Hypotension Kills

[linkin06]

How about the other end? In young, healthy patients, 60 is fine I think.

---

Members don't see this ad.

 

[leviathan]

Statistical significance doesn't imply clinical significance. Also, as you know it depends on how the results were defined and whether they did ad hoc or post hoc analysis. There's a lot of garbage being published these days.

A statistically significant result in a small sample size implies a very large effect. Nobody said the two are the same, my response was to the person saying "oh it's only a small study" as if that changes how a P value is calculated.

Clinical significance is a different discussion than the one I was having, but I agree with you on that.

 

[deleted697535]

Can someone explain to me why fluid is a treatment for hypotension and what the patient benefits are post induction in an elective patient?

What im getting at is fluid doesnt carry oxygen. These people arent septic or leaky capillaries. How will IV fluid benefit them?
I do it all the time but i dont know why

 

[nimbus]

Can someone explain to me why fluid is a treatment for hypotension and what the patient benefits are post induction in an elective patient?

What im getting at is fluid doesnt carry oxygen. These people arent septic or leaky capillaries. How will IV fluid benefit them?
I do it all the time but i dont know why

The assumption is that patients are hypovolemic from the preop fast. But I agree fluids rarely work in this situation where the postinduction blood pressure is 75/40. They need vasopressor and/or inotropes and an incision.

 

[Psai]

Keeps the vessels open and maintains perfusion pressure. Doesn't matter how many rbcs you have if you have no fluid for them to run through.

You're not treating hypotension, you're treating the cause of hypotension which is hypovolemia and vasodilation.

 

[deleted59964]

Can someone explain to me why fluid is a treatment for hypotension and what the patient benefits are post induction in an elective patient?

What im getting at is fluid doesnt carry oxygen. These people arent septic or leaky capillaries. How will IV fluid benefit them?
I do it all the time but i dont know why

Simplistically
Do2=CaO2 x CO
CO = sv x hr
SV varies with preload.contractility/afterload

Giving fluid increases preload ... Increases SV ... increases CO ... increases DO2

 

[leviathan]

Simplistically
Do2=CaO2 x CO
CO = sv x hr
SV varies with preload.contractility/afterload

Giving fluid increases preload ... Increases SV ... increases CO ... increases DO2

A patient who is now vasoplegic after induction has a supraphysiologic DO2 and high cardiac output state. They need a vasopressor, not fluid.

 

[deleted59964]

A patient who is now vasoplegic after induction has a supraphysiologic DO2 and high cardiac output state. They need a vasopressor, not fluid.

i'm not advocating fluids over pressors, was merely answering Newtwo's question by describing the impact of giving fluids on oxygen delivery.

any evidence that post induction hypotension exists with a high CO state?

also need to be careful about terms like "vasoplegia" -- our agents venodilation as well as causing arteriolar vasodilation. venodilation sets up a relative physiological hypovolaemia --- which can be treated with fluids or pressors.

 

[nimbus]

In the common OR scenario, I’ve rarely if ever seen a fluid bolus actually work to rapidly correct hypotension. How much fluid does one need to give to correct postinduction hypotension? Fluid bolus alone is never the right answer at least in adults. I think an argument could be made that postinduction hypotension is rarely fluid responsive and fluid boluses are overutilized.

 

[Psai]

Well they are fluid down and should be drinking clears until 2 hours prior to surgery instead of everyone being npo forever. Postinduction hypotension is often iatrogenic and related to sympathetic tone. I doubt it is high co.

 

[vector2]

I'm of the opinion that post induction hypotension is probably related to almost solely GA blunting of adrenergic, vasopressinergic, and RAS activity leading to some CO depression but mostly SVR drop secondary to decreased arteriolar and venous tone. The concept of NPO deficit/MIVF is almost certainly outdated and should be thrown in the garbage (seriously, what's the evidence that the average healthy person is clinically hypovolemic after an 8hr snooze?). The problem is that only a small number of pts can receive effective GDT since it requires vigileo, echo, some other device etc. for the time being, so there's probably no harm in bolusing 500-1000cc crystalloid to attenuate some of the preload decrease 2/2 venodilation. However, the mainstay of post induction treatment should be vasopressors.

