Hypotension

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As FFP said, HTN causes a shift of the auto regulatory curve. Drummond at UCSD recommends or suggests the bottom of that curve in a chronic hypertensive is near 70 - so I tried to keep these HTN patients above 70 (MAP).

In MOST cases, patients tolerate hypertension much more than they do hypOtension. Just remember that.

I almost always give 10mg ephedrine, and 100mcg of phenylephrine together (depending on HR of course).

Also, as was mentioned, most hypotension is a vascular resistance issue. Struggling with BP? Give fluid.
 
Also, as was mentioned, most hypotension is a vascular resistance issue.

Agree

Struggling with BP? Give fluid.

Disagree. If the problem is vascular resistance - then fix the vascular resistance i.e. phenylephrine. Never made sense to me to flood the patient just to try to fill up the now dilated vascular bed when it's so easy to just restore vascular tone to normal. I've also never really been impressed by fluid's ability to improve anesthetic induced hypotension.
 
Agree



Disagree. If the problem is vascular resistance - then fix the vascular resistance i.e. phenylephrine. Never made sense to me to flood the patient just to try to fill up the now dilated vascular bed when it's so easy to just restore vascular tone to normal. I've also never really been impressed by fluid's ability to improve anesthetic induced hypotension.
Yup. We're too often taught that vasopressors are the devil and masking something that's going wrong. In certain situations that may be correct, but that's why we're anesthesiologists. To know which situation is which. If your GA is causing vascular relaxation, give something to counteract that effect. Just like you give glyco with neostigmine.
 
Agree



Disagree. If the problem is vascular resistance - then fix the vascular resistance i.e. phenylephrine. Never made sense to me to flood the patient just to try to fill up the now dilated vascular bed when it's so easy to just restore vascular tone to normal. I've also never really been impressed by fluid's ability to improve anesthetic induced hypotension.
That hasn't been my experience at all.

I find that if I don't give fluid, they continually need chemical correction of MAP, but with administration of fluid, they stabilize.

Try it sometime. I bet you'll be pleasantly surprised.
 
That hasn't been my experience at all.

I find that if I don't give fluid, they continually need chemical correction of MAP, but with administration of fluid, they stabilize.

Try it sometime. I bet you'll be pleasantly surprised.
Of course, they'll need chemical correction though. They're under continual general anesthesia.
 
Disagree. If the problem is vascular resistance - then fix the vascular resistance i.e. phenylephrine. Never made sense to me to flood the patient just to try to fill up the now dilated vascular bed when it's so easy to just restore vascular tone to normal. I've also never really been impressed by fluid's ability to improve anesthetic induced hypotension.

Couldn't agree more.

Others here are advocating treating a problem of vascular tone with fluid, as opposed to, y'know, a vascular tone agent. Hmmm.
 
Couldn't agree more.

Others here are advocating treating a problem of vascular tone with fluid, as opposed to, y'know, a vascular tone agent. Hmmm.

I'm also pretry firmly in the tone camp, but it should be acknowledged that volatile does have direct calcium-mediated vasodilating (including venodilating) activity that attenuates smooth muscle response to catecholamines. It's not unreasonable to give a fluid bolus after a phenylephrine challenge to counteract decreased preload from venous pooling. But as was pointed out earlier, unless the case has ongoing fluid losses then 1-2L is enough.
 
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As a specialty, we have to start switching our mindset from short-term benefits to long-term.

Long-term, many surgical patients benefit from having been kept relatively dry intraop. Don't chase urine output. Don't chase the BP with (just) fluids. Don't overestimate surgical field evaporation losses. Don't overestimate NPO losses. Be mindful when giving fluids (and pressors); replace blood loss but not much else (and don't pump the patient full with fluids that will leak out in 1.5-2 hours - that applies for colloids, too, except blood); if the blood loss is significant, give some blood, not just fluids. Try not to give more crystalloid than 20-30 ml/kg plus 2-3 x blood losses.

All fluids we give are pro-inflammatory, and inflammation causes endothelial leaks, hence edema. If that edema happens in the belly, it can cause intra-abdominal hypertension and decreased urine output, leading to more fluids being given by urine output-chasers, leading to more IAH and AKI, and so on. If the edema is in the lung, it will cause respiratory issues, up to ARDS (especially after a few hours of great anesthetist care at 10 ml/kg Vt and zero PEEP) . IV fluids are good until they are not. I have seen more people harmed with IV fluids than with lack of them. Yes, the numbers look good during the surgery, but that's the short-term mindset. Think about the big picture, for every patient. Before just giving more fluids, make sure that you have fixed everything else that can be fixed (anesthetic depth, temperature, coags, vascular resistance etc.).

