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Are we targeting too high a blood pressure intraop?

vector2

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The recently released MAP 65 Trial has certainly raised some questions in the critical care community this year, namely whether we just pulled a "MAP of 65 mmHg" out of our collective a$$es and have been targeting that number for years for no other reason than trying to normalize numbers for the sake of normalizing numbers.

The trial was multicenter and randomized 2600 patients aged 65 and older with vasodilatory shock to a MAP of 60-65 or to usual standard of care aka a MAP at the discretion of the clinician. Bottom line results: 90 day mortality difference was non-significant (41% in permissive group vs 43.8% in standard of care), as was serious adverse events including acute renal failure and arrhythmia. The biggest weakness of the trial is that the intervention group still spent a lot of time with a MAP above 70, however the standard of care group spent a lot of time with a MAP above 80, so at least the differential was preserved.

Both PulmCCM and PulmCrit have excellent analyses of the trial.

From PulmCCM:
" Targeting a lower mean arterial pressure does not necessarily deprive tissues of perfusion and may actually improve flow if critical closing pressures fall below mean arterial pressure. The trouble is that each organ has its own conductance curve and the slope of each organ’s curve adapts differently to an equally dynamic physiological milieu within and between patients. A patient with a 90% left main stenosis has a very low, and fixed, cardiac conductance; therefore, vasodilation of other tissue beds poses an existential risk. Whereas an 18-year old with pneumococcal bacteremia and anaphylaxis from amoxicillin will have high total body tissue conductance, a low mean arterial pressure and, potentially, preserved organ perfusion. To the credit of the 65 Trial, enrolling those at least 65 years of age is anticipated to concentrate the former, rather than the latter patient, yet mortality was lower in the permissive hypotension group [absolute risk difference, −2.85%; 95% CI, −6.75 to 1.05; P = .15] and these patients received fewer vasoactive medications. "



Personally, based on the classic teaching of the shift in autoregulatory curves, I've always been of the opinion that it's better to run geriatric pts at a MAP of ~80, especially if they have history of HTN, CAD, CVA, CKD etc. Same goes for older folks on CPB and I've always thought the general rule of "MAP = Age" while on pump is a sound idea. We've known for awhile that this logic may be dubious because as PulmCCM points out, perfusion at the local tissue bed is what really matters, but I've always seen running a slightly higher MAP at the very least as not causing any harm.

Does everyone else out there also run older pts at a slightly higher blood pressure? Does the fact that a slightly lower MAP didn't worsen mortality in critically ill geriatric pts (let alone relatively healthy and/or optimized geriatric pts coming for elective surgery) change your thinking? Or are the results of this trial not generalizable at all due to the fact that volatile anesthetics disrupt autoregulation curves?
 
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dchz

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Tl;DR: yes, most of the time our intraop MAP goals are higher than necessary. But it's done so to build in margin of error.

To think of it theoretically: BP is a proxy measure for oxygen(blood) delivery. Most of the time in the OR you don't have enough info to know oxygen delivery, so we err on the higher side by setting an arbitrary map of 65.

As more information is presented to me, I am more comfortable with lower MAP: I see that the pt has no wall motion abnormalities on TEE, BIS of 35, SVO2 of 71%, NIR head sats ~ baseline, but the MAP is 45, i'm fine with a map of 45 in the short term. This clinical picture has told me my anesthetic has lowered CMRO2, Cardiac oxygen demand, and total body oxygen demand so low that my lower supply is still fine. However, I am also aware that my margin for error is much lower, I would be very uncomfortable if the MAP went lower to say 35, even though i don't believe there is any harm for the pt at this MAP at this moment in the clinical picture, there is no benefit in risking going to a map of 35. So in the end, I always treat the MAP of 45, even though i know the pt is fine, just to increase my margin for error. But there are times where I wouldn't treat it: we are going on CPB soon and the increase BP might increase dissection risk, the pt is bleeding from a surgical bleed and increasing BP might be detrimental, etc.

With regards to the MAP = Age for CPB cases, I don't agree with that. On CPB you can set your own CO and oxygenation, BP on CPB is designed to get the blood to the brain and organs. Having higher MAP on CPB as a rule can def cause harm - case in point: the perfusionist sometimes just target a MAP and disregard the CO. If i was on the pump i'd rather have a 2.4 index with a map 55 than a 1.8 index with MAP 80, or sometimes they go to an index of 1.4 just to keep a MAP of 70. Also, if you're hemodiluting just to keep a certain MAP and CO, some would argue that's even worse.

"Does the fact that a slightly lower MAP didn't worsen mortality in critically ill geriatric pts let alone relatively healthy geriatric pts coming for elective surgery change your thinking?"
No, different pt population with different pathology. Violates one of the basic rules of applying evidence based medicine: are my pt population similar to those of the study? No.

"Or are the results of this trial not generalizable at all due to the fact that volatile anesthetics disrupt autoregulation curves? "
Yes, that and none of these pts in the study are having planned surgical trauma with sometimes huge fluid shifts.

