surgeons can't see if there's bleeding....
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Shoulder Surgery
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surgeons can't see if there's bleeding....
There-in lies the problem. We will never again run systolics in the 80-90's in the beach-chair position.
OK you have mentioned an article. What many of us here do is discuss the article and how it pertains to the subject. Could you start this discussion?
Maybe this will give us a "clue".
You, I and Jet have mentioned the BS/Dogma a few times. It would be much more believable to fellow anesthesiologists if we were to explain why we think something is BS/Dogma. Rather than just calling it so and expecting people to believe us. We are anonymous, why should they believe us?
The vasodilating and myocardial depressant effects of anesthetics reduce stroke vol. and cardiac output. Many quote by 20%. BP in the non-anesthetized pt in the sitting position either is unchanged or increases slightly as opposed to the decrease that occurs when anesthetized.
CPP decreases in the sitting position (possibly 15%) in the unanesthetized and by more under anesthesia due to the vasodilating effects, impaired venous return, etc. Then ventilation has an effect on CPP as well. Spontaneous ventilation increases venous return by inspiratory subatmospheric pressure and this is partially offset by PPV.
This is the best explanation I have. Do you have a better one to refute it?
militaryMD ---
you have to take into consideration cerebral blood flow and what are the determinant factors for cerebral perfusion...
the issue with sitting(beach chair) shoulders is that frequently the surgeons whine because there is a bit of blood in their view... then the gas-passer gives a few hits of labetalol, dials up the gas a bit and lets the pressure drop.. you basically end up vaso-dilating the poor patient and a lot of their blood is pooling below the neck... the cases of hypoxic injury (while rare) in the seated position should give us pause
there was a guy during my anesthesia training (who we all worshipped but despised by most of the surgeons) who would write 90/60 with a big black marker on a sheet of paper and then tape it over the monitor (and then turn off the monitor).... he would then proceed to tell the surgeon that the blood pressure is now perfect for the surgery...
Mil MD - what would you do if BP is 75/40 and the shoulder is still bleeding - lower the BP even more to make your surgeons happy... come on ....
you have to take into consideration cerebral blood flow and what are the determinant factors for cerebral perfusion...
the issue with sitting(beach chair) shoulders is that frequently the surgeons whine because there is a bit of blood in their view... then the gas-passer gives a few hits of labetalol, dials up the gas a bit and lets the pressure drop.. you basically end up vaso-dilating the poor patient and a lot of their blood is pooling below the neck... the cases of hypoxic injury (while rare) in the seated position should give us pause
there was a guy during my anesthesia training (who we all worshipped but despised by most of the surgeons) who would write 90/60 with a big black marker on a sheet of paper and then tape it over the monitor (and then turn off the monitor).... he would then proceed to tell the surgeon that the blood pressure is now perfect for the surgery...
Mil MD - what would you do if BP is 75/40 and the shoulder is still bleeding - lower the BP even more to make your surgeons happy... come on ....
You're right, I would not, but then my cutters don't ask for anything less than SBP of 100 mmHg.
I'm at work right now, so I gotta go, but BP control and regulation is one of my areas of interest when I had time and access to the library.
I need to apologize to anyone who is offended by my off hand (after 2 bourbon) remark about bp and what we do.....because I really feel that what we do with bp is not literature or evidence based...but based on what gets perpetuated during training.
more later when I get home.
Vent,
Let's continue with our banter now....This something that is of interest to me.
So there is that dreaded "cerebral autoregulation" curve that we all have been taught.
Now I spent quite a few hours trying to track down where that original data came from, and I was unable to....this includes talking to old, gray hair guys.
Anyone who knows the original data, please post up.
OK...now based on this autoregulation data.....where did the +/- 20% of baseline come from?
Once again, I've spent many hours trying to identify the source without success.
So here also, anyone with the original data, please post up.
OK, now, let's ASSUME that all this is true, and we have a case where we NEED to lower to bp below the 20%.....How long does someone's BP needed to be treated before the curve is shifted....AND where is that data?
and ASSUMING that this is ALL true, why is it that when we go on bypass and after bypass, we tolerate such lower BP's??