Also, don't forget that anything that reduces blood viscosity can cause hypotension, by reducing SVR, and that may not be fixed easily by pressors. That's why 1-2 units of blood (or plasma or other colloid) will do miracles occasionally, because of the viscosity. Don't dilute the blood too much with crystalloids, unless you are sure the patient can tolerate it.

Fluid management is not easy, except for people who don't know fluid management.
 
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Couldn't agree more.

Others here are advocating treating a problem of vascular tone with fluid, as opposed to, y'know, a vascular tone agent. Hmmm.

well good luck then.

I'd much rather give 500ml bolus of LR then give phenylephrine every few minutes for 2 hours.
 
well good luck then.

I'd much rather give 500ml bolus of LR then give phenylephrine every few minutes for 2 hours.

Easy thing, rather than the right thing? :poke:

Put the syringe on a pump or squirt some in a bag on a pump and let it go at 25 mcg/min.

There, you don't even need weight-based dosing!



And you're not really suggesting that a 500 mL bonus of LR is going to fix the hypotension for two hours, are you?

500 mL every 20-30 minutes for 2 hours might work (or it might not). But then you're talking liters.
 
And you're not really suggesting that a 500 mL bonus of LR is going to fix the hypotension for two hours, are you?

I suspect his bolus is finishing about the same time as the initial incision, and it's really the catechol bump from the surgery starting that's fixing the hypotension.


Oh, and :=|:-): for this one:
There, you don't even need weight-based dosing!
 
Had the same problem friday with a psych patient for a carotid: after induction and cerv block his pressure tanked with no response to 10mg of ephedrine.
So we started an epinephrine pump which by the time the BP was stabilized was running at 100cc/h @4mcg/cc. Dude was on ACEI and a bunch of anti-psycotic meds one of which he took sub-cu 1/week...
I switched to norepi at that point because he was getting tachycardic from all the epi.

Completely resolved once awake.
 
Had the same problem friday with a psych patient for a carotid: after induction and cerv block his pressure tanked with no response to 10mg of ephedrine.
So we started an epinephrine pump which by the time the BP was stabilized was running at 100cc/h @4mcg/cc. Dude was on ACEI and a bunch of anti-psycotic meds one of which he took sub-cu 1/week...
I switched to norepi at that point because he was getting tachycardic from all the epi.

Completely resolved once awake.

You intubate and do a cervical plexus block?
 
I want to know who started this dogma that says phenylephrine is somehow safe through a PIV and NE is not. I've looked pretty hard, and though there aren't any huge studies, pretty much everything I've found says that they're both safe when used in a good IV monitored closely. Assuming the mechanism of harm is intense, sustained vasoconstriction in the area of extravasation, I would think that a direct alpha agonist would be the most harmful agent, and that something like Epi would be even less harmful--though I suppose a lot depends on the concentration of the infusion.
 
I want to know who started this dogma that says phenylephrine is somehow safe through a PIV and NE is not. I've looked pretty hard, and though there aren't any huge studies, pretty much everything I've found says that they're both safe when used in a good IV monitored closely. Assuming the mechanism of harm is intense, sustained vasoconstriction in the area of extravasation, I would think that a direct alpha agonist would be the most harmful agent, and that something like Epi would be even less harmful--though I suppose a lot depends on the concentration of the infusion.

I had a critical care attending tell me that you can't use epi or norepi for push dose pressors like you can for phenylephrine and ephedrine which I thought was bs.

Pulm crit has a nice discussion regarding peripheral pressors: PulmCrit- Do phenylephrine and epinephrine require central access?

Apparently you can run peripheral pressors for days as long as you're using a decent size vein and catheter. Three cases of skin necrosis exist in the literature (2 for phenylephrine, 1 for epinephrine), all in the distal leg and without major sequelae. Last one was from 50 years ago. Also people have injected epipens into their fingers with no lasting adverse effects.

