Critical Care Topic of the Month

Akulahawk

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I'm not the smartest guy either, but I don't think you quite understand this.
Finally we get somewhere. So then, in theory your basically saying two things (that I'm not quite sure I'd agree with at this point) :

1.we'd rather see impaired gas exchange at the cellular level lending toward the direction of acidosis (i.e CO2 going up and O2 dropping - > as opposed to increased fluid loss? And,
You seem to have this reversed. As fluid loss continues, there'll be impaired gas exchange at the cellular level because blood flow slows at the capillary beds because... there's no volume. Yes, we want to stabilize the volume but as long as the leak is still there, anything we do to increase flow is going to keep the leak open.
2. how do you suppose this mitigates the tendency to develop a rather profound tachy (and hence possibly put ourselves in a not-so-good place) IF the "permissive" hypotension (as it has been put) turns into profound and uncontrolled hypotension to where we see a profound ventricular compenstation? (which is increasingly more likely over time as shock eventually sets in.) Would seem less problematic to me just to keep a relatively normalized pressure that perhaps wouldn't quite be labeled "hypotension" say per, despite being lower as compared to the majority norm. (say around 100/70 or so) and just keep up with the blood product infusions, if you ask me.

And to clarify what I mean by aldosterone dump, aldosterone is one of the precursors of adrenaline/epinephrine. Hence, Adrenaline dump = Aldosterone and DHEA dump as conversion to adrenaline/epinephrine takes place.
The point of permissive hypotension is to allow the body's clotting ability to seal off leaks while keeping the MAP high enough to perfuse vital organs while also keeping it low enough to not pop clots off those leaks. What's been found is that keeping the patient a bit dry is far more helpful than chasing even a low-normal BP. In the field we don't usually have access to whole blood or access to platelets and FFP so increasing volume via crystalloids (any of them) dilute the body's clotting factors setting up a coagulopathy that can ultimately be lethal, all because you want to maintain blood flow at the capillary beds.

Most of the body can tolerate low perfusion states for a few hours. Certain organs can't. The body protects those. Given a choice between trying to maintain a certain BP using crystalloids and keeping the MAP just high enough to perfuse the heart, lungs, and brain I'd go with the second option. Sure I'll plant large bore IV catheters if I can, but that's not for the purpose of flooding the patient with fluids that don't support clotting or oxygen transport. I'm going to give very small amounts of fluid, stop any leaks I can, and get the patient to a surgeon that can do damage control to stop the leaks. Until the leaks are sealed, keep the patient dry. If the patient exanguinates in the time it takes me to get from the scene to the OR despite what I do to maintain core circulation, the patient wasn't going to survive anyway. Turning the blood into "Kool-aid" doesn't help when you get a patient that's injured this profoundly.

Oh, and pressors may be useful to a point, but you don't want to be so generous as to bring the BP up to something approaching normal because that pops clots, restarts hemorrhage, and now you've caused your patient to lose blood that used to be available. You end up emptying the tank by squeezing it to maintain a number and when you can't squeeze the tank any further, things really go south fast.

Since you're thinking we can keep up with the leaks by doing blood infusions, how much blood do you have on hand in the field? I mean whole blood or PRBCs, FFP and platelets... do you have enough to keep up with a leak that won't seal because you're keeping the BP up?

The better trauma facilities don't have their EDs do much of anything... including blood transfusions because of the above as that wastes blood that belongs to the patient AND transfused blood. By the time the patient hits the OR, they're well out of our hands and in the hands of those that do trauma resus. Those of us that work in the field or in the ED aren't experts at this.
 

Carlos Danger

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Finally we get somewhere. So then, in theory your basically saying two things (that I'm not quite sure I'd agree with at this point) :

1.we'd rather see impaired gas exchange at the cellular level lending toward the direction of acidosis (i.e CO2 going up and O2 dropping - > as opposed to increased fluid loss? And,

2. how do you suppose this mitigates the tendency to develop a rather profound tachy (and hence possibly put ourselves in a not-so-good place) IF the "permissive" hypotension (as it has been put) turns into profound and uncontrolled hypotension to where we see a profound ventricular compenstation? (which is increasingly more likely over time as shock eventually sets in.) Would seem less problematic to me just to keep a relatively normalized pressure that perhaps wouldn't quite be labeled "hypotension" say per, despite being lower as compared to the majority norm. (say around 100/70 or so) and just keep up with the blood product infusions, if you ask me.