Now, as for measuring the BP, JNCVII describes VERY clearly how BP is to be measured.....sitting position, with arm at the side....essentially micmicking a position MORE extreme than the beachchair position.
So the BP you find in the outpatient medical record reflects a BP measured IN the seated upright position measured at the level of the heart...so why should we change where the BP is measured just because we are in the Operating room.
The data on BP treatment is quite clear.....longer and LOWER the bp is...the less likely a patient with have either a STROKE or Heart attack....from the Framingham study group....there's that controversial J-curve issue, but we generally don't treat BP the that part of the curve.
I always thought that the reason we tolerate lower MAPs on bypass was due to decreases in O2 consumption secondary to the hypothermia that accompanies a CPB run. IE, organs use less O2, so they tolerate less perfusion.
Correct.
Nope, there are many cases now where CPB is not instituted and patient is kept warm.
And patients are rewarmed before separating from bypass.
well , at least, where I trained.
Perhaps BP ain't the whole story... Could it be that that pt, suffered from an air embolism causing an air lock in a small cerebral vessel causing the stroke. In the beach chair position, the shoulder is above the heart. Air can be entrained into the circulation. Everybody wants to blame it on BP, let's blame it on a small air embolism that travels to the brain and doesn't cause any hemodynamic instability. Regards, ---Zippy
Sometimes we do tolerate it and sometimes we don't, "Pump Head".
Yeah, there's a lot of pump head out there. And, patients don't always fully recover from it. Not a good counterpoint. Plus, these patients are (as someone already mentioned) chilled to the point that CMRO2 is significantly decreased, even more so than just with the anesthetic agent alone. You don't do this on "beating heart" cases. Also why the routine use of hemodilution/hypotension techniques have all but been abandoned.
-copro
Cerebral autoregulation has been thought to maintain cerebral blood flow constant b/w MAP of 50 - 150 mmHg. This value probably came from a 1953 publication by McCall.
http://www.ncbi.nlm.nih.gov/pubmed/13104502
I'll save you guys the trouble of looking it up if you wish. 42 pregnant women (24 pre-eclamptic and 18 normal) were treated with hydralazine or Veratrum viride. MAP in the 2 normal groups of 9 pts each was reduced to 57 mmHg with Veratrum viride and 64 mmHg with hydralazine, CBF remained constant in the former group and actually increased in those treated with hydralazine. This article was referenced again by LAssen in 1959, and according to Drummond , has been quoted ever since to support the "presumed" 50 mmHg as Lower Limit.
Yes, I found that one, but where is the one that it shifts with chronic HTN....and that it shifts back after you treat it....and how long do you need to treat it before it shifts back...
And for this particular 1953 article....how was CBF measured? and how did the upper limit get measured (150 mmHg)?
And where did the 20% number come from?
As for "pump" head....researchers have been look at a number of different presumed causes....I don't think BP has been definitively identified as the culprit.
Neurologic complications has been compared between normothermic and hypothermic CPB.....hypothermic DID NOT prevent "pump" head....I believe it came out of Duke.
off-pump bypass? heard of it?
Hemodilution has pretty much been abandoned because it is just not cost-effective....a lot of work to save a very small volume of blood...and in this day and age of extremely safe banked blood, it just doesn't seem warranted.....or is there data to say that hemodilution was abandoned because of safety reasons.
as for deliberate hypotension....is NOT abandoned....blue cross pays for using this technique.
Now lets continue with the cerebral autoregulation topic. Human studies since the early 1970's document a range of the lower limit of autoregulation (LLA) b/w 70 and 90 mmHg, with a mean of 80 mmHg rather than the usually quoted 50 mmHg.
