How would you do this case?

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epidural man said:
Just curious as the Titan of TIVA - why would you all want gas? Is it for the benefits of preconditioning that the fluranes provide?
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Off topic, but interestingly the ACC recommends volatile anesthetic rather than IV anesthetic for all cardiac patients under GA. The recommendation is extrapolated from the better outcomes seen after cardiac bypass when volatile is used versus propofol.

Anecdotally, I also think propofol at equipotent doses as volatile causes more hypotension.
 
dipriMAN said:
Off topic, but interestingly the ACC recommends volatile anesthetic rather than IV anesthetic for all cardiac patients under GA. The recommendation is extrapolated from the better outcomes seen after cardiac bypass when volatile is used versus propofol.

Anecdotally, I also think propofol at equipotent doses as volatile causes more hypotension.
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Well this was my point/question! I was suggesting that maybe better outcomes would be from the possible cardio protection of volatiles.
 
dipriMAN said:
Off topic, but interestingly the ACC recommends volatile anesthetic rather than IV anesthetic for all cardiac patients under GA. The recommendation is extrapolated from the better outcomes seen after cardiac bypass when volatile is used versus propofol.

Anecdotally, I also think propofol at equipotent doses as volatile causes more hypotension.
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I remember that UTDOL posted this study in their whats new section for anesthesia awhile back

www.ncbi.nlm.nih.gov

PubMed

PubMed® comprises more than 38 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full text content from PubMed Central and publisher web sites.
www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov

I havent looked into it too closely but they found the volatile group required more pressor post-pump and there were no differences in outcome vis a vis "preconditioning."

I just find it very difficult to get over my anecdotal experience of how much more rock stable neuro/spine case hemodynamics (neuromonitoring vs none) are on 1 MAC volatile vs 125-200 mcg/kg/min propofol, respectively. Universally the latter needs a phenylephrine gtt. The former maybe 25-50% of the time.
 
vector2 said:
I remember that UTDOL posted this study in their whats new section for anesthesia awhile back

www.ncbi.nlm.nih.gov

PubMed

PubMed® comprises more than 38 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full text content from PubMed Central and publisher web sites.
www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov

I havent looked into it too closely but they found the volatile group required more pressor post-pump and there were no differences in outcome vis a vis "preconditioning."

I just find it very difficult to get over my anecdotal experience of how much more rock stable neuro/spine case hemodynamics (neuromonitoring vs none) are on 1 MAC volatile vs 125-200 mcg/kg/min propofol, respectively. Universally the latter needs a phenylephrine gtt. The former maybe 25-50% of the time.
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This is just one study. There are numerous studies looking at post CPB, the majority showing less pressor needed and less troponin rise postop. I think it is unequivocal that for CPB a volatile should be used, because there is a known ischemic insult.

For non CPB cases, there should be no ischemic insult. As far as I remember there aren’t any studies showing a benefit in non cardiac surgery.
 
woopedazz said:
So basically his pacemaker was picking up signals from his enormous sympathetic drive from severe pain that we'd clearly underestimated. Ppm max rate was 130. So it took off from 60 --> 130 in a single beat and just carried on.

Telling the surgeons to chill, slugging him with another 200 fent and we were golden. 2 hours into the case at this point...

Trops at their baseline (elevated baseline) post-op.

Still **** myself though
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Explain to me how the pacemaker picks up sympathetic drive from severe pain, please.
 
Just my approach but I would rather place the FIB block preoperatively and give my own sympathetic agent. I find that CHF pts don’t have much sympathetic reserves. They are tapped out pretty much.

I also prefer volatile agents in these cases to TIVA or some combo. With volatile agents I can get rid of it faster. And I think they require less sympathetic agents.
 
sidefx said:
Not entirely clear from the hx if this low EF is a new finding or if he is known to have chronic HFrEF. Assuming it's chronic and he's not having a severe acute decompensation (we don't have physical exam findings, but CT scan from yesterday doesn't suggest pulmonary vascular congestion or any significant pulmonary edema) I'd say the most likely scenario is that he's on Entresto GDMT for HFrEF and that BNP is "falsely" elevated
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Come to think of it, 4.4 is pretty high for chronic heart failure.
 
