EMT City: Paramagic - Viewing Profile - EMT City

It's an interesting question, and not, I would think, one that is going to be answered anytime soon due to the massive numbers of confounding variables that come in to play in pre-hospital cardiac arrest.

Personally, I do not routinely push fluids during the arrest unless I have reason to suspect that volume depletion is an underyling cause of the arrest (eg PEA as presenting rhythm), but I will allow it to run TKVO and to use as a flush following drug boluses.

However we have been inducing hypothermia for several years now with 2 litres of ice cold normal saline given as rapidly as possible, and our experience has been that there has not been the problems with pulmonary edema that many were expecting. Now, part of the rationale behind using ice-cold fluid as opposed to other methods is that we are mounting a three pronged attack in the post-arrest patient: Hypothermia (which we should all be conversant with now), Hypertension (to maintain adequate cerebral perfusion - hypertension being a relative term, we are looking for 'normal' BP/MAP rather than just accepting any kind of perfusion as adequate) and finally, Hemodilution.

The main cause of further neurolgical injury in the post-arrest patient is reperfusion injury. Following the arrest there are large amounts of nasty stuff like calcium, glutamate and so on that is suddenly being moved around the brain to areas that may not have initally been as ischaemic or injured. The principle in managing this is to dilute these factors to minimize their impact: in essence 'flushing them out' before they can cause further injury.

As a result of our aggressive management of the post-arrest patient (as well as public education, co-response from fire, and a tiered system with well trained EMTs) we have a survival to neurologically intact discharge rate from bystander witnessed VF/VT of about 30%

We are soon to start a trial of cold saline induced hypothermia during the arrest, in effect managing the reperfusion injury before the reperfusion injury takes place, so it will be interesting to see how this pans out. It will take a number of years to complete however.

chbare, on 04 July 2010 - 06:24 AM, said:

Hmmm... volatile agents in an ambulance, curious. Lungs will kill him before the kidneys will, so it may be worth a shot. IV morphine, IM fentanyl, no IV fentanyl? Odd. Can you get on to OLMC and get permission for some IV fentanyl?

Mechanism (in relatoin to motor vechicle collisions) is a poor predictor of injury. Mechanism alone is not sufficient to warrant the risk of running emergent to a trauma center. Mechanism should be used as a cue to alert you to look for specific patterns of injuries, not as a reason to not treat appropriately.

armymedic571, on 09 February 2010 - 05:02 AM, said:

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That's a good question. They certainly have been used to deal with the fluid shift, but on the erroneous assumption that there is an overload of fluid. The key term is 'fluid shift'. Eliminating the fluid in the system does not necessarily correct the fluid shift (it's not systemic overload we are usually worried about with ACPE - it's fluid in the wrong place, not too much fluid) and can lead to further problems with electrolytes (K+ in particular of course) and long term poor outcomes. Nitrates and ACEI's all serve to better correct the imbalance between hydrostatic and colloid oncotic forces that are the main problem to allow the fluid to shift back (or rather be taken up by the lymphatic system) and CPAP splints alveoli open to improve oxygenation and the problems that come from the V/Q mismatch (and shunt if really bad) (hopefully someone else can explain that better than me)

Regarding long term CHF patients with an exacerbation, there are two schools of thought. One is that diuretics are appropriate as this may at least in part be a problem that has overload as a contributing factor. The other is that in the face of the sometimes quite substantial amounts of furosemide that these patients are taking alreadsy, a small amount may just be peeing into the wind and not achieving anything.

To be honest, I am not sure how much data there is or isn't to support either of these positions. I currently am coming down in favor of giving the frusemide to these patients, but really, I'm not sure whether that is to make them feel better or me feel better... And it is only in cases of documented fluid overload that I consider it. I certainly would like to think that the potential to do harm with furosemide that we have in the true acute cases is not there for the acute on chronic cases. I stand to be corrected on this though, so if anyone else has a position, or better some data to support one way or another I would love to see it.

That probably doesn't help a great deal though does it?

I'll have a fossick around tomorrow and dig up some studies to support my ramblings.

Paramagic

armymedic571, on 09 February 2010 - 02:50 AM, said:

Thanks, long time lurker, first time poster....

At this stage, generally speaking, I would be in favour of removing lasix from the drug box, at least for the setting of suspected pulmonary edema - nitrates, CPAP and ACE Inhibitors are first line treatment for this, and irrespective of the difficulties with differentiating ACPE from pneumonia, it probably leads to worse outcomes. However, while there seems to be less and less of a role for it in the setting of ACPE, that is not to say that it does not have uses elswhere in pre-hospital care (hyperkalemia for example) although these instances may be rare, and a cost/benefit analysis should probably be undertaken.

I am, however, firmly against protocolisation (is that a word?) of emergency medicine as the sole form of clinical risk management. The first line of clinical risk management should always be education. In some cases further protocolisation may be required, but it shoud be a last resort.

Something else we need to be careful of is being against losing 'skills' or drugs for reasons other than patient care (ie. ego). There often seems to be an attitude that removal of a particular drug or procedure somehow reflects badly on us as paramedics (not that I am trying to imply that this is your stance; this is just a general observation) Now, if this has occured because, say we have been unable to differentiate between the decapitated/non-decapitated patient, then fair enough, we should be ashamed. However if it has occured because the best available evidence demonstrated no benefit, or even harm from using it, then we should happily wave it goodbye and maybe give it a Viking Burial at sea. We need to practice emergency medicine, not massive egotism.

The studies quoted earlier in the thread seem to me to relate to a systemic problem in the diagnosis and management of a particular cohort of patients in a particular service. One needs to be careful with making generalisations regarding our own practice or service from these kinds of studies without having read and understood the study in it's entirety, including any methodological errors before making decisions regarding it's applicability to our own specific circumstances. When we just read abstracts we end up with blanket statements being made like "RSI is bad, mmmmkay" that may not be appropriate depending on ones circumstances.