kevkei

Hmmm, interesting way of looking at it ... are you saying then that the harder the narcan has to compete to bind to receptors, the shorter the half life, primarily due to it 'working so hard'? That doesn't make much sense to me, because that would imply narcan is equatable to a living cell using energy exponitiously, when we all know that it's purely a chemical.

Technically however (and I may be wrong here ... but this is how I understand it), serum concentration and half-life refers only to unbound drugs. If the drug is bound to a receptor, depending on the cells activity, it will either be utilized quickly or slowly, and then made available for biotransformation and elimination ... the rest, will simply attempt to find an open receptor and slowly (as I was actually taught narcans half-life is anywhere between 30 and 81 minutes) be eliminated. Therefore, the serum concentration of the narcan is not affected by the serum concentration of the opiate.

peace

Take a patient that has been given two seperate doses of a narcotic but all other things being equal, say 10 mg and 20 mg respectively of morphine. If you administer 2 mg of narcan IVP to both situations, your saying that the effects of the narcan will last 45 minutes in both situations? I say I disagree. The affinity that a drug has for a receptor is influenced primarily by two factors: 1) the natural affinity the free drug has for the receptor, 2) the concentration of the drug. Other factors include things like pH, bioavailability.

In this situation, although narcan typically has a higher natural affinity to mu and kappa receptors than most opioids, it is competing with a higher drug concentration. The higher plasma drug concentration the higher it's said affinity for the receptor site and it's ability to actually remove the narcan from the receptor. This will result in less bound narcan and more free drug, which leads to metabolization and elimination.

Even though Narcans half life is shorter then most opiates, it's still pretty long. 45 minutes or so,

I disagree. Narcan doesn't have a specific half life if it is bound. As long as it is competatively binding to a receptor site, it's affinity depends on the affinity and concentration of the drug it is competing with.

For example, if a patient has 10 mg of morphine in his system versus 20 mg, the narcan will wear off faster in the 20 mg scenario due to the plasma concentrations of the morphine.

What do yall think about EMT intermediates being able to administer Noloxone to an overdose?

.... At any rate...what to you think about Narcan..... .... :?:

NO, NO, NO, NO, NO. Did I say NO?

As a healthcare professional that is supposed to do no harm, unless you can also give a benzodiazepine, no. Does an Intermediate do this????

On the genius topic of Romazicon, NO, NO, NO, NO, NO, NO, NO, NO, NO, NO. Unless you can give a different anticonvulsant like Dilantin, no. Can an Intermediate do this either???

Ever seen a flash pulmonary edema after narcan administration? How would you treat that?

Unless you can accept the fact that there is no 'safe' or 'benign' medication and understand why, then no.

Have you tried looking on PubMed?

Look here, without sorting, I found 109 articles entering 'prehsopital entonox'

Prehospital Entonox Use

In the future we may see more providers administering & assisting with IN Narcan in the field.

Actually, there is a program in our inner City called Street Works that is training laypersons from the community to recognize and administer IM narcan. Basically, they are a known narcotic user and found unresponsive.

Seizures, acute withdrawal, combativeness...The half life of narcan is generally significantly shorter than the narcotic so a constant infussion titrated to effect (respiratory depression) and/or a monitored patient is required.

Agreed. These things are bad m'kay.

Who do you think is the better medic? The guy who works for Toronto, does 8 calls a shift, but never sees a truly acute patient? Or the medic who works for Thunder Bay, does 1 call every 3 or 4 days, but every patient is at least a ctas 2?

Sorry, but quality isn't any better than quantity. In Edmonton, I will see at least one CTAS-2 every 4 days and in between see 6-8 others a day (1,3,4,5). You need patient contact to become a better caregiver. You also need a strong background, the right personality, good training (each institution has something to offer to different types of students, so one is really no better than others) and experience. Experience takes years if you only see 1 patient every 3-4 days, regardless of their acuity.

A very wise Paramedic once told me that Paramedics save lives and good EMT's save Paramedics.

This has got to be the stupidest and most nieve saying there is. :roll: I have yet to see anyone qualify or substantiate this statement.

Absolutely correct someone if they are wrong, just be 100% certain that you are right and they are wrong. I have had people of the same level of care and lower try to tell me that I was wrong when in fact they were in the wrong and found out such by doing a little studying and research. At the same time, I've had people say "hey, have you thought of this" or "did you know this..." It's all about tact and diplomacy, and has been stated, how you broach the subject. Team work is suggestive of two or more people working together for a common goal.

We have all made mistakes and we learn from them and it makes us better as caregivers.

Is capnography included in ALS programs? Or is it still too new in the EMS setting...?

Either way, another illustration of how all EMS issues come back to education.

Yes, it is in the standards for Paramedics. Not only that, but also tailoring and treating to qualitative benchmarks dependent on underlying factors and pathophysiology.

Sure BiPap and PEEP, but not in an arrest. That's where you'll really run into trouble. We've been hearing about doing this around here for a while although it's not in protocols or standard of care.

Another little trick in a known or suspected asthmatic arrest is dropping some epi down the tube once they are intubated, even with IV access. It works great for direct Beta II stimulation.

I hear that Hawaii is beautiful at this time of year. I think that my favorite location on the islands to enjoy a Mount & Do would have to be ComeonIwannalayyou. :^o

If there was anything I learned at a CBRN (Chemical, Biological, Radiological and Nuclear) course, it was: "The solution to polution is dilution."