Noyac said:
Just my approach but I would rather place the FIB block preoperatively and give my own sympathetic agent. I find that CHF pts don’t have much sympathetic reserves. They are tapped out pretty much.
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The presence of a beta blocker and/or ace inhibitor wouldn't be unlikely in this patient though and the choice of slogging the heart with your inopressor or risking a post op pain problem is sort of a guess. I think I agree with the pre op block and just accept that he'll probably go to the unit on something for his cardiac output. Either way, it's putting lipstick on a pig...
 
dipriMAN said:
This is just one study. There are numerous studies looking at post CPB, the majority showing less pressor needed and less troponin rise postop. I think it is unequivocal that for CPB a volatile should be used, because there is a known ischemic insult.

For non CPB cases, there should be no ischemic insult. As far as I remember there aren’t any studies showing a benefit in non cardiac surgery.
Click to expand...

I use volatile for CPB cases. The four institutions I've trained and work at all use volatile. Every cardiac anesthesiologist I know uses volatile. That still doesn't justify using the terminology that it's unequivocal that for CPB a volatile must be used.

Bench research studies on ischemic preconditioning, troponin leak, and pressor requirement have not translated to a (large majority of studies showing a) difference in weaning from CPB failure, intubation duration, ICU length of stay, reinfarct rates, or mortality. Again, I don't disagree with using volatile 100% of the time for pump cases, but I wouldn't necessarily go around saying that the debate is settled when multiple large studies (including MYRIAD, listed below, which was just published in NEJM, and I believe the one UTDOL was referring to- not the one I first quoted) and metanalyses can't demonstrate as such.


-------------------
RESULTS
A total of 5400 patients were randomly assigned: 2709 to the volatile anesthetics group and 2691 to the total intravenous anesthesia group. On-pump CABG was performed in 64% of patients, with a mean duration of cardiopulmonary bypass of 79 minutes. The two groups were similar with respect to demographic and clinical characteristics at baseline, the duration of cardiopulmonary bypass, and the number of grafts. At the time of the second interim analysis, the data and safety monitoring board advised that the trial should be stopped for futility. No significant difference between the groups with respect to deaths from any cause was seen at 1 year (2.8% in the volatile anesthetics group and 3.0% in the total intravenous anesthesia group; relative risk, 0.94; 95% confidence interval [CI], 0.69 to 1.29; P=0.71), with data available for 5353 patients (99.1%), or at 30 days (1.4% and 1.3%, respectively; relative risk, 1.11; 95% CI, 0.70 to 1.76), with data available for 5398 patients (99.9%). There were no significant differences between the groups in any of the secondary outcomes or in the incidence of prespecified adverse events, including myocardial infarction.


--------------------------

CONCLUSIONS:
In the authors' experience, patients undergoing noncardiac surgery did not benefit from anesthesia based on halogenated anesthetics. Further studies are necessary to evaluate the cardioprotective effects of volatile agents in noncardiac surgery.

www.ncbi.nlm.nih.gov

Volatile agents for cardiac protection in noncardiac surgery: a randomized controlled study - PubMed

In the authors' experience, patients undergoing noncardiac surgery did not benefit from anesthesia based on halogenated anesthetics. Further studies are necessary to evaluate the cardioprotective effects of volatile agents in noncardiac surgery.
www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
------------------------------------
CONCLUSIONS:
Anesthesia with sevoflurane reduced cardiac biomarker release and length of hospital stay after CABG with cardiopulmonary bypass surgery compared with propofol-based TIVA with a possible reduction in 1-year mortality.

www.ncbi.nlm.nih.gov

Sevoflurane Versus Total Intravenous Anesthesia for Isolated Coronary Artery Bypass Surgery With Cardiopulmonary Bypass: A Randomized Trial - PubMed