Makes me wonder what else academia is teaching me that's total bull****
 
I had a critical care attending tell me that you can't use epi or norepi for push dose pressors like you can for phenylephrine and ephedrine which I thought was bs.

This is nonsense.
 
I want to know who started this dogma that says phenylephrine is somehow safe through a PIV and NE is not. I've looked pretty hard, and though there aren't any huge studies, pretty much everything I've found says that they're both safe when used in a good IV monitored closely. Assuming the mechanism of harm is intense, sustained vasoconstriction in the area of extravasation, I would think that a direct alpha agonist would be the most harmful agent, and that something like Epi would be even less harmful--though I suppose a lot depends on the concentration of the infusion.
I had a critical care attending tell me that you can't use epi or norepi for push dose pressors like you can for phenylephrine and ephedrine which I thought was bs.

Pulm crit has a nice discussion regarding peripheral pressors: PulmCrit- Do phenylephrine and epinephrine require central access?

Apparently you can run peripheral pressors for days as long as you're using a decent size vein and catheter. Three cases of skin necrosis exist in the literature (2 for phenylephrine, 1 for epinephrine), all in the distal leg and without major sequelae. Last one was from 50 years ago. Also people have injected epipens into their fingers with no lasting adverse effects.

Makes me wonder what else academia is teaching me that's total bull****
Oops, you guys really need to look better. Phenylephrine can extravasate and not much will happen; there are a handful of case reports in the last 50-70 years. If norepi extravasates, it can be a tragedy, and there are many more than 1-2 case reports. I am a big fan of peripheral pressors, but it takes some well-placed IVs in closely-monitored big veins with long catheters and phentolamine (and/or nitroglycerine, or terbutaline and other vasodilators) immediately available at bedside, to avoid serious complications.

This is one of the recent studies showing that it can be done: Safety of peripheral intravenous administration of vasoactive medication. - PubMed - NCBI , but they had an excellent protocol which involved everybody in the ICU (residents, nurses, pharmacy etc.).

And this is the largest review to date on the subject: Mythbuster: Administration of Vasopressors Through Peripheral Intravenous Access - R.E.B.E.L. EM - Emergency Medicine Blog . The important part:

"Results:
  • 85 articles with 270 patients and 325 separate local tissue injury and extravasation events included
  • 318 events were from PIV administration
    • 204 local tissue injury events (179 skin necrosis, 5 tissue necrosis, and 20 gangrene)
      • 85.3% of adverse events occurred from PIVs located at sites distal to antecubital or popliteal fossae
      • 96.8% of adverse events occurred after 4 hrs of infusion from PIV
      • Major disability and mortality in 9 (4.4%) and 4 (2.2%) of cases respectively
    • 114 extravasation events
      • 75.4% did not result in any tissue injury
      • 75% of adverse events were distal to antecubital and popliteal fossae
      • Major disability 3 cases (2.7%), and mortality 1 case (0.9%)
    • 7 events were from CVC administration
      • 4 local tissue injury events (3 skin necrosis & 1 gangrene)
        • Long-term sequelae 3 cases and minor disability 2 cases
        • Mortality in 1 case
      • 3 extravasation events
        • No injuries reported"
When it happens, it looks ugly like here: Well recognised but still overlooked: norepinephrine extravasation -- Kim et al. 2012 -- BMJ Case Reports

F1.medium.gif


Just Google "norepinephrine extravasation", and look at the Images, and you'll find a number of scary ones. I have seen one of these extravasations myself, and the patient was screaming in pain.

It is true that most case reports are from back when they used to run elephant doses of norepi (70-100 mcg/min) for days in the ICU. I would say that running norepi through a PIV for a few hours, especially in the OR (or any other closely-monitored setting), should be fine, but please do realize the potential for harm. I wouldn't do it in some community hospital that doesn't have an IV team specialized in treating extravasations immediately. Epi (or dopamine) isn't much different at pressor doses. The drugs that can be always run peripherally are the inodilators.

Btw, I have personally used peripheral pressors for mild sepsis for less than a day, so I am all for it, whenever possible. Many of the problems result from not noticing that the IV is getting infiltrated, or from using short (less than 2 inch-long) catheters with poor IV placement technique (through and through, or other damage to the vein) and slow flowing IV, where the pressor can leak back to the insertion site and through the hole on the posterior wall of the vein.
 
