"Is Prehospital EMS (PHEMS) a Profession?"

Handsome Robb

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Finally, why are we so hell bent on diuresing this patient? While probably needed eventually, this isn't going to help us out short-term very much.

Because he's an ICU nurse :rofl:

Sorry just had to point that out there dude. Your angle seems to be geared towards inhospital care rather than in the acute prehospital setting.
 

TatuICU

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Because he's an ICU nurse :rofl:

Sorry just had to point that out there dude. Your angle seems to be geared towards inhospital care rather than in the acute prehospital setting.

No my angle has to do with not killing your patient and actually doing something to help them. And in addition to being an ICU nurse I'm also a practicing paramedic. is there something funny about working in an ICU that I am unaware of?

So your contention is that diuresis would not help the the patient in this crisis?
 

Veneficus

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I wouldn't use Dig either. I don't know of anyone in or out of a hospital that would use Dig for this instance first line especially since, according to this scenario, Lasix has been ineffective suggesting that perhaps there are some serious renal issues happening.

But this is not first line, we are discussing what to do when the therapies in the given scenario are not working.

I also mentioned the renal failure possibility in my original reply in response to the lasix not being effective.

Epi is not a hail mary in this instance. Epi will worsen this patient's condition. The increase in afterload even at a lower dose would increase SVR and offset whatever increase in contractile force it would provide, which would probably not be very much, because as a patient with a heart this diseased probably has an LV that's as stiff as a board.

From: http://www.aic.cuhk.edu.hk/web8/inotropes.htm


"Epinephrine
Pharmacokinetics
Admin: IV/IM/infiltration
Elim: mostly degraded by conjugation with glycuronic and sulphuric acids and excreted in the urine. Smaller part is oxidised by amine oxidase and inactivated by o-methyl-transferase
Pharmacodynamics
- stimulates alpha1 and both beta1 and beta2 receptors. Effects are mediated by stimulation of adenyl cyclase resulting in an increase in cAMP
- beta2 receptors more sensitive to epinephrine than alpha1
CVS
- positive inotrope and chronotrope (NB. mediated by all 3 receptors not just beta1)
- increases incidence of dysrhythmias by increasing irritability of automatic conducting system
- constricts vessels of skin, mucosae, subcutaneous tissues, splanchnic area, kidneys (alpha effects)
- vessels of muscle and liver are dilated at physiological doses (beta effect) but are constricted at higher doses.
- cerebral and pulmonary arteries are constricted
- may precipitate angina in patients with IHD
- CVS effects reduced by acidosis
- at low doses causes: increased cardiac output, slight reduction in SVR, increase in effective circulating volume and increased venous return. Net result: systolic BP rises but diastolic falls
- higher doses: rise in SVR, decreased cardiac output and rise in both systolic and diastolic BP"


Who said the tube would be a solution? I'm saying that a tube is most likely the most effective therapy in which to assure adequate ventilation. And nothing is going to matter if you don't fix your pump problem (long shot here from the scenario described.)

The person who posted the scenario implied that when many prehospital treatments failed, that the tube would be a beneficial treatment.

My point was just as you said, attempting to address the pump is the solution to this problem.

Most units I've seen or worked on do carry dobutamine and every unit carries dopamine which could also be used here for inotropic support. Milrinone, you're right.

Could you please tell me who carries dobutamine?

I detect an air on condescension here, any particular reason why? Again, who said anything about intubation being a "magic bullet?" Please show where in my post that I suggested intubation was going to be the intervention to correct this patient's condition and I will certainly go back and edit it out. Intubation is not going to be the magic bullet for this patient and in fact there is no pathology that I know of where intubation is a magic bullet that fixes anything.

Sorry, I thought you were trying to argue in favor of intubation being a helpful treatment in resolving the underlying pathology.

Intubation is a therapy, and in this case I feel an appropriate one, to insure adequate ventilation for this patient. You're also assuming that a patient in this extremis is able to protect their airway.

There are many ways to protect an airway. I would suggest a gradual escalation, especially in this patient which is listed as semiconscious. Even if you planned to move right to RSI, we would have to account for the difficulty of the intubation, which may preclude that option, and then we would be back to managing an airway without intubation.
 

TatuICU

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Dopa is going to be only slightly less harmful than epi,
Finally, why are we so hell bent on diuresing this patient? While probably needed eventually, this isn't going to help us out short-term very much.