Drummond has argued that if MAP is being discussed, the LLA normally is not less than 70 mmHg. MAP is usually used b/c true CPP (MAP - ICP or CVP) is usually unknown. If the normal ICP is 10 -15 mmHg in the supine pt, the LLA expressed as MAP is 70 and when expressed as CPP it is 55 -60 mmHg (70 minus 10-15). Although studies have shown normal cerebral oxygen metabolism can be maintained down to a CPP of 30 - 40 mmHg with deliberate hypotension, values this low leave no room for error.
http://www.anesthesiology.org/pt/re...6XpQ9Zqtcn1BZbZn!-383192544!181195628!8091!-1
Drummond has argued that if MAP is being discussed, the LLA normally is not less than 70 mmHg. MAP is usually used b/c true CPP (MAP - ICP or CVP) is usually unknown. If the normal ICP is 10 -15 mmHg in the supine pt, the LLA expressed as MAP is 70 and when expressed as CPP it is 55 -60 mmHg (70 minus 10-15). Although studies have shown normal cerebral oxygen metabolism can be maintained down to a CPP of 30 - 40 mmHg with deliberate hypotension, values this low leave no room for error.
http://www.anesthesiology.org/pt/re...6XpQ9Zqtcn1BZbZn!-383192544!181195628!8091!-1
I'm not sure but in this thread we are interested in the LLA b/c of the beach chair position and surgeons asking for the BP to be lowered.
Naw, edumecate me.
(I actually did one today.) What I was trying to say is that you don't drop the blood pressures into the SBP 80-90 range for this technique. At least we don't at our institution. Your "cerebral protection" is limited by your agent (i.e. decrease in cerebral metabolic oxygen rate), not by hypothermia. My bad for the confusing thought structure in the other post.
Who said abandoned? I said "all but" been abandoned. I'm sure there are a lot of yokels out there who are still routinely practicing 1970's anesthesia.
But, you're right. CellSaver and better, safer blood supply has probably obviated the need for this, which is the main reason why it's no longer done...
http://www.corronline.com/pt/re/cor...dJrwgnmG2Pnh0hJR!-809317659!181195629!8091!-1
Again, I'm not talking about dropping the blood pressure for a few minutes so an orthopod can put glue on a bone. I'm talking about entire case plans where this is done. I'm sure people still do this as well, but you're messing with physiology in a potentially dangerous way, especially if (like many of my patients) their regular SBP is in the 140-150 range.
http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Why do it, aside for the fact that BC still pays for it? We going to also neuromonitor every patient that we want to do this technique to? How much additional cost is that going to add (for little additional benefit) to an already failing healthcare system rife with patients who already don't pay?
These techniques are just, quite frankly, no longer routinely necessary, taught, or used. I've never even heard anyone suggest them.
-copro
These articles can help answer some of these questions.
http://stroke.ahajournals.org/cgi/reprint/15/3/413.pdf
http://circ.ahajournals.org/cgi/content/abstract/circulationaha;53/4/720
http://ajpheart.physiology.org/cgi/content/full/274/3/H1023 (this one explains a lot)
I'm going to ignore the last ten or so posts and focus on the original message.
1. Lateral and beachchair; depends on the procedure. If it's open, it's beachchair; if it's a scope, lateral. If it's both, lateral to beachchair (assisted with a beanbag). +/- Schlein headrest
2. BP isn't an issue as long as it's "normal." Generally, the surgeons would prefer that it's kept under 100mm systolic unless the patient is a vasculopath. Vision tends to be an issue when the pressure goes high -- like 160+. Sometimes it's just a matter of increasing pump pressure to fix things.
3. BPs are measured in the opposite arm. Pulse ox on usually on the opposite arm or on the foot, depending on cord length and laziness. I don't think I've ever used an a-line for a shoulder case since going into private practice. The last time that I did was for a big shoulder disarticulation on a 70 year old pulmonary cripple as a resident, and that was just for post-op blood gases/ICU blood samples.
Pain management varies from intraarticular shots of marcaine and morphine at the end of the scope to shooting a ton of local down the drain at the end of the case, clamping it, and pulling it out in recovery to simply straight systemic narcotics with toradol. Usually nobody gets an interscalene block unless it's an open procedure and even then, it's just for post-op pain relief -- everyone still goes to sleep.
