined by either reaching treatment endpoints (BP < 165/90, < 1 PVC / 5 min, no ST/T wave changes, and orthostatic hypotension not worse than 80/45 standing) or development of side effects (reflex tachycardia, nasal congestion, nausea, or abdominal pain).

Perioperative mortality is greatly reduced with preoperative therapy with alpha blockers.

Reversal of ECG changes and myocarditis is possible [Miller 6th ed, p 1042]: For patients who exhibit ST-T changes on ECG, long-term preoperative and preprocedure α-adrenergic receptor blockade (1 to 6 months) has produced ECG and clinical resolution of catecholamine-induced myocarditis.
/ end

 

[urge]

Preoperatively, I feel much better if my pheos for adrenalectomy are orthostatic.

How many are we talking about? That sounds like you do them on a weekly basis!

I have only seen 1, ever.

Do you live next to a nuclear power plant or something that causes pheos?

PS: Good discussion of a highly testable but rare disease.

 

[Idiopathic]

ive done probably 10 in the OR as a resident and attending - taken care of a few postoperatively in the ICU who werent very well optimized, you can definitely tell as they remain difficult to control in that setting

 

[Mman]

we do about 1-2 pheos a month, though as a referral center for more than 2 million people we get them from all over. 2 ivs, arterial line, and that's about it. With a well alpha blocked patient and a good surgeon it is a routine case > 95% of the time.