" Personally, based on the classic teaching of the shift in autoregulatory curves, I've always been of the opinion that it's better to run geriatric pts at a MAP of ~80, especially if they have history of HTN, CAD, CVA, CKD etc"
This is true only if you can guarantee their cardiac output doesn't change when you get their MAPs there. If you're getting their maps there with an increase in HR and lower CO you might very well be hurting the organ you're trying to protect.

Why is this propagated? If you're the attending with your license on the line, you'd rather the CRNA/resident err on the side of safety. How many residents would you trust with enough clinical acumen to understand certain situations may be ok to have a lower MAP? Even worse, sometimes if you try to explain this idea, next thing you know, everyone says "Dr.DCHZ says it's ok to keep a MAP of 45 for all 80+ years old pts...."
 
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nimbus

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Ever since Epic I’ve been running a lot more intraop norepi infusions for medicolegal reasons. I haven’t noticed that patients are doing any better.

Sharrock did a whole bunch of studies during the 1990’s examining hypotensive epidural anesthesia targeting MAP=50 in old folks getting total hips. No difference in postop complications.


 
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vector2

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As more information is presented to me, I am more comfortable with lower MAP: I see that the pt has no wall motion abnormalities on TEE, BIS of 35, SVO2 of 71%, NIR head sats ~ baseline, but the MAP is 45, i'm fine with a map of 45 in the short term. This clinical picture has told me my anesthetic has lowered CMRO2, Cardiac oxygen demand, and total body oxygen demand so low that my lower supply is still fine. However, I am also aware that my margin for error is much lower, I would be very uncomfortable if the MAP went lower to say 35, even though i don't believe there is any harm for the pt at this MAP at this moment in the clinical picture, there is no benefit in risking going to a map of 35. So in the end, I always treat the MAP of 45, even though i know the pt is fine, just to increase my margin for error. But there are times where I wouldn't treat it: we are going on CPB soon and the increase BP might increase dissection risk, the pt is bleeding from a surgical bleed and increasing BP might be detrimental, etc.

In your example, I think at a MAP of 45 you can be relatively confident that brain perfusion is OK (NIRS baseline), heart perfusion is OK (TEE), and perhaps global oxygen balance is wnl (SvO2), but even all those things still don't account for regional tissue perfusion and oxygenation. Even with all those monitors, you don't know that the kidneys, liver, gut, etc are tolerating that MAP of 45 (nor will you likely know til later that day or the next). Now, think of the number of cases (aka the vast majority) where we don't have any information from NIRS, swan, or TEE. One of the clinical counters to your point that comes to mind is the case of beach chair position and CVA. Many of the cases where pts have stroked out or gone blind were ones in which the MAP at the arm was normal (making the MAP at the brain ~40-50s), pulse ox 100%, and ETCO2 (surrogate for CO) wnl. Furthermore, we have some evidence that even short episodes of intraoperative MAP of <55 mmHg are associated with acute kidney injury and myocardial injury after a noncardiac surgery.. My biggest fear is that we don't know what we don't know when it comes to how the organs we're not monitoring are handling the decreased MAP.

With regards to the MAP = Age for CPB cases, I don't agree with that. On CPB you can set your own CO and oxygenation, BP on CPB is designed to get the blood to the brain and organs. Having higher MAP on CPB as a rule can def cause harm - case in point: the perfusionist sometimes just target a MAP and disregard the CO. If i was on the pump i'd rather have a 2.4 index with a map 55 than a 1.8 index with MAP 80, or sometimes they go to an index of 1.4 just to keep a MAP of 70. Also, if you're hemodiluting just to keep a certain MAP and CO, some would argue that's even worse.

Obviously increasing vascular resistance and sacrificing CI and SvO2 down to critical levels just to artificially inflate the MAP to 80 when using a centrifugal pump is stupid. Same for giving liters of volume if the pt is already in an acceptable range. I'm more or less saying all other things being equal, would you rather have your 80 year old closer to a MAP of 70 or 50 while on pump? Maybe that's even the wrong question to be asking, because interestingly enough, age may not even be one of the factors that matters if you look at transcranial doppler studies of various MAPs on CPB

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"Does the fact that a slightly lower MAP didn't worsen mortality in critically ill geriatric pts let alone relatively healthy geriatric pts coming for elective surgery change your thinking?"
No, different pt population with different pathology. Violates one of the basic rules of applying evidence based medicine: are my pt population similar to those of the study? No.

Which studies or sources of evidence based medicine are you using for your current practice? So many basic tenets of anesthesia are so poorly studied that we many times have to make extrapolations from associative data or from data where the study population isn't perfectly matched to the patient we're currently caring for. That being said, I didn't ask "are you going to change your practice?" - I merely asked about your "thinking." Yes, the patient populations are different in the MAP 65 trial, but I think it should at least be hypothesis generating for you that a population which is very susceptible to organ malperfusion and multisystem organ failure did not fare significantly worse with a lower MAP, therefore "normal" geriatric pts may very well fare OK too. Of course, more study is needed.

