I’m not sure I’d agree would this - but don’t disagree either.The hemodynamic and amnestic effects of 0.7 mac volatile are infinitely more predictable IMO than a tiva titration
I mean sure - for amnesia - but not sure about hemodynamics.
I’m not sure I’d agree would this - but don’t disagree either.The hemodynamic and amnestic effects of 0.7 mac volatile are infinitely more predictable IMO than a tiva titration
Oh I never said that.I though you wanted to stop saying stupid things?
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.Just curious as the Titan of TIVA - why would you all want gas? Is it for the benefits of preconditioning that the fluranes provide?
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.
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.
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.I remember that UTDOL posted this study in their whats new section for anesthesia awhile back
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Comparison of propofol-based versus volatile-based anaesthesia and postoperative sedation in cardiac surgical patients: a prospective, randomized, study - PubMed
The use of volatile-based anaesthesia and postoperative sedation did not confer any cardioprotection compared with propofol-based anaesthesia and sedation in patients who had good left ventricular function and were undergoing CABG.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.
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
Come to think of it, 4.4 is pretty high for chronic heart failure.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
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.
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.
I have lost interest in etomidate. I like neofol.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.
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.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.
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.Explain to me how the pacemaker picks up sympathetic drive from severe pain, please.
Pain is the best pressor...Sometimes a little stimulation helps things!
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?I have lost interest in etomidate. I like neofol.
In extreme circumstances I like epifol.
I agree. I’m just stating that I don’t use it much. Nothing wrong with etomidate.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?
I haven’t used it since my cardiac days.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.
+1. Btw, etomidate can drop the pressure, too (for those of us who use it as if it were holy water).I agree. I’m just stating that I don’t use it much. Nothing wrong with etomidate.
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.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.
Watched a person die the other day after the ER pushed 5 of midazolam and 30 of etomidate.+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.
Interesting, the choice of that much midaz and that much etomidate makes no sense to me. How big was the patient? How old?Watched a person die the other day after the ER pushed 5 of midazolam and 30 of etomidate.
That's a pretty big call to GA every #NOFIts 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.
That's a pretty big call to GA every #NOF
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.
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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.
... 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.Watched a person die the other day after the ER pushed 5 of midazolam and 30 of etomidate.
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.... 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
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.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.
Which do you think was the problem? /SocratesWatched a person die the other day after the ER pushed 5 of midazolam and 30 of etomidate.
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?"
Watched a person die the other day after the ER pushed 5 of midazolam and 30 of etomidate.
Long time ago, when mommy dropped the EM resident on his head.Yikes. Was it a trauma case?
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.
Single vehicle MVC at high speed. Alcohol involved.Yikes. Was it a trauma case?
Milrinone???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.
Totally. Not to bag on the trauma resident but wtf does this guy/girl really know about theses agents. All they do is sit back and point fingers.The blind leading the blind...
Not very big. Probably in 60s. Already inebriated and declining mental status.Interesting, the choice of that much midaz and that much etomidate makes no sense to me. How big was the patient? How old?
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.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.
I would be careful with this, because I have seen people go into bradycardia and arrest with this recipe.... 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
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.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.
I would be careful with this, because I have seen people go into bradycardia and arrest with this recipe.