Preop Diastolic HTN

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osoprop28

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So we had a pt for a kidney transplant, and her preop BP was something like 180s/110s. My attending refused to go back until the diastolic was lowered. Which it eventually did with labetalol and hydralazine.

I didn't get a chance to debrief with him, but he was only focused on diastolic and I was wondering why? I feel like usually people freak out over high systolic since that can lead to strokes, MI and whatnot from the high afterload, but is there something specific regarding diastolic HTN that I'm missing? Thanks
 
I'm guessing it's because people with hypertension have increased intraoperative lability (causing scarring affecting renal viability), higher risk of perioperative renal dysfunction, higher risk of stroke and mortality. Coronary perfusion should be good though 😛

2017 aha/acc guidelines say people should be treated for htn at 130/80.
 
Agreed, acutely lowering the pressure before induction doesn’t do anything for you. Can’t delay the case. BP will be labile, but will definitely come down after induction.
 
So we had a pt for a kidney transplant, and her preop BP was something like 180s/110s. My attending refused to go back until the diastolic was lowered. Which it eventually did with labetalol and hydralazine.

I didn't get a chance to debrief with him, but he was only focused on diastolic and I was wondering why? I feel like usually people freak out over high systolic since that can lead to strokes, MI and whatnot from the high afterload, but is there something specific regarding diastolic HTN that I'm missing? Thanks
MAP = 1/3* SBP + 2/3 * DBP. At normal heart rates, diastole is twice as long as systole. Hence the DBP matters more.

People tend to focus on the SBP because it's the bigger number. Between those two, the DBP of 110 clearly mattered more; not enough to delay a case in my book, but that's a different story. Also the DBP correlates better with SVR.
 
So we had a pt for a kidney transplant, and her preop BP was something like 180s/110s. My attending refused to go back until the diastolic was lowered. Which it eventually did with labetalol and hydralazine.

I didn't get a chance to debrief with him, but he was only focused on diastolic and I was wondering why? I feel like usually people freak out over high systolic since that can lead to strokes, MI and whatnot from the high afterload, but is there something specific regarding diastolic HTN that I'm missing? Thanks

Giving a patient longer-acting antihypertensives like labetalol and hydralazine before a kidney transplant is probably one of the dumber things I have read regarding horror stories in academia.

The name of the game is perfusion of the new kidney, and you do that by maintaining their baseline blood pressure, ideally without the use of vasoactive agents (traditional teaching is to avoid alpha agonism due to potential for decreased renal blood flow). If you load them with anti-hypertensives to meet some arbitrary value that your attending has picked out and then you induce GA, what do you think will happen?

For whatever it's worth, I trained at one of the busiest transplant centers. The way I have shifted to doing kidney transplants is to induce patients and start the case without any opioid to avoid dropping their pressure (propofol + lidocaine + cisatracurium +/- esmolol). Maybe titrate in 25 mcg here and there as needed if patient is getting particularly stimulated. At the end of the case, when they are closing, you can titrate in your opioid of choice. I have seen way too many people do a "normal" induction with 50-100 mcg of fentanyl, only to see them chasing the BP with liters of fluids and vasoactive agents all case long. It is surprising how little pain most of these patients have afterwards, probably in no small part to the slug of steroid we give them beforehand as well.

Funny enough I just did a kidney transplant a couple days back whose preoperative BP was 210/130 or something...
 
Don't you want to get in a decent amount of fluid? I think we give 2-3 L a case
 
LOL, 50-100mcg of fentanyl doesn't cause a renal transplant patient to get hypotensive post-induction. Most of them never drop >20 pts below their baseline pressure, but when they do it's because they're hypovolemic from just being dialyzed and/or 100% of them are on an ace-i/arb for HTN
 
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LOL, 50-100mcg of fentanyl doesn't cause a renal transplant patient to get hypotensive post-induction. Most of them never drop >20 pts below their baseline pressure, but when they do it's because they're hypovolemic from just being dialyzed and/or 100% of them are on an ace-i/arb for HTN

As I said, I trained at one of the busiest transplant centers in the country and I find the above to be the best way. I'm not going to argue with you as to outcome difference, since I am sure there is none, but you definitely less hypotension this way. You can try to explain the hypotension you get with dialysis or ACEis/ARBs, I don't care. The way we did these cases was to keep the patient's blood pressure at baseline or +20% without the use of vasoactive agents.