 

[Robotic Wis-Hipple]

A patient who is now vasoplegic after induction has a supraphysiologic DO2 and high cardiac output state. They need a vasopressor, not fluid.

It’s not as simple or straight forward as either of these explanations. I wouldn’t call a post induction period of hypotension vasoplegic, it’s a combo of myocardial depression, functional hypovolemia secondary to reduced SVR or actual hypovolemia due to the fasting state, decreased sympathetic tone, etc. Many patients do respond to fluids, many patients are beta blocked and don’t/can’t create a high cardiac output state reflexively etc.

 

[Psai]

How can you call something outdated and promote goal directed therapy in the same post with a straight face?

 

[vector2]

How can you call something outdated and promote goal directed therapy in the same post with a straight face?

I'm calling the concept of weight based NPO deficit (4/2/1 rule) and running MIVF at some arbitrary 100cc/hr rate outdated. GDT involves bolusing to meet a predetermined CO/CO-surrogate improvement target.

 

[deleted59964]

can't say i'm excited by the turn this thread has taken. post induction hypotension can be explained quite well by the content of any undergrad pharmacology and physiology text.

yawn

 

[deleted697535]

You can blame me for that. But really was it ever not going to go that way. Any discussion on hypotension kills is going to lead to how to treat it.

I don't think fluid is a great answer all the time

 

[dannyboy1]

If heart rate is high give phenylephrine, if low give ephedrine. Enough said.

 

[parcus]

A statistically significant result in a small sample size implies a very large effect. Nobody said the two are the same, my response was to the person saying "oh it's only a small study" as if that changes how a P value is calculated.

Clinical significance is a different discussion than the one I was having, but I agree with you on that.

Even though there is truth to what you are saying, small sample sizes get more error both ways (tends towards more false negatives?). Using my phone now and can’t find the article from the OP, but I believe it assessed high risk patients only, about 300 pts; sounds decent to me ( although I don’t know what the ideal n would be), But I can understand why someone would be skeptical.

 

[drmwvr]

If heart rate is high give phenylephrine, if low give ephedrine. Enough said.

All things being equal, a "high" heart rate (assuming it is sinus) in the face of hypotension needs fluid first, not vasomotor tone. That need may follow, but first things first.

 

[deleted59964]

you might as well argue over whether to fix bland food by adding salt or pepper.

 

[Consigliere]

Go Eagles!

 

[nimbus]

All things being equal, a "high" heart rate (assuming it is sinus) in the face of hypotension needs fluid first, not vasomotor tone. That need may follow, but first things first.

I’d argue it’s better to correct hypotension with pressor first. Has anybody seen a 250-500ml fluid bolus do anything?

 

[CopaceticOne]

I’d argue it’s better to correct hypotension with pressor first. Has anybody seen a 250-500ml fluid bolus do anything?

Yeah. (In a 20kg kiddo )

 

[drmwvr]

I’d argue it’s better to correct hypotension with pressor first. Has anybody seen a 250-500ml fluid bolus do anything?

If the hypotension you want to treat is from a lack of volume, using a bolus pressor as a stop-gap while you get the volume in is defensible. Probably a good idea. But it doesn't "correct" the hypotension. Euvolemia does.

Giving a pressor when the patient needs volume is a bad habit.

 

[nimbus]

If the hypotension you want to treat is from a lack of volume, using a bolus pressor as a stop-gap while you get the volume in is defensible. Probably a good idea. But it doesn't "correct" the hypotension. Euvolemia does.

Giving a pressor when the patient needs volume is a bad habit.

I’m saying often the hypotension is not primarily from hypovolemia.

If they are normotensive with a normal heart rate prior to induction of anesthesia and hypotensive after induction, the hypotension is more likely to be caused by vasoplegia and myocardial depression secondary to anesthesia. They don’t suddenly become hypovolemic from the induction of anesthesia. And an incision often cures postinduction hypotension with no fluids given. Many patients require vasopressor during anesthesia and then are completely normotensive after emergence despite what I consider minimal intraoperative fluids(600-700ml for a 90min case). I don’t assume that most elective surgery patients are hypovolemic from the preop fast.

