# Critical Care Topic of the Month



## VFlutter (Mar 27, 2017)

Just brain storming as I sit here doing a write up about balloon pumps and browsing the forum. This forum really is great place to learn with providers of various levels and expertise. It would be kind of cool to have a monthly critical care topic where members could discuss, educate, ask questions etc. It would nice to liven up the HEMS/Critical Care section and maybe work towards building a sticky or resource section. 

Not sure how it would work necessarily or how topics would be chosen or voted but just thought I would throw it out there.


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## DesertMedic66 (Mar 27, 2017)

Since I am just now starting to get into critical care I really like this idea.


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## TransportJockey (Mar 27, 2017)

I like the idea a lot 

Sent from my SM-N920P using Tapatalk


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## NysEms2117 (Mar 28, 2017)

i'm not a critical care provider but i work on a critical care rig, so I can talk about equipment and things like that, I'm down to learn


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## VentMonkey (Mar 28, 2017)




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## StCEMT (Mar 29, 2017)

I might not work in the Critical Care world, but I'd love to learn a thing or two from whatever topics would come from this.


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## GMCmedic (Mar 29, 2017)

Im in. As soon as I can hold an illinois cert again I want to fly. (36 months to get it back if you let it lapse. I didnt do anything illegal)

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## VFlutter (Mar 29, 2017)

GMCmedic said:


> Im in. As soon as I can hold an illinois cert again I want to fly. (36 months to get it back if you let it lapse. I didnt do anything illegal)
> 
> Sent from my SAMSUNG-SM-G920A using Tapatalk



Illinois is the worst. Took me a while to get my RN license. And now I work on the IL side


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## GMCmedic (Mar 29, 2017)

Chase said:


> Illinois is the worst. Took me a while to get my RN license. And now I work on the IL side


It is. I only let it go cause I couldnt get in touch with our illinois medical director and Its not required at my current job. 

Plus I didnt want to keep track of my hours for 4 years at a time. 

Sent from my SAMSUNG-SM-G920A using Tapatalk


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## E tank (Mar 30, 2017)

I'll throw a topic out there. Maybe should be a new thread but someone can move it if needed. 

In any patient that is hypotensive (MAP less than 65ish), what specific steps do folks move through to systematically treat and/or advise receiving hospital of needs of the patient on arrival?


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## VFlutter (Mar 30, 2017)

E tank said:


> I'll throw a topic out there. Maybe should be a new thread but someone can move it if needed.
> 
> In any patient that is hypotensive (MAP less than 65ish), what specific steps do folks move through to systematically treat and/or advise receiving hospital of needs of the patient on arrival?



1. Assess my patient. Do they look adequately perfused? Mental status, skin quality, ETCO2, etc. Yes, proceed to number 2.  No, proceed to number 3. 

2. Assess my equipment. Is this a NIBP or Arterial line? Is my patients arm bent or in an awkward position? Did my transducer fall on the floor? Retake, re-zero, confirm manually. 

3.  Critically think. Is this unexpected or a downward trend? Is your patient peri-arrest? Push dose pressors to buy time. What is the patients disease process? What medications are they on? What do they need to be on? When in doubt give volume. Add pressors and inotropes as need. Correct arrhythmias if indicated. 

4. Re-evaluate your interventions 

5. Contact hospital and med control. 


17. Grab the Methlyene Blue.


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## StCEMT (Apr 1, 2017)

E tank said:


> I'll throw a topic out there. Maybe should be a new thread but someone can move it if needed.
> 
> In any patient that is hypotensive (MAP less than 65ish), what specific steps do folks move through to systematically treat and/or advise receiving hospital of needs of the patient on arrival?


With the other week being the most recent instance. this was the gist...

1. Vitals. Pulse, confirm pressure with a manual verification, mental status, perfusion, MAP estimate.
2. IV accessx2 and fluids started on scene.
3. Causes? None stood out at the time, but her history was beyond anything I had heard of. Didn't seem to be cardiac related. If so, treat accordingly.
4. Reassess. Think about pressors, but city transports are usually done by the time I get any meaningful amount of fluids in someone.
2-5. Anytime. Call a doc and get an opinion on the best treatment path or for permission for something I want to do. In her case, fluids were fine for the 5 minute drive. If someone looks like they are spiraling before I can even leave, it's not in my protocols to use push dose pressors or other temporizing measures. Fluids only. This would be where I'd fast track a bit and call sooner rather than later on the advice/permission and hopefully get options.