"Or are the results of this trial not generalizable at all due to the fact that volatile anesthetics disrupt autoregulation curves? "
Yes, that and none of these pts in the study are having planned surgical trauma with sometimes huge fluid shifts.

I would argue that pts in septic shock receiving 30 ml/kg resuscitation also have a significant inflammatory component and fluid shifts going on, but yes, if you want to go to an extreme example like a liver resection instead of say a lap chole then obviously the results of the trial are less generalizable to anesthesia practice.

" Personally, based on the classic teaching of the shift in autoregulatory curves, I've always been of the opinion that it's better to run geriatric pts at a MAP of ~80, especially if they have history of HTN, CAD, CVA, CKD etc"
This is true only if you can guarantee their cardiac output doesn't change when you get their MAPs there. If you're getting their maps there with an increase in HR and lower CO you might very well be hurting the organ you're trying to protect.

It is very unlikely within a range of HR 50-130 that an increasing heart rate would lower CO. Did you mean increased MAP and lower HR thus compromising CO?

You are correct though that I am making an educated guess that maintaining a MAP of 80 using vasopressors does not adversely affect CO. However I tend not to be worried if I've maintained the HR within a reasonable range of their baseline, given a bit of an empiric fluid bolus, and because alpha1 ags at low doses are typically are either CO neutral or increase CO because they help maintain preload by changing unstressed venous reservoir volume to stressed.

Why is this propagated? If you're the attending with your license on the line, you'd rather the CRNA/resident err on the side of safety. How many residents would you trust with enough clinical acumen to understand certain situations may be ok to have a lower MAP? Even worse, sometimes if you try to explain this idea, next thing you know, everyone says "Dr.DCHZ says it's ok to keep a MAP of 45 for all 80+ years old pts...."

In addition to the reason you give, it's also because low blood pressure is associated with bad outcomes. But obviously this is a chicken-egg problem, i.e. correlation is not causation.
 
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pgg

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Ever since Epic I’ve been running a lot more intraop norepi infusions for medicolegal reasons. I haven’t noticed that patients are doing any better.

Sharrock did a whole bunch of studies during the 1990’s examining hypotensive epidural anesthesia targeting MAP=50 in old folks getting total hips. No difference in postop complications.
When I was a resident (2006-9) we routinely ran nitroprusside infusions on total hip patients to minimize bleeding. Seems silly in retrospect.

I too run a lot of phenylephrine and norepi infusions in older people; it makes my own chest hurt to walk into a room and see people letting old people ride with MAPs of 50 or 55. Even though I know these patients aren't having events. (Well, I think they aren't, I'm not checking troponins on everyone in PACU.)

I don't think I'll change my practice. Insofar as my thinking changes, it's just a reminder that patients are individuals, that tissue delivery can be poor despite a pleasing BP on the monitor, and that most of the time I don't actually have all the info needed to determine if a lowish BP is "enough". It's easy enough to run it higher, and the above comments on margins are on point too.
 
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deleted171991

The recently released MAP 65 Trial has certainly raised some questions in the critical care community this year, namely whether we just pulled a "MAP of 65 mmHg" out of our collective a$$es and have been targeting that number for years for no other reason than trying to normalize numbers for the sake of normalizing numbers.

The trial was multicenter and randomized 2600 patients aged 65 and older with vasodilatory shock to a MAP of 60-65 or to usual standard of care aka a MAP at the discretion of the clinician. Bottom line results: 90 day mortality difference was non-significant (41% in permissive group vs 43.8% in standard of care), as was serious adverse events including acute renal failure and arrhythmia. The biggest weakness of the trial is that the intervention group still spent a lot of time with a MAP above 70, however the standard of care group spent a lot of time with a MAP above 80, so at least the differential was preserved.

Both PulmCCM and PulmCrit have excellent analyses of the trial.

From PulmCCM:
" Targeting a lower mean arterial pressure does not necessarily deprive tissues of perfusion and may actually improve flow if critical closing pressures fall below mean arterial pressure. The trouble is that each organ has its own conductance curve and the slope of each organ’s curve adapts differently to an equally dynamic physiological milieu within and between patients. A patient with a 90% left main stenosis has a very low, and fixed, cardiac conductance; therefore, vasodilation of other tissue beds poses an existential risk. Whereas an 18-year old with pneumococcal bacteremia and anaphylaxis from amoxicillin will have high total body tissue conductance, a low mean arterial pressure and, potentially, preserved organ perfusion. To the credit of the 65 Trial, enrolling those at least 65 years of age is anticipated to concentrate the former, rather than the latter patient, yet mortality was lower in the permissive hypotension group [absolute risk difference, −2.85%; 95% CI, −6.75 to 1.05; P = .15] and these patients received fewer vasoactive medications. "



Personally, based on the classic teaching of the shift in autoregulatory curves, I've always been of the opinion that it's better to run geriatric pts at a MAP of ~80, especially if they have history of HTN, CAD, CVA, CKD etc. Same goes for older folks on CPB and I've always thought the general rule of "MAP = Age" while on pump is a sound idea. We've known for awhile that this logic may be dubious because as PulmCCM points out, perfusion at the local tissue bed is what really matters, but I've always seen running a slightly higher MAP at the very least as not causing any harm.