 

[fakin' the funk]

The immediate post-induction circulatory state:
- low preload from positive pressure ventilation, actual hypovolemia, mild/relative hypovolemia from venodilation, or all of the above
- low HR, from opioids, anesthetics, and withdrawal of awake sympathetic tone, and a blunted baroreceptor
- normal or impaired contractility, from anesthetics
- low SVR, from anesthetics, and withdrawal of awake sympathetic tone

All of the above independent of patient and surgical factors.

There's a lot more going on than "preoperative fasting."

Fluid only fixes one of those parameters, and lasts many hours to days, when what you have is a number of minutes-to-hours problems.

 

[BLADEMDA]

The immediate post-induction circulatory state:
- low preload from positive pressure ventilation, actual hypovolemia, mild/relative hypovolemia from venodilation, or all of the above
- low HR, from opioids, anesthetics, and withdrawal of awake sympathetic tone, and a blunted baroreceptor
- normal or impaired contractility, from anesthetics
- low SVR, from anesthetics, and withdrawal of awake sympathetic tone

All of the above independent of patient and surgical factors.

There's a lot more going on than "preoperative fasting."

Fluid only fixes one of those parameters, and lasts many hours to days, when what you have is a number of minutes-to-hours problems.

Nice post. The IMMEDIATE solution is still the same: Pressors. A volume bolus with crystalloids would take too long to be of any immediate benefit and the hypotension may remain uncorrected.

 

[deleted59964]

The immediate post-induction circulatory state:
- low preload from positive pressure ventilation, actual hypovolemia, mild/relative hypovolemia from venodilation, or all of the above
- low HR, from opioids, anesthetics, and withdrawal of awake sympathetic tone, and a blunted baroreceptor
- normal or impaired contractility, from anesthetics
- low SVR, from anesthetics, and withdrawal of awake sympathetic tone

All of the above independent of patient and surgical factors.

There's a lot more going on than "preoperative fasting."

Fluid only fixes one of those parameters, and lasts many hours to days, when what you have is a number of minutes-to-hours problems.

I like a little salt, a little pepper, sometimes some garlic, and sometimes some chilli.
Multifactorial problems as you've highlighted above respond best to multifactorial solutions.

 

[drmwvr]

The immediate post-induction circulatory state:
- low preload from positive pressure ventilation, actual hypovolemia, mild/relative hypovolemia from venodilation, or all of the above
- low HR, from opioids, anesthetics, and withdrawal of awake sympathetic tone, and a blunted baroreceptor
- normal or impaired contractility, from anesthetics
- low SVR, from anesthetics, and withdrawal of awake sympathetic tone

All of the above independent of patient and surgical factors.

There's a lot more going on than "preoperative fasting."

Fluid only fixes one of those parameters, and lasts many hours to days, when what you have is a number of minutes-to-hours problems.

Nothing to argue with here, of course, but the post induction, pre-incision period and post incision period are different entities as far as "fixing" hypotension goes. A stepwise approach, putting HR and volume ahead of a pressor is important especially when beta blockers, acei/arb, CCB's etc. are complicating things.

 

[Tularemia-bunny]

They need vasopressor and/or inotropes and an incision.

MS4 level ignorance here: why an incision? Is that because it causes a sympathetic response which will raise the pressure?

 

[nimbus]

MS4 level ignorance here: why an incision? Is that because it causes a sympathetic response which will raise the pressure?

Yes

 

[leviathan]

It’s not as simple or straight forward as either of these explanations. I wouldn’t call a post induction period of hypotension vasoplegic, it’s a combo of myocardial depression, functional hypovolemia secondary to reduced SVR or actual hypovolemia due to the fasting state, decreased sympathetic tone, etc. Many patients do respond to fluids, many patients are beta blocked and don’t/can’t create a high cardiac output state reflexively etc.

