Case for tomorrow

[cchoukal]

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65 yo M w/ CAD, CHF, Afib, hypothyroidism for total shoulder arthroplasty.

CAD-> CABG + mitral valve annuloplasty in 2010, uncomplicated post-op course.
CHF-> last EF 20%, severe LV enlargement, global hypo, moderate MR. Can walk 1 flight of stairs. Bi-V pacer/ICD.
AFib-> on warfarin.
hypothyroidism-> not taking his synthroid.

on ASA, statin, furosemid, carvedilol, and I think an ACE-I, plus a bunch of herbs.

Labs are more or less NL, but his Cr is 1.6 (baseline).

On exam, he's thin, frail-looking, interacts normally.
airway exam is reassuring.
cardiopulmonary exam does not reveal crackles, S3, JVD, or peripheral edema. Extremities are warm.

What's your plan?

Anything else you want to know?

 

[bawer234]

code status? j/k

 

[sevoflurane]

Anything else you want to know?

Vitals, CXR, INR, TSH, CBC, BMP to start. I'm assuming ECHO and functional status is @ baseline and not worse. Is he dependant on his pacer in any way? Can it be inerrogated and reprogramed? Bovie will buy him some volts if not... especially if it's a L. TSA.

R/B detailed in chart.

A-line (transducer placed at the level of his ears) especially in beach chair, 2 lines (one for possible pressors if you were to need it- I'd consider external IJ just to ward off evil spirits), block.

R/B conversation detailed in the chart.

Nice easy anesthestic with a good block should get you through.

 

[sevoflurane]

Couple things I left out: estimated PA pressures, recent cath report (if worsening echo) and why is this dude off his synthroid? Is he still optimized for this elective surgery?

 

[cchoukal]

Vitals, CXR, INR, TSH, CBC, BMP to start. I'm assuming ECHO and functional status is @ baseline and not worse. Is he dependant on his pacer in any way? Can it be inerrogated and reprogramed? Bovie will buy him some volts if not... especially if it's a L. TSA.

R/B detailed in chart.

A-line (transducer placed at the level of his ears) especially in beach chair, 2 lines (one for possible pressors if you were to need it- I'd consider external IJ just to ward off evil spirits), block.

R/B conversation detailed in the chart.

Nice easy anesthestic with a good block should get you through.

CXR shows a big heart, clear lungs.

INR 2.6, now bridged on enox.

He's not pacer-dependent from a rhythm perspective (he's A-sensed, Bi-V paced the majority of the time), but he reportedly had improvement in his symptoms when the Bi-V was inserted. So I'd say his stroke volume is pacer-dependent.

What do you want the interrogator to tell you? What would you have her reprogram it to (It's presently DDDR)?

 

[BLADEMDA]

65 yo M w/ CAD, CHF, Afib, hypothyroidism for total shoulder arthroplasty.

CAD-> CABG + mitral valve annuloplasty in 2010, uncomplicated post-op course.
CHF-> last EF 20%, severe LV enlargement, global hypo, moderate MR. Can walk 1 flight of stairs. Bi-V pacer/ICD.
AFib-> on warfarin.
hypothyroidism-> not taking his synthroid.

on ASA, statin, furosemid, carvedilol, and I think an ACE-I, plus a bunch of herbs.

Labs are more or less NL, but his Cr is 1.6 (baseline).

On exam, he's thin, frail-looking, interacts normally.
airway exam is reassuring.
cardiopulmonary exam does not reveal crackles, S3, JVD, or peripheral edema. Extremities are warm.

What's your plan?

Anything else you want to know?

I see this type of patient twice a week in practice; I'm located in the Medicare capital of the world.

Believe it or not the onlly thing which seems out of the ordinary here is "not taking his synthroid." This type of patient is usually very compliant. I'd ask why and how many doses he has missed.

1. U/S guided ISB (piece of cake on him) single shot with decadron.
2. Arterial Line
3. Cerebral Oximetry
4. LMA (i've done hundreds this way- total shoulders after a block)
5. Maintain mean BP at the cuff level greater than 70-75
6. Careful induction (how about 0.5 mg/kg of propofol after Arterial line placement then mask him a bit if needed with agent)
7. Magnet for AICD if non pacer dependent. If pacer dependent turn off AICD and set pacemaker to non-synchronous rate.
8. If BP drops below mean of 70 I'd use low dose Epi to maintain BP just like Hospital for Special Surgery in New York City. (you don't get tachycardic with low dose epi)
9. I assume INR is within range (less than 1.5 or 1.6 for total joint replacement)

I know some of you would insist on an ETT here for a sitting position total shoulder. Fine. You may even argue that CO2 is better controlled avoiding acidosis; I'd counter that Brain perfusion is actually better with some acidosis while myocardial perfusion is maintained with some hypercarbia via an LMA.


I'm confused as to why an Orthopedic Surgeon would want to do an elective total shoulder with such a high INR of 2.6. Yes, it can done but why? Another day or 2 off Coumadin and the INR will fall easily below 2 if not 1.5.

 

[sevoflurane]

CXR shows a big heart, clear lungs.

INR 2.6, now bridged on enox.

He's not pacer-dependent from a rhythm perspective (he's A-sensed, Bi-V paced the majority of the time), but he reportedly had improvement in his symptoms when the Bi-V was inserted. So I'd say his stroke volume is pacer-dependent.

What do you want the interrogator to tell you? What would you have her reprogram it to (It's presently DDDR)?

Manufacturer, model, battery status, is the pacer appropriately sensing, pacing/capturing?, get it reprogramed so that the bovie won't interfere with the pacer/defibrillator and inappropriately activate it. What happens when a magnet is placed? Does it convert to asynchronous mode? Do you need to reprogram it once you take the magnet off? What happens to his B.P. and stroke volume once you go to VOO/DOO? Antitachycardia functions? What happens if he goes into an malignant rhythm? Does taking off the magnet ensure the AICD will fire? (make sure you can shock by some other means if not).