And you really need to do more cases if you think 100 mcg of fentanyl doesn't cause a patient's blood pressure to drop...

Edit: Since you're a new attending anyway, maybe you should brush up a bit on some residency pearls that you may have missed also: UCSF Anesthesia Resident Pearls: Renal Transplant | UCSF Dept of Anesthesia
  • Opioid- Mainstay is fentanyl. Recommend opioid loading at the end of the case, and no (or little) opioid with induction (see Esmolol). Once fascia is divided, there is very little surgical stimulus. Opioid up front may contribute to relative hypotension. Average amount of fentanyl 200- 250mcg/case.
 
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Don't you want to get in a decent amount of fluid? I think we give 2-3 L a case

Yep, I am mainly talking about post-induction hypotension. As I said above, we would try to keep patients' blood pressures between baseline and +20% ideally, without the use of pressors.
 
Thats kind of odd because i dont see hypotension in these patients more than any other patient at all. and we do a lot of transplants here

They don't get any more hypotensive than any other patient, but for 99% of surgeries you don't care if their pressures drops a bit. And for most other surgeries, if it gets too low you can just hit them with your vasopressor of choice.
 
Umm. You should have close to 2 hours from induction until the time of the unclamping of the renal artery. Plenty of time for both the fentanyl and phenylephrine to have worn off..
Also BP tends to drop a bit with reperfusion, our surgeons just care about the number on the BP not if we are using any pressors.
 
Umm. You should have close to 2 hours from induction until the time of the unclamping of the renal artery. Plenty of time for both the fentanyl and phenylephrine to have worn off..
Also BP tends to drop a bit with reperfusion, our surgeons just care about the number on the BP not if we are using any pressors.

The harm in using pressors is more theoretical than anything else, but the traditional teaching was to avoid them.

Again, you can do it any way you want, I don’t care if you give fentanyl for induction or not. I was presenting my way of doing it and that other guy for some reason took issue with me saying fentanyl decreases blood pressure (which it does).
 
Agree with @Urzuz. I don’t do any transplants but I’ve gone to completely opioid free anesthetics for many nonpainful procedures (e.g. afib ablations) and I use a lot less phenylephrine now than when I’d give 100mcg of fentanyl up front.
 
As I said, I trained at one of the busiest transplant centers in the country and I find the above to be the best way. I'm not going to argue with you as to outcome difference, since I am sure there is none, but you definitely less hypotension this way. You can try to explain the hypotension you get with dialysis or ACEis/ARBs, I don't care. The way we did these cases was to keep the patient's blood pressure at baseline or +20% without the use of vasoactive agents.

And you really need to do more cases if you don't think 100 mcg of fentanyl doesn't cause a patient's blood pressure to drop...

Edit: Since you're a new attending anyway, maybe you should brush up a bit on some residency pearls that you may have missed also: UCSF Anesthesia Resident Pearls: Renal Transplant | UCSF Dept of Anesthesia
  • Opioid- Mainstay is fentanyl. Recommend opioid loading at the end of the case, and no (or little) opioid with induction (see Esmolol). Once fascia is divided, there is very little surgical stimulus. Opioid up front may contribute to relative hypotension. Average amount of fentanyl 200- 250mcg/case.