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## E tank (Apr 1, 2017)

Here's one way to look at it that can be useful. These steps need to be taken in order: If you have hypotension that you want to treat

1. HR -Too slow? Fix that first

2. Rhythm - not perfusing? Fix that next.

3.Pre-load - volume. Depending on your setting you may have an A line or be able to assess pulse wave variation in ventilated patients. History  and assessment will help determine if there have been volume losses.

4. After load -  vasomotor tone. Pick one... Phenylepherine, vasopressin then norepinephrine

5. Contractility - Epinepherine

So, the point here is not to give a pressor before you have decided that volume isn't the problem anymore or at all. Likewise, you wouldn't want to start an inotrope before you determined that the vasomotor tone was OK. Obviously, you can do many of these things simultaneously. But they should be taken in that order.


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## VFlutter (Apr 1, 2017)

A few random thoughts. In catecholamine depleted and severely acidotic patients Vasopressin is very effective. Although controversial if your patient is known to be severely acidotic and is non-responsive to vasopressors then it may be one of the few times IV push Bicarb is necessary, it should improve hemodynamics briefly. 

Calcium can be very helpful as well especially if your patient has been massively transfused.

Epinephrine drips can be extremely useful when used correctly. Post ROSC and Massive PEs  (That RV squeeeze) 

If you are unfortunate to not have Push Dose Pressors, like me, then initiate a Levo/Epi drip prior to intubating a shocky patient. Avoid peri-intubation hypotension and arrest.


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## E tank (Apr 1, 2017)

Chase said:


> A few random thoughts. In catecholamine depleted and severely acidotic patients Vasopressin is very effective. Although controversial if your patient is known to be severely acidotic and is non-responsive to vasopressors then it may be one of the few times IV push Bicarb is necessary, it should improve hemodynamics briefly.
> 
> Calcium can be very helpful as well especially if your patient has been massively transfused.
> 
> Epinephrine drips can be extremely useful when used correctly. Post ROSC and Massive PEs  (That RV squeeeze)



All good points. I give a half unit vasopressin the first time to see what the response will be. Sometimes it works too well. And as far as I'm concerned, giving bicarb to make catechol drips work better isn't controversial. It works. You just need to make sure that you are giving adequate ventilation for the added CO2 load.


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## TXmed (Apr 1, 2017)

Im curious to knkw more about what people are using vasopressin drips for now and days (other than 2nd line in sepsis) i recently listened to a podcast from flight bridge that vasopressin may be a good drug to use in traumatic shock.


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## VFlutter (Apr 1, 2017)

Vasopressin is great for any shock that involves derrangment of Adrenergic receptors. As mentioned acidosis severely reduces receptors affinity for catecholamines. Also like how Milrinone works in similar situations.


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## E tank (Apr 2, 2017)

TXmed said:


> Im curious to knkw more about what people are using vasopressin drips for now and days (other than 2nd line in sepsis) i recently listened to a podcast from flight bridge that vasopressin may be a good drug to use in traumatic shock.



So, the stock answer is refractory vasoplegia, but that doesn't mean a whole lot to folks. It implies that you've gone through phenylephrine and norepi and you still need something that isn't an inotrope. One that I can think of right off the bat is a patient on an ACE inhibitor or ARB that is having some kind of insult that is affecting their blood pressure. 

These drugs make the patient uniquely refractory to more conventional efforts at restoring vasomotor tone....thus Vasopressin.


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## 8jimi8 (May 5, 2017)

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.



E tank said:


> Here's one way to look at it that can be useful. These steps need to be taken in order: If you have hypotension that you want to treat
> 
> 1. HR -Too slow? Fix that first
> 
> ...