It is? A lower dose 5mcg/kg/min would not only increase inotropy but could also help stimulate dopaminergic receptors within the nephron of the kidney would could potentially promote diuresis.

And why diuresis? Well because that's how you'd effectively decrease preload and afterload without hitting a shocky patient who most likely has a MAP<65 with continuous NTG? Not sure why we wouldn't look to start diuresis?
 

Veneficus

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It is? A lower dose 5mcg/kg/min would not only increase inotropy but could also help stimulate dopaminergic receptors within the nephron of the kidney would could potentially promote diuresis.

Just so you know, renal dose dopamine has been debunked for many years in several studies, including a Cochran Review.
 

Handsome Robb

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It is? A lower dose 5mcg/kg/min would not only increase inotropy but could also help stimulate dopaminergic receptors within the nephron of the kidney would could potentially promote diuresis.

And why diuresis? Well because that's how you'd effectively decrease preload and afterload without hitting a shocky patient who most likely has a MAP<65 with continuous NTG? Not sure why we wouldn't look to start diuresis?

Not much evidence supporting its use in the prehospital setting when compared to patient outcomes.
 

TatuICU

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But this is not first line, we are discussing what to do when the therapies in the given scenario are not working.

I also mentioned the renal failure possibility in my original reply in response to the lasix not being effective.



From: http://www.aic.cuhk.edu.hk/web8/inotropes.htm


"Epinephrine
Pharmacokinetics
Admin: IV/IM/infiltration
Elim: mostly degraded by conjugation with glycuronic and sulphuric acids and excreted in the urine. Smaller part is oxidised by amine oxidase and inactivated by o-methyl-transferase
Pharmacodynamics
- stimulates alpha1 and both beta1 and beta2 receptors. Effects are mediated by stimulation of adenyl cyclase resulting in an increase in cAMP
- beta2 receptors more sensitive to epinephrine than alpha1
CVS
- positive inotrope and chronotrope (NB. mediated by all 3 receptors not just beta1)
- increases incidence of dysrhythmias by increasing irritability of automatic conducting system
- constricts vessels of skin, mucosae, subcutaneous tissues, splanchnic area, kidneys (alpha effects)
- vessels of muscle and liver are dilated at physiological doses (beta effect) but are constricted at higher doses.
- cerebral and pulmonary arteries are constricted
- may precipitate angina in patients with IHD
- CVS effects reduced by acidosis
- at low doses causes: increased cardiac output, slight reduction in SVR, increase in effective circulating volume and increased venous return. Net result: systolic BP rises but diastolic falls
- higher doses: rise in SVR, decreased cardiac output and rise in both systolic and diastolic BP"




The person who posted the scenario implied that when many prehospital treatments failed, that the tube would be a beneficial treatment.

My point was just as you said, attempting to address the pump is the solution to this problem.



Could you please tell me who carries dobutamine?



Sorry, I thought you were trying to argue in favor of intubation being a helpful treatment in resolving the underlying pathology.



There are many ways to protect an airway. I would suggest a gradual escalation, especially in this patient which is listed as semiconscious. Even if you planned to move right to RSI, we would have to account for the difficulty of the intubation, which may preclude that option, and then we would be back to managing an airway without intubation.

Bear with me, I can't do multiple quotes from my phone:

With regard to the dig, it doesn't matter which line as there is no line for dig in this situation and I'm unsure off why dig was ever brought up.

Ill pm a list of services here that carry doubt amine and will send you our protocol for it as well.

The rest will have to wait a bit, headed to work
 

Veneficus

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With regard to the dig, it doesn't matter which line as there is no line for dig in this situation and I'm unsure off why dig was ever brought up.

Says who?
 

TatuICU

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Just so you know, renal dose dopamine has been debunked for many years in several studies, including a Cochran Review.

Just so you know 5 is not a "renal dose" it's a low inotropic dose that can promote diuresis. Renal doses were argued to be predicated upon increasing renal messenteric blood flow, not necessarily by direct action on te nephron.
 
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Handsome Robb

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No my angle has to do with not killing your patient and actually doing something to help them. And in addition to being an ICU nurse I'm also a practicing paramedic. is there something funny about working in an ICU that I am unaware of?

So your contention is that diuresis would not help the the patient in this crisis?

There's nothing funny about being an ICU nurse. Slow your roll.

Your advocating using meds that are not readily available to most EMS crews, that's why I said it.