Does everyone else out there also run older pts at a slightly higher blood pressure? Does the fact that a slightly lower MAP didn't worsen mortality in critically ill geriatric pts (let alone relatively healthy and/or optimized geriatric pts coming for elective surgery) change your thinking? Or are the results of this trial not generalizable at all due to the fact that volatile anesthetics disrupt autoregulation curves?
My view of this is: First Do No Harm.

So I target the patient's lowest recent baseline MAP +/- 20-25%, because that seems not to be associated with bad outcomes (also our BPs naturally drop during sleep without negative consequences). It goes both ways: I am not obsessed about a MAP of 65 in a 19 year-old female with baseline BP of 80/50, but I will aim for at least 75 in a 70 year-old with a baseline BP of 130/80.

One thing I always remember is that the MAP is just a number that has little to do with tissue perfusion. Pressure does not equal flow, especially when the resistance is increased. One can have an ischemic periphery with a nice central number. It's a matter of risks vs benefits. Pressors are not some benign holy water. They each decrease tissue perfusion in some territories, especially in higher doses. So, if the patient requires a lot of pressors to maintain that quasi-baseline MAP, I will try to find a lower number, that's usually still over 65-75, that allows me to maintain that tissue perfusion. Why 65-75? Because 65 is the number that does not produce change in survival (NOT end-organ damage) in most (not all) patients, and 75 is the number that's associated with fewer AKIs than 65, at least in ICU studies. And we all know that the kidney is very sensitive to poor perfusion, and that AKI is associated with decrease in survival, so targeting at least 75, especially in the elderly and hypertensive, sounds like the right thing to do. Again, First Do No Harm.

Of course, it's not that easy to judge peripheral perfusion, but there are a few surrogates I use, if I must, such as urine output (I don't chase it, though, because both mechanical ventilation and increased abdominal pressures decrease it, for example), pulse oximeter signal, upper extremity color and temperature. I would love to have a better monitor, such as gastric tonometry or some peripheral capillary microscope.

This kind of question also leads to what's better to counteract the decrease in SVR from volatile anesthetics: pressors or fluids, and how much of each. And we know that too much of either is bad, but we also know that a little of each does not cause harm. So again, I try to use a bit of both, while keeping in mind that both NPO and intraop fluid losses have been overestimated in studies, and that IV fluids are pro-inflammatory and not benign.

One thing a lot of CRNAs and residents forget about, is keeping the patient euvolemic at all times. I personally watch the blood loss like a hawk, hence also the pressor requirements. I don't just sit at the head of the table; I walk around periodically, and assess the blood loss for myself. I don't rely on what the surgeon says, unless it's measurable (i.e. they used X amount for irrigation) or likely true. I trust my eyes and my judgment more, because I have the perspective and am more detached. And if I feel that I cannot restore volume and flow with some crystalloids and some pressors, I do give blood (transplant). Again, it's a matter of risks vs benefits (e.g. I am more reticent to give blood in a younger or cancer patient). Everything I do tends to be patient- and situation-dependent, not based on some universal number. People are not machines.

So this paper will not change my practice. The current one seems to work pretty well, both in the OR and in the ICU, and not just based on survival, but also on end-organ damage. I especially care about the brain, the heart, the kidneys, the liver, and the gut.

If anything, I think the paper is dangerous, because it will induce the same number-based comfort level as with MAP over 65, especially for lazy/stupid/uneducated people who think very unidimensionally. "The MAP is over 65, ergo the patient is OK." "The MAP is 60 [in this hypertensive patient with baseline of 160/90], what's the big deal, you didn't read that new study that says that we don't need 65." Etc. Personally, I think generalizations in medicine are dangerous, and that every patient is a different many-many variable-equation.
 
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Lidolover

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All is relative I believe. Intra-op, I try hard to resemble the preop state aka if pt presented with systolic in 200s with MAP in the 90s, I allow an approximately 20% range, and if I have to give ephedrine, neo or whatever to achieve it (even if it above map 65), I do it even though ppl look at me surprised
 

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Within 20% of the patients regular BP seems a reasonable goal. That being said we have all worked with colleagues or CRNA’s who are not so fastidious and their patients seem to do just fine.....
In all likelihood we are not with these patients long enough for it to make a difference.....
 
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deleted162650

If you are needing pressors intraop, you are giving too much gas (outside of blood loss, compressing vessels, other extenuating circumstances, etc)

Yes and no. There are some people who’s bodies can’t handle the amount of anesthesia their brain requires. If you don’t want to, or are unable to paralyze these folks, you’re gonna need a little pressor. Shouldn’t need much though.
 