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## Carlos Danger (May 5, 2017)

TXmed said:


> Im curious to knkw more about what people are using vasopressin drips for now and days (other than 2nd line in sepsis) i recently listened to a podcast from flight bridge that vasopressin may be a good drug to use in traumatic shock.


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

And why would you use a vasopressor in a hemorrhagic patient anyway?


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## E tank (May 5, 2017)

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.



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.


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## 8jimi8 (May 5, 2017)

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?


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## Carlos Danger (May 5, 2017)

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.


I'm quite familiar with vasopressin, but I'd like to know why it would be appropriate to use in s bleeding patient.


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## 8jimi8 (May 5, 2017)

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.


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## 8jimi8 (May 5, 2017)

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.




Peripheral vasoconstriction.


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## E tank (May 5, 2017)

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.



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.


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## 8jimi8 (May 5, 2017)

My bad. Old habits.


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## 8jimi8 (May 5, 2017)

8jimi8 said:


> My bad. Old habits.


I appreciate the deescalation. I have enough people to argue with already.


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## E tank (May 5, 2017)

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.



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?


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## Brandon O (May 5, 2017)

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)...
> 
> ...



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).


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## E tank (May 5, 2017)

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).



Sorry, when was that?


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## Brandon O (May 5, 2017)

E tank said:


> Sorry, when was that?



Maybe not then. That has certainly been my experience.


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## E tank (May 5, 2017)

Brandon O said:


> Maybe not then. That has certainly been my experience.



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.


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## Brandon O (May 5, 2017)

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.



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.


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## Carlos Danger (May 5, 2017)

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)...
> 
> ...



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.


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## E tank (May 5, 2017)

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.



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.


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## E tank (May 5, 2017)

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.
> 
> ...



Well, this would require  situational awareness.


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## MonkeyArrow (May 5, 2017)

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.


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## E tank (May 6, 2017)

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.



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.


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## Medic27 (Aug 10, 2017)

Definitely interested, I love learning.


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## bakertaylor28 (Aug 10, 2017)

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.
> 
> 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.



The thing is that without proper load, pressing isn't going to do much anyways. The "leak" in the system will self-limit the net effect of the pressor at some point. Where we're going to have our first major problem however, is in that we are also diluting sodium and potassium with the massive amounts of fluid. (least we forget: hypokalemia / hyponatremia = eventual arrhythmia. its a matter of WHEN not IF) The problem becomes since total load can only be estimation at best (and most probably  a crappy estimation.) We really have no way of calculating the when.  It will then become that our real solution in trauma cases is blood products or electrolytes or electrolytes plus blood products depending upon the given state.  If we've infused more than a pre-defined amount of fluids then we need to be dealing with electrolytes in some way or another. (and with particularly large amounts of fluids we might be dealing with this problem sooner than later.)   Really either way we go, until we plug the hole, we're going to have trade-offs involved that we're just going to have to learn to deal with in turn. Hence, we need to be thinking in more of a holistic approach to this as opposed to limiting ourselves to any one technique.


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## E tank (Aug 10, 2017)

bakertaylor28 said:


> The thing is that without proper load, pressing isn't going to do much anyways. The "leak" in the system will self-limit the net effect of the pressor at some point. Where we're going to have our first major problem however, is in that we are also diluting sodium and potassium with the massive amounts of fluid. (least we forget: hypokalemia / hyponatremia = eventual arrhythmia. its a matter of WHEN not IF) The problem becomes since total load can only be estimation at best (and most probably  a crappy estimation.) We really have no way of calculating the when.  It will then become that our real solution in trauma cases is blood products or electrolytes or electrolytes plus blood products depending upon the given state.  If we've infused more than a pre-defined amount of fluids then we need to be dealing with electrolytes in some way or another. (and with particularly large amounts of fluids we might be dealing with this problem sooner than later.)   Really either way we go, until we plug the hole, we're going to have trade-offs involved that we're just going to have to learn to deal with in turn. Hence, we need to be thinking in more of a holistic approach to this as opposed to limiting ourselves to any one technique.