I'm in a physician-only group and our turnaround times are generally ten minutes at our sites; interscalenes just aren't an option for every case. They just slow things down, even if I could routinely get them all in from prep to removal of the pulse ox in five mins. Also, I'm very aware of the surgeon's skills and block preferences; I never force a block down the throat of a patient whose surgeon is either anti-block or is simply technically lousy or careless.
Despite hypertensive adaptation of CBF autoregulation,
antihypertensive treatment generally is not associated
with a risk of inducing cerebral ischaemia. On
the contrary, the brain is the organ that has benefited
most from modern antihypertensive treatment. It is
now universally agreed that even moderate degrees of
hypertension should be treated, in order to protect a
substantial proportion of the patients against the disaster
of stroke. The reasons why cerebral ischaemia is so
seldom caused by antihypertensive treatment are at
least three: First, despite hypertensive adaptation of
CBF autoregulation, there is still in most patients considerable
room for therapeutic blood pressure lowering
before CBF is jeopardized. Typically, in acute, controlled
hypotension the pressure can be lowered around
25% before the lower limit of autoregulation is reached
and around 50% before symptoms of brain hypoperfusion
are encountered.
antihypertensive treatment generally is not associated
with a risk of inducing cerebral ischaemia. On
the contrary, the brain is the organ that has benefited
most from modern antihypertensive treatment. It is
now universally agreed that even moderate degrees of
hypertension should be treated, in order to protect a
substantial proportion of the patients against the disaster
of stroke. The reasons why cerebral ischaemia is so
seldom caused by antihypertensive treatment are at
least three: First, despite hypertensive adaptation of
CBF autoregulation, there is still in most patients considerable
room for therapeutic blood pressure lowering
before CBF is jeopardized. Typically, in acute, controlled
hypotension the pressure can be lowered around
25% before the lower limit of autoregulation is reached
and around 50% before symptoms of brain hypoperfusion
are encountered.
16 Second, during long-term
treatment, as mentioned above, some hypertensive patients
readapt their CBF autoregulation towards normal.
And third, even though the blood pressure falls
somewhat below the lower limit of autoregulation, the
brain can compensate for the fall in flow by increasing
the oxygen extraction from the blood. Thus, in the
internal jugular venous blood, oxygen saturation typically
is around 60% whereas e.g. in the coronary sinus
it is 20-30%.2I This difference may well explain why
treatment, as mentioned above, some hypertensive patients
readapt their CBF autoregulation towards normal.
And third, even though the blood pressure falls
somewhat below the lower limit of autoregulation, the
brain can compensate for the fall in flow by increasing
the oxygen extraction from the blood. Thus, in the
internal jugular venous blood, oxygen saturation typically
is around 60% whereas e.g. in the coronary sinus
it is 20-30%.2I This difference may well explain why
antihypertensive
Correct me if I'm wrong:
because we observed that there is a lower limit of autoreg in preg/pih'ers in the 1950's...using a technique that may or maynot be validated ...where Cerebral metabolic RATE IS ASSUMED to be constant ....in an UNanesthetized patient....and where there is NO clinical endpoint studied.....
We now use that physiology and the "20%" number to guide our clinical practice..
Whereas while there is solid data that links higher BP's with adverse clinical outcomes (stroke/mi) and solid data linking LOWER BP to decreasing ENDPOINTS....as low as sbp of 100 mmHg (which is what I call induced hypotension) before the J-curve hypothesis is even a possibility...we don't use that to guide our clinical practcie.....
And the solid data is collected from patients in a manner that is similar to our beach chair position....
and Zippy is right on ...as usual.
because we observed that there is a lower limit of autoreg in preg/pih'ers in the 1950's...using a technique that may or maynot be validated ...where Cerebral metabolic RATE IS ASSUMED to be constant ....in an UNanesthetized patient....and where there is NO clinical endpoint studied.....
We now use that physiology and the "20%" number to guide our clinical practice..
Whereas while there is solid data that links higher BP's with adverse clinical outcomes (stroke/mi) and solid data linking LOWER BP to decreasing ENDPOINTS....as low as sbp of 100 mmHg (which is what I call induced hypotension) before the J-curve hypothesis is even a possibility...we don't use that to guide our clinical practcie.....