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If you are needing pressors intraop, you are giving too much gas (outside of blood loss, compressing vessels, other extenuating circumstances, etc)

This is a huge, somewhat dangerous generalization.

There’s a difference between needing pressors and having a margin for error (see @dchz post above). Also, though I know you didn’t mean it like this, your post paints you as someone who will ride a MAP of 45 in a CAD, CKD geriatric patient and not give pressors because dogmatically “if you need pressors you’re giving too much anesthesia”
 
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If you are needing pressors intraop, you are giving too much gas (outside of blood loss, compressing vessels, other extenuating circumstances, etc)

In people with double or triple antihypertensive therapy? I assume you're including those in the "other extenuating circumstances, etc" qualifier, which are the majority of my patients.
 

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If you are needing pressors intraop, you are giving too much gas (outside of blood loss, compressing vessels, other extenuating circumstances, etc)
100% disagree. We know all our anesthetics cause vasodilation, blunting of sympathetic tone, some cause bradycardia. All of these have the effect of decreasing BP at the very least and potentially CO as well. Why would you not use a low-dose vasopressors to counteract the shock state you've induced with general anesthesia. Instead we resort to volume in patients that probably don't need it in the first place.
 
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vector2

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This recommendation is considered Grade 2C (meaning the evidence behind it is very weak, and is considered more a suggestions rather than recommendation).


Determination of target blood pressure values — There is no consensus regarding specific intraoperative BP target values. In most patients, we attempt to maintain BP within 20 percent of the patient's baseline and keep mean arterial pressure (MAP) >65 mmHg, rather than targeting a specific BP value. This approach was examined in a randomized trial in 298 patients undergoing major abdominal surgery (82 percent had chronic hypertension) [7]. The intervention group was treated to maintain systolic BP within 10 percent of the individual's normal resting baseline value, including use of a norepinephrine infusion to increase BP when necessary. The control group was treated to maintain systolic BP ≥80 mmHg or to prevent a 40 percent decrease in BP below baseline. Attempting to maintain systolic BP within 10 percent of baseline led to fewer complications, defined as a composite of systemic inflammatory response syndrome with renal, respiratory, cardiovascular, or neurologic dysfunction (relative risk 0.73; 95% CI 0.56-0.94) [7].

In a study of more than 10,000 noncardiac surgical patients, both absolute decrease and relative maximum decrease in MAP were predictive of perioperative complications of myocardial injury or AKI [8]. A 2018 systematic review of 42 cohorts including various types of noncardiac surgery noted that both duration and degree of intraoperative hypotension (using both absolute and relative definitions) were associated with adverse postoperative outcomes [9]. Even a short duration of MAP <65 mmHg was associated with increased overall mortality, AKI, myocardial injury, and stroke; a MAP <80 mmHg for ≥10 minutes was associated with a small but statistically significant increase in overall mortality. By contrast, a subsequently published retrospective study of more than 138,000 patients noted that the association of intraoperative MAP with postoperative AKI depended upon whether or not preoperative risk factors were present [10]. There was no relationship between MAP and AKI in patients without preoperative risk factors; conversely, an association between even mild intraoperative hypotension and postoperative AKI was present in those with high baseline risk.

For chronically hypertensive patients with high baseline blood pressures (eg, MAP >100 mmHg), a MAP target of 65 mmHg may be too low. In a retrospective study of 57,315 patients undergoing noncardiac surgery, low MAP values <65 mmHg or MAP values <20 percent of the individual patient's baseline were associated with myocardial and kidney injury, and such injury was more likely in those with chronic hypertension [11]. In a trial of older adults with chronically elevated MAP (approximately 100 mmHg), maintaining an intraoperative MAP target of 80 to 95 mmHg produced a lower incidence of AKI compared with a lower target of 65 to 79 mmHg or a higher target of 96 to 110 mmHg (6.3 versus 13.5 and 12.9 percent, respectively) [12]. However, intraoperative lability of BP values is common in chronically hypertensive patients, and both severe hypertension and severe hypotension may occur. To avoid undesirable large shifts in BP, short-acting vasoactive medications are selected and are administered in small, carefully titrated doses to treat unacceptably high or low BP values.

Notably, it is unclear which component of BP measurements (eg, systolic BP, diastolic BP, or MAP) should be targeted for monitoring and treatment during the intraoperative period. One retrospective review of more than 18,000 noncardiac surgical patients noted that 30-day mortality was associated with both the degree and the duration of intraoperative hypotension, regardless of whether systolic hypotension <70 mmHg, diastolic hypotension <30 mmHg, or low MAP <50 mmHg was used to define hypotension [13]. Similar findings were noted in a separate retrospective cohort [14].

Futier E, Lefrant JY, Guinot PG, et al. Effect of Individualized vs Standard Blood Pressure Management Strategies on Postoperative Organ Dysfunction Among High-Risk Patients Undergoing Major Surgery: A Randomized Clinical Trial. JAMA 2017; 318:1346.