I've never had the experience of giving so much crystalloid (or colloid) that I ended up causing a dilutional hypokalemia or natremia, especially given that we use balanced salt solution. I have seen hyperchloremic acidosis from the days when we used to poison patients with NS. A lot of IV fluid is not really the way we treat most hypotensive trauma patients anyway, at least we shouldn't be. What is far more likely and common is hemodilution and dilutional coagulopathy.


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## bakertaylor28 (Aug 10, 2017)

E tank said:


> I've never had the experience of giving so much crystalloid (or colloid) that I ended up causing a dilutional hypokalemia or natremia, especially given that we use balanced salt solution. I have seen hyperchloremic acidosis from the days when we used to poison patients with NS. A lot of IV fluid is not really the way we treat most hypotensive trauma patients anyway, at least we shouldn't be. What is far more likely and common is hemodilution and dilutional coagulopathy.



True, that. UNLESS the patient had hypo- kalemia / -natremia to begin with. (curiously, I've heard of it happening, though never personally seen it.)  I was more speaking in hypothetical / theoretical terms for some of the Basics on here that aren't quite familiar with some of the theory that comes behind these things. In theory, given pump dynamics, pressors should decrease the need for load and in turn load should decrease the need for pressors. Therefore, Fluid Replacement (preferably NOT NS because of the Cloride Ion) plus Blood Products Plus  pressors, in basic theory.


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## Carlos Danger (Aug 11, 2017)

bakertaylor28 said:


> The thing is that without proper load, pressing isn't going to do much anyways.


Actually it is a myth that the best way to increase preload is to give volume. Because the venous side of the vascular circuit is so "soft" and elastic, it has great capacity for storing volume with minimal increase in pressure. Hence the sometimes-used term "capacitance vessels". 

A much more efficient way to increase preload is to tighten the venous side up with vasopressors, and then you have the added benefit of avoiding hemo dilution and electrolyte overload.



bakertaylor28 said:


> The "leak" in the system will self-limit the net effect of the pressor at some point.



Doing anything to raise BP (fluid loading OR vasopressors) will probably increase bleeding. That's why permissive hypotension is used by the most progressive trauma programs.


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## bakertaylor28 (Aug 11, 2017)

Remi said:


> Actually it is a myth that the best way to increase preload is to give volume. Because the venous side of the vascular circuit is so "soft" and elastic, it has great capacity for storing volume with minimal increase in pressure. Hence the sometimes-used term "capacitance vessels".
> 
> A much more efficient way to increase preload is to tighten the venous side up with vasopressors, and then you have the added benefit of avoiding hemo dilution and electrolyte overload.
> 
> ...



But then the  question becomes (for the sake of teaching the basics) , how then do we keep a decent ventricular load, as to keep control of the increased rate? It's going to seem like we're going to see an increased ventricular rate (i.e. sinus tach or at least some form or another of a tachy arrhythmia, for sake of the basic pont.) If we allow low pressure, which also in turn is going to increase loss, since we know that low pressure = native increased rate if we are to attempt to maintain homeostasis and keep flow as close to the same as possible. Thus, it would seem that low pressure might not be the best idea in the world, under the circumstances.


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## Carlos Danger (Aug 11, 2017)

bakertaylor28 said:


> But then the  question becomes (for the sake of teaching the basics) , *how then do we keep a decent ventricular load, as to keep control of the increased rate?* It's going to seem like we're going to see an increased ventricular rate (i.e. sinus tach or at least some form or another of a tachy arrhythmia, for sake of the basic pont.) If we allow low pressure, which also in turn is going to increase loss, since we know that low pressure = native increased rate if we are to attempt to maintain homeostasis and keep flow as close to the same as possible. Thus, it would seem that low pressure might not be the best idea in the world, under the circumstances.



I don't know what you are talking about.


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## VFlutter (Aug 11, 2017)

bakertaylor28 said:


> But then the  question becomes (for the sake of teaching the basics) .