And to clarify what I mean by aldosterone dump, aldosterone is one of the precursors of adrenaline/epinephrine. Hence, Adrenaline dump = Aldosterone and DHEA dump as conversion to adrenaline/epinephrine takes place.
Look, no one is going to take the time to discuss this with you if you are going to argue with everything everyone says and keep muddying up the discussion with irrelevant and incorrect statements.

If you don't want to insist that it's better to flood bleeding patients with crystalloid when pretty much all the research done on the topic clearly says otherwise, fine. I'm not going to argue with you about it.

I suggest you learn some basic physiology, read about some critical care principles and damage control resuscitation and the evidence behind it, and gain some experience taking care of sick patients.

Then we can have a discussion on this stuff.
 
OP
VFlutter

VFlutter

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Finally we get somewhere. So then, in theory your basically saying two things (that I'm not quite sure I'd agree with at this point) :

1.we'd rather see impaired gas exchange at the cellular level lending toward the direction of acidosis (i.e CO2 going up and O2 dropping - > as opposed to increased fluid loss? And,

2. how do you suppose this mitigates the tendency to develop a rather profound tachy (and hence possibly put ourselves in a not-so-good place) IF the "permissive" hypotension (as it has been put) turns into profound and uncontrolled hypotension to where we see a profound ventricular compenstation? (which is increasingly more likely over time as shock eventually sets in.) Would seem less problematic to me just to keep a relatively normalized pressure that perhaps wouldn't quite be labeled "hypotension" say per, despite being lower as compared to the majority norm. (say around 100/70 or so) and just keep up with the blood product infusions, if you ask me.

And to clarify what I mean by aldosterone dump, aldosterone is one of the precursors of adrenaline/epinephrine. Hence, Adrenaline dump = Aldosterone and DHEA dump as conversion to adrenaline/epinephrine takes place.
Patient's survive surgery with aortic cross clamp times significantly longer then most trauma patients will be hypotensive. Mild acidosis is easy to manage and more tolerable than significant coagulopathy.

Either tachycardic with a poor SV or normal HR with a normal SV its still the same cardiac output. Most patients can tolerate the increase in oxygen demand. You will likely never be able to give enough NS to mitigate compensatory tachycardia in a trauma patient.
 

bakertaylor28

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Either tachycardic with a poor SV or normal HR with a normal SV its still the same cardiac output. Most patients can tolerate the increase in oxygen demand. You will likely never be able to give enough NS to mitigate compensatory tachycardia in a trauma patient.
But yet it would seem that tachy plus increased O2 demand is just going to result in the tachy gradually increasing, as a infinite loop, since increased demand feeds the tachy which in turn feeds the increased demand of the tachy itself. So what might limit the tachy as to keep things within a sinus rhthm. If my mind serves me right I remember hearing something in an ACLS class years ago that if rate increases enough that sinus tachy will always turn into SVT or V-tach.
 

bakertaylor28

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Look, no one is going to take the time to discuss this with you if you are going to argue with everything everyone says and keep muddying up the discussion with irrelevant and incorrect statements.

If you don't want to insist that it's better to flood bleeding patients with crystalloid when pretty much all the research done on the topic clearly says otherwise, fine. I'm not going to argue with you about it.

I suggest you learn some basic physiology, read about some critical care principles and damage control resuscitation and the evidence behind it, and gain some experience taking care of sick patients.

Then we can have a discussion on this stuff.
Oh, so you never question the "research"? Interesting, considering the fact that if we never challenged the current thinking we'd still think the world to be Flat. On the upside- Apollo 1, Challenger, and Columbia wouldn't have happened either. There's an old yet wise expression- When you THINK you have the answers, keep asking WHY. Eventually, you will find a question that doesn't come with a pre-packaged answer.

Oh, and failing to question the research is not always a good idea either- as it often has this way of turning out to be wrong for non-obvious reasons. Take for example ACLS protocol- did we change things because "the research proved the research wrong"? OR (more likely) did we change things because some "idiot" did it wrong and got (pleasantly) unexpected results? OR perhaps we have a third (more remote) possibility- someone acted on a predefined hypothesis in the moment after conventional wisdom failed. I can see you have yet to figure out that logic is limited where not challenged.
 