Not that it really matters as far as the evidence is concerned but I trained at a top 3 by volume liver transplant center and did a fair number of renal tx and open nephrectomies as well. Opioid sparing and opioid free anesthetics had become all the rage when I started, and certainly I’m not going to argue with anyone who wants to do a multimodal approach. However, one should be aware this concern about avoiding opioid hypotension in RTX comes from the concern about pressors and graft function. Unfortunately, that concern is based on 20 yr old rat kidney data (or highly confounded human studies in which inotrope/pressor choice and dose is not differentiated) and has nothing to do with actual clinical management. Just like the stupid plastic surgeons who once thought 100 mcgs of phenylephrine would kil their flap and who have mostly been debunked in the last ten years, my bet is the body of evidence will eventually show low dose vasopressors to counteract anesthetic vasodilation are also safe in transplant, and thus give whatever opioid you want.

Comparison of norepinephrine and dopamine in kidney... : European Journal of Anaesthesiology (EJA)
 
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just lower the gas, it helps raise the pressure. the more fentanyl on board the more you can lower it.

but yea here the surgeons dont like pressors. but we dont really care about what they like. it's not like we use it for no reason. if pressure is low we will use it.
 
I would definitely not delay a transplant for that DBP, especially when essentially all anesthetic medications he will be receiving will be working to lower that.
 
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Not that it really matters as far as the evidence is concerned but I trained at a top 3 by volume liver transplant center and did a fair number of renal tx and open nephrectomies as well. Opioid sparing and opioid free anesthetics had become all the rage when I started, and certainly I’m not going to argue with anyone who wants to do a multimodal approach. However, one should be aware this concern about avoiding opioid hypotension in RTX comes from the concern about pressors and graft function. Unfortunately, that concern is based on 20 yr old rat kidney data (or highly confounded human studies in which inotrope/pressor choice and dose is not differentiated) and has nothing to do with actual clinical management. Just like the stupid plastic surgeons who once thought 100 mcgs of phenylephrine would kil their flap and who have mostly been debunked in the last ten years, my bet is the body of evidence will eventually show low dose vasopressors to counteract anesthetic vasodilation are also safe in transplant, and thus give whatever opioid you want.

Comparison of norepinephrine and dopamine in kidney... : European Journal of Anaesthesiology (EJA)

You can practice whatever way you want, as I said, I’m sure there is zero difference in outcome. The issue I have is your response of “LOL, 50-100mcg of fentanyl doesn't cause a renal transplant patient to get hypotensive post-induction” because 1) you come off sounding like a condescending douche, since ironically and more importantly, 2) you’re wrong, it DOES cause the patient’s blood pressure to drop post induction (you yourself just referenced opioid hypotension in this most recent post of yours!)
 
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So we had a pt for a kidney transplant, and her preop BP was something like 180s/110s. My attending refused to go back until the diastolic was lowered. Which it eventually did with labetalol and hydralazine.

I thought that was what the propofol was for?😕
 
I have noticed as well that in residency that we usually always dumped fluids or pressors post induction with opioid used, and now with me doing opioid free, I rarely ever have to use either, unless some surgical issues or I got a little too happy with precedex
 
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You can practice whatever way you want, as I said, I’m sure there is zero difference in outcome. The issue I have is your response of “LOL, 50-100mcg of fentanyl doesn't cause a renal transplant patient to get hypotensive post-induction” because 1) you come off sounding like a condescending douche, since ironically and more importantly, 2) you’re wrong, it DOES cause the patient’s blood pressure to drop post induction (you yourself just referenced opioid hypotension in this most recent post of yours!)

You're reading your own interpretation into what I actually wrote. I referenced 'this concern' (aka yours) about opioid hypotension, not 'my' concern cause I'm honestly not convinced the phenomenon exists when we're talking about 1 mcg/kg fentanyl doses as part of a balanced anesthetic. The whole prospect that a slug of opioids (let alone of whiff of 50mcg fentanyl) is causing some profound hypotension post-induction is absurd. Yes, opioids cause some sympathetic blunting, but prolonged hypotension post-induction is 9 times/10 vasodilation from a mac of volatile plus PPV decreasing preload, and (in the renal case) a bit of hypovolemia and HTN med effect.