Post-op you need to interrogate and restore pacing/defribillator function.

INR is a weee bit high.

 

[sevoflurane]

Nice case cchoukal!

Thanks for posting...! 👍

 

[sevoflurane]

I know some of you would insist on an ETT here for a sitting position total shoulder. Fine. You may even argue that CO2 is better controlled avoiding acidosis; I'd counter that Brain perfusion is actually better with some acidosis while myocardial perfusion is maintained with some hypercarbia via an LMA.

This is why I'd like to know PA pressures. ETT might be reasonable if he's in the 50-80 range. On the other hand, mild acidosis will unload O2 to the tissues. I like permessive hypercarbia if no PA issues.

 

[BLADEMDA]

Manufacturer, model, battery status, is the pacer appropriately sensing, pacing/capturing?, get it reprogramed so that the bovie won’t interfere with the pacer/defibrillator and inappropriately activate it. What happens when a magnet is placed? Does it convert to asynchronous mode? Do you need to reprogram it once you take the magnet off? What happens to his B.P. and stroke volume once you go to VOO/DOO? Antitachycardia functions? What happens if he goes into an malignant rhythm? Does taking off the magnet ensure the AICD will fire? (make sure you can shock by some other means if not).

Post-op you need to interrogate and restore pacing/defribillator function.

INR is a weee bit high.

http://emedicine.medscape.com/article/285265-overview

There are dissenting views on how to handle AICDs and most of the reps will tell you our ASA guidelines are way too conservative.

 

[sevoflurane]

CXR shows a big heart, clear lungs.

INR 2.6, now bridged on enox.

He's not pacer-dependent from a rhythm perspective (he's A-sensed, Bi-V paced the majority of the time), but he reportedly had improvement in his symptoms when the Bi-V was inserted. So I'd say his stroke volume is pacer-dependent.

What do you want the interrogator to tell you? What would you have her reprogram it to (It's presently DDDR)?

Agree, Blade... but the above deserves special attention.

 

[BLADEMDA]

Agree, Blade... but the above deserves special attention.

The Heart Rhythm Society (HRS)/American Society of Anesthesiologists (ASA) Expert Consensus Statement on the perioperative management of patients with implantable defibrillators, pacemakers and arrhythmia monitors: facilities and patient management: executive summary this document was developed as a joint project with the American Society of Anesthesiologists (ASA), and in collaboration with the American Heart Association (AHA), and the Society of Thoracic Surgeons (STS).

George H Crossley; Jeanne E Poole; Marc A Rozner; Samuel J Asirvatham; Alan Cheng; Mina K Chung; T Bruce Ferguson; John D Gallagher; Michael R Gold; Robert H Hoyt; et al. (Profiled Author: Alan Cheng)
St. Thomas Research Institute and University of Tennessee College of Medicine, Nashville, Tennessee, USA.
Heart rhythm : the official journal of the Heart Rhythm Society 2011;8(7):e1-18.

 

[BLADEMDA]

Agree, Blade... but the above deserves special attention.

I'd turn off the AICD portion and leave the pacemaker at DDDR. Modern pacemakers are resistant to bovie interference anyway. In addition, the Rep can check the pacemaker and turn the AICD back on in the PACU.

Most would place Defib pads in the O.R. or Preop once the AICD is turned off.

 

[pgg]

I know some of you would insist on an ETT here for a sitting position total shoulder. Fine. You may even argue that CO2 is better controlled avoiding acidosis; I'd counter that Brain perfusion is actually better with some acidosis while myocardial perfusion is maintained with some hypercarbia via an LMA.

I'd go with an ETT. If you want a bit of acidosis you can be precise and deliberate with an ETT - there's no reason you can't park his ETCO2 at 45 if that's where you want it. I don't see any advantage to the LMA.

An interscalene catheter might be nice too, though their postop anticoagulation plan might present issues there.

 

[sevoflurane]

I'd turn off the AICD portion and leave the pacemaker at DDDR. Modern pacemakers are resistant to bovie interference anyway. In addition, the Rep can check the pacemaker and turn the AICD back on in the PACU.

Most would place Defib pads in the O.R. or Preop once the AICD is turned off.

How would you do that?

 

[BLADEMDA]

I'd go with an ETT. If you want a bit of acidosis you can be precise and deliberate with an ETT - there's no reason you can't park his ETCO2 at 45 if that's where you want it. I don't see any advantage to the LMA.

An interscalene catheter might be nice too, though their postop anticoagulation plan might present issues there.

No Problem PGG. You can have your ETT.



http://forums.studentdoctor.net/showthread.php?t=917317&highlight=cerebral+perfusion+pressure

This is worth re-reading.

 

[BLADEMDA]

How would you do that?

I'd have the Manufacturer Rep come to holding and assist me in turning off the AICD while leaving the pacer portion at DDDR. In addition, if you have any questions why not call an EP specialist or the person who placed this device? I can usually reach an EP specialist in less than 15 minutes for a discussion.

I find the Reps to be quite helpful here and I have called the company directly if I have questions (I get a very good rep there).

 

[sevoflurane]

I'd have the Manufacturer Rep come to holding and assist me in turning off the AICD while leaving the pacer portion at DDDR. In addition, if you have any questions why not call an EP specialist or the person who placed this device? I can usually reach an EP specialist in less than 15 minutes for a discussion.

I find the Reps to be quite helpful here and I have called the company directly if I have questions (I get a very good rep there).

👍

Exactly.

 

[sevoflurane]

and sometimes that is not a luxury @ 3am during a free air/esophageal perforation/spetic patient....