Anesthesia with sevoflurane reduced cardiac biomarker release and length of hospital stay after CABG with cardiopulmonary bypass surgery compared with propofol-based TIVA with a possible reduction in 1-year mortality.
www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
-------------------------------------
CONCLUSION:
This meta-analysis demonstrates sevoflurane and desflurane reduce the postoperative rise in cTnI. Sevoflurane-mediated reduction in cardiac troponin was associated with improved long-term outcomes in one study. This meta-analysis was not able to show that these positive effects on troponin were translated into improved clinical outcomes. Well-designed large randomized control trials are needed to further elucidate the differential cardio-protective effects of volatile anesthetics.

www.ncbi.nlm.nih.gov

The effects of volatile anesthetics on cardiac ischemic complications and mortality in CABG: a meta-analysis - PubMed

This meta-analysis demonstrates sevoflurane and desflurane reduce the postoperative rise in cTnI. Sevoflurane-mediated reduction in cardiac troponin was associated with improved long-term outcomes in one study. This meta-analysis was not able to show that these positive effects on troponin were...
www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
 
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Personally would do a low dose spinal. But if everyone insists on GA.... etomidate, roc, tube and tell surgeon to be quick. Patient will survive.
 
Is anybody using dobutamine intra-op for cases like this? I've obviously used it in cardiac cases, but never in a general case. Maybe try and counteract some of the negative intropic effects of the anesthetic. Hypotension being an obvious concern, but it might be a better option than phenylephrine.
 
Ronin786 said:
Is anybody using dobutamine intra-op for cases like this? I've obviously used it in cardiac cases, but never in a general case. Maybe try and counteract some of the negative intropic effects of the anesthetic. Hypotension being an obvious concern, but it might be a better option than phenylephrine.
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Epi is usually faster to get (and God's pressor), so if I need an inotrope intraop, that's my usual go-to. That little bit of alpha-1 can be rather helpful to counteract the beta-2 dilation if you need anything more than a trickle of beta-agonist.

Sent from my SM-G930V using SDN mobile
 
urge said:
Explain to me how the pacemaker picks up sympathetic drive from severe pain, please.
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Every pacemaker code that contains the letter R (for Rate Adaptive/Rate Modulation) is fitted with one or more sensors that allow it to adapt its rate to match sympathetic drive.
 
Noyac said:
I have lost interest in etomidate. I like neofol.
In extreme circumstances I like epifol.
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Why the disdain against etomidate? If you have a sick patient and you’re worried about hypotension or cardiac arrest, why not give an anesthetic that’s much more forgiving and less likely to drop BPs?
 
MoMoGesiologist said:
Why the disdain against etomidate? If you have a sick patient and you’re worried about hypotension or cardiac arrest, why not give an anesthetic that’s much more forgiving and less likely to drop BPs?
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I agree. I’m just stating that I don’t use it much. Nothing wrong with etomidate.
 
Ronin786 said:
Is anybody using dobutamine intra-op for cases like this? I've obviously used it in cardiac cases, but never in a general case. Maybe try and counteract some of the negative intropic effects of the anesthetic. Hypotension being an obvious concern, but it might be a better option than phenylephrine.
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I haven’t used it since my cardiac days.
 
Noyac said:
I agree. I’m just stating that I don’t use it much. Nothing wrong with etomidate.
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+1. Btw, etomidate can drop the pressure, too (for those of us who use it as if it were holy water).

+1 on using epi, too. I know it much better than dobutamine, it's in the cart, and it's easy to titrate. Keep an eye on O2 consumption and one should be fine. If concerneed about tachycardia, I add (or replace it with) norepi.
 
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Ronin786 said:
Is anybody using dobutamine intra-op for cases like this? I've obviously used it in cardiac cases, but never in a general case. Maybe try and counteract some of the negative intropic effects of the anesthetic. Hypotension being an obvious concern, but it might be a better option than phenylephrine.
Click to expand...
Dobutamine is very arrythmogenic and can vasodilate. Unlikely that you would be able to use it on its own as a pressor. I also think epi works better and is more reliable.
 