Again, if 'opioid hypotension' is a big problem, it leaves me wondering how my last couple hundred inductions in the highest risk pts (cardiac surg) using moderate dose opioid (1.5-3mcg/kg fent) plus a whiff of propofol and/or vapor could have been quite so stable.
 
You're reading your own interpretation into what I actually wrote. I referenced 'this concern' (aka yours) about opioid hypotension, not 'my' concern cause I'm honestly not convinced the phenomenon exists when we're talking about 1 mcg/kg fentanyl doses as part of a balanced anesthetic. The whole prospect that a slug of opioids (let alone of whiff of 50mcg fentanyl) is causing some profound hypotension post-induction is absurd. Yes, opioids cause some sympathetic blunting, but prolonged hypotension post-induction is 9 times/10 vasodilation from a mac of volatile plus PPV decreasing preload, and (in the renal case) a bit of hypovolemia and HTN med effect.

Again, if 'opioid hypotension' is a big problem, it leaves me wondering how my last couple hundred inductions in the highest risk pts (cardiac surg) using moderate dose opioid (1.5-3mcg/kg fent) plus a whiff of propofol and/or vapor could have been quite so stable.

See above peoples’ responses.

Or, you know, you can continue insisting you’re right.

I told you how I do kidney transplants and for some reason you found to need to criticize it. Then I showed you how they do it at UCSF, other peoples’ experiences on this board, etc. with inductions, yet for some reason you want to continue debating.

Humility goes a long way, especially for a new attending. Hope for your own sake you learn to accept that others’ experiences may be different than yours.
 
Guys, don't fight. It's pure physiology.

The problem with opiates is that they can produce bradycardia, and blunt compensatory sympathetic responses. (Opiates don't cause vasodilation AFAIK.) Hence, when coupled with inappropriately-dosed propofol and/or inhalational anesthetics, they block the tachycardic reflex and decrease cardiac output, possibly causing hypotension.

All of us have witnessed post-induction hypotension in residency, from some dear attending who pushed 100 mg of Lidocaine, 150-200 mcg of Fentanyl, and 1.5-2 mg/kg of propofol. Like MAC, mixing induction agents is an art. Giving 50-100 mcg of Fentanyl shouldn't be an issue in most patients, provided it's coupled with appropriate dose reductions in other agents, including gases. Give it to the normotensive elderly who's on beta-blockers with a HR of 60 at baseline, and you're almost guaranteed to get bradycardia and hypotension. It's a matter of good judgment and art.

So everybody is both right and wrong. 🙂
 
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See above peoples’ responses.

Or, you know, you can continue insisting you’re right.

I told you how I do kidney transplants and for some reason you found to need to criticize it. Then I showed you how they do it at UCSF, other peoples’ experiences on this board, etc. with inductions, yet for some reason you want to continue debating.

Humility goes a long way, especially for a new attending. Hope for your own sake you learn to accept that others’ experiences may be different than yours.

I agree with you totally that either method probably doesn't affect renal allograft function, but let's be clear, you are offering your opinion and I am offering mine. I think reasonably dosed opioids can be part of a balanced renal transplant induction based on my experience; you don't. If you're posting with the sole intent of just having everyone pat you on the back every time you offer one of your pearls, I don't know what to tell you. Could I have phrased my incredulity better? Sure. So, if my "LOL" offended your sensibilities, I truly apologize for the slight of laughing out loud.

You posted one UCSF guideline and pointed to two posters and are shocked that I could have any skepticism about it? I love guidelines and use them frequently but I don't consider one guideline in isolation to be the end-all-be-all of anesthesia, echocardiography, or critical care. That being said, I don't know you and you don't know me; for instance, I traveled halfway across the country to do fellowship in a different place with different attendings using different methodologies because there's always a different (and likely equally acceptable) way to skin a cat. I've been here for over 10 years and have learned a ton from the greats, even some things which have significantly changed my practice. At the end of the day, your judgement of whether I am humble enough or not based on a cursory search of my post history is relatively meaningless to me.