If you exclude people with pre-existing LV dysfunction, or aortic stenosis, even in cardiac cases when you do TEE the majority have hyperdynamic hearts with high cardiac output after induction. I agree that some get myocardial depression or significant drops in preload due to positive intrathoracic pressure, but I personally haven't seen it that often. Functional hypovolemia should be treated with pressors, not fluids, to increase the stressed volume. Even with that functional hypovolemia the cardiac output still generally increases due to the overall net effect of a much lower SVR and associated increased ejection fraction and higher heart rate. So giving fluids if the CO is already high might increase your blood pressure but doesn't change the physiology. In my mind, giving pressors will get the same effect without the harm of a positive fluid balance.

 

[Robotic Wis-Hipple]

If you exclude people with pre-existing LV dysfunction, or aortic stenosis, even in cardiac cases when you do TEE the majority have hyperdynamic hearts with high cardiac output after induction. I agree that some get myocardial depression or significant drops in preload due to positive intrathoracic pressure, but I personally haven't seen it that often. Functional hypovolemia should be treated with pressors, not fluids, to increase the stressed volume. Even with that functional hypovolemia the cardiac output still generally increases due to the overall net effect of a much lower SVR and associated increased ejection fraction and higher heart rate. So giving fluids if the CO is already high might increase your blood pressure but doesn't change the physiology. In my mind, giving pressors will get the same effect without the harm of a positive fluid balance.

I agree with the vast majority of this post, however, for the sake of all potential readers I will note that increased EF (if it occurs) does not equal increased stroke volume and thus any increase in HR (if this can occur depending on degree of beta blockade etc) does not necessarily lead to an equal let alone greater CO.

My point was simply that it is not as simple as “give pressor” or “give fluid”. We all likely went thru a period as residents, and I’ve seen it as a Fellow and as an Attending, where we move from phenylephrine to norepi and have a pressure that looks great when in reality the Pt was/is dry and volume is likely to at the least decrease your pressor requirement. With that said, there’s a great post here somewhere discussing phenylephrine and how it not only increases SVR, but also decreases venous capacitance and therefore improves RV preload which aids CO in much the same way the idea that giving additional fluid would. So again, pressors may be the best initial response but they are not the end all be all and if used as such may lead to a scenario where your numbers on the monitor look good but perfusion suffers.

 

[wickedskillz]

Who here would enroll their dad in a study where blood pressure wasn't treated until it fell below 80 systolic?!? I wouldn't. They pass of their 'control group' as standard of care, but I've never met a single person who thought a treatment threshold of sbp 80 was sufficient , especially in high risk patients. Imo they created an abnormal effect size by providing sub standard care to their 'control' arm. Useless study and shouldn't have been approved by IRB. it's like comparing a infection risk in an antibiotic coated central line vs central line placed without wearing gloves. A ****ty control will make any intervention look great!

 

[wickedskillz]

I agree with basic premise that individualized blood pressure parameters are likely more physiologically sensible considering shifts in auto regulation curves, but no need to create a shoddy study with sub standard care to make your point!!!

 

[pgg]

Who here would enroll their dad in a study where blood pressure wasn't treated until it fell below 80 systolic?!? I wouldn't. They pass of their 'control group' as standard of care, but I've never met a single person who thought a treatment threshold of sbp 80 was sufficient , especially in high risk patients. Imo they created an abnormal effect size by providing sub standard care to their 'control' arm. Useless study and shouldn't have been approved by IRB. it's like comparing a infection risk in an antibiotic coated central line vs central line placed without wearing gloves. A ****ty control will make any intervention look great!

I see people let systolics in the 80s ride all the time between induction and incision.

 

[Robotic Wis-Hipple]

I see people let systolics in the 80s ride all the time between induction and incision.

People push waaaay too much propofol quite often. You can induce a lot of people with 100-150mg, especially if they got their “2 and 2” before heading back.

 

[wickedskillz]

I see people let systolics in the 80s ride all the time between induction and incision.

