Critical Care Topic of the Month

8jimi8 said:
For sepsis we currently treat hypotension with pressors and fluid simultaneously. We don't "fill the tank" we press early. And we use levophed first. Vasopressin is our last intervention.
Click to expand...

Yeah, like I said you can do things simultaneously but the point was ignoring a previous step altogether or addressing it prematurely is to the detriment of the physiology. It's a big reason why Levophed earned the nick name "Leave 'em dead". It was used to maintain perfusion pressure instead of volume. The consequence of that was irreversible renal damage.

And the reality is that when we start a pressor, we intitially do increase the pre-load with a significant recruitment of volume from different vascular beds. From a pre hospital perspective that might be enough, but volume is critical to maintain end organ perfusion with pressor use.

The trick is determining just how much volume.
 
Vasopressin is the most powerful peripheral vasoconstrictor. It is last line for us because it increases afterload. Trauma is typically going to be your only subset of otherwise healthy patients.

Remi said:
Why would vasopressin be better for trauma than any other pressor?

And why would you use a vasopressor in a hemorrhagic patient anyway?
Click to expand...
 
8jimi8 said:
Vasopressin is the most powerful peripheral vasoconstrictor. It is last line for us because it increases afterload. Trauma is typically going to be your only subset of otherwise healthy patients.
Click to expand...
I'm quite familiar with vasopressin, but I'd like to know why it would be appropriate to use in s bleeding patient.
 
I don't disagree with some if what you said. Repeating the levophed euphemism; however is ridiculous and it reveals a stunning misunderstanding of how the drug should be used. Note I stated fluid and press simultaneously.

Making the tank smaller IS treating tachycardia. Your hypothetical patient said nothing about tachycardia. It said hypotensive. And I gave a very specific example. I didnt say we treat all hypotension. With pressors and fluid simultaneously.

E tank said:
Yeah, like I said you can do things simultaneously but the point was ignoring a previous step altogether or addressing it prematurely is to the detriment of the physiology. It's a big reason why Levophed earned the nick name "Leave 'em dead". It was used to maintain perfusion pressure instead of volume. The consequence of that was irreversible renal damage.

And the reality is that when we start a pressor, we intitially do increase the pre-load with a significant recruitment of volume from different vascular beds. From a pre hospital perspective that might be enough, but volume is critical to maintain end organ perfusion with pressor use.

The trick is determining just how much volume.
Click to expand...
 
Remi said:
I'm quite familiar with vasopressin, but I'd like to know why it would be appropriate to use in s bleeding patient.
Click to expand...


Peripheral vasoconstriction.
 
8jimi8 said:
I don't disagree with some if what you said. Repeating the levophed euphemism; however is ridiculous and it reveals a stunning misunderstanding of how the drug should be used. Note I stated fluid and press simultaneously.

Making the tank smaller IS treating tachycardia. Your hypothetical patient said nothing about tachycardia. It said hypotensive. And I gave a very specific example. I didnt say we treat all hypotension. With pressors and fluid simultaneously.
Click to expand...

Weird...getting a confrontational vibe here...just one medical pro to another talking about treating hypotension in a septic patient. Not casting judgment on your system's directives on treating these patients...just adding my 0.02 and knowledge of the physiology. Adding to the conversation for the purposes of enriching it, not criticizing.

As far as the moniker "leave 'em dead" (not really a euphemism) that was a little history lesson for anyone that wasn't aware of it. Sounds like you're not. So I'll just say that treatment for sepsis 15 or 20 years ago involved fluid restriction, not resuscitation. But patients still had hypotension from the sepsis so the treatment was...Levophed. Which was pretty effective right up to the point where patients died.

Hope that clears some of the confusion.
 
My bad. Old habits.
 
Remi said:
I'm quite familiar with vasopressin, but I'd like to know why it would be appropriate to use in s bleeding patient.
Click to expand...

Never really heard of this, and just throwing it out there for consideration...no literature at all to support it...but...

Given the morbidity and mortality of coagulopathy in trauma, and given that too much crystalloid is a contributor to that (and too much crystalloid can be more than about 2 liters)...