I'm confused who you are trying to "teach the basics" to? Or are you trying to teach the EMT-Basics of the site? Either way, you sould probably have logical train of thought. That post makes no sense what so ever


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## VentMonkey (Aug 11, 2017)

Chase said:


> I'm confused who you are trying to "teach the basics" to? Or are you trying to teach the EMT-Basics of the site? Either way, you sould probably have logical train of thought. That post makes no sense what so ever


I'd wondered the same. And if he is trying to teach the basics he sure knows how to come across...

Perhaps he meant teach fundamentals //shrugs//. If you were in fact referring to the EMT-basics on this site, @bakertaylor28 you once again sound extremely arrogant, and condescending. 

Congrats though, you've managed to stump two of the more formally educated forum members on here; both of whom manage to get their points across in non-jargon filled rants just fine. I suggest you try this method some time, cheers.


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## VFlutter (Aug 11, 2017)

Technically, I am an EMT-Basic....


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## VentMonkey (Aug 11, 2017)

Chase said:


> Technically, I am an EMT-Basic....


...technically, I'm not that smart.


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## E tank (Aug 11, 2017)

VentMonkey said:


> Congrats though, you've managed to stump two of the more formally educated forum members on here.



Make that three...


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## NomadicMedic (Aug 11, 2017)




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## bakertaylor28 (Aug 12, 2017)

VentMonkey said:


> I'd wondered the same. And if he is trying to teach the basics he sure knows how to come across...
> 
> Perhaps he meant teach fundamentals //shrugs//. If you were in fact referring to the EMT-basics on this site, @bakertaylor28 you once again sound extremely arrogant, and condescending.
> 
> Congrats though, you've managed to stump two of the more formally educated forum members on here; both of whom manage to get their points across in non-jargon filled rants just fine. I suggest you try this method some time, cheers.



AS IN  in the EMT-B's that come across these posts and often haven't the clue as to where we're going with these things. Truth is that you can frame up ANYTHING to be "condescending and arrogant" as you put it. Truth is, your just trying to pick a fight, and I'm not bitting. So yeah, do yourself a favor, and go smoke a bowl. :-D


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## bakertaylor28 (Aug 12, 2017)

Remi said:


> I don't know what you are talking about.


I'm Talking about that nice little law of pump dynamics that people seem to overlook:

Pressure(Rate)  = Net Flow 

Where for our purposes here, Flow is a near constant because  of homeostasis.


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## bakertaylor28 (Aug 12, 2017)

VentMonkey said:


> ...technically, I'm not that smart.



Technically your just trying to be difficult. [mind you that's the censored version of what I really wanted to say, which was something more along the lines of using less letters to say it. ]   ;-) But really can you quit trolling already?


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## VFlutter (Aug 12, 2017)

bakertaylor28 said:


> I'm Talking about that nice little law of pump dynamics that people seem to overlook:
> 
> Pressure(Rate)  = Net Flow
> 
> Where for our purposes here, Flow is a near constant because  of homeostasis.



I have heard of Ohm's Law, Poiseuille's Law, Laplace's Law, etc but never the "Law of Pump Dynamics". Care to educate us?  

Yes, cardiac output and blood pressure remain fairly constant due to the body's ability to modulate HR, SV, and vascular tone. That is not a hard concept..



bakertaylor28 said:


> AS IN  in the EMT-B's that come across these posts and often *haven't the clue as to where we're going with these things.* Truth is that you can frame up ANYTHING to be "condescending and arrogant" as you put it. Truth is, your just trying to pick a fight, and I'm not bitting. So yeah, do yourself a favor, and go smoke a bowl. :-D



I think most of the EMT-Bs on this site can offer far more constructive and logical contributions than you have in this thread. And not sure who "we" is referring to. You seem to be the only speaking in circle and creating confusion. Nothing being discussed is overly difficult. 

Also, please learn to use multi-quote...


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## bakertaylor28 (Aug 12, 2017)

Chase said:


> I have heard of Ohm's Law, Poiseuille's Law, Laplace's Law, etc but never the "Law of Pump Dynamics". Care to educate us?
> 
> Yes, cardiac output and blood pressure remain fairly constant due to the body's ability to modulate HR, SV, and vascular tone. That is not a hard concept..
> 
> ...