Ok, I can see that. Wouldn't do it, but I can see it. Especially if map was over 60. But hypotension most likely also has a duration related effect in addition to absolute/relative value. Have you seen someone go the entire case not pushing pressors unless sbp falls below 80?

Sent from my SM-G950U using Tapatalk

 

[wickedskillz]

Ok, I can see that. Wouldn't do it, but I can see it. Especially if map was over 60. But hypotension most likely also has a duration related effect in addition to absolute/relative value. Have you seen someone go the entire case not pushing pressors unless sbp falls below 80?

Sent from my SM-G950U using Tapatalk

We're talking about case durations of minimum 2 hours, and their study had lots of people going near 4 hours, and some over that too. I don't think I've seen people let patients run in 80s for multiple hours?

Sent from my SM-G950U using Tapatalk

 

[rakotomazoto]

I see people let systolics in the 80s ride all the time between induction and incision.

Agreed. As a resident, we often get sent to do lunch breaks, bathroom breaks, research meeting breaks, etc. Can't even count how many times I walk into a room with a hypotensive patient (SBP 70-80's) and either they didn't notice or weren't concerned. This is over a wide variety of patient ages and ASA scores.

I also see a lot of excessive propofol pushing on induction. I always have some pressors (phenylephrine, ephedrine) drawn up and ready, it's like a reflexive part of drawing up propofol. It will be interesting to see how my practices change in a new environment in July.

 

[wickedskillz]

I think we're confusing transient hypotension with an entire case of running someone with an sbp goal of 80. Huge difference.

Sent from my SM-G950U using Tapatalk

 

[Psai]

I think we're confusing transient hypotension with an entire case of running someone with an sbp goal of 80. Huge difference.

Sent from my SM-G950U using Tapatalk

There's some data that says that even one 5 minute period of hypotension can lead to worsened outcomes. I like to recheck the bp and if it is still ****ty, I give a push of pressors. I've been thinking about leaning towards vasopressin as well over phenylephrine as well.

 

[dhb]

There's some data that says that even one 5 minute period of hypotension can lead to worsened outcomes.

And you believe it?

 

[wickedskillz]

I think that's a major reason why inpress has flown mostly without major criticism for their horrible control group. There's a lot of 'data' around which is essentially all retrospective analysis of records with plenty of room for confounders. This may be the first good prospective study (at least that I can find), which seems absurd considering how common this problem is

Sent from my SM-G950U using Tapatalk

 

[Hamhock]

How can you call something outdated and promote goal directed therapy in the same post with a straight face?

I could promote peri-operative GDT and not get laughed at in many CCM circles.
There is a difference between peri-operative GDT in critically ill patients and "Rivers EGDT" for patients admitted from the ED with septic shock that started hours or even days before hospitalization.

HH

 

[anbuitachi]

Simplistically
Do2=CaO2 x CO
CO = sv x hr
SV varies with preload.contractility/afterload

Giving fluid increases preload ... Increases SV ... increases CO ... increases DO2

Giving fluid decreases hgb concentration which decreases cao2. You increased one and decreased the other.

 

[vector2]

Giving fluid decreases hgb concentration which decreases cao2. You increased one and decreased the other.

This is true, but luckily the change isn't proportional or else we'd be killing people left and right with a 2l bolus. If we go back to the vastly oversimplified hgb/do2=boxcar analogy, let's say that each stroke volume contained 10 box cars in a hypovolemic patient. If we hemodiluted someone that was on the wrong side of the starling curve then each new stroke volume would only contain 9. However, if the ventricle augments SV with the newly increased preload from fluid, the new SV might go up as much as 30%, ergo even with dilution the new SV would now have increased to ((0.3*9)+9)= 12 boxcars per stroke volume.

The relationship between oxygen delivery and consumption during fluid resuscitation of hypovolemic and septic shock. - PubMed - NCBI


People much smarter than me are working on computer models to see where exactly this DO2/hemodilution/SV inflection point is, but unfortunately I can't access the paper right now

Tissue perfusion in Fluid therapy - IEEE Conference Publication