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Critical Care Topic of the Month

Discussion in 'HEMS and Air Medical Transport' started by Chase, Mar 27, 2017.

  1. bakertaylor28

    bakertaylor28 Forum Lieutenant

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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.
     
  2. E tank

    E tank Forum Captain

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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.
     
  3. bakertaylor28

    bakertaylor28 Forum Lieutenant

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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.
     
    TXmed likes this.
  4. Remi

    Remi Forum Deputy Chief Premium Member

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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.

    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.
     
    VentMonkey likes this.
  5. bakertaylor28

    bakertaylor28 Forum Lieutenant

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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.
     
  6. Remi

    Remi Forum Deputy Chief Premium Member

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    I don't know what you are talking about.
     
  7. Chase

    Chase Flight Nurse

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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
     
  8. VentMonkey

    VentMonkey Crackpot Premium Member

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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.
     
    Chimpie likes this.
  9. Chase

    Chase Flight Nurse

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    Technically, I am an EMT-Basic....
     
    NomadicMedic and VentMonkey like this.
  10. VentMonkey

    VentMonkey Crackpot Premium Member

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    ...technically, I'm not that smart.
     
  11. E tank

    E tank Forum Captain

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    Make that three...
     
    VentMonkey likes this.
  12. NomadicMedic

    NomadicMedic formerly DEmedic

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  13. bakertaylor28

    bakertaylor28 Forum Lieutenant

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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
     
  14. bakertaylor28

    bakertaylor28 Forum Lieutenant

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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.
     
  15. bakertaylor28

    bakertaylor28 Forum Lieutenant

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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?
     
  16. Chase

    Chase Flight Nurse

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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..

    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...
     
  17. bakertaylor28

    bakertaylor28 Forum Lieutenant

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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)
     
    Last edited by a moderator: Aug 13, 2017
  18. Remi

    Remi Forum Deputy Chief Premium Member

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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.
     
    Last edited: Aug 12, 2017
    GMCmedic likes this.
  19. bakertaylor28

    bakertaylor28 Forum Lieutenant

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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.
     
  20. Chimpie

    Chimpie Site Administrator Community Leader

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    Keep the discussion on topic and civil, please.
     

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