Vernooij LM, van Klei WA, Machina M, et al. Different methods of modelling intraoperative hypotension and their association with postoperative complications in patients undergoing non-cardiac surgery. Br J Anaesth 2018; 120:1080.

Wesselink EM, Kappen TH, Torn HM, et al. Intraoperative hypotension and the risk of postoperative adverse outcomes: a systematic review. Br J Anaesth 2018; 121:706.

Mathis MR, Naik BI, Freundlich RE, et al. Preoperative Risk and the Association between Hypotension and Postoperative Acute Kidney Injury. Anesthesiology 2020; 132:461.

Salmasi V, Maheshwari K, Yang D, et al. Relationship between Intraoperative Hypotension, Defined by Either Reduction from Baseline or Absolute Thresholds, and Acute Kidney and Myocardial Injury after Noncardiac Surgery: A Retrospective Cohort Analysis. Anesthesiology 2017; 126:47.

Wu X, Jiang Z, Ying J, et al. Optimal blood pressure decreases acute kidney injury after gastrointestinal surgery in elderly hypertensive patients: A randomized study: Optimal blood pressure reduces acute kidney injury. J Clin Anesth 2017; 43:77.

Monk TG, Bronsert MR, Henderson WG, et al. Association between Intraoperative Hypotension and Hypertension and 30-day Postoperative Mortality in Noncardiac Surgery. Anesthesiology 2015; 123:307.

Ahuja S, Mascha EJ, Yang D, et al. Associations of Intraoperative Radial Arterial Systolic, Diastolic, Mean, and Pulse Pressures with Myocardial and Acute Kidney Injury after Noncardiac Surgery: A Retrospective Cohort Analysis. Anesthesiology 2020; 132:291.
 
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deleted171991

Real q: Does anyone know where this "20%" number actually came from?
To be honest, I don't remember.

I use that number (20-25%) because of both standard of care issues and because it has worked well for me (as in I haven't hurt a patient with it yet). Also, I am a strong believer that Nature is much smarter than I, so the closer I keep the patient to his/her own baseline homeostasis, and the less I disturb things, the better the outcome.
 
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urge

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The recently released MAP 65 Trial has certainly raised some questions in the critical care community this year, namely whether we just pulled a "MAP of 65 mmHg" out of our collective a$$es and have been targeting that number for years for no other reason than trying to normalize numbers for the sake of normalizing numbers.

The trial was multicenter and randomized 2600 patients aged 65 and older with vasodilatory shock to a MAP of 60-65 or to usual standard of care aka a MAP at the discretion of the clinician. Bottom line results: 90 day mortality difference was non-significant (41% in permissive group vs 43.8% in standard of care), as was serious adverse events including acute renal failure and arrhythmia. The biggest weakness of the trial is that the intervention group still spent a lot of time with a MAP above 70, however the standard of care group spent a lot of time with a MAP above 80, so at least the differential was preserved.

Both PulmCCM and PulmCrit have excellent analyses of the trial.

From PulmCCM:
" Targeting a lower mean arterial pressure does not necessarily deprive tissues of perfusion and may actually improve flow if critical closing pressures fall below mean arterial pressure. The trouble is that each organ has its own conductance curve and the slope of each organ’s curve adapts differently to an equally dynamic physiological milieu within and between patients. A patient with a 90% left main stenosis has a very low, and fixed, cardiac conductance; therefore, vasodilation of other tissue beds poses an existential risk. Whereas an 18-year old with pneumococcal bacteremia and anaphylaxis from amoxicillin will have high total body tissue conductance, a low mean arterial pressure and, potentially, preserved organ perfusion. To the credit of the 65 Trial, enrolling those at least 65 years of age is anticipated to concentrate the former, rather than the latter patient, yet mortality was lower in the permissive hypotension group [absolute risk difference, −2.85%; 95% CI, −6.75 to 1.05; P = .15] and these patients received fewer vasoactive medications. "



Personally, based on the classic teaching of the shift in autoregulatory curves, I've always been of the opinion that it's better to run geriatric pts at a MAP of ~80, especially if they have history of HTN, CAD, CVA, CKD etc. Same goes for older folks on CPB and I've always thought the general rule of "MAP = Age" while on pump is a sound idea. We've known for awhile that this logic may be dubious because as PulmCCM points out, perfusion at the local tissue bed is what really matters, but I've always seen running a slightly higher MAP at the very least as not causing any harm.

Does everyone else out there also run older pts at a slightly higher blood pressure? Does the fact that a slightly lower MAP didn't worsen mortality in critically ill geriatric pts (let alone relatively healthy and/or optimized geriatric pts coming for elective surgery) change your thinking? Or are the results of this trial not generalizable at all due to the fact that volatile anesthetics disrupt autoregulation curves?
What do critical care patients with vasodilatory shock have to do with the average intra op patient?
 

vector2

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What do critical care patients with vasodilatory shock have to do with the average intra op patient?