 

[sevoflurane]

I'd go with an ETT. If you want a bit of acidosis you can be precise and deliberate with an ETT - there's no reason you can't park his ETCO2 at 45 if that's where you want it. I don't see any advantage to the LMA.

An interscalene catheter might be nice too, though their postop anticoagulation plan might present issues there.

Yes. You know I like my LMA's... but in critical patients like the one described, that is one less thing to worry about if things start heading south. This dude is prolly edentulous anyways...

.... and I usually tube my TSA's.

 

[BLADEMDA]

and sometimes that is not a luxury @ 3am during a free air/esophageal perforation/spetic patient....

Yes. But, outcome isn't as good at 0300 either. In an emergency you must decide to place a magnet or not as the rep won't be avail. It is your call to make. But be aware that a magnet over an AICD will turn off the Defib portion but leave the pacer portion susceptible to interference or reprogrammng from the bovie. If a patient is pacer dependent then this can be problematic (I have seen the magnet removed and the pacer function restored).

 

[sevoflurane]

65 yo M w/ CAD, CHF, Afib, hypothyroidism for total shoulder arthroplasty.

CAD-> CABG + mitral valve annuloplasty in 2010, uncomplicated post-op course.
CHF-> last EF 20%, severe LV enlargement, global hypo, moderate MR. Can walk 1 flight of stairs. Bi-V pacer/ICD.
AFib-> on warfarin.

He's lost his atrial kick (hopefully rate controlled), global dysnfxn, severe LV enlargement, MR (and likely pulmn htn... with low starting BPs') + pacer dependant...?

I'm thinking this (or worse):

May not be a bad idea to do a quick transthoracic to take a peak the am of surgery....

Not a case I would take lightly... and if his pacer is contributing to his CO/SV... then I wouldn't just throw on a magnet and go.... some might though. If you don't manage this guy appropriately you could easily throw him into CHF.

 

[cincincyreds]

I see this type of patient twice a week in practice; I'm located in the Medicare capital of the world.

Believe it or not the onlly thing which seems out of the ordinary here is "not taking his synthroid." This type of patient is usually very compliant. I'd ask why and how many doses he has missed.

1. U/S guided ISB (piece of cake on him) single shot with decadron.
2. Arterial Line
3. Cerebral Oximetry
4. LMA (i've done hundreds this way- total shoulders after a block)
5. Maintain mean BP at the cuff level greater than 70-75
6. Careful induction (how about 0.5 mg/kg of propofol after Arterial line placement then mask him a bit if needed with agent)
7. Magnet for AICD if non pacer dependent. If pacer dependent turn off AICD and set pacemaker to non-synchronous rate.
8. If BP drops below mean of 70 I'd use low dose Epi to maintain BP just like Hospital for Special Surgery in New York City. (you don't get tachycardic with low dose epi)
9. I assume INR is within range (less than 1.5 or 1.6 for total joint replacement)

I know some of you would insist on an ETT here for a sitting position total shoulder. Fine. You may even argue that CO2 is better controlled avoiding acidosis; I'd counter that Brain perfusion is actually better with some acidosis while myocardial perfusion is maintained with some hypercarbia via an LMA.


I'm confused as to why an Orthopedic Surgeon would want to do an elective total shoulder with such a high INR of 2.6. Yes, it can done but why? Another day or 2 off Coumadin and the INR will fall easily below 2 if not 1.5.

I was wondering. If you do a really good ultrasound block, could you just do it under a straight block if the patient is reasonable and cooperative and avoid the LMA/general addition to the block?

I've done single shot ISBs with ultrasound guidancealong with propofol sedation for shoulder arthroplasties in COPDers and I've done fine. We have our patients lateral rather than beachchair. I would assume the lateral position is better for the patient than beachchair. Just curious as to your opinions on this?

 

[BLADEMDA]

I was wondering. If you do a really good ultrasound block, could you just do it under a straight block if the patient is reasonable and cooperative and avoid the LMA/general addition to the block?

I've done single shot ISBs with ultrasound guidancealong with propofol sedation for shoulder arthroplasties in COPDers and I've done fine. We have our patients lateral rather than beachchair. I would assume the lateral position is better for the patient than beachchair. Just curious as to your opinions on this?

I've done awake rotator cuff repairs under straight block. I've never done a complete total shoulder under MAC plus block but it seems very doable. I woud block the cervical plexus and infiltrate the skin over the incision site. I have no doubt a little ketafol combined with the ISB, cervical plexus and skin infiltration and I could get through the case.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989124/

89 percent performed under ISB alone (no GA)

Take a look

 

[SexPanther]

I was under the impression that a magnet (in general) disables the tachyarrhythmia fxn of the AICD but has no effect on the pacemaker. The only definitive way you could make sure there was no interference in pacemaker fxn intra-op would be pre-op programming to an asynchronous mode which may be deleterious in this patient.

I've had several cases lately with Medtronic AICDs and if a tachyarrhythmia occurs intra-op, the magnet can be removed with return of AICD fxn in a matter if seconds. I still call the rep and document this discussion each time I encounter it though.

 

[SexPanther]

I've done awake rotator cuff repairs under straight block. I've never done a complete total shoulder under MAC plus block but it seems very doable. I woud block the cervical plexus and infiltrate the skin over the incision site. I have no doubt a little ketafol combined with the ISB, cervical plexus and skin infiltration and I could get through the case.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989124/

89 percent performed under ISB alone (no GA)

Take a look

That is pretty cool and I've wondered about that. I have met a lot of resistance even suggesting LMAs on shoulders (inc. scopes) so I can only imagine the reaction to doing it just under block.

I assume the superficial cervical plexus block is for the supraclavicular nerve? I've never done one of these, is this an US guided technique? Would there be any concerns about inadequate blockage of the inferior trunk with an ISB + SCP? To my knowledge, there shouldn't be any innervation coming from there to the shoulder.