And since you brought up some guidelines, here's a section from the UTD article on anesthesia for renal transplant, written by a Stanford anesthesia professor and edited by the transplant nephrology director at Hopkins. Maybe it'll help you understand where my original post came from vis a vis the acceptability of opioids in transplant and my emphasis on volume status and other causes of hypotension such as ace-i (which have been known since the early 2000s to confer a mortality benefit in ESRD, hence my saying 100% of ESRD pts are on one at the time of transplant is barely an exaggeration):






"
We typically induce general anesthesia with IV propofol 1 to 2.5 mg/kg because the pharmacokinetic and pharmacodynamic responses to this agent are not markedly altered by ESRD [18,19]. We reduce and titrate the propofol dose in patients who may be hypovolemic since a standard induction dose administered as a bolus may result in profound hypotension due to venous and arterial dilation. Induction doses of propofol are also reduced in patients with known coexisting heart failure or older age [20-22]. (See "Anesthesia for dialysis patients", section on 'Induction' and "General anesthesia: Intravenous induction agents", section on 'Propofol'.)

During induction in most patients, we also administer adjuvant medications to blunt tachycardia due to the sympathetic response to laryngoscopy and endotracheal intubation (eg, fentanyl 1 to 2 mcg/kg and/or lidocaine 1 mg/kg), as well as a neuromuscular blocking agent (NMBA). Some ESRD patients require rapid sequence induction and intubation (RSII) due to gastroparesis with risk of aspiration of gastric contents. Succinylcholine (SCh) can be safely used as the NMBA to facilitate laryngoscopy if potassium concentration is <5.5 mEq/L and there are no electrocardiographic (ECG) changes [23]. If potassium is ≥5.5 mEq/L in a patient who requires RSII, we use a relatively large dose of rocuronium (1 mg/kg) rather than SCh. A remifentanil intubation technique is an alternative that facilitates laryngoscopy while avoiding any NMBA. (See "Anesthesia for dialysis patients", section on 'Induction' and "Rapid sequence induction and intubation (RSII) for anesthesia".)

Hydration status is assessed immediately before induction, including whether dialysis was recent and whether there is any deviation from the target dry weight (see 'Volume overload' above). For patients with likely hypovolemia, we suggest volume expansion before administration of anesthetic induction agents, with rapid IV administration of 1 to 2 L of isotonic crystalloid solution (eg, normal [0.9 percent] saline or an acetate-buffered, chloride-reduced solution such as Normosol-R, Ringer's lactate [also termed Hartmann's solution], or Plasmalyte). (See 'Fluid management' below.)"

..

"We supplement an inhalation-based anesthetic technique with intermittent bolus doses of an opioid (eg, fentanyl or sufentanil) titrated to treat hemodynamic parameters indicating sympathetic responses to pain (eg, tachycardia and/or hypertension). (See "Anesthesia for dialysis patients", section on 'Opioids' and "Perioperative uses of intravenous opioids in adults".)"
 
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You're reading your own interpretation into what I actually wrote. I referenced 'this concern' (aka yours) about opioid hypotension, not 'my' concern cause I'm honestly not convinced the phenomenon exists when we're talking about 1 mcg/kg fentanyl doses as part of a balanced anesthetic. The whole prospect that a slug of opioids (let alone of whiff of 50mcg fentanyl) is causing some profound hypotension post-induction is absurd. Yes, opioids cause some sympathetic blunting, but prolonged hypotension post-induction is 9 times/10 vasodilation from a mac of volatile plus PPV decreasing preload, and (in the renal case) a bit of hypovolemia and HTN med effect.

Again, if 'opioid hypotension' is a big problem, it leaves me wondering how my last couple hundred inductions in the highest risk pts (cardiac surg) using moderate dose opioid (1.5-3mcg/kg fent) plus a whiff of propofol and/or vapor could have been quite so stable.

My favorite is when cardiac CRNAs routinely run the gas at 1.3 MAC with all the fentanyl on board and are puzzled as to why the patient is hypotensive, and then dump crystals and albumin to "fix" it. I brought it up to the attending after I took over this particular case and he said you just have to pick your battles.
 