FFP said:
+1. Btw, etomidate can drop the pressure, too (for those of us who use it as if it were holy water).

+1 on using epi, too. I know it much better than dobutamine, it's in the cart, and it's easy to titrate. Keep an eye on O2 consumption and one should be fine. If concerneed about tachycardia, I add (or replace it with) norepi.
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Watched a person die the other day after the ER pushed 5 of midazolam and 30 of etomidate.
 
abolt18 said:
Watched a person die the other day after the ER pushed 5 of midazolam and 30 of etomidate.
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Interesting, the choice of that much midaz and that much etomidate makes no sense to me. How big was the patient? How old?
 
My recipe for floor intubations as a resident was one 10 cc syringe, half filled with etomidate and half filled with paralytic. Push and tube. Never had a problem.
 
I would induce with etomidate and roc ; not sure sux should be given in this patient with history of CVA would have to eyeball him. I would definately place an ETT and just drop off to the ICU intubated; unlikely you will get the guy off the ETT quickly due to all the mucus plugging and lung pathology. Could try suggamadex but its a gamble. Have discussion with family

Make sure ICD/PPM is functioning and what functions it has. and also have all pressors drawn up and ready to go . A line is a plus .

Maybe try some pulmonary toilet before induction to help against mucus plugging
 
Its just too much of a hassle to do an epidural or spinal in the lateral position and it may not give you the analgesia you want. I have seen it work successfully and seen it fail horribly.
 
interscalene said:
Its just too much of a hassle to do an epidural or spinal in the lateral position and it may not give you the analgesia you want. I have seen it work successfully and seen it fail horribly.
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That's a pretty big call to GA every #NOF
 
Spinal all the way. DOne
This case is a supine case on the fracture table.

If you dont want to do that, slip an LMA in with No or minimal narcotic.
DONE!
preop art line.
 
@woopedazz could you see pacer spikes? And was the pacer detection feature of your monitor enabled (assuming it has one)?

Reason I’m asking is, wondering how many ppl would try a small slug of esmolol for a wide complex tach WITH pacer spikes? Would your decision change if the BP is normal, low, or very low?

Paced WCT with normal pressure, even in a heart with EF 20% I might trickle in 10mg esmolol at a time. The negative inotropy won’t kill the patient as long as you dose it slowly and cautiously, despite popular belief
 
psychbender said:
Epi is usually faster to get (and God's pressor), so if I need an inotrope intraop, that's my usual go-to. That little bit of alpha-1 can be rather helpful to counteract the beta-2 dilation if you need anything more than a trickle of beta-agonist.

Sent from my SM-G930V using SDN mobile
Click to expand...

dipriMAN said:
Dobutamine is very arrythmogenic and can vasodilate. Unlikely that you would be able to use it on its own as a pressor. I also think epi works better and is more reliable.
Click to expand...

My concern with epi is the variable receptor effects. You have somebody with pHTN and RV dysfunction. With epi you could be rolling the dice with whether or not they're going to have a significant alpha response or not. IMO dobutamine +/- vaso or norepinephrine is a more predictable option.
 
abolt18 said:
Watched a person die the other day after the ER pushed 5 of midazolam and 30 of etomidate.
Click to expand...
... that dosing makes no sense. If someone is that sick you’re inducing with midaz or etomidate, you don’t need more than 1-2mg midaz OR 10mg etomidate, not whopping doses of both. If someone can tolerate 30 etomidate, just give a small amount of propofol instead.

Also if someone is super sick and out of it, feel free to use paralytic only. These people don’t remember anything of what happened to them. Probably a survival mechanism to help us forget our traumas
 
As people are saying, this case is dependent on where you are and who's holding the knife. Keep it simple if you in a PP with good ortho surgeons. Go HAAm if you're in an academic with slow residents (including your own).
 