And the solid data is collected from patients in a manner that is similar to our beach chair position....
and Zippy is right on ...as usual.
agreed that a LOT of the literature on BP and Cardiac Work is poor - especially since most of it is based on old canine studies or other studies done in the 30s-60s with poor equipment/statistics etc...
however there is a real phenomenon where the brain of a vasculopath does require higher pressures to perfuse properly...
i think the best examples are those patients who have mental status changes when they drop their blood pressure... ie the old lady who was put on a new anti-hypertensive comes to the ER totally out of it - her BP is 120/80 - gets worked up with nothing revealing itself - goes to the ICU where they put her on a phenylephrine drip - as soon as her BP gets to 160/100 she starts mentating perfectly normal again...
now when the BP gets measured at the arm in an awake patient you aren't dealing with pooling, vasodilation like you see while under anesthesia...
probably the best way to really evaluate this would be to put somebody in a beach-chair - anesthetize them - place an EEG (a real one - not a BIS) and start lowering their BP - see what happens - that should provide us with some info... don't think that has been done
however there is a real phenomenon where the brain of a vasculopath does require higher pressures to perfuse properly...
i think the best examples are those patients who have mental status changes when they drop their blood pressure... ie the old lady who was put on a new anti-hypertensive comes to the ER totally out of it - her BP is 120/80 - gets worked up with nothing revealing itself - goes to the ICU where they put her on a phenylephrine drip - as soon as her BP gets to 160/100 she starts mentating perfectly normal again...
now when the BP gets measured at the arm in an awake patient you aren't dealing with pooling, vasodilation like you see while under anesthesia...
probably the best way to really evaluate this would be to put somebody in a beach-chair - anesthetize them - place an EEG (a real one - not a BIS) and start lowering their BP - see what happens - that should provide us with some info... don't think that has been done
From a practical point of view and away from all the metaphysical abstract thinking that has been taking place on this thread it makes sense for each clinician to establish personal comfort levels with what is considered acceptable BP taking in consideration each patient's unique circumstances(Preexisting disease, baseline BP, volume status, risk factors, type of surgery...).
These comfort levels currently should be based on available data, on common sense and a good portion of clinical judgment until someone comes up with clear guidelines.
Further more, deliberate hypotension is rapidly becoming a thing of the past and is being replaced by maintaining BP and avoiding hypertension which is what we do all day on every patient.
These comfort levels currently should be based on available data, on common sense and a good portion of clinical judgment until someone comes up with clear guidelines.
Further more, deliberate hypotension is rapidly becoming a thing of the past and is being replaced by maintaining BP and avoiding hypertension which is what we do all day on every patient.
I think thats an over generalization, with all due respect, Plank.
Additionally, it appears that whats taught in residency is not based on available literature.
I think it is very obvious to all of us after doing thousands of cases that a low BP, say 100 systolic, in a patient under general anesthesia, is very well tolerated by just about every patient..regardless of their preoperative BP reading...which is in direct conflict with what we are taught.
It is rare to see intraoperative myocardial ischemia as evidenced by intraoperative ST changes.
It is rare that patients wake up with evidence of cerebral ischemia.
I'd say in my experience that when it comes to manipulating BP to a higher number intraoperatively, I've done it more when concerned about renal function than for any other reason.
Regional for C sections is completely different. I am liberal with sympathomimetics and vasopressors....I give ephedrine immediately after spinal placement regardless of starting BP....but only because I've found it reduces the incidence of nausea/vomiting in the parturient.
I don't think thats a great example, Tenes, since the example you are basing your reasoning on is not a patient under anesthesia.
Your post is exactly what I was referring to when I mentioned personal comfort levels, You have used your experience, your knowledge, and what you could salvage from what they taught you in residency to come up with a plan of action that you feel is best for your patients.
1. Depends on the surgeon, most do lateral but some do beach chair
2. Yes, more than a few complain if they see a BP that is higher than they think it should be (whether there is bleeding or not). I turn my monitor away from them. During the case I keep an eye on their scope monitor, if I see bleeding, I see where I am at BP wise and if I have anyway room to safely decrease it I do. One thing to do in these cases is pay attention to the scope monitor, if you can't see neither can they. If you can, try to help their situation before they ask.