 

[IlDestriero]

I think i would tell them that the shoulder is the least of this dude's problems. Go home and start picking out headstones. What's he going to do, go play golf? Can he even do pt? He's one bag of potato chips and a Victoria's Secret commercial away from the fatal mi.
This is why I dumped adults. What a mess.🙁

 

[cchoukal]

So when I actually met the guy in pre-op, he looked a lot better than his chart. To follow up on a couple issues:

The INR had been from a few days prior and he'd been bridged with enox, last dose the night before the OR.

Lots of great discussion on whether he needs GA or not. In residency, I did a lot of shoulder scopes/rotator cuffs under block + mac, but never a total shoulder. In my current shop (the VA), things take a little longer, the likelihood of blood is a little higher, and the default is GA via ETT.

Also a lot of great discussion about his device. It is true that a magnet applied to an ICD (all ICDs CAN pace, but this one was a little different) will disable tachy-therapy and leave the pacing function (DDDR) alone. The reason I perceived that to be inadequate in THIS case was that, by report, his CHF/symptoms improved quite a bit when he initiated Bi-V pacing, and my concern was that if the pacing were left alone and EMI interfered with sensing, he'd lose ventricular synchrony. So while he wasn't pacer-dependent, per se, he sort of was. My plan, then, was to have the EP folks disable tachy-therapy and go DOO on the pacer.

After seeing him in pre-op and realizing he was reasonably vigorous, the case seemed a little less complex. We did use an a-line and a central line (we ended up giving him some norepi during the case, and stared at a couple ScvO2s of 80%), and had a great interscalene block placed by the resident (a CA1, no less). Easy, Peasy, Japanese-y

 

[loveoforganic2]

CHF-> last EF 20%, severe LV enlargement, global hypo, moderate MR.
cardiopulmonary exam does not reveal crackles, S3, JVD, or peripheral edema. Extremities are warm.

Anything else you want to know?

Q - Is the lack of an S3 significant in any way given that you already know the presence of the terrible EF and LV dilation?

 

[BLADEMDA]

I was under the impression that a magnet (in general) disables the tachyarrhythmia fxn of the AICD but has no effect on the pacemaker. The only definitive way you could make sure there was no interference in pacemaker fxn intra-op would be pre-op programming to an asynchronous mode which may be deleterious in this patient.

I've had several cases lately with Medtronic AICDs and if a tachyarrhythmia occurs intra-op, the magnet can be removed with return of AICD fxn in a matter if seconds. I still call the rep and document this discussion each time I encounter it though.

Correct. But with a magnet on the device bovie is more likely to interfere with pacemaker function. I've seen it happen

 

[BLADEMDA]

So when I actually met the guy in pre-op, he looked a lot better than his chart. To follow up on a couple issues:

The INR had been from a few days prior and he'd been bridged with enox, last dose the night before the OR.

Lots of great discussion on whether he needs GA or not. In residency, I did a lot of shoulder scopes/rotator cuffs under block + mac, but never a total shoulder. In my current shop (the VA), things take a little longer, the likelihood of blood is a little higher, and the default is GA via ETT.

Also a lot of great discussion about his device. It is true that a magnet applied to an ICD (all ICDs CAN pace, but this one was a little different) will disable tachy-therapy and leave the pacing function (DDDR) alone. The reason I perceived that to be inadequate in THIS case was that, by report, his CHF/symptoms improved quite a bit when he initiated Bi-V pacing, and my concern was that if the pacing were left alone and EMI interfered with sensing, he'd lose ventricular synchrony. So while he wasn't pacer-dependent, per se, he sort of was. My plan, then, was to have the EP folks disable tachy-therapy and go DOO on the pacer.

After seeing him in pre-op and realizing he was reasonably vigorous, the case seemed a little less complex. We did use an a-line and a central line (we ended up giving him some norepi during the case, and stared at a couple ScvO2s of 80%), and had a great interscalene block placed by the resident (a CA1, no less). Easy, Peasy, Japanese-y

Correct about the magnet and AICD. There is some debate about the best default setting of the pacemaker when the AICD is disabled. I have used both DDD and DOO with the rep telling me asynchronous isn't really necessary due to the bovie because the magnet isn't being utilized here.

 

[sevoflurane]

So when I actually met the guy in pre-op, he looked a lot better than his chart. To follow up on a couple issues:

The INR had been from a few days prior and he'd been bridged with enox, last dose the night before the OR.

Lots of great discussion on whether he needs GA or not. In residency, I did a lot of shoulder scopes/rotator cuffs under block + mac, but never a total shoulder. In my current shop (the VA), things take a little longer, the likelihood of blood is a little higher, and the default is GA via ETT.

Also a lot of great discussion about his device. It is true that a magnet applied to an ICD (all ICDs CAN pace, but this one was a little different) will disable tachy-therapy and leave the pacing function (DDDR) alone. The reason I perceived that to be inadequate in THIS case was that, by report, his CHF/symptoms improved quite a bit when he initiated Bi-V pacing, and my concern was that if the pacing were left alone and EMI interfered with sensing, he'd lose ventricular synchrony. So while he wasn't pacer-dependent, per se, he sort of was. My plan, then, was to have the EP folks disable tachy-therapy and go DOO on the pacer.

After seeing him in pre-op and realizing he was reasonably vigorous, the case seemed a little less complex. We did use an a-line and a central line (we ended up giving him some norepi during the case, and stared at a couple ScvO2s of 80%), and had a great interscalene block placed by the resident (a CA1, no less). Easy, Peasy, Japanese-y

Great thread so far...