There are several laws of pump dynamics and that is but one of them. I wasn't specifically naming the name of a law involved, but I susepcted you arelady knew that, and are just trying to troll and stir the pot.  (For those whom might really want to know google it.) 

And the point is that all of this is all good and all But the fact is that Total Output (i.e. flow)  is going to decrease over time if we allow hypotension in the setting of a major bleed, Plus the fact that we KNOW we're guaranteed the initial pressor effect. (thanks to adolsterone dump.) On top of that you have the issue of an even bigger dump effect in attempt to overcome hypotension. Hence, if we're not careful, we're likely to  end up with an adisonian state down the road.

_(moderator snip)_


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## Carlos Danger (Aug 12, 2017)

bakertaylor28 said:


> There are several laws of pump dynamics and that is but one of them. I wasn't specifically naming the name of a law involved, but I susepcted you arelady knew that, and are just trying to troll and stir the pot.  (For those whom might really want to know google it.)
> 
> And the point is that all of this is all good and all But the fact is that Total Output (i.e. flow)  is going to decrease over time if we allow hypotension in the setting of a major bleed, Plus the fact that we KNOW we're guaranteed the initial pressor effect. (thanks to adolsterone dump.) On top of that you have the issue of an even bigger dump effect in attempt to overcome hypotension. Hence, if we're not careful, we're likely to  end up with an adisonian state down the road.



With all due respect, you seem to be misunderstanding the physiology in question here.

As far as the cardiodynamics ("pump dynamics") go, yes, a low flow state causes poor preload which makes the heart work inefficiently. I think that's what you were trying to get across? The thing is......we don't care. It's OK given the bigger clinical picture. Because until we control bleeding, we don't want a big, efficient CO pushing blood out of the vascular defect.

The "initial pressor effect" you are talking about has already come and gone once we get to the point where we are thinking about how/whether to treat hypotension. Once hypotension develops, then by definition the sympathetic, vasopressinergic, and RAAS (which I think is what you mean by "aldosterone dump"?) compensatory mechanisms have already failed to maintain perfusion, which is why we are now in hypotensive _decompensated_ shock.

Acute adrenal insufficiency is commonly encountered in the ICU setting but is not a consideration in the initial stages of resuscitation.


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## bakertaylor28 (Aug 12, 2017)

Remi said:


> With all due respect, you seem to be misunderstanding the physiology in question here.
> 
> As far as the cardiodynamics ("pump dynamics") go, yes, a low flow state causes poor preload which makes the heart work inefficiently. I think that's what you were trying to get across? The thing is......we don't care. It's OK given the bigger clinical picture. Because until we control bleeding, we don't want a big, efficient CO pushing blood out of the vascular defect.
> 
> ...



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.


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## Chimpie (Aug 13, 2017)

*Keep the discussion on topic and civil, please. *


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## Akulahawk (Aug 13, 2017)

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


bakertaylor28 said:


> 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.


bakertaylor28 said:


> 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.


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## Carlos Danger (Aug 13, 2017)

bakertaylor28 said:


> 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,
> 
> ...



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.


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## VFlutter (Aug 13, 2017)

bakertaylor28 said:


> 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,
> 
> ...



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.


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## bakertaylor28 (Aug 13, 2017)

Chase said:


> 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.


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## bakertaylor28 (Aug 13, 2017)

Remi said:


> 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.
> 
> ...



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.


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## Akulahawk (Aug 13, 2017)

bakertaylor28 said:


> 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?


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## Akulahawk (Aug 13, 2017)

bakertaylor28 said:


> 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.


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## VentMonkey (Aug 13, 2017)

@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 (Aug 13, 2017)

VentMonkey said:


> @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.


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## bakertaylor28 (Aug 13, 2017)

Akulahawk said:


> 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.
> 
> ...



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.


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## bakertaylor28 (Aug 13, 2017)

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.


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## Akulahawk (Aug 13, 2017)

bakertaylor28 said:


> 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:FFPlatelets. 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.


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## TXmed (Aug 13, 2017)

Chase said:


> 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.


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## CANMAN (Aug 14, 2017)

TXmed said:


> 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 (Aug 14, 2017)

CANMAN said:


> 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.