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I still don't see anything addressing the relative safety of NE vs phenylephrine. I agree there's risk with both, but I just doubt the risk is much different between the two. Again, I think the concentration of the infusion is probably more important.

One of those links mentioned nitro paste for treatment, which I had never heard of and will keep in mind--much more available than phentolamine.

Oops, you guys really need to look better. Phenylephrine can extravasate and not much will happen; there are a handful of case reports in the last 50-70 years. If norepi extravasates, it can be a tragedy, and there are many more than 1-2 case reports. I am a big fan of peripheral pressors, but it takes some well-placed IVs in closely-monitored big veins with long catheters and phentolamine (and/or nitroglycerine, or terbutaline and other vasodilators) immediately available at bedside, to avoid serious complications.

This is one of the recent studies showing that it can be done: Safety of peripheral intravenous administration of vasoactive medication. - PubMed - NCBI , but they had an excellent protocol which involved everybody in the ICU (residents, nurses, pharmacy etc.).

And this is the largest review to date on the subject: Mythbuster: Administration of Vasopressors Through Peripheral Intravenous Access - R.E.B.E.L. EM - Emergency Medicine Blog . The important part:

"Results:
  • 85 articles with 270 patients and 325 separate local tissue injury and extravasation events included
  • 318 events were from PIV administration
    • 204 local tissue injury events (179 skin necrosis, 5 tissue necrosis, and 20 gangrene)
      • 85.3% of adverse events occurred from PIVs located at sites distal to antecubital or popliteal fossae
      • 96.8% of adverse events occurred after 4 hrs of infusion from PIV
      • Major disability and mortality in 9 (4.4%) and 4 (2.2%) of cases respectively
    • 114 extravasation events
      • 75.4% did not result in any tissue injury
      • 75% of adverse events were distal to antecubital and popliteal fossae
      • Major disability 3 cases (2.7%), and mortality 1 case (0.9%)
    • 7 events were from CVC administration
      • 4 local tissue injury events (3 skin necrosis & 1 gangrene)
        • Long-term sequelae 3 cases and minor disability 2 cases
        • Mortality in 1 case
      • 3 extravasation events
        • No injuries reported"
When it happens, it looks ugly like here: Well recognised but still overlooked: norepinephrine extravasation -- Kim et al. 2012 -- BMJ Case Reports

F1.medium.gif


Just Google "norepinephrine extravasation", and look at the Images, and you'll find a number of scary ones. I have seen one of these extravasations myself, and the patient was screaming in pain.

It is true that most case reports are from back when they used to run elephant doses of norepi (70-100 mcg/min) for days in the ICU. I would say that running norepi through a PIV for a few hours, especially in the OR (or any other closely-monitored setting), should be fine, but please do realize the potential for harm. I wouldn't do it in some community hospital that doesn't have an IV team specialized in treating extravasations immediately. Epi (or dopamine) isn't much different at pressor doses. The drugs that can be always run peripherally are the inodilators.

Btw, I have personally used peripheral pressors for mild sepsis for less than a day, so I am all for it, whenever possible. Many of the problems result from not noticing that the IV is getting infiltrated, or from using short (less than 2 inch-long) catheters with poor IV placement technique (through and through, or other damage to the vein) and slow flowing IV, where the pressor can leak back to the insertion site and through the hole on the posterior wall of the vein.
 
I still don't see anything addressing the relative safety of NE vs phenylephrine. I agree there's risk with both, but I just doubt the risk is much different between the two. Again, I think the concentration of the infusion is probably more important.

One of those links mentioned nitro paste for treatment, which I had never heard of and will keep in mind--much more available than phentolamine.
I don't know what to tell you, except that the number of case reports is many times higher for norepi than for phenylephrine (219 vs 6 in Loubani's review paper), and I personally still have to see one of the latter, while having witnessed the damage norepi can do.
 
Couple of things that I didn't see described in the story so far...

What was the TV/peep?
Neck dissection, so did you put the head of the bed up for the surgeon? Or did he do it unknowns to you? Even with a shoulder roll?

Within reason you can create any spurious bp you want (non pharmacologically) by just fiddling around with the vent and Trendelenburg.
 
I don't know what to tell you, except that the number of case reports is many times higher for norepi than for phenylephrine (219 vs 6 in Loubani's review paper), and I personally still have to see one of the latter, while having witnessed the damage norepi can do.
Are most of those case reports from the ICU or the OR? I'd bet on the ICU.