This is looking like a sticky...👍

 

[BLADEMDA]

In particular the Medtronic people are adamant that our approach to AICD/Pacemaker management is overkill. They state their device is the best on the market and all I need to do is place a magnet over the AICD to deactivate it. The pacer portion will remain functional and highly unlikely to be interfered with by a bovie. They then ask me if I have ever seen a Medtronic device malfunction due to a bovie in the OR.
With an N of about 1,000 my answer is no. I have seen the other brands do some weird stuff but not a Medtronic device.

Our ASA recommends deactivating the AICD and changing the pacing function to DOO. But, the EP specialists aren't as adamant about this approach in all patients. They state it may be advisable to do this in pacemaker dependent patients but careful thought should be put into the consequences of a DOO mode vs leaving a DDD mode in place.

Anyway, the OP did a good job here. I would like to read about his thought of mean BP in this patient and where he would place the arterial line transducer and why.

 

[cchoukal]

I would like to read about his thought of mean BP in this patient and where he would place the arterial line transducer and why.

Unlike many seemingly end-stage CHF patients who manage to generate systolic BPs in the 80s and 90s, this patient's were generally in the 130s prior to surgery. As such, I didn't spend a ton of time thinking about what I would "accept." My general approach is to keep people close to where they live. Inhalational anesthetics are powerful vasodilators, so on the one hand, hypotension may be from decreased afterload, meaning there may be no net change in flow or perfusion (thus the age-old question: is a MAP of 70 on shiite-tons of pressor really any better, perfusion-wise, than a MAP of 50 on nothing?).

On the other hand, they are potent myocardial depressants, and so in these patients, hypotension could also be from that, and could certainly lead to hypoperfusion. I used the ScvO2 to try to keep a handle on this, and it never dipped below 80% (was he merely shunting like in the septic patient? No, he didn't have that kind of physiology, and he cont'd to make urine).

As for the transducer, I'll dodge the question by saying the case was done essentially supine. People seem to go back and forth on where to put the transducer in beach-chair cases, thinking that if they place the transducer at the level of the head, then their MAP is actually CPP, and they have some guarantee of adequate cerebral perfusion. I haven't read the literature on this, but I don't think it passes the physiologic rationale.

First, people's baseline BP is determined in the clinic, where it's measured with the patient roughly in the beach-chair position. So if their baseline in the clinic was good enough to keep their brain happy in that position...

Of course (second), "anesthesia" lowers the BP, so maybe CPP does go down, but measuring the MAP with the transducer at the head doesn't measure CPP anyway, so I'm not sure this covers you. (CPP = MAP - ICP). Plus, inhalational anesthetics actually increase CBF, so is there really a net change in perfusion? I don't know.

I take care of sick high-ICP patients in the ICU all the time, and no one's putting the transducer at the head (for whatever that's worth); it doesn't seem to represent a real physiologic construct.

Nihilistic perhaps, or maybe naive. Blade, could you share some literature on the transducer height issue?

 

[sevoflurane]

Case Presentation
A 47-year-old, healthy female underwent general anesthesia for shoulder arthroscopy. Preoperative blood pressure (BP) was 125/83 mmHg. After premedication with 50 mg of meperidine, 40 mg hydroxyzine, and 0.2 mg glycopyrrolate intramuscularly, anesthesia was induced with 200 mg propofol, 100 mg succinylcholine, and 30 mg lidocaine. Because she was hypertensive, just prior to induction, 50 mg of labetalol was given intravenously. Anesthesia was maintained with 2% isoflurane, 60% nitrous oxide, and oxygen. The patient was placed in the "barbershop" position for the surgery. Twenty minutes into the case, blood pressure decreased to 100/60 mmHg and then remained in the 80-90 mmHg systolic range for the remainder of the case. Oxygen saturation was 100% and end tidal CO2 values were in the 30s throughout the case. Upon arrival in the post-anesthesia care unit (PACU), her blood pressure was 113/60 mmHg but she did not awaken. Naloxone 0.1 mg was given intravenously, but she remained unresponsive and did not move her extremities. Another 0.1 mg of naloxone was given 35 min after arrival in the PACU followed by 3 more doses of naloxone and 2 doses of physostigmine. During this time, her trachea remained intubated and she was well oxygenated. Neurologic evaluation suggested a diencephalic syndrome, possibly brain infarction. She was unresponsive to voice commands or painful stimuli, and reflexes were decreased bilaterally. A computer axial tomography (CAT) scan of the head was normal initially, but 5 days later suggested brain swelling and obliteration of the cistern. Magnetic resonance imaging (MRI) 1 week later showed changes in both cerebral hemispheres suggesting cortical infarcts, involvement of the anterior and medial temporal lobe bilaterally, no significant edema, and no significant herniation. At no time was there any evidence of an intracranial bleed. After 2 weeks, her Glasgow coma scale was 3; her fundi were clear and crisp. She had corneal reflexes, a positive gag, and negative doll's eyes; she was hyperreflexive with increased tone and was unresponsive to noxious stimuli in all 4 extremities. She is expected to remain in a persistent vegetative state.


"Despite its low incidence, intraoperative stroke associated with shoulder surgery, particularly in healthy patients at no risk for stroke, is a totally unexpected and devastating complication. Patients in the beach chair position are at risk for an intraoperative stroke if borderline low BPs, as measured in the arm, are used without appreciating the effect on CPP and CBF. Because of the specific physiologic changes associated with the sitting position, great care should be applied when using and interpreting BP cuff measurements in the nonoperative arm or, even more so, if leg measurements of BP must be used. Blood pressure values <80% of preoperative resting values should be treated aggressively to enhance the margin of safety. Deliberate hypotension must be avoided. A thorough understanding of the physiologic changes associated with the upright position, and the physical effects of gravity on BP in the brain is crucial to prevent catastrophic neurologic outcome during shoulder surgery in the sitting position."

http://www.apsf.org/newsletters/html/2007/summer/01_beach_chair.htm

From the anesthesia patient safety foundation.