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## TXmed (Aug 14, 2017)

@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 (Aug 15, 2017)

TXmed said:


> @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...


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## TXmed (Aug 15, 2017)

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.


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## CANMAN (Aug 15, 2017)

TXmed said:


> @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 ?



Yes, our kits do allow us to transduce for ART line if desired.


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## CANMAN (Aug 15, 2017)

TXmed said:


> 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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## TXmed (Aug 15, 2017)

CANMAN said:


> Correct. Our kits are 7fr and 64cm in length, with two ports, one for balloon occlusion and the other for transducing an arterial waveform.



So in theory a critical/unstable trauma patient should just have this thrown in regardless of if you use the balloon occlusion or not, more of just a safe thing to have correct?


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## CANMAN (Aug 15, 2017)

TXmed said:


> So in theory a critical/unstable trauma patient should just have this thrown in regardless of if you use the balloon occlusion or not, more of just a safe thing to have correct?



Idk if I would say all of that. I think the decision for REBOA with our Trauma Surgeon's is very assessment & provider based prior to placement and I don't think, or at least haven't seen them arbitrarily just placing them for a just in case scenario. If the patient is a candidate then the decision to REBOA would be a quick one and would look something like this when patient arrives: Decision to intubate/not intubate, bilateral manual blood pressures with declaration of shock/no shock, rapid trauma assessment. If mechanism or assessment findings are suggestive of waist down trauma then patient gets a portable pelvis x-ray in the bay, and if time allows/stable enough they will shoot a quick chest. If abdomen is a concern we are likely looking at doing a DPL.  If patient has been declared hypotensive and in shock, TXA and 2 units is given, and pelvic x-ray shows considerable fractures/trauma then REBOA would be the next line if not going to be something we can control with pelvic binder. Regardless if patient gets a binder or REBOA, if they continue with hypotension they will go straight to the OR to get opened up within 15 minutes or less of hitting the door. Depending on who is doing the REBOA I have seen start to finish in about 5-8 minutes total time spent in bay, I have also seen the REBOA procedure take 8 minutes in and of itself for someone who isn't the most familiar with the kit...

That answer your question?


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## Carlos Danger (Aug 15, 2017)

CANMAN said:


> Idk if I would say all of that. I think the decision for REBOA with our Trauma Surgeon's is very assessment & provider based prior to placement and I don't think, or at least haven't seen them arbitrarily just placing them for a just in case scenario. If the patient is a candidate then the decision to REBOA would be a quick one and would look something like this when patient arrives: Decision to intubate/not intubate, bilateral manual blood pressures with declaration of shock/no shock, rapid trauma assessment. If mechanism or assessment findings are suggestive of waist down trauma then patient gets a portable pelvis x-ray in the bay, and if time allows/stable enough they will shoot a quick chest. If abdomen is a concern we are likely looking at doing a DPL.  If patient has been declared hypotensive and in shock, TXA and 2 units is given, and pelvic x-ray shows considerable fractures/trauma then REBOA would be the next line if not going to be something we can control with pelvic binder. Regardless if patient gets a binder or REBOA, if they continue with hypotension they will go straight to the OR to get opened up within 15 minutes or less of hitting the door. Depending on who is doing the REBOA I have seen start to finish in about 5-8 minutes total time spent in bay, I have also seen the REBOA procedure take 8 minutes in and of itself for someone who isn't the most familiar with the kit...
> 
> That answer your question?



DPL? Really? Lol


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## E tank (Aug 15, 2017)

Aortic occlusion balloons are pretty useful for ruptured AAA's. But with these, they have to be put in under fluoro because of the risk of trans migration of the wire/sheath through the damaged aorta. 

Never used one in trauma...is fluoro used in that situation or is it a blind placement?


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## CANMAN (Aug 15, 2017)

Remi said:


> DPL? Really? Lol



Old school hospital man, some of the stuff I shake my head at. It's not frequent, we have ultrasound as well, just depends who all is on.