3. My Limit? Good question with no proven answer. Sometimes there is a reason for dogma. The 20% from mean number may not be clinically proven but alot of what we do is not. Sometimes we do things because it makes sense physiologically. Sometimes we go with the best data that is available as unreliable as that may be. As for me, if I have a patient with known CAD, PVD, or has not very well controlled hypertension, it is reasonable to expect that they probably need a higher pressure to perfuse their end organs. In these patients, I talk to the surgeon before the case about my plans for BP management. That saves me from any intraop arguements. I do try to keep these patients within that 20%. As for healthy normotensive patients, I try to keep their mean between 60-70. These are the means I would shoot for in the ICU, I feel like they should work in the OR. As for the beach chair position, I take away about 10 from the mean showing and manage the BP accordingly. Again no hard data for these numbers. Until there is hard data this is what I will do.
4. BP usually measured with cuff on opposite arm.
5. Risks? I think positioning and CPP are the biggest issues with these cases. I know air embolism has been mentioned and is a concern but to me it is down on the list. I think it becomes more of a concern with open procedures but I feel it would be rare for a joint full of fluid (arthroscopic) to be a source of an air embolism.
Great thread, relevant to every day practice, great discussion
pd4
jet - that was an example of cerebral perfusion and pressure -
if you want an example of cerebral perfusion UNDER anesthesia look at what happens with carotids while being neuro-monitored....
i mean we drive the pressure way up to keep good flow to the brain - and you can actually see EEG changes as we drive the blood pressure higher...
bottom line - one of the points of anesthesia is to keep the noggin' perfused so they can wake up without a stroke/hypoxic injury --- if the patient doesn't wake up after shoulder surgery and it goes to court what will the accepted standard of care be? pre-op BP is 150/80 and peri-procedure BP 100/60.... you gotta be careful
the other reason i can think of to explain post-op neurologic deficit is that somehow the pressure was high enough to be flushing their saline/fluid intra-arterially and somehow it flushed back into the central system and got into the carotid.... however with those types of injuries it is usually a hemispheric problem versus a global hypoxic event.
if you want an example of cerebral perfusion UNDER anesthesia look at what happens with carotids while being neuro-monitored....
i mean we drive the pressure way up to keep good flow to the brain - and you can actually see EEG changes as we drive the blood pressure higher...
bottom line - one of the points of anesthesia is to keep the noggin' perfused so they can wake up without a stroke/hypoxic injury --- if the patient doesn't wake up after shoulder surgery and it goes to court what will the accepted standard of care be? pre-op BP is 150/80 and peri-procedure BP 100/60.... you gotta be careful
the other reason i can think of to explain post-op neurologic deficit is that somehow the pressure was high enough to be flushing their saline/fluid intra-arterially and somehow it flushed back into the central system and got into the carotid.... however with those types of injuries it is usually a hemispheric problem versus a global hypoxic event.
perioperative stroke NOT related to carotid and/or CABG is extremely rare...and when they do occur...I don't think they are watershed strokes....the kind you see from hypotension.....
We had one in 2000....colon resection surgery...did a huge lit review on it.
we're all talking here like hypotension will lead to hypoperfusion....well, then the strokes should be watershed strokes....
but they aren't...they're strokes in vascular supply regions like where clots go.
We had one in 2000....colon resection surgery...did a huge lit review on it.
we're all talking here like hypotension will lead to hypoperfusion....well, then the strokes should be watershed strokes....
but they aren't...they're strokes in vascular supply regions like where clots go.
We do these cases under MAC, believe it or not, in our surgicenter.
ISB and some propofol. You can talk to the patient if you'd like, but I keep em fairly "deep."
You can just talk to em to test out their brain function. Zap em with a smidge of K if for Komfort.
Plus you dont obtund their autoregulation (cerebral, cardiac, or renal) because there is no volatile.
No hx of CVA that anyone knows of doing this operation at the surgicenter under the above technique.