Dose, duration, vigilance, patient population could account for much of the difference. I virtually never see NE used in the OR outside of cardiac cases (which have central lines). And I virtually never see phenylephrine used in the ICU.

Coincidentally, Friday night was the first time I've used NE through a PIV in as long as I can remember. Gave it through a RIC and paid attention.
 


Both studies demonstrate association but not causation.

"In conclusion, an overall causal relation between IOH and 1-yr mortality could not be demonstrated in the current study."

The IOH groups were older and more likely to have CAD/DM/Htn. We all know sicker patients are more likely to experience IOH. That does not mean IOH increases mortality or that treating or preventing IOH decreases mortality. The most prevalent cause of 1year mortality was cancer. That does not mean IOH caused increased mortality from cancer.

To show causation you need a prospective trial comparing different BP management strategies in risk matched cohorts.
 
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Are most of those case reports from the ICU or the OR? I'd bet on the ICU.

Dose, duration, vigilance, patient population could account for much of the difference. I virtually never see NE used in the OR outside of cardiac cases (which have central lines). And I virtually never see phenylephrine used in the ICU.

Coincidentally, Friday night was the first time I've used NE through a PIV in as long as I can remember. Gave it through a RIC and paid attention.


Agree. And in my experience, many of the crap IVs that come from the floor or the ICU are just not tolerated in the OR. That may be the difference.
 
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Both studies demonstrate association but not causation.

"In conclusion, an overall causal relation between IOH and 1-yr mortality could not be demonstrated in the current study."

The IOH groups were older and more likely to have CAD/DM/Htn. We all know sicker patients are more likely to experience IOH. That does not mean IOH increases mortality or that treating or preventing IOH decreases mortality. The most prevalent cause of 1year mortality was cancer. That does not mean IOH caused increased mortality from cancer.

To show causation you need a prospective trial comparing different BP management strategies in risk matched cohorts.

Sure, I agree there are lots of holes in the study. But, I agree with the conclusion as will 99% of your peer-reviewed colleagues:

Clinical Implications

we believe that there is strong evidence that intraoperative hypotension, namely SBP < 70 mmHg, MAP < 50 mmHg, and DBP < 30 mmHg, is associated with excess operative morbidity and mortality


In the largest (33,330 noncardiac surgeries) and most recently published study, Walsh et al.7 reported that patients with a MAP < 55 mmHg for 1 to 5, 6 to 10, 11 to 20, and more than 20 min had graded increases in their risk for acute kidney injury or myocardial injury.

Clinical Pearl for Residents and Junior Attendings:

HYPOTENSION KILLS
 
New CA1 here had a case the other day that still has me wondering what happened.

56 yo male, history of HTN and B-cell lymphoma comes in for a neck dissection/lymph node biopsy.

Patient was induced uneventfully with 120mg propofol, 50 of fentanyl and succinylcholine. No BP issues at this point.

Placed a cobra ETT and the plan was to keep the patient on the deeper side as the surgeon doesn't want the patient paralyzed.

I get the patient to 1.1 MAC and give 50 of fentynl just before incision. Prior to this the BP had been in the 110's.

Within 1 minute his BP tanks and his MAP falls to the 50's. Over the next few minutes I try giving phynlephrine, ephedrine even levophed with no/minimal response. I reduce the gas to 0.8 MAC and hes still hypotensive and nothing is working. Finally I ended up giving epinephrine and was able to get his BP back up.

I ended up having to give intermittent bonuses of epi 1mcg at a time as he wouldn't respond to anything else.

My attending was in the room by the time I was giving levophed and epi and he was thinking it was an adverse reaction to possibly the ancef.

This was a short case (45 min) and magically once we woke the patient up his BP was in the 130's systolic and he was totally fine.

My question is how often do you run across these patients that get profoundly hypotensive and only respond to epinephrine? Is this somewhat common?

This is a classic response to General Anesthesia for some patients taking ARBs or ACE inhibitors. You will see it again and again so learn how to properly deal with it in the O.R.

