Critical Care Topic of the Month

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.
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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.
 
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.
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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.
 
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.
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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.
 
bakertaylor28 said:
The thing is that without proper load, pressing isn't going to do much anyways.
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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.
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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.
 
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.



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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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.
 
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.
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I don't know what you are talking about.
 
bakertaylor28 said:
But then the question becomes (for the sake of teaching the basics) .
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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
 
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
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I'd wondered the same. And if he is trying to teach the basics he sure knows how to come across:confused:...

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

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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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
 
Remi said:
I don't know what you are talking about.
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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.
 
VentMonkey said:
...technically, I'm not that smart.
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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?
 
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.
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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
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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...
 
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..



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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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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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.
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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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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.

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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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.
 
Keep the discussion on topic and civil, please.
 
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