I agree with you totally that either method probably doesn't affect renal allograft function, but let's be clear, you are offering your opinion and I am offering mine. I think reasonably dosed opioids can be part of a balanced renal transplant induction based on my experience; you don't. If you're posting with the sole intent of just having everyone pat you on the back every time you offer one of your pearls, I don't know what to tell you. Could I have phrased my incredulity better? Sure. So, if my "LOL" offended your sensibilities, I truly apologize for the slight of laughing out loud.

You posted one UCSF guideline and pointed to two posters and are shocked that I could have any skepticism about it? I love guidelines and use them frequently but I don't consider one guideline in isolation to be the end-all-be-all of anesthesia, echocardiography, or critical care. That being said, I don't know you and you don't know me; for instance, I traveled halfway across the country to do fellowship in a different place with different attendings using different methodologies because there's always a different (and likely equally acceptable) way to skin a cat. I've been here for over 10 years and have learned a ton from the greats, even some things which have significantly changed my practice. At the end of the day, your judgement of whether I am humble enough or not based on a cursory search of my post history is relatively meaningless to me.

And since you brought up some guidelines, here's a section from the UTD article on anesthesia for renal transplant, written by a Stanford anesthesia professor and edited by the transplant nephrology director at Hopkins. Maybe it'll help you understand where my original post came from vis a vis the acceptability of opioids in transplant and my emphasis on volume status and other causes of hypotension such as ace-i (which have been known since the early 2000s to confer a mortality benefit in ESRD, hence my saying 100% of ESRD pts are on one at the time of transplant is barely an exaggeration):






"
We typically induce general anesthesia with IV propofol 1 to 2.5 mg/kg because the pharmacokinetic and pharmacodynamic responses to this agent are not markedly altered by ESRD [18,19]. We reduce and titrate the propofol dose in patients who may be hypovolemic since a standard induction dose administered as a bolus may result in profound hypotension due to venous and arterial dilation. Induction doses of propofol are also reduced in patients with known coexisting heart failure or older age [20-22]. (See "Anesthesia for dialysis patients", section on 'Induction' and "General anesthesia: Intravenous induction agents", section on 'Propofol'.)

During induction in most patients, we also administer adjuvant medications to blunt tachycardia due to the sympathetic response to laryngoscopy and endotracheal intubation (eg, fentanyl 1 to 2 mcg/kg and/or lidocaine 1 mg/kg), as well as a neuromuscular blocking agent (NMBA). Some ESRD patients require rapid sequence induction and intubation (RSII) due to gastroparesis with risk of aspiration of gastric contents. Succinylcholine (SCh) can be safely used as the NMBA to facilitate laryngoscopy if potassium concentration is <5.5 mEq/L and there are no electrocardiographic (ECG) changes [23]. If potassium is ≥5.5 mEq/L in a patient who requires RSII, we use a relatively large dose of rocuronium (1 mg/kg) rather than SCh. A remifentanil intubation technique is an alternative that facilitates laryngoscopy while avoiding any NMBA. (See "Anesthesia for dialysis patients", section on 'Induction' and "Rapid sequence induction and intubation (RSII) for anesthesia".)

Hydration status is assessed immediately before induction, including whether dialysis was recent and whether there is any deviation from the target dry weight (see 'Volume overload' above). For patients with likely hypovolemia, we suggest volume expansion before administration of anesthetic induction agents, with rapid IV administration of 1 to 2 L of isotonic crystalloid solution (eg, normal [0.9 percent] saline or an acetate-buffered, chloride-reduced solution such as Normosol-R, Ringer's lactate [also termed Hartmann's solution], or Plasmalyte). (See 'Fluid management' below.)"

..

"We supplement an inhalation-based anesthetic technique with intermittent bolus doses of an opioid (eg, fentanyl or sufentanil) titrated to treat hemodynamic parameters indicating sympathetic responses to pain (eg, tachycardia and/or hypertension). (See "Anesthesia for dialysis patients", section on 'Opioids' and "Perioperative uses of intravenous opioids in adults".)"