As I said to dchz earlier

"Yes, the patient populations are different in the MAP 65 trial, but I think it should at least be hypothesis generating for you that a population which is very susceptible to organ malperfusion and multisystem organ failure did not fare significantly worse with a lower MAP, therefore "normal" geriatric pts may very well fare OK too. Of course, more study is needed."
 

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Ever since Epic I’ve been running a lot more intraop norepi infusions for medicolegal reasons. I haven’t noticed that patients are doing any better.

Sharrock did a whole bunch of studies during the 1990’s examining hypotensive epidural anesthesia targeting MAP=50 in old folks getting total hips. No difference in postop complications.



How long did you follow your patients after surgery?
 
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Let’s step back for a moment to the real world:

1. Minimum MAC is 0.5 for most and 0.7 MAC for some. I use 0.7 MAC to be cautious and cover my ass. Recall must be prevented. Anything over 0.7 MAC is up to the provider and the situation based on vitals

2. Any poor outcomes may cause a review of the record and your care will be scrutinized. That means a low BP will be an easy marker for the bad outcome. You will lose the lawsuit without question. Thus, in this environment a mean BP of 70-75 is very prudent in most situations especially in elderly patients.
I think a 20 percent reduction of BP is overly cautious because many of our patients are very hypertensive preop with MAP over 110. Even in that subgroup I wouldn’t increase my pressors just to maintain the 20 percent rule.

3. We know patients are dehydrated preop. That has been know for the past 4 decades. A bag of fluid like LR seems quite reasonable for the vast majority of patients prior to starting any pressors/drips.

4. If I have learned anything over the past 3 decades it is not to alter my practice based on any one study. Time and time again these studies are proven incorrect or simply inconclusive. It is the sum of the body of evidence combined with our experience in the OR as a specialty that should help guide our decisions.
 
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MoMoGesiologist

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Let’s step back for a moment to the real world:

1. Minimum MAC is 0.5 for most and 0.7 MAC for some. I use 0.7 MAC to be cautious and cover my ass. Recall must be prevented. Anything over 0.7 MAC is up to the provider and the situation based on vitals

2. Any poor outcomes may cause a review of the record and your care will be scrutinized. That means a low BP will be an easy marker for the bad outcome. You will lose the lawsuit without question. Thus, in this environment a mean BP of 70-75 is very prudent in most situations especially in elderly patients.
I think a 20 percent reduction of BP is overly cautious because many of our patients are very hypertensive preop with MAP over 110. Even in that subgroup I wouldn’t increase my pressors just to maintain the 20 percent rule.

3. We know patients are dehydrated preop. That has been know for the past 4 decades. A bag of fluid like LR seems quite reasonable for the vast majority of patients prior to starting any pressors/drips.

4. If I have learned anything over the past 3 decades it is not to alter my practice based on any one study. Time and time again these studies are proven incorrect or simply inconclusive. It is the sum of the body of evidence combined with our experience in the OR as a specialty that should help guide our decisions.
You wrote such a reasonable response, I am willing to ignore your corona posts over the last several months
 
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coffeebythelake

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100% disagree. We know all our anesthetics cause vasodilation, blunting of sympathetic tone, some cause bradycardia. All of these have the effect of decreasing BP at the very least and potentially CO as well. Why would you not use a low-dose vasopressors to counteract the shock state you've induced with general anesthesia. Instead we resort to volume in patients that probably don't need it in the first place.

Reminds me of flaps and surgeons complaining when using pressors.
They don't seem to understand such basics.
 
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deleted171991

What’s the controversy in saying volatile or anesthetic overdose contributes to hypotension?
Nothing. Don't let them bully you, especially certain people who specialize in it. I see the problem all the time, especially with CRNAs, at 1.2-1.5 MAC. Then I give them a break, reduce the volatile to 0.7, add some low-dose opiate, and there is no more hypotension. Surprise!

Need for pressor infusions is, many times, the mark of a poorly balanced anesthetic, especially nowadays with the non-opiate mania. Stop using semi-useless vasodilators with minimal analgesic or hypnotic activity (e.g. precedex), think about every drug and its needed dose, including the gas, and one will have much less hypotension.

Watch the blood loss like a hawk, replace volume loss properly (that includes blood, if appropriate), give glyco for bradycardia etc., and there won't be a need for pressor infusion. If your patient is on more than 20 mcg/min of phenylephrine, I will question your anesthetic skills. Same for using any pressor infusion in an ambulatory surgery (except for obvious situations like shoulders).

Btw, a person who just sets and forgets that gas dial is the kind of anesthesiologist I wouldn't want to have.
 
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MoMoGesiologist

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Nothing. Don't let them bully you. I see the problem all the time, especially with CRNAs, at 1.2-1.5 MAC. Then I give them a break, reduce the volatile to 0.7, add some low-dose opiate, and there is no more hypotension. Surprise!

Need for pressor infusions is, many times, the mark of a poorly balanced anesthetic, especially nowadays with the non-opiate mania. Stop using semi-useless vasodilators with minimal analgesic or hypnotic activity (e.g. precedex), think about every drug and its needed dose, and one will have much less hypotension.