MoMoGesiologist said:
... that dosing makes no sense. If someone is that sick you’re inducing with midaz or etomidate, you don’t need more than 1-2mg midaz OR 10mg etomidate, not whopping doses of both. If someone can tolerate 30 etomidate, just give a small amount of propofol instead.

Also if someone is super sick and out of it, feel free to use paralytic only. These people don’t remember anything of what happened to them. Probably a survival mechanism to help us forget our traumas
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I agree entirely. I showed up during the code. Reportedly already AMS and declining upon arrival. HD stable initially but had positive FAST exam. Induce and Tube. Code during that induction. Chest tubes and lines. ROSC. Code again a few minutes later. Rinse and repeat multiple times. I'm leaving out details that would be even more damning but they get very specific and I'd prefer to not make the situation easily identifiable to others who were there.

Anyway, during a moment of calm the EM resident asked of the trauma surgery chief resident "do you think I overdid it with the midaz and etomidate?"

Even in a totally stable and awake patient, I've never given 30mg of etomidate. That PLUS the midaz was just icing on the cake.
 
Ronin786 said:
My concern with epi is the variable receptor effects. You have somebody with pHTN and RV dysfunction. With epi you could be rolling the dice with whether or not they're going to have a significant alpha response or not. IMO dobutamine +/- vaso or norepinephrine is a more predictable option.
Click to expand...
You're really not, though. Epi in low doses is going to have very little, if any, alpha-1 agonism (function almost the same as dobutamine initially, then just enough alpha-1 to offset the beta-2 dilation). At the doses where you are going to see some alpha agonism, you should still have enough beta-1 to help the RV overcome the slight increase in PVR. Dobutamine plus vaso is a really nice combo, but probably not necessary. I'd still just titrate the epi carefully.

Sent from my SM-G930V using SDN mobile
 
Is there anyway that you could do this with an epidural? I would put a probe on to eval fluid status with that BNP. Look at RV f(x) and sub xiphoid IVC. A line just before epdiural placement. PPV with mask as poor man's CPAP, low dose propfol as sedation with very small titrations of opioid throughout the case, like 25 mcg at a time. Also have bolus stick of NE ready in room with gtt as well.

I'd be scared to really put him under general given his co-morbidities and his potential for crumpage just after landing in ICU. I don't think you have a great amount of time to optimize him, either.
 
What technique did you pick? Howd the patient do?
DrOwnage said:
Hey guys heres a case.

65 y.o. 77kg, 5'11" BMI 23, with previous medical history of CAD, MI x3 (last in 2017); s/p DES to OM (6/07); periprocedure thalamic CVA x 2 with right-sided weakness; s/p CABG (LIMA-LAD, SVG-RCA/PDA in 4/2010) and DES x4 (OM1 6/2017, LAD 5/2008 and 2017, LCx 5/2015) with ischemic cardiomyopathy, h/o VT and CHB s/p AICD (pacemaker dependent); infected AICD, lead extraction 4/26/2019 and generator change with leadless single chamber pacemaker; chronic stable angina, OSA (on home CPAP) and syncope. From SNG for acute right leg pain after falling out of his wheelchair. Found to have Comminuted fracture of the proximal femur metadiaphysis, with displacement and overriding of the fragments

Plan for open reduction internal fixation, IM nail fixation (R) Hip.

Echocardiogram: Date: 10/23/19
LV ejection fraction (%): 20
Valve Assessment
mild aortic insufficiency
moderate mitral regurgitation
moderate tricuspid regurgitation
Pulmonary Pressure (mmHg): 55, Moderate Pulm Htn
Other: CONCLUSIONS
1. Definity contrast agent was given intravenously to enhance visualization.
2. Mildly increased left ventricular size.
3. Borderline concentric left ventricular hypertrophy.
4. There are no normally-contracting wall segments.
5. The calculated ejection fraction (Simpson's) is 20 %.
6. Upper normal right ventricle in size.
7. Moderately reduced RV systolic function.
8. Severely dilated left atrium in size.
9. Moderately dilated right atrium in size.
10. At least moderate mitral valve regurgitation. If clinically indicated and if management of a patient will alter, a transesophageal echocardiogram (TEE) may be considered.
11. Moderate tricuspid regurgitation.
12. Mild aortic regurgitation.
13. Moderately elevated PA systolic pressure.
14. Elevated right-sided filling pressure.