Ok man, last post I am going to make on this thread because it has gone pretty far off topic. I am going to try to make this as simple as possible since you have created so many straw men that I am having trouble understanding what exactly you are "debating".

1) You need to go back and re-read the thread and all of my posts. The only thing that I disagreed with you on was where in your original post where you found it laughable that giving opioid with induction causes a decrease in blood pressure. It does. If you don't give opioids, the drop in pressure you see with the induction of anesthesia is less. Try it out sometime if you care to experiment. Now, whether or not the drop in pressure impacts graft function is a completely separate matter. I personally like keeping the pressure between baseline and +20%. Once again, probably no difference in outcome, but that is how I practice.

2) CAN you give opioid with induction and throughout the case as part of a balanced anesthetic? YES. So I am completely confused when you say, "I think reasonably dosed opioids can be part of a balanced renal transplant induction based on my experience; you don't". Where did I ever even suggest that? I have maintained from the beginning that this is the way I prefer to do my inductions, but there is probably no difference in outcome regardless of how you do it. Again, straw man you have created.

3) Yes, propofol causes venous and arterial dilation. Yes, these patients are hypovolemic. Yes, hydration is important. Yes, you can get ACE and ARB-induced hypotension. I agree with all of the above (again, another straw man you argued with). Once again, this is all completely exclusive of my point #1. In my first response to you I said that you can explain the hypotension you get in whatever way YOU want. But the avoidance of opioid takes at least one possibility out of the equation for me, and in my experience, I have less patients who are left with a relative hypotension.

4) I don't care who pats me on the back and who doesn't. I am comfortable with my knowledge and practice, thanks.

Ultimately I think you misunderstood me offering my way of doing things as me saying it is the ONLY way to do things. I am not rigid at all, and I know anesthesiology is a field that has a ton of leeway in how you practice. Next time, if you want to actually debate what the better way of doing something is, I am all for it and we can debate physiology and outcomes. But your original post didn't seem to suggest you cared to debate outcome, and you honed in on opioids causing/not causing hypotension with induction.
 
Today I gave 50mcg of fentanyl to a stable patient mid-case and the bp went down. I can’t believe this doesn’t happen to anyone else. That’s all I have to say.
 
My favorite is when cardiac CRNAs routinely run the gas at 1.3 MAC with all the fentanyl on board and are puzzled as to why the patient is hypotensive, and then dump crystals and albumin to "fix" it. I brought it up to the attending after I took over this particular case and he said you just have to pick your battles.
That's a pretty important battle to pick. Why are they in the heart room, again?
 
That's a pretty important battle to pick. Why are they in the heart room, again?

Academic center, many rooms so need the CRNAs to cover and also to teach the srna's. The funny part is many days there is only 1 attending assigned to each room so theoretically they should be able to do their own cases but they are usually just hanging around in the lounge while the resident\fellow\crna is freezing to death, they don't even give breaks most of the time. Regarding battles, lost cause I guess... And can't anger your workforce?
 
Ok man, last post I am going to make on this thread because it has gone pretty far off topic. I am going to try to make this as simple as possible since you have created so many straw men that I am having trouble understanding what exactly you are "debating".

1) You need to go back and re-read the thread and all of my posts. The only thing that I disagreed with you on was where in your original post where you found it laughable that giving opioid with induction causes a decrease in blood pressure. It does. If you don't give opioids, the drop in pressure you see with the induction of anesthesia is less. Try it out sometime if you care to experiment. Now, whether or not the drop in pressure impacts graft function is a completely separate matter. I personally like keeping the pressure between baseline and +20%. Once again, probably no difference in outcome, but that is how I practice.

2) CAN you give opioid with induction and throughout the case as part of a balanced anesthetic? YES. So I am completely confused when you say, "I think reasonably dosed opioids can be part of a balanced renal transplant induction based on my experience; you don't". Where did I ever even suggest that? I have maintained from the beginning that this is the way I prefer to do my inductions, but there is probably no difference in outcome regardless of how you do it. Again, straw man you have created.