Like I said, in the prehospital field I'm looking for NTG before Lasix because there is little evidence that supports the use of lasix in the field when compared to patient outcome.
 

TatuICU

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Says who?

Are u serious??? You want to use dig in a patient with renal failure? Why in the world would u choose dig in this instance?
 
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Veneficus

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Are u serious??? You want to use dig in a patient with renal failure?

that is not a part of the assumption

If you are going with the 30 minute transport with acute and critical CHF, with renal failure at 55, whatever underlying patholgy, and a potential unstable airway, you might be better off with just some versed and morphine in high dose. It will probably be kinder than treating the crazy elevated K+ in addition to the rest of this.
 
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TatuICU

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that is not a part of the assumption

So even though you assumed it it's not part of the assumption? And you guys are arguing that dobutrex is not practical because you don't carry it but dig is because you guys carry it? Digoxin but not dobutrex? Most services carry dobutamine, none that I know of carry dig


At work will return later
 
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Handsome Robb

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So even though you assumed it it's not part of the assumption? And you guys are arguing that dobutrex is not practical because you don't carry it but dig is because you guys carry it? Digoxin but not dobutrex? Most services carry dobutamine, none that I know of carry dig


At work will return later

Who is this "you guys" you speak of?

I never said anything about dig.

Our flight service carries dobutamine, our ground service does not. We don't carry dig either.

I'm not the only person that has said they don't carry dobutamine. I've never heard of 911 units carrying dobutamine. IFT/CCT makes sense.

It seems like you're getting frustrated which is making you grumpy as well.
 

usalsfyre

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It is? A lower dose 5mcg/kg/min would not only increase inotropy but could also help stimulate dopaminergic receptors within the nephron of the kidney would could potentially promote diuresis.
Which is why I'd choose dopa over epi. I think the diuresis is going to be more about increased renal perfusion though.

And why diuresis? Well because that's how you'd effectively decrease preload and afterload without hitting a shocky patient who most likely has a MAP<65 with continuous NTG? Not sure why we wouldn't look to start diuresis?
So you want vasodilation from dobtamine (tied dose wise to your inotropy) but not from NTG (an independent factor you can adjust)? Which is it?

Diuresis is going to be important in say...20 minutes or so. In the next five while we're in the oxygenation death spiral its not going to help fast enough. You've got to get the afterload off and clear the LV right now to give the CPAP a chance to do its job.

Ultimately she needs a baloon pump.
 

Veneficus

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So even though you assumed it it's not part of the assumption? And you guys are arguing that dobutrex is not practical because you don't carry it but dig is because you guys carry it? Digoxin but not dobutrex? Most services carry dobutamine, none that I know of carry dig


At work will return later

I think you are misunderstanding or interpreting the original discussion.

I presented a potential course when you don't have the perfect solution. Based on what is commonly carried on a US ALS unit when after your primary treatments have failed.

The original argument was that intubation would somehow help.

Since then, I have seen an argument against what I said, based most likely off of what you have seen or assume, as I have posted the very mechanism as to why epi might be a long shot.

Giving dig to increase cardiac contractility in advanced CHF is in every medical text I have ever seen that talks about the subject.

There are several studies showing it does not improve mortality. But at least one that demonstrates a reduction in ICU admission. If it can be used chronically, it can be used acutely by the same mechanism.

I have said it many times, in medicine, it is not "what" that makes a difference, it is "why."

http://jasn.asnjournals.org/content/15/8/2195.full

http://www.ncbi.nlm.nih.gov/pubmed/21180781

and as for inciting renal toxicity, in acute kidney injury, there are treatments in order to help mitigate that as nicely explained here.

http://www.ncbi.nlm.nih.gov/pubmed?term=N-GAL: Diagnosing AKI as soon as possible

and in the full publication of this:

Ren Fail. 2012;34(1):130-3. Epub 2011 Oct 20.

Using NGAL as an early diagnostic test of acute kidney injury.

We can make the scenario as complex as you like.

Just state what you want it to be.
 

RocketMedic

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From a new paramedic's point of view, I'd still think that a secure airway and good ventilation would be things to need.

Another great reason for prehospital ETT- anaphalaxis or deep FBAO.
 

Veneficus

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From a new paramedic's point of view, I'd still think that a secure airway and good ventilation would be things to need.

Another great reason for prehospital ETT- anaphalaxis or deep FBAO.

could I just inquire why you have this fascination with intubation?
 
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