What if you maintained a MAP of around 65 with pressor after giving judicious crystalloid until a 1:1:1 replacement strategy could be started? It would be for a short period of time and it would cut down on the ridiculous amount of fluid that bleeding patients get in the field where no blood is available. Even where pre-hospital blood is available (assuming no FFP here) it's in PRBC form, not WB so while the problem of coagulopathy is mitigated to a degree, it is still a problem.

It is very discouraging to bring a bleeding patient to the OR that has received 4 liters of NS(ughhhh, another post) and maybe packed cells and nothing that clots blood.

Maybe a couple of different issues in the mix, but...

Thoughts?
 
E tank said:
Never really heard of this, and just throwing it out there for consideration...no literature at all to support it...but...

Given the morbidity and mortality of coagulopathy in trauma, and given that too much crystalloid is a contributor to that (and too much crystalloid can be more than about 2 liters)...

What if you maintained a MAP of around 65 with pressor after giving judicious crystalloid until a 1:1:1 replacement strategy could be started? It would be for a short period of time and it would cut down on the ridiculous amount of fluid that bleeding patients get in the field where no blood is available. Even where pre-hospital blood is available (assuming no FFP here) it's in PRBC form, not WB so while the problem of coagulopathy is mitigated to a degree, it is still a problem.

It is very discouraging to bring a bleeding patient to the OR that has received 4 liters of NS(ughhhh, another post) and maybe packed cells and nothing that clots blood.

Maybe a couple of different issues in the mix, but...

Thoughts?
Click to expand...

I think if you reflect back upon the times when someone tried to treat hypovolemic shock with pressors, you'd remember that it didn't work very well, didn't last very long, and in the end was a temporizing measure at best and perhaps a smokescreen at worst (i.e. treating the number without actually improving cardiac output and perfusion).
 
Brandon O said:
I think if you reflect back upon the times when someone tried to treat hypovolemic shock with pressors, you'd remember that it didn't work very well, didn't last very long, and in the end was a temporizing measure at best and perhaps a smokescreen at worst (i.e. treating the number without actually improving cardiac output and perfusion).
Click to expand...

Sorry, when was that?
 
Brandon O said:
Maybe not then. That has certainly been my experience.
Click to expand...

Sure, it would be if you did that for 6 or 8 or 24 hours. The question is would there be some benefit in the trade-off of mitigating the effect of a lot of crystalloid by using pressor as a stop-gap for an hour or so until blood component therapy or WB was available.
 
E tank said:
Sure, it would be if you did that for 6 or 8 or 24 hours. The question is would there be some benefit in the trade-off of mitigating the effect of a lot of crystalloid by using pressor as a stop-gap for an hour or so until blood component therapy or WB was available.
Click to expand...

I think there are certainly times when it's appropriate, or at least inevitable. I think we're just disagreeing about timeframe. For me this would be in the realm of minutes (pushing some pressor while you await blood, or, yes, a fluid bolus), basically to prevent arrest.

Pushing it much beyond that and the picture I usually see is this: the pressors rapidly escalate with little response. Before long you're maxing multiple pressors. A little after that the patient codes. This is like, a classic overnight intern thing to do in the ICU.

When you need fluid, you need fluid. (Also, as I said, I have a suspicion that even in the short-medium term you're discussing, I am not sure how much you're truly improving perfusion. If nothing's coming out of the heart, you can squeeze it all you want without helping the organs.)

I won't say I haven't seen people sitting on prolonged pressor drips for (presumed) hypovolemic shock, but in most cases I suspect there was another etiology at play.
 
E tank said:
Never really heard of this, and just throwing it out there for consideration...no literature at all to support it...but...

Given the morbidity and mortality of coagulopathy in trauma, and given that too much crystalloid is a contributor to that (and too much crystalloid can be more than about 2 liters)...

What if you maintained a MAP of around 65 with pressor after giving judicious crystalloid until a 1:1:1 replacement strategy could be started? It would be for a short period of time and it would cut down on the ridiculous amount of fluid that bleeding patients get in the field where no blood is available. Even where pre-hospital blood is available (assuming no FFP here) it's in PRBC form, not WB so while the problem of coagulopathy is mitigated to a degree, it is still a problem.