CT Chest yesterday:
IMPRESSION:
1. Interval development of peripheral lobulated masslike consolidation within the left lower lobe/lingula, small to moderate left pleural effusion and prominent mediastinal lymph nodes. This raises concern for malignancy/lung cancer. Recommend further
evaluation with contrast-enhanced CT and/or, left pleural fluid analysis or lung biopsy depending on clinical scenario.
2. Nodular consolidative opacities in the right lung apex are of indeterminate etiology. Possibility include infection or malignancy
3. Scattered areas of airways impaction, most prominently in the right lower lobe, likely aspiration.
4. Cardiomegaly. Coronary stents. Leadless ICD in the right ventricle

Hgb 10.1
BNP 4.4k
Creatinine 1.22
INR 1.3

This being done at an ortho hospital without intraop TEE. There is a cath lab.

Epidural, a line, central line w/ MAC? General with preinduction a line, central line w/ PAC? What would you guys do? Thanks ahead of time.
Click to expand...
 
Ronin786 said:
My concern with epi is the variable receptor effects. You have somebody with pHTN and RV dysfunction. With epi you could be rolling the dice with whether or not they're going to have a significant alpha response or not. IMO dobutamine +/- vaso or norepinephrine is a more predictable option.
Click to expand...
Milrinone???
 
dipriMAN said:
Interesting, the choice of that much midaz and that much etomidate makes no sense to me. How big was the patient? How old?
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Not very big. Probably in 60s. Already inebriated and declining mental status.
 
abolt18 said:
Single vehicle MVC at high speed. Alcohol involved.

@FFP I'm thinking both did it. Either one by itself, at lower doses may have been better tolerated.
Click to expand...
Yep. People tend to forget that midazolam is a vasodilator. Using a ton of etomidate for induction "stability", then adding a ton of midazolam = one really stupid resident, the kind that shouldn't be allowed even to wipe the patient's butt unsupervised. Let's not mention whoever was "supervising" him. I don't remember ever pushing more than 20 mg of etomidate; one actually needs 2 vials to draw up 30, which should have rung a bell in the wide empty space.

I am actually glad that patients have started suing trainees too for malpractice. Every healthcare worker should concentrate on first doing no harm.
 
Last edited by a moderator:
MoMoGesiologist said:
... that dosing makes no sense. If someone is that sick you’re inducing with midaz or etomidate, you don’t need more than 1-2mg midaz OR 10mg etomidate, not whopping doses of both. If someone can tolerate 30 etomidate, just give a small amount of propofol instead.

Also if someone is super sick and out of it, feel free to use paralytic only. These people don’t remember anything of what happened to them. Probably a survival mechanism to help us forget our traumas
Click to expand...
I would be careful with this, because I have seen people go into bradycardia and arrest with this recipe.
 
FFP said:
Yep. People tend to forget that midazolam is a vasodilator. Using a ton of etomidate for induction "stability", then adding a ton of midazolam = one really stupid resident, the kind that shouldn't be allowed even to wipe the patient's butt unsupervised. Let's not mention whoever was "supervising" him. I don't remember ever pushing more than 20 mg of etomidate; one actually needs 2 vials to draw up 30, which should have rung a bell in the wide empty space.

I am actually glad that patients have started suing trainees too for malpractice. Every healthcare worker should concentrate on first doing no harm.
Click to expand...
Ours are 20mL vials with 2mg/mL so that's not applicable here. But I also have never given that much even in non-trauma patients.
 
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