Vasoplegic Syndrome and Renin-Angiotensin System Antagonists

Medscape: Medscape Access

http://www.anesthesiologynews.com/R...gs-In-the-Perioperative-Period/35357/ses=ogst

Refractory hypotension during general anesthesia despite preoperative discontinuation of an angiotensin receptor blocker
 
Sure, I agree there are lots of holes in the study. But, I agree with the conclusion as will 99% of your peer-reviewed colleagues:

Clinical Implications

we believe that there is strong evidence that intraoperative hypotension, namely SBP < 70 mmHg, MAP < 50 mmHg, and DBP < 30 mmHg, is associated with excess operative morbidity and mortality


In the largest (33,330 noncardiac surgeries) and most recently published study, Walsh et al.7 reported that patients with a MAP < 55 mmHg for 1 to 5, 6 to 10, 11 to 20, and more than 20 min had graded increases in their risk for acute kidney injury or myocardial injury.

Clinical Pearl for Residents and Junior Attendings:

HYPOTENSION KILLS

"First and most importantly, this is an observational study and therefore can only address association and not causality."


Again there is an association. Most patients do not experience that level of hypotension. The ones who are already at death's door are more likely to experience that level of hypotension. Can you reduce mortality by treating hypotension? Can you reduce kidney injury? Would treating hypotension have any effect on mortality? Could it increase mortality? Can some maneuvers to treat hypotension be causing more harm while I am treating a number? Who knows. The question is not answered and needs to be.

I treat and try to prevent hypotension because it is the dogma but it's a wild guess as to whether I'm doing more harm than good.
 
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Again there is an association. Most patients do not experience that level of hypotension. The ones who are already at death's door are more likely to experience that level of hypotension. Can you reduce mortality by treating hypotension? Can you reduce kidney injury? Would treating hypotension have any effect on mortality? Who knows. The question is not answered and needs to be.

In my part of the world the question has been answered until I see evidence to the contrary. Hypotension is bad and severe hypotension is potentially lethal. Any delay in treating severe hypotension may worsen outcome for a particular patient. I believe it is my job and obligation to use the best evidence we have to date to take care of patients in a clinical setting. For me, that means maintaining BP at an appropriate level. Hypertension (which we used to worry about a lot as well) is well tolerated most of the time unlike hypotension which we now have good evidence (you call "association") will worsen outcome for our most vulnerable patients.

Every Resident needs to know that the "association" between bad outcomes has been linked to hypotension and in particular, the duration of that hypotension in the O.R. Be prepared to defend that automated Electronic record which displays long periods of hypotension.
 
If hypotension is that bad, it should be easy to show that treating hypotension improves outcomes but that has not been done.
 
In my part of the world the question has been answered until I see evidence to the contrary. Hypotension is bad and severe hypotension is potentially lethal. Any delay in treating severe hypotension may worsen outcome for a particular patient. I believe it is my job and obligation to use the best evidence we have to date to take care of patients in a clinical setting. For me, that means maintaining BP at an appropriate level. Hypertension (which we used to worry about a lot as well) is well tolerated most of the time unlike hypotension which we now have good evidence (you call "association") will worsen outcome for our most vulnerable patients.

Every Resident needs to know that the "association" between bad outcomes has been linked to hypotension and in particular, the duration of that hypotension in the O.R. Be prepared to defend that automated Electronic record which displays long periods of hypotension.

What do you define as hypotension and severe hypotension? This feels like sepsis where we kinda know what it is and how to treat it but getting an exact definition is a little murky.
 
If hypotension is that bad, it should be easy to show that treating hypotension improves outcomes but that has not been done.
Hypotension leads to complications. So common sense tells me that avoiding it is probably usually a good thing. I haven't seen a study showing that looking both ways before crossing the street improves outcomes, but my spidey sense tells me I should do it.
 
Hypotension leads to complications. So common sense tells me that avoiding it is probably usually a good thing. I haven't seen a study showing that looking both ways before crossing the street improves outcomes, but my spidey sense tells me I should do it.

Some things we do based on common sense are eventually proven to be harmful. Or we do things like start beta blockade on a wide swath of patients to prevent perioperative ischemic events and learn later on that it increases all cause mortality. You wouldn't know this without a prospective trial.

I do wonder exactly what level of hypotension is beneficial to treat. Would love to see a trial comparing different treatment strategies....say comparing treatment for a MAP of 70 vs more permissive MAPs of 60 and 50. And also comparing treatment by controlling anesthetic depth vs pressors vs inotropes and even volume. They are all very basic questions that remain unanswered. So we still rely on common sense.
 
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