3) Yes, propofol causes venous and arterial dilation. Yes, these patients are hypovolemic. Yes, hydration is important. Yes, you can get ACE and ARB-induced hypotension. I agree with all of the above (again, another straw man you argued with). Once again, this is all completely exclusive of my point #1. In my first response to you I said that you can explain the hypotension you get in whatever way YOU want. But the avoidance of opioid takes at least one possibility out of the equation for me, and in my experience, I have less patients who are left with a relative hypotension.

4) I don't care who pats me on the back and who doesn't. I am comfortable with my knowledge and practice, thanks.

Ultimately I think you misunderstood me offering my way of doing things as me saying it is the ONLY way to do things. I am not rigid at all, and I know anesthesiology is a field that has a ton of leeway in how you practice. Next time, if you want to actually debate what the better way of doing something is, I am all for it and we can debate physiology and outcomes. But your original post didn't seem to suggest you cared to debate outcome, and you honed in on opioids causing/not causing hypotension with induction.

Speaking of strawmen, I think you're now being a pedant considering you're trying to imply that I said opioids don't cause any decrease in blood pressure, when this entire time we've been talking about opioids and their causality in relation to significant post-induction hypotension. To be very clear, <=1 mcg/kg of fentanyl may prevent a MAP rise due to laryngoscopy, or even possibly drop the avg pt's MAP 5-10 pts if they're sensitive- what it doesn't do is cause the protracted 20% drop from the baseline that you're worried about if they are administered with an otherwise balanced anesthetic.

I did read your posts, and while you now are conveniently implying in 2) that you've held a "both sides" opinion of using opioids in transplant, any honest reading of your earlier post would infer an authoritative, prescriptive declaration when you said "I have seen way too many people do a "normal" induction with 50-100 mcg of fentanyl, only to see them chasing the BP with liters of fluids and vasoactive agents all case long." An honest reading of that statement does, indeed, seem like you don't think opioids can be part of a transplant induction given the harm you've seen "way too many" times. But if you want to go back now and say 'oh, I really just want to talk about outcomes,' or 'oh, in fact opioids are fine and you can do what you want,' I guess that's your prerogative.

I would love to debate physiology and outcomes, hence why I posted the study of norepinephrine and dopamine on graft survival. FFP had an excellent exposition of a balanced anesthetic and how to relates to the physiology of post-induction hypotension, and that's the kind of discussion I'd be happy to continue. So don't be disingenuous as you're peacing out and imply I have no interest in these kind of debates.
 
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Academic center, many rooms so need the CRNAs to cover and also to teach the srna's. The funny part is many days there is only 1 attending assigned to each room so theoretically they should be able to do their own cases but they are usually just hanging around in the lounge while the resident\fellow\crna is freezing to death, they don't even give breaks most of the time. Regarding battles, lost cause I guess... And can't anger your workforce?
1:1 with an attending that is barely present. Total waste of money, and a big reason I dislike academia. It's not just the OR, though. I've seen academic places with 6-8 patient "non-teaching" ICU services with one attending and two NPs/PAs, when really just the one attending is necessary to run that service.
 
Academic center, many rooms so need the CRNAs to cover and also to teach the srna's. The funny part is many days there is only 1 attending assigned to each room so theoretically they should be able to do their own cases but they are usually just hanging around in the lounge while the resident\fellow\crna is freezing to death, they don't even give breaks most of the time. Regarding battles, lost cause I guess... And can't anger your workforce?

I will never understand this. 3 people in a room that only needs 1 and two of them don't even belong there. Insanity.
 
1:1 with an attending that is barely present. Total waste of money, and a big reason I dislike academia. It's not just the OR, though. I've seen academic places with 6-8 patient "non-teaching" ICU services with one attending and two NPs/PAs, when really just the one attending is necessary to run that service.
Who's gonna write the notes!?
 
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