Akulahawk

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But yet it would seem that tachy plus increased O2 demand is just going to result in the tachy gradually increasing, as a infinite loop, since increased demand feeds the tachy which in turn feeds the increased demand of the tachy itself. So what might limit the tachy as to keep things within a sinus rhthm. If my mind serves me right I remember hearing something in an ACLS class years ago that if rate increases enough that sinus tachy will always turn into SVT or V-tach.
Why should I limit the rate to a sinus rhythm? Why would Sinus Tach always convert to SVT or VTach? Here's a hint: it doesn't. Damage control resus accepts that we're not fully resuscitating a patient fully back to normal physiology.

Here's the other thing you're missing: trauma resus isn't an ACLS situation. In ACLS, the heart is damaged. In most trauma, the heart is fairly healthy and something else is the problem. Most of the body's tissues can tolerate zero flow for hours. What kind of damage control is done in the ED? REBOA or cross clamping (if those procedures are needed) and off the patient goes to OR. One of the hospitals I used to take patients to (no longer exists, unfortunately) was a Level II Trauma Center. They routinely had faster door to OR times than either of the Level I facilities in the region, and those other facilities had fairly short times... partly this was due to two things. One is the Trauma OR was directly connected to the ED. Care to guess what the other reason why their door to OR times were so short?
 

Akulahawk

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Oh, so you never question the "research"? Interesting, considering the fact that if we never challenged the current thinking we'd still think the world to be Flat. On the upside- Apollo 1, Challenger, and Columbia wouldn't have happened either. There's an old yet wise expression- When you THINK you have the answers, keep asking WHY. Eventually, you will find a question that doesn't come with a pre-packaged answer.

Oh, and failing to question the research is not always a good idea either- as it often has this way of turning out to be wrong for non-obvious reasons. Take for example ACLS protocol- did we change things because "the research proved the research wrong"? OR (more likely) did we change things because some "idiot" did it wrong and got (pleasantly) unexpected results? OR perhaps we have a third (more remote) possibility- someone acted on a predefined hypothesis in the moment after conventional wisdom failed. I can see you have yet to figure out that logic is limited where not challenged.
I have followed trauma care for about 30 years now. I've seen many changes over those 30 years, all based on research and real-world application. Just 30 years ago the conventional wisdom was that we flood trauma patients with crystalloids to maintain blood pressure. We were turning blood into Kool-Aid but the heart had something to pump, even though it wasn't carrying oxygen. Just 20 years ago we started to revise our thought to let's limit the fluids boluses to maintain a BP of around 90 systolic. We were doing better but we still lost many patients and the blood was less like Kool-Aid. Thanks to military experiences, current practices include tourniquet, rapid cross-clamping, REBOA, or other similar measures, and keeping the patient dry until damage control surgery is performed. By the way, none of this research was done under the AHA, and therefore isn't a part of ACLS. It's (hopefully) getting into ITLS and it's certainly a part of PHTLS in their TCCC stuff.
 

VentMonkey

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@Akulahawk, @Remi, and @Chase thanks for keeping the thread topic on track and "medic-friendly".

Are any of your guys' respective areas actively utilizing REBOA? I know this was trending heavily about a year or two ago. I'm curious to obtain any current literature, or firsthand knowledge with said procedure in the traumatic resuscitation population.
 
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VFlutter

VFlutter

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@Akulahawk, @Remi, and @Chase thanks for keeping the thread topic on track and "medic-friendly".

Are any of your guys' respective areas actively utilizing REBOA? I know this was trending heavily about a year or two ago. I'm curious to obtain any current literature, or firsthand knowledge with said procedure in the traumatic resuscitation population.
Both of the level one trauma centers we frequently fly into have REBOA but only one seems to be aggressive with utilizing it. The hospital is a C-STARS center so I am sure that plays into their familiarity with it. Recently had them place one intra-arrest on a trauma patient we brought in with pelvic fracture and hemorrhage. It is usually utilized for non-compressible sub diaphragmatic hemorrhage with impending arrest and is a great alternative to thoracotomy and cross clamp. I have yet to see it outside of the level one centers but I think it will good once referring facilities start to utilize it to stabilize prior to transport. The literature is there for military medicine and austere environments but I think there is a lack of research for its use in-hospital and urban areas.
 

bakertaylor28

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I'm not the smartest guy either, but I don't think you quite understand this.