Anypoops,
We still haven't answered how one figures out what the absolute safe "low" bp is. I suppose, as an above poster noted, you could slap an EEG on gramps and look for changes that evolve from dipping below critical CBF. Hell, slap an SVO2 monitor on there too. Go nuts with the damn thing.
ISB and some propofol. You can talk to the patient if you'd like, but I keep em fairly "deep."
You can just talk to em to test out their brain function. Zap em with a smidge of K if for Komfort.
Plus you dont obtund their autoregulation (cerebral, cardiac, or renal) because there is no volatile.
No hx of CVA that anyone knows of doing this operation at the surgicenter under the above technique.
Anypoops,
We still haven't answered how one figures out what the absolute safe "low" bp is. I suppose, as an above poster noted, you could slap an EEG on gramps and look for changes that evolve from dipping below critical CBF. Hell, slap an SVO2 monitor on there too. Go nuts with the damn thing.
No one can give you an exact answer to this.
Have you seen BP holters; when you sleep your BP can drop to these kind of level. Despite of this we treat our "asleep" patients as if they are "awake"... 😕
Exactly the part I was most interested in when reading that article. And then the bold depicts a very important point. Which is why people have more MI's from hypotension than strokes.
True story: Me and another locums guy was down in Texas years ago and had 2 declots of AV fistulas. He had one in his room and I had the other AT THE SAME TIME. I give my lady 1 mg versed and 1cc of fentanyl and surgeon did local infiltration at the arm site. The other locums uses GA with LMA. Both surgeons used the same strange technique of forcing heparin soln distally to proximally with a 60 cc syringe with considerable force. My lady had LOC with BIGTIME hemodynamic instability. I tube her and pushed some EPI and threw her in the unit with consults to neuro and ICU docs. She eventually recovers with no neuro sequelae. The other locums dude's male pt. never woke up and they threw him over in ICU and CT/MRI scans revealed that he had a CVA. He never had any hemodynamic instability at all during the entire case. Last I had heard was they were ruminating about makin' him an organ donor. Some of these experiences lend me to believe that this shoulder stuff(it is rather rare) is an embolic phenomenon rather than a BP/CBF/autoregulation phenomenon. Regards, ---- Zippy
We moved right through this topic pretty promptly and went directly to CPP but I do want to make sure everyone understands something very important in these cases. That where you are measuring the BP.
Read this:
http://www.anesthesia-analgesia.org/cgi/content/full/97/4/1198
Read this:
http://www.anesthesia-analgesia.org/cgi/content/full/97/4/1198
that guy had his bp measured in the EXACT position and way JNCVII recommends....and I submit that yes...he had problems and it is true / true / and unrelated.
look what zippy says.
I agree that embolism may very well be the cause of these injuries but I haven't seen any data describing it. The vast majority information is dealing with hypotension. So why is it mostly shoulder surgery in the sitting position that this occurs in? Why is it more prevalent in the sitting position than when lateral? Can you show me a case where this happened in the lateral position?
are there really that many?
we had one in town that I know off that happened to a YOUNG guy in the LATERAL position...never woke up.....I don't know the details...but our bone MD's ask for only 100mmHg of deliberate hypotension (and when I say I do it....that's all that I ever offer)....
so it happened to a young guy in the lateral position....and it's in PP, so I know it is not going to be in any case reports.
the sitting stuff has some academic guy interested in it.....does that really mean that we have a "new" problem.....OR a "problem" at all..
Shi t happens....just because some one decides to make noise about it, doesn't mean that we're doing something wrong.
Look at the blindness from prone surgery thing....it started out with "we're doing something wrong"....now we know...s hit happens when you have surgery face down for a long time.
Very good example.
These two issues are very similar IMHO.
But I have become more vigilant in my long prone spine cases b/c of the whole blindness issue. Has it made a difference? I don't know b/c to date I haven't had a case of blindness. Just like I haven't had an issue in shoulder surgery. But I don't want to have one either and I will do whatever it is I can do to avoid it. And that may mean employing tactics that aren't proven but that may make some sense "to me".
