Off Label

Not all systems do transport those patients you describe. From the question, I'm guessing where you are there is not protocol for determining a death in the field in these circumstances?

cold water drowning, any hypothermic arrest. A colleague of mine took care of a young lady who went for a walk in 15 degree weather after drinking too much one evening and was found at sun up the next day... her clothes were literally frozen to the ground. Brought to the hospital in full arrest, placed on cardiopulmonary bypass and slowly rewarmed. She didn't miss any school as it happened on Christmas break.

If more folks took this approach, maybe the field intubation debate wouldn't have occurred.

I'd ask him/her to consider a true alpha agonist to augment your epinephrine in cardiogenic shock. Epi and something like phenylephrine covers contractility and vasomotor tone very well. Dobutamine improves cardiac output thru enhanced contractility, but does risk hypotension via mild beta 2 agonism. That would be hard to tease out in the pre-hospital setting IMO. If the heart needs unloading, I'd prefer something like NTG if tolerable.

Nearly 10 years later, maybe an update... Dopamine...dirty drug. Sometimes you get what you want, sometimes more than you asked for...ie tachycardia when all you want is more blood pressure. Dose varies. I don't use it. Epinepherine first line..inotrope of choice for me for contractility issues Norepi...excellent drug for correction of loss of vasomotor tone. Bad reputation comes from the days when septic patients were relatively fluid restricted and squeezed to death with this drug, ie, end organ damage because of poor perfusion (lack of intravascular volume). We've learned a bit since those days. Vasopressin...excellent drug when vasoplegia from whatever cause is refractory to NE or phenylephrine. Not first line, but very effective. Dobutamine...an OK inotrope but could require a pressor for blood pressure as well. I'd pick epi first.

The cardiac transplant patient won't feel the pain of ischemia for the same reason anticholinergics don't work. The nerves are cut. Direct acting sympathomimetics work because of the receptors present on the transplanted heart. Further, cardiac transplant patients have a higher resting heart rate, so 90 is normal for them. Two P waves, one from the native atrial remnant and one from the graft, can be seen as well.

Sounds like a problem using the 3 way stop cock. But I'm still trying to figure out, all these years later, why they needed to bolus from a 500 cc bag plugged into a line where they had a 1000 cc bag already hanging.

If it doesn't delay care or is too expensive, ETCO2 can be useful. Interfacility or prolonged transport of intubated patients would benefit from the enhanced safety if immediate recognition of an extubation. Correct tube placement in a patient not in full arrest is easier to confirm with ETCO2. For systems that don't have long transport times or intubations, not worth it. Nasal cannula or mask ETCO2 sets are just really expensive respiratory monitors. Very much qualitative as opposed to quantitative.

In trauma, too much of any crystalloid is bad... it causes hemodilution, dilutional coagulopathy, raises blood pressure which breaks clots etc. This is not the thinking of 30 years ago and anecdotal evidence isn't good enough. We really don't learn this stuff unless we study it. War time accelerates our understanding, but without formal investigations, we have no basis for what we can say with confidence.

Intubations in the ED or field that require an "induction agent" require muscle relaxant for the vase majority of cases. What that induction agent is really doesn't matter in these cases, as long as the proper dose is given. Hypotension after an induction of anesesthesia (which is what is called for prior to direct laryngoscopy) is an expected event that should be anticipated and treated accordingly if necessary. If the patient meets medical criteria for intubation, short full arrest or an otherwise flaccid patient, muscle relaxant should be mandatory. Versed is as stable as any other agent with the possible exception of etomidate, and even then, hypotention can occur. The caveat is that the proper dose needs to be given which is about .2 to .3 mg/kg. Otherwise, don't use it.

Read Poiseuille's law I'd give vasopressin over epi if I could. Contractility isn't his problem, loss of vasomotor tone is.

The value of alpha agonist in this case would be less treating the neurohumeral causes of her symptoms (i.e. inflammatory mediators, cytokines) and more just treating her severe vasoplegia that is a result of them. I have to say that I'm surprised metaraminol is still being used or talked about in EM/pre-hospital care, as it is largely ignored in my neck of the woods in CC and by the anesthesia folks. Having been away from pre-hospital/emergency/trauma care for many years, I can't really comment on the reasons for this. That being said, vasopressin, which every ALS ambulance has, is an excellent treatment for vasoplegia and hypotension refractory to pressors, inopressors and volume.

If you have the type of iv catheter that you can put on the end of a syringe, advancing it with the plunger pulled back to create some negative pressure is a good way to get your flash.

Norepinepherine (levophed) is the first line pressor of choice in the setting of septic shock at most places I'm aware of. If there are no significant contractility issues, epinephrine doesn't make sense. NE is usually chosen over phenylephrine because, theoretically, raises CO more.

Intrapulmonary AVM?

This was far more of an issue when we gave a lot more crystalloid for all kinds of things. It only really matters now in a couple of settings. If giving less that 1.5 liters or so of crystalloid, the fluid doesn't matter. It's an issue when giving several liters over a couple of hours. It that situation, Plasmalyte/Normosol is superior to LR which is superior to NS. The reason being that acidosis is far easier to manage. The fall in pH isn't as profound with Plas/Norm as it is with LR in situations where there is a lot of blood loss and clamping and unclamping of the aorta, iliacs etc in an OR setting. That said, again, we don't give a lot of crystalloid anymore, so the argument really doesn't apply in most settings.

Who says you won't be able to use your new found skills and knowledge in a 911 setting? And how would they know if they didn't hold that certification? Clearly there are skills that are limited to a critical care setting, but the knowledge involved in the care of those patients crosses over in many places. As patients live in the community with more and more complex diseases, how can advanced training not be practically applied in your setting? Right off the bat, I can say that the number of patients in the community with implantable LVADs is increasing meteorically. Some folks can't see beyond their own narrow horizons...don't listen to 'em.