 

[sevoflurane]

Before we took over a recent ortho ASC, the anesthesiologist staffing that site had a patient wake up with a stroke from a shoulder scope/rotator cuff repair. This was last year.

These things happen.

 

[sevoflurane]

However, significant changes can develop when patients are moved to the upright position. Mean arterial pressure (MAP), central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP), stroke volume, cardiac output, and PaO2 all decrease while the alveolar-arterial oxygen gradient (PAO2-PaO2), pulmonary vascular resistance, and total peripheral resistance increase. Under nonanesthetized conditions, these effects are compensated for by an increase in systemic vascular resistance by up to 50-80%. However, this autonomic response is blocked by vasodilating anesthetics, which further exacerbate and compromise cardiac output. Blood pressure remains unchanged or increases slightly in nonanesthetized patients in the sitting position but decreases in the anesthetized state. Cerebral perfusion pressure (CPP) decreases by approximately 15% in the sitting position in non-anesthetized patients and could further decrease under anesthesia because of vasodilation and impaired venous return. Venous return from the cerebral circulation is usually increased by inspiratory subatmospheric pressure during spontaneous ventilation, but this mechanism is nullified by positive pressure ventilation. Obstruction of the internal jugular veins in the sitting position may also impede cerebral venous drainage, especially with unfavorable positions of the head and neck, such as flexion of the head. Pohl and Cullen reported a series of cases in 2005 that documented blood pressure decreases ranging from 28-42%; consequently, hypotension was thought to be a likely cause of ischemic brain injury. Given the potential for peripheral vasodilatation and myocardial depression that can occur in patients who are anesthetized with potent intravenous and inhalational drugs, the effects of the upright position and anesthesia synergize.

 

[BLADEMDA]

Unlike many seemingly end-stage CHF patients who manage to generate systolic BPs in the 80s and 90s, this patient's were generally in the 130s prior to surgery. As such, I didn't spend a ton of time thinking about what I would "accept." My general approach is to keep people close to where they live. Inhalational anesthetics are powerful vasodilators, so on the one hand, hypotension may be from decreased afterload, meaning there may be no net change in flow or perfusion (thus the age-old question: is a MAP of 70 on shiite-tons of pressor really any better, perfusion-wise, than a MAP of 50 on nothing?).

On the other hand, they are potent myocardial depressants, and so in these patients, hypotension could also be from that, and could certainly lead to hypoperfusion. I used the ScvO2 to try to keep a handle on this, and it never dipped below 80% (was he merely shunting like in the septic patient? No, he didn't have that kind of physiology, and he cont'd to make urine).

As for the transducer, I'll dodge the question by saying the case was done essentially supine. People seem to go back and forth on where to put the transducer in beach-chair cases, thinking that if they place the transducer at the level of the head, then their MAP is actually CPP, and they have some guarantee of adequate cerebral perfusion. I haven't read the literature on this, but I don't think it passes the physiologic rationale.

First, people's baseline BP is determined in the clinic, where it's measured with the patient roughly in the beach-chair position. So if their baseline in the clinic was good enough to keep their brain happy in that position...

Of course (second), "anesthesia" lowers the BP, so maybe CPP does go down, but measuring the MAP with the transducer at the head doesn't measure CPP anyway, so I'm not sure this covers you. (CPP = MAP - ICP). Plus, inhalational anesthetics actually increase CBF, so is there really a net change in perfusion? I don't know.

I take care of sick high-ICP patients in the ICU all the time, and no one's putting the transducer at the head (for whatever that's worth); it doesn't seem to represent a real physiologic construct.

Nihilistic perhaps, or maybe naive. Blade, could you share some literature on the transducer height issue?

Was hoping you would do the research here; oh well:

Controversy surrounds this area of interest but most agree that maintaining BP is important in the Beach Chair position. Many Anesthesiologists believe baseline BP should not be allowed to be reduced more than 25% based on cuff readings. Others want even tighter BP control.

Those who argue for tight BP control do so because CPP is lower in the cerebral hemispheres compared to cuff pressure when in the sitting position.

You can place the transducer at the cuff level (maintain BP within 25% of baseline or no less than 70 mmHg mean); or, as per Dr. Drummond, place the transducer at the level of the tragus realizing that these readings will be lower than the cuff pressure. Even at the level of the tragus the mean BP should be maintained at 50 or more at all times- perhap even a bit higher.

Here is a example:

5'11" male in the beach chair. Mid point of cerebral hemispheres is about 12-15 inches above the cuff. Mean BP at the cuff 95/50= 60 (too low) vs mid cerebral blood pressure of 34-40 (too low).

Hence, where you place the transducer will affect the acceptable mean BP before starting vasopressors (Noreip or low dose Epi). While I use Cerebral Oximetry the mean BP should not be allowed to drift below a mean of 70 (at the cuff) at any point or use a mean of 50 at the tragus. Remember, those are the minimum numbers and a few extra points higher should be your goal.

 

[BLADEMDA]

Cerebral autoregulation is the primary homeostatic mechanism that maintains blood flow to the brain despite changes in blood pressure, and is preserved in the sitting position.10,11 As Dr. Drummond previously observed, the lower limit of autoregulation varies with the individual and can range from 33 to 113 mm Hg.12 However, a decrease below the lower limit of autoregulation does not necessarily mean ischemia will occur, or that infarction will develop. Inadequate blood flow can be compensated with increased oxygen extraction, and there is a margin between ischemia and infarction (the ischemic penumbra). This consideration has prompted growing interest in using cerebral oximetry as a surrogate to monitor adequacy of blood flow to the brain. However, results of these studies raised questions about the importance of blood pressure management in these cases. Murphy et al.13 showed that cerebral desaturation occurred more frequently in the BCP compared with the lateral decubitus position, but the patients were managed in a similar manner, with no difference in blood pressure. Similarly, YaDeau et al.14 could not demonstrate a relationship between blood pressure and cerebral oximetry in patients undergoing shoulder surgery in the sitting position when hypotension occurred in 76% of the observations. Moreover, cerebral desaturation was present in only 0.77% of observations. Assuming that cerebral oximetry monitors the adequacy of blood flow to the brain, these observations suggest that blood pressure within the clinical range considered to be acceptable (within 25% of baseline) during anesthesia is well tolerated. Genomic factors may render an individual more susceptible to the effects of systemic hypotension, but are beyond the scope of this editorial.