So until we have a good answer for these issues, we need to all review what is available and make our own informed decisions, which is the point of this thread. Well done everyone. Thank You.
at our institution (where I'm a resident), the culture is to place a shoulder block for post-op pain, and then induce GA for beachchair shoulders...often with an LMA, sometimes a tube, almost always with (albiet minimal amounts of) sevo....
let me ask u guys a couple questions:
pretend we have a patient who has a history of CVA/TIA (and not watershed in distribution, so presumably not from hypotension, more likely from embolic phenomena)....or a hx of significant carotid stenosis.....or some hx that makes you feel the pt may have reduced risk from an aggressive strategy that maximizes cerebral perfusion while minimizing cerebral metabolic rate
1) If we did a GA w/ propofol (as compared with sevo), do you think we would see more or less blood flow to the brain in beachchair?
2) What would the necessary dose of propofol be to begin to meaningfully decrease cerebral metabolic rate? Probably the dose it takes to induce GA, right?
3) There's some emerging literature that precedex decreases cerebral metabolic rate, but I'm not sure if the general vibe is that you would have to give so much precedex to get this decrease in cerebral metabolic rate, that you end up decreaseing cerebral perfusion b/c that dose would decrease the BP so much.....any thoughts on propofol vs dexmedetomidine vs volatile for beachchair anesthetics? (impairment of cerebral autoregulation, cerebral perfusion, metabolic rate considerations, etc)
it would be interesting to look at a case series of consecutive pts who had beachchair anesthetics that have a prior history of watershed infarcts...
let me ask u guys a couple questions:
pretend we have a patient who has a history of CVA/TIA (and not watershed in distribution, so presumably not from hypotension, more likely from embolic phenomena)....or a hx of significant carotid stenosis.....or some hx that makes you feel the pt may have reduced risk from an aggressive strategy that maximizes cerebral perfusion while minimizing cerebral metabolic rate
1) If we did a GA w/ propofol (as compared with sevo), do you think we would see more or less blood flow to the brain in beachchair?
2) What would the necessary dose of propofol be to begin to meaningfully decrease cerebral metabolic rate? Probably the dose it takes to induce GA, right?
3) There's some emerging literature that precedex decreases cerebral metabolic rate, but I'm not sure if the general vibe is that you would have to give so much precedex to get this decrease in cerebral metabolic rate, that you end up decreaseing cerebral perfusion b/c that dose would decrease the BP so much.....any thoughts on propofol vs dexmedetomidine vs volatile for beachchair anesthetics? (impairment of cerebral autoregulation, cerebral perfusion, metabolic rate considerations, etc)
it would be interesting to look at a case series of consecutive pts who had beachchair anesthetics that have a prior history of watershed infarcts...
I think that's been my point all along....
There is no data (that I know of, so please post up if anyone knows) that supports anything ....in the anesthesia literature...just opinions on how "doing certain things" ...."makes sense".
However, PLENTY of data in the medicine literature that says LOWER the bp , the better things are for these types of patients....excluding the J-curve hypothesis.
One Caveat....when I say deliberate hypotension...I 'm talking SBP of 90 mmHg......which I was not clear on early in the posts.
There is no data (that I know of, so please post up if anyone knows) that supports anything ....in the anesthesia literature...just opinions on how "doing certain things" ...."makes sense".
However, PLENTY of data in the medicine literature that says LOWER the bp , the better things are for these types of patients....excluding the J-curve hypothesis.
One Caveat....when I say deliberate hypotension...I 'm talking SBP of 90 mmHg......which I was not clear on early in the posts.
D
DuckhuntingDoc
Position? Both
BP- is as low as I'm comfortable with for that patient. No one size fits all.
US guided ISB for most unless they refuse.
Risk? Bleeding, infection, nerve injury, seizure, problems with the heart and lungs, allergic reactions, etc.
BP- is as low as I'm comfortable with for that patient. No one size fits all.
US guided ISB for most unless they refuse.
Risk? Bleeding, infection, nerve injury, seizure, problems with the heart and lungs, allergic reactions, etc.