You seem to have this reversed. As fluid loss continues, there'll be impaired gas exchange at the cellular level because blood flow slows at the capillary beds because... there's no volume. Yes, we want to stabilize the volume but as long as the leak is still there, anything we do to increase flow is going to keep the leak open.

The point of permissive hypotension is to allow the body's clotting ability to seal off leaks while keeping the MAP high enough to perfuse vital organs while also keeping it low enough to not pop clots off those leaks. What's been found is that keeping the patient a bit dry is far more helpful than chasing even a low-normal BP. In the field we don't usually have access to whole blood or access to platelets and FFP so increasing volume via crystalloids (any of them) dilute the body's clotting factors setting up a coagulopathy that can ultimately be lethal, all because you want to maintain blood flow at the capillary beds.

Most of the body can tolerate low perfusion states for a few hours. Certain organs can't. The body protects those. Given a choice between trying to maintain a certain BP using crystalloids and keeping the MAP just high enough to perfuse the heart, lungs, and brain I'd go with the second option. Sure I'll plant large bore IV catheters if I can, but that's not for the purpose of flooding the patient with fluids that don't support clotting or oxygen transport. I'm going to give very small amounts of fluid, stop any leaks I can, and get the patient to a surgeon that can do damage control to stop the leaks. Until the leaks are sealed, keep the patient dry. If the patient exanguinates in the time it takes me to get from the scene to the OR despite what I do to maintain core circulation, the patient wasn't going to survive anyway. Turning the blood into "Kool-aid" doesn't help when you get a patient that's injured this profoundly.

Oh, and pressors may be useful to a point, but you don't want to be so generous as to bring the BP up to something approaching normal because that pops clots, restarts hemorrhage, and now you've caused your patient to lose blood that used to be available. You end up emptying the tank by squeezing it to maintain a number and when you can't squeeze the tank any further, things really go south fast.

Since you're thinking we can keep up with the leaks by doing blood infusions, how much blood do you have on hand in the field? I mean whole blood or PRBCs, FFP and platelets... do you have enough to keep up with a leak that won't seal because you're keeping the BP up?

The better trauma facilities don't have their EDs do much of anything... including blood transfusions because of the above as that wastes blood that belongs to the patient AND transfused blood. By the time the patient hits the OR, they're well out of our hands and in the hands of those that do trauma resus. Those of us that work in the field or in the ED aren't experts at this.
That's certainly one way of looking at things... which perhaps is workable as a strategy , BUT IF we think out / work out the ratio of blood products to Fluids in order to acceptably cancel out the hemo-dilution effect ENOUGH to get the job done with hopefully transient effects, combined with decreased transport time, we're quite possibly in a better place overall, perhaps with a bit more time on our side AND a "B" plan, than taking permissive hypotension upfront, getting a clot formation if we're lucky, and then at the slightest raise of pressure, having the inherent possible risk of a rather large and catastrophic clot embolism.
 

bakertaylor28

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The point on this is being that the "studies" really show nothing, because they don't control for the underlying trauma severity as an absolute- (This can be subjective at best in establishing criteria to attempt to objectify the severity of a given case via comparison.) Therefore, they can't show method A Vs. Method B to be anything BUT a mere correlation to outcome. Hence, it becomes that the research isn't well controlled, and in reality is quite meaningless beyond casual correlation.
 

Akulahawk

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That's certainly one way of looking at things... which perhaps is workable as a strategy , BUT IF we think out / work out the ratio of blood products to Fluids in order to acceptably cancel out the hemo-dilution effect ENOUGH to get the job done with hopefully transient effects, combined with decreased transport time, we're quite possibly in a better place overall, perhaps with a bit more time on our side AND a "B" plan, than taking permissive hypotension upfront, getting a clot formation if we're lucky, and then at the slightest raise of pressure, having the inherent possible risk of a rather large and catastrophic clot embolism.
That ratio has already been pretty well worked out. Whole blood or 1:1:1 PRBC:FFP:platelets. Crystalloid and colloid fluids that aren't what I just mentioned in the previous sentence will dilute the blood its clotting factors. We do have a large body of ideas about what doesn't work (flooding the patient with fluids) and a large body of ideas that do work - permissive hypotension in the field with hemorrhage control beginning in the field along with beginning WB or 1:1:1 transfusions upon arrival at a trauma center with rapid movement to an OR for damage control surgery. War teaches us a LOT about trauma. Unfortunately we have had a LOT of experience with wartime conditions, more than a decade of it, but our trauma care as advanced quite rapidly because of it.
 