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## CANMAN (Aug 15, 2017)

E tank said:


> Aortic occlusion balloons are pretty useful for ruptured AAA's. But with these, they have to be put in under fluoro because of the risk of trans migration of the wire/sheath through the damaged aorta.
> 
> Never used one in trauma...is fluoro used in that situation or is it a blind placement?



Blind no fluro


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## Brandon O (Aug 15, 2017)

E tank said:


> Aortic occlusion balloons are pretty useful for ruptured AAA's. But with these, they have to be put in under fluoro because of the risk of trans migration of the wire/sheath through the damaged aorta.
> 
> Never used one in trauma...is fluoro used in that situation or is it a blind placement?



Just measured based on anatomy. They try to hit various "zones" based upon the site of injury.


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## VFlutter (Jul 21, 2019)

Bump.  HEMS/Critical Care section has been lagging lately. Anyone have requests on topics? Devices to cover? Interesting flights?


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## StCEMT (Jul 21, 2019)

Something peds may be good.


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## Peak (Jul 21, 2019)

Field management of the pre-Glenn single ventricle?


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## VentMonkey (Jul 22, 2019)

VFlutter said:


> Bump.  HEMS/Critical Care section has been lagging lately. Anyone have requests on topics? Devices to cover? Interesting flights?


//shrugs// had a good MVA polytrauma v. STEMI “chicken or the egg” a few weeks ago. 

Bought a tube, got good care on our end, and watched the trauma center work the pt., drop a cortis and do their best a few weeks back.


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## GMCmedic (Jul 22, 2019)

One of our crews had a recent Head on MVA, one driver intoxicated and dead on impact, the driver they flew had a hole in his right ventricle (you could fit 3 fingers in it) 

About the most interesting thing Ive heard or seen recently. He is still alive.


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## VentMonkey (Jul 26, 2019)

Has anyone heard of/ gone over the EPIC Trial? I breezed through the article and found it interesting on a broad provider scale.









						Association of Traumatic Brain Injury Treatment Guidelines With Patient Survival Following Traumatic Brain Injury
					

This study evaluates the association of implementing the nationally vetted, evidence-based, prehospital treatment guidelines with outcomes in moderate, severe, and critical traumatic brain injury.




					jamanetwork.com


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## GMCmedic (Jul 27, 2019)

VentMonkey said:


> Has anyone heard of/ gone over the EPIC Trial? I breezed through the article and found it interesting on a broad provider scale.
> 
> 
> 
> ...


Full disclosure, I did not read the study but I listened to Dr. Jarvis do a breakdown on the lighthouse podcast. I would have better luck understanding a bible written in Japanese.

I didnt find the study to be very informative as far as current practice that im used too, I could see several services local that could learn something. I thought overall the way they conducted the study and used the imformation was impressive.


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## StCEMT (Jul 30, 2019)

One thing I haven't learned much about are the impella devices. I could read up on it myself, but some first-hand knowledge and pearls would be good as well to supplement that with.


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## GMCmedic (Jul 30, 2019)

StCEMT said:


> One thing I haven't learned much about are the impella devices. I could read up on it myself, but some first-hand knowledge and pearls would be good as well to supplement that with.


biomed has some impella courses online that are free. I think there are 5 of them.


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## TXmed (Jul 30, 2019)

Theres an impella app for Android and I phones that's very detailed


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## VFlutter (Jul 30, 2019)

StCEMT said:


> One thing I haven't learned much about are the impella devices. I could read up on it myself, but some first-hand knowledge and pearls would be good as well to supplement that with.



Any specific questions? Probably deserves a write up. Lots to talk about with them. Just had a tandem (CP and RP) a few weeks ago


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## StCEMT (Jul 30, 2019)

VFlutter said:


> Any specific questions? Probably deserves a write up. Lots to talk about with them. Just had a tandem (CP and RP) a few weeks ago


I understand the very basic idea of what it does, but I think this is a case of not knowing what I don't know. Off the top of my head IABP vs Impella (when and why specifically), any unique complications to be aware of and how to fix them, and how your treatments of patients varies between the two (different approach with pressors for example). Otherwise....whatever is particularly relevant and useful knowledge.


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