 

[pgg]

Before we took over a recent ortho ASC, the anesthesiologist staffing that site had a patient wake up with a stroke from a shoulder scope/rotator cuff repair. This was last year.

These things happen.

Patients are lucky it doesn't happen more often.

A while ago I was quietly asked "keep an eye on" a new locums anesthesiologist who'd had a sentinel event his first day on the job. I peeked in on one of his cases, a sitting shoulder to see him running his BP in the low 80/ range. After a 😱 moment I asked him about it, and he very patiently explained to me, like he was speaking to a child, that deliberate hypotension reduces surgical bleeding and improves the surgeon's view ...

 

[cchoukal]

50 mg of labetalol was given intravenously. Anesthesia was maintained with 2% isoflurane, 60% nitrous oxide, and oxygen.

So was it the normal BP in a normal position, or the massive anesthetic overdose (combined with some un-described comorbidity?) that caused her stroke?

Is the rate of stroke in the beachchair higher than the rate of stroke under GA in general?

 

[BLADEMDA]

http://www.cairnsanaes.org/downloads-2/files/Soeding.PDF

This is the BEST study in the literature to date. The authors used an arterial line placed at the level of the tragus. They were aggressive in treating mean BP below 65-70 (level of tragus). Even though there is only an indirect relationship between Cerebral Blood flow/CPP and MAP the authors state that CBF is preserved when a MAP of 70 (at the level of the tragus) is maintained.

For your high risk patients this can mean a mean BP at the cuff of 90.

Read the attached study.

 

[BLADEMDA]

http://www.anesthesia-analgesia.org/content/114/6/1156.long#ref-10

 

[BLADEMDA]

To put the issue in perspective, particularly as it applies to stroke in the BCP, one must take into account the following facts.

1. The incidence of perioperative stroke in noncardiac, non-neurosurgical procedures is low, and even lower, between 0.05% and 0.4%, when patients with apparent stroke risk factors are excluded.5 Most of these strokes are considered thromboembolic in origin. Even in patients with symptomatic carotid stenosis >70%, whereby hemodynamic impairment from hypotension could be detrimental, arterial-to-arterial emboli have been shown to be an important etiologic factor in watershed infarcts.6
2. Approximately 200,000 shoulder surgery cases are performed in the BCP in the United States annually, yet the incidence of intraoperative cerebrovascular events is estimated to be only approximately 0.004%.7 Furthermore, based on the statistical analysis of the results of the survey, there is no apparent difference in the incidence of stroke between patients in the BCP and the lateral decubitus position.7
3. Many shoulder procedures are performed in the BCP, and not infrequently hypotensive anesthesia is used to minimize blood loss and improve surgical conditions. Recently, YaDeau et al.8 observed no cerebrovascular complications in 4169 patients undergoing shoulder surgery using regional anesthesia in the BCP with deliberate hypotension, even though 47% of patients were hypotensive, as defined by a decrease of MAP by 30%, MAP <66 mm Hg, or systolic blood pressure <90 mm Hg. Because neurologic complication is a rare event, these numbers remain consistent with an incidence of a perioperative stroke rate of 0.07%. Even when deliberate hypotensive anesthesia is not used, it has been observed that patients on antihypertensive medications experience more hypotension in the BCP.9 Although we do not condone such practice of "benign neglect" or "permissible hypotension," one can nevertheless surmise that a large cohort of patients undergoing shoulder surgery in the BCP indeed experience systemic hypotension without neurologic sequelae. Certainly, sustained hypotension in a susceptible patient can cause ischemia. Whether this ischemia would result in an infarction may be determined by the risk factors associated with the patient, both physiologic and genomic.
4. Cerebral autoregulation is the primary homeostatic mechanism that maintains blood flow to the brain despite changes in blood pressure, and is preserved in the sitting position.10,11 As Dr. Drummond previously observed, the lower limit of autoregulation varies with the individual and can range from 33 to 113 mm Hg.12 However, a decrease below the lower limit of autoregulation does not necessarily mean ischemia will occur, or that infarction will develop. Inadequate blood flow can be compensated with increased oxygen extraction, and there is a margin between ischemia and infarction (the ischemic penumbra). This consideration has prompted growing interest in using cerebral oximetry as a surrogate to monitor adequacy of blood flow to the brain. However, results of these studies raised questions about the importance of blood pressure management in these cases. Murphy et al.13 showed that cerebral desaturation occurred more frequently in the BCP compared with the lateral decubitus position, but the patients were managed in a similar manner, with no difference in blood pressure. Similarly, YaDeau et al.14 could not demonstrate a relationship between blood pressure and cerebral oximetry in patients undergoing shoulder surgery in the sitting position when hypotension occurred in 76% of the observations. Moreover, cerebral desaturation was present in only 0.77% of observations. Assuming that cerebral oximetry monitors the adequacy of blood flow to the brain, these observations suggest that blood pressure within the clinical range considered to be acceptable (within 25% of baseline) during anesthesia is well tolerated. Genomic factors may render an individual more susceptible to the effects of systemic hypotension, but are beyond the scope of this editorial.
5. The definition of "hypotension" under general anesthesia remains controversial. A study comparing the nadir during natural sleep to decrease in blood pressure after induction of general anesthesia suggests that a 30% decrease compared with normal blood pressure is acceptable, because this is comparable to what happens during the natural sleep cycle.15 Furthermore, hypotensive anesthesia continues to be practiced by some anesthesiologists, even in elderly patients, with apparently good results, and in one study, no cognitive deficits were demonstrated.16 Although these patients were not in the BCP, a decrease in cerebral perfusion pressure occurring from systemic hypotension should have placed them at similar risk of cerebral ischemia. Moreover, although the BCP will lead to a decrease in the blood pressure at the brain (when compared with cuff on the arm), this is partially offset by the decrease in intracranial pressure in this position, mitigating the overall decrease in cerebral perfusion pressure.
6. The other potentially important factor cited by Drummond et al. is the anatomic variant in the circle of Willis. Although this undoubtedly can be a contributing factor, it must be noted that a complete circle of Willis is present in only 35% to 45% of the population,17&#8211;19 and the anatomic variant as described probably occurred in approximately 20% of the population (Bart Keogh, MD, PhD, personal communication, Swedish Neuroscience Institute). Given the high frequency of mild hypotension during anesthesia, and the common use of induced hypotension, one might expect to see a higher incidence of stroke, yet the frequency of perioperative stroke remains low. According to a recent review of the American College of Surgeons National Surgical Quality Improvement Program, the incidence of perioperative stroke in noncardiac, non-neurologic patients is approximately 0.1%, and multivariate analysis fails to establish perioperative hypotension as a risk factor.20
7. The collaterals in the circle of Willis are primarily useful when there is existing stenosis or occlusion. In the absence of hemodynamically significant lesions, collaterals are only potential conduits. Thus, all regions of the brain are potentially at risk during global hypotension, regardless of the presence or absence of collaterals, as the inflow artery into the collateral is subjected to the same driving pressure. Thus, the posterior circulation cannot supply blood flow to the right hemisphere via the small posterior communicating artery any more than it can to the left hemisphere, because the driving pressure is equally low in the anterior and posterior circulation. These considerations, and the distribution of the infarct, do not exclude systemic hypotension as the primary cause, but do suggest that embolic causes cannot be ruled out. Furthermore, venous air embolism during the BCP is a potential complication and fatality has been reported.21&#8211;24
8. Finally, we must recognize that it is difficult to avoid hypotension, although it can and should be treated. The benefits of preventing hypotension, however, must be balanced against the risks of prophylactic vasopressor therapy. Additionally, there is debate on the appropriate vasopressor for blood pressure support to improve cerebral perfusion.25 However, there are simple maneuvers that we should adopt. Anesthesiologists do not routinely correct for the hydrostatic change in blood pressure between the cuff on the arm and perfusion to the brain in the sitting position, and we should. This would be particularly important if the cuff is placed on the lower limb (a practice that is best avoided).