TXmed

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Both of the level one trauma centers we frequently fly into have REBOA but only one seems to be aggressive with utilizing it. The hospital is a C-STARS center so I am sure that plays into their familiarity with it. Recently had them place one intra-arrest on a trauma patient we brought in with pelvic fracture and hemorrhage. It is usually utilized for non-compressible sub diaphragmatic hemorrhage with impending arrest and is a great alternative to thoracotomy and cross clamp. I have yet to see it outside of the level one centers but I think it will good once referring facilities start to utilize it to stabilize prior to transport. The literature is there for military medicine and austere environments but I think there is a lack of research for its use in-hospital and urban areas.
Both level 1s in my area perform it. Idk about ben taub but a hermann ER doc told me they perform anywhere from 1-3 a month. Ive also heard the folks at baltimore shock trauma hoave the process down to a quick simple procedure.
 

CANMAN

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Both level 1s in my area perform it. Idk about ben taub but a hermann ER doc told me they perform anywhere from 1-3 a month. Ive also heard the folks at baltimore shock trauma hoave the process down to a quick simple procedure.
We are doing about the same numbers, if not a little more in D.C. where I work, and Baltimore Shock Trauma is likely seeing higher numbers than we are. We get 1-2 GSW a day, they see 3-5 depending on the day. The entire city has become a warzone. We have had two incidents of balloon ruptures in the REBOA kits, and they are trying to drill down the RCA on those patients. Both ended up getting cracked and cross-clamped. We had gotten away from dropping in crash central line/cordis in our trauma bays, so the initial ramp up with REBOA again took a little bit, but the doc's are back in the swing of things and can accomplish it fairly quickly now depending on who the trauma fellow is.

Chase, I don't know about the referral pattern where you fly, but other than level 1's I doubt we ever see another facility do REBOA's around here. Most of our places we retrieve from will not even put in an art line for patient's on pressors smh.
 
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VFlutter

VFlutter

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Chase, I don't know about the referral pattern where you fly, but other than level 1's I doubt we ever see another facility do REBOA's around here. Most of our places we retrieve from will not even put in an art line for patient's on pressors smh.
Ya it's a far stretch but it would be nice if it eventually made it's way to smaller facilities. To me that is where REBOA makes the most sense as a relatively simple percutanous option when defintive surgery is not immediately accessible and they are not willing to do a thoracotomy. That's somewhat the military model as a bridge to definitive treatment.
 

TXmed

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@CANMAN is the reboa able to monitor arterial pressures now?

Like if you decide not to inflate the baloon are you able to use it as an art line ?
 
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VFlutter

VFlutter

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@CANMAN is the reboa able to monitor arterial pressures now?

Like if you decide not to inflate the baloon are you able to use it as an art line ?
Not sure if all the kits are standardized but i think they use a 12fr sheath as the introducer so assuming they removed the baloon it could be capped and transduced like any other sheath. But a 12fr sheath is significantly larger, and shorter, then the standard long 4fr catheters they commonly use for femoral arterial lines so I'm not sure how great the waveform would be. Obviously better then nothing. You could transduce the old school IABP introducers without issues which were 7-9fr.

I wouldn't be surprised if they eventually become fiber optic and able to transduce pressures as the technology evolves. I mean isn't it pretty much an IABP catheter you leave inflated...
 

TXmed

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Dont take my word on this, but i beleive they have been able to use a 7fr now, vascular damage was a significant concern in the earlier stages.

And yea but less length and more width. Just straight occlusion.
 

CANMAN

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Dont take my word on this, but i beleive they have been able to use a 7fr now, vascular damage was a significant concern in the earlier stages.

And yea but less length and more width. Just straight occlusion.
Correct. Our kits are 7fr and 64cm in length, with two ports, one for balloon occlusion and the other for transducing an arterial waveform.
 

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