It is very discouraging to bring a bleeding patient to the OR that has received 4 liters of NS(ughhhh, another post) and maybe packed cells and nothing that clots blood.

Maybe a couple of different issues in the mix, but...

Thoughts?
Click to expand...

I suppose if you frame it as though giving a pressor is "less bad" then diluting clotting factors and platelets with large volumes of fluid and PRBC's, then there definitely might be something to the idea.

But I'm a big fan of the idea of permissive hypotension in hemorrhagic shock. I know the military research supports it pretty solidly, though it still hasn't really caught on in the civilian world. Also, I haven't seen the papers on it but I understand that Shock Trauma has had great results with their no crystalloid / hypotensive resuscitation of trauma patients. I think they do 1:1:1 only plus vasopressors, but by the time they start that protocol the patient is on the way to the OR for surgical control.

I just don't see raising the pressure in a container when the container has a leak being beneficial, if your goal is to minimize volume loss from the container. Pressure doesn't necessarily equate to flow, and I don't know if reducing flow through the cerebral and hepatic and renal vessels by constriction is any better than reducing flow as a result of volume loss, especially when you consider that higher pressure is going to mean more volume being driven to areas of less resistance - the leaks in the vessels.
 
Remi said:
I suppose if you frame it as though giving a pressor is "less bad" then diluting clotting factors and platelets with large volumes of fluid and PRBC's, then there definitely might be something to the idea.

But I'm a big fan of the idea of permissive hypotension in hemorrhagic shock. I know the military research supports it pretty solidly, though it still hasn't really caught on in the civilian world. Also, I haven't seen the papers on it but I understand that Shock Trauma has had great results with their no crystalloid / hypotensive resuscitation of trauma patients. I think they do 1:1:1 only plus vasopressors, but by the time they start that protocol the patient is on the way to the OR for surgical control.

I just don't see raising the pressure in a container when the container has a leak being beneficial, if your goal is to minimize volume loss from the container. Pressure doesn't necessarily equate to flow, and I don't know if reducing flow through the cerebral and hepatic and renal vessels by constriction is any better than reducing flow as a result of volume loss, especially when you consider that higher pressure is going to mean more volume being driven to areas of less resistance - the leaks in the vessels.
Click to expand...

Right, so the idea would be permissive hypotension with the pressor. MAP 60-65. I think lower than that, in the civilian world, ie, lots of comorbidities, would be a little dicey.
 
Brandon O said:
I think there are certainly times when it's appropriate, or at least inevitable. I think we're just disagreeing about timeframe. For me this would be in the realm of minutes (pushing some pressor while you await blood, or, yes, a fluid bolus), basically to prevent arrest.

Pushing it much beyond that and the picture I usually see is this: the pressors rapidly escalate with little response. Before long you're maxing multiple pressors. A little after that the patient codes. This is like, a classic overnight intern thing to do in the ICU.

When you need fluid, you need fluid. (Also, as I said, I have a suspicion that even in the short-medium term you're discussing, I am not sure how much you're truly improving perfusion. If nothing's coming out of the heart, you can squeeze it all you want without helping the organs.)
.
Click to expand...

Well, this would require situational awareness.
 
MonkeyArrow said:
This is actually a fairly concise clinical review I read a few weeks ago on the topic:
http://www.joacp.org/article.asp?is...olume=33;issue=1;spage=3;epage=8;aulast=Gupta

However, the quality of evidence behind a lot of the recommendations made is poor since this topic has not been recently studied.
Click to expand...

If there is one thing that strikes me in a conversation about guidelines, whether they have to do with sepsis or trauma or blood sugar, it is that the addition of 5-10 years makes them nearly unrecognizable from their previous iteration. That isn't to say that what we have isn't useful, it's just that it's important to recognize that it isn't dogma.

Kind of a no brainer, but that realization took a couple of decades for me.
 
You must log in or register to reply here.
Back
Top