 

[sevoflurane]

... After a 😱 moment....

That was funny. 😀

 

[sevoflurane]

...he very patiently explained to me, like he was speaking to a child, that deliberate hypotension reduces surgical bleeding and improves the surgeon's view ...

This is not. 😡

 

[sevoflurane]

So was it the normal BP in a normal position, or the massive anesthetic overdose (combined with some un-described comorbidity?) that caused her stroke?

Is the rate of stroke in the beachchair higher than the rate of stroke under GA in general?

These bad outcomes are usually multifactorial.

Hard to tell what happened without reviewing the anesthesia record. I don't know what happened after laryngoscopy... maybe she shot up to 220/90 and thus was given 50mg of labatolol (I always start slow and work my way up....usually start with 10mg).

Maybe she had bad protoplasm (like your patient), sitting position, GA (and it's negative hemodynamic effects)... and I don't know let say she had a recent mastectomy and BPs were being measured in the lower extremity.... Letting her ride @ 90 systolic via BP cuff didn't help... oh and she was on an ACE inhibitor and was NPO for 16 hours.

The one thing we can do with these cases is just to be aware and practice defensively. Hence, I am always keeping my MAPs at or above pre-op levels (especially when BPs are taken at the arm). I educate my surgeons if I have to... and remind them of the adverse event that happened last year.

Regarding incidence of stroke in BC vs Supine. I'm not sure. What I do know, is that I have heard of this complication more than one occasion... and sometimes in perfectly healthy patients.

 

[cchoukal]

Blade's source above seems to suggest that stroke in beach chair shoulders is no worse than supine shoulders and, in fact, lower than the estimate of stroke under GA in all-comers. Maybe beach chair is protective.

 

[BLADEMDA]

Blade's source above seems to suggest that stroke in beach chair shoulders is no worse than supine shoulders and, in fact, lower than the estimate of stroke under GA in all-comers. Maybe beach chair is protective.

Sure. Good luck with your defense at the deposition hearing when the expert, John Drummond, MD, testifies that your mean BP was "unacceptably too low and increased the risk for stroke in this patient."

It is perfectly clear that even though the incidence of stroke is no greater in Beach Chair position too much fuss has been published about this position making your care that much more reviewable. I recommend a mean BP of at least 60-70 (at least 70 per Drummond) in all your high risk patients (like the one posted here). Rather than do any math calculations or risk a midlevel provider getting confused as to mean BP in the brain consider placing an arterial line with the transducer at the level of the tragus and instructing your staff to maintain the mean BP around 65-70 (insist on being callred if BP goes below a mean of 65). Yes, the good saturation reading on your cerebral oximetry is reassuring but I still insist on a mean BP of 65 on all my high risk patients having surgery in the beach chair position (preferred inotropes are Norepi or low dose Epi).

 

[proman]

There's an ongoing study looking at the effect of beach chair vs lateral position on cerebral autoregulation and cardiac output. It'll help answer many of our questions

http://clinicaltrials.gov/ct2/show/NCT01225185?term=hogue&rank=6