Btw, a person who just sets and forgets that gas dial is the kind of anesthesiologist I wouldn't want to have.
Thank you. I feel surprised so few people here have found gas to be a frequent cause of intraop hypotension. Why do so many residents/CRNAs think you need one MAC to prevent awareness? Do people not understand what “MAC” actually measures/means? 0.7 is my goal, but I’ll tolerate 0.5 based on surgeon and patient and anesthetic factors.

Also agree: patient does not need dexmed, ketamine, robaxin, IV Tylenol, and toradol to wake up comfortable. K. I. S. S!
 
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deleted171991

Thank you. I feel surprised so few people here have found gas to be a frequent cause of intraop hypotension. Why do so many residents/CRNAs think you need one MAC to prevent awareness? Do people not understand what “MAC” actually measures/means? 0.7 is my goal, but I’ll tolerate 0.5 based on surgeon and patient and anesthetic factors.

Also agree: patient does not need dexmed, ketamine, robaxin, IV Tylenol, and toradol to wake up comfortable. K. I. S. S!
Monkey see, monkey do (NOT monkey think). Only "fleas" think, and round, and care about the long-term welfare of their patients. That's the explanation.

It drives me nuts when I see geniuses giving a ton of analgesics in the middle of surgery, then fighting hypotension and having most of those medications wear off by the time the patient wakes up (dizzy and in pain). People also tend to worry more about their phones than their patients, so it's much easier to just set the gas high and run pressors, than watch the surgical field and adjust the gas appropriately.

People can get upset all they want, but the amount of knee-jerk, one size fits all, people in ORs is scary.
 
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coffeebythelake

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Thank you. I feel surprised so few people here have found gas to be a frequent cause of intraop hypotension. Why do so many residents/CRNAs think you need one MAC to prevent awareness? Do people not understand what “MAC” actually measures/means? 0.7 is my goal, but I’ll tolerate 0.5 based on surgeon and patient and anesthetic factors.

Yep, I see this all the time and it annoys the hell out of me. 1 MAC of gas and a phenylephrine gtt running
0.7 MAC is goal. nothing more needed if muscle relaxants used judiciously
 
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BLADEMDA

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volatile anesthetics disrupt autoregulation curves
 
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anbuitachi

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Thank you. I feel surprised so few people here have found gas to be a frequent cause of intraop hypotension. Why do so many residents/CRNAs think you need one MAC to prevent awareness? Do people not understand what “MAC” actually measures/means? 0.7 is my goal, but I’ll tolerate 0.5 based on surgeon and patient and anesthetic factors.

Also agree: patient does not need dexmed, ketamine, robaxin, IV Tylenol, and toradol to wake up comfortable. K. I. S. S!

who here likes doing cases on 75% nitrous + paralysis and call it a day ?

got your 0.7 mac there, and no movement! yay K I S S
 
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drmwvr

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Also agree: patient does not need dexmed, ketamine, robaxin, IV Tylenol, and toradol to wake up comfortable. K. I. S. S!

No they don't...they can wake up at 4 in the afternoon in a narcotic/benzo stupor. No mention in this discussion of different incisions meaning different analgesia/anesthesia requirements? A thorocotomy isn't a knee scope...not picking on you, but the broad generalizations in this thread is really surprising.
 

MoMoGesiologist

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No they don't...they can wake up at 4 in the afternoon in a narcotic/benzo stupor. No mention in this discussion of different incisions meaning different analgesia/anesthesia requirements? A thorocotomy isn't a knee scope...not picking on you, but the broad generalizations in this thread is really surprising.
Yep. Depends on surgeon and patient factors. But maybe it’s where I work, but I have seen plenty of times people getting a bunch of adjuncts when pt has epidural or block on board and it doesn’t make sense to me
 
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When I was in training, it was almost gospel in my department to give at least 2mcg/kg fentanyl or its equivalent for every anesthetic. Frequently we gave 5-10mcg/kg and it was often a goal to have the patients breathing spontaneously at 8-10 breath/min at the end of the case. However, one day I was working with one of the faculty luminaries who was instrumental in describing fluorinated volatile anesthetics. I remember giving 100mcg fentanyl out of habit to a patient having FESS. His words to me were, “you’ve just ruined a perfectly good anesthetic” and he was right.
 
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MoMoGesiologist

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When I was in training, it was almost gospel in my department to give at least 2mcg/kg fentanyl or its equivalent for every anesthetic. Frequently we gave 5-10mcg/kg and it was often a goal to have the patients breathing spontaneously at 8-10 breath/min at the end of the case. However, one day I was working with one of the faculty luminaries who was instrumental in describing fluoridated volatile anesthetics. I remember giving 100mcg fentanyl out of habit to a patient having FESS. His words to me were, “you’ve just ruined a perfectly good anesthetic” and he was right.
Do you give fentanyl at induction? What’s your typical analgesic plan for a straight forward case? Give any long acting narcotics?

For the FESS you’re describing, did your attending not plan to give any opiate?
 
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