Contralaterally, the more 'card carrying people' and the more 'volunteers' (polution)you have, the more diluted the workforce is (supply and demand) and the less you can demand as a profession (solution) and as employee's. Yes there may be a need for volunteers on a few and very isolated cases, but to justify volunteer services beacuse the cost can't be supported is false.

I wholeheartedly agree with Bledsoe. These are the same reasons why many of us up north of you brag about our programs and why sometimes we come off as arrogant and eletist. More than that, it's because we are proud of our training. Personally, I used 18 textbooks for my program, I'm sitting at 4000 hours worth of training to become a Paramedic. Does this mean I know it all? Well, yes, but that's besides the point (kidding).

The moment we think we know it all, or stop making the effort to learn is the day we die as a good caregiver. On the subject of 'grandfathering' and 'I've been doing this for 10 years' our regulatory College requires all caregivers to upgrade their training because of a National Competency Profile as well as increasing our scope of practice ( seeAlberta GAP Training ). If you don't want to or refuse to do this, you lose your right to practice. Here is what is comprised in the upgrades, at each respective level.

EMR - Airway Module, Pharmacology Module, Trauma and MCI Module.

EMT - Airway Module, Cardiac Monitoring Module, IV Therapy Module, Pharmacology Module, Trauma and MCI Module,

EMT-P - Arterial Blood Gas Samples Module, Blood Products Module, Chest Tubes Module, Femoral Venipuncture Module, Intraosseous Module, Intrapartal Exam Module, Nasotracheal Intubation Module, Suturing and Hemostat Module

TCP Module, Urinary Catheterization Module.

The good thing with these areas is it will be a significant wakeup call for those that think they know it all or haven't picked up a textbook or journal or attended rounds in eons.

Haven't we already beaten this subject to death ????????????????????????????????

Not only left lateral recumbent but also a slight Trendelenberg position.

Anyone interested in Edmonton's, send me a PM with an e-mail address and I'll see what I can do.

"Dude, we weren't sleeping! We were having sex!"

:twisted:

Dude, wasn't your last parter also male? :twisted:

Check jems.com to start.

The author was referencing the hypokalemia that can happen when patients self administer albuterol for an extended period. Potassium is maintained in a pretty narrow range in the body, so small changes in either direction can cause huge problems.

Before Dustdevil weighs in, -5 for posting an ALS subject in the BLS forum.

At most, continuous (keep in mind this is over 2-3 hours) albuterol has been shown to decrease serum potassium up to 0.3 - 0.5 mmol/L, or 10% of normal limits. Also remember that treatment of moderate to severe hyperkalemia is multifacited.

Also, because the lowering of potassium from albuterol use/administration is self limiting and reverses after the albuterol has been metabolized. Why? Because the potassium never leaves the body, it is only redistributed into the cell. Unless you give lasix, a potassium resin (Kaexolate) or dialysis, the potassium remains in the body and it is only temporary.

So this confirms what we all already suspected. So what? I think it is unrealistic to summise that we discontinue on the basis that during transit, compression quality deteriorates. There are more influential and supportive arguments than this for this practice.

There are also certain patients that we can't call on scene and therefore have to transport. Don't get me wrong, my preference is to work a code to it's fullest and if appropriate, discontinue on scene.

I was so sick last night and I didn't get much sleep :pukeleft: :pottytrain5: :pukeright: but I didn't want to burden the service :wink: with a sick call in so I motivated myself to come in for the good of the department. :-({|= (If you sell it well enough, and can mimic symptoms, they may send you some out of sympathy) :wink: (NOT)

OK, so now I am MOST definately confused. If it were hypotonic, wouldn't it draw water into the interstital space, and not the vascular space? This was the debate that we had, some said that the sugar draws water into the interstital space by the cells rapidly using the sugar, hence the water follows,decreasing preload. Some said the the sugar remains in the blood stream, causing water to be pulled into the vascular space, (hypertonic), diuresing the pulmonary edema. I know the concentration is too low to make a difference, but it is in our protocols for a reason. This debate was after class let out, therefore we didn't get to ask the question.

Kevin

Sorry about that. I should have read what I wrote before submitting, but we got called out. It should have read more like this:

Actually, D5W although initially is isotonic, once the glucose is taken up at the cellular level (which is quickly) or processed into glycogen, it becomes hypotonic and will eventually worsen circulatory volume by first drawing water into the interstitial compartment due to osmosis (natural movement of solute and solvent) and oncotic (pull) pressure, but that fluid will eventually re-distribute into the vascular system. The only way to get rid of volume overload is third spacing (temporary), diuresis or dialysis. Keep in mind that osmosis and oncotic gradients cause fluid to continually move back and forth until an equilibrium is established.

I think that in reality, the dextrose in the solution does not stay in the vascular system for long enough to make a sensible change insofar as drawing interstitial fluid into the vasculature. What it does do is add whatever volume of water you administer to the total body volume that eventually ends up somewhere.

I know albumin is a heavy protein, and thus it pulls interstitial fluid back into the vascular space, (reduction of edema).

As for the CHF patient's you are talking about, where is the edema occuring that you are trying to correct? If it is pulmonary (left heart failure), attempts to redistribute fluid into the interstitium or vasculature won't really help. What you want to do is potentially decrease preload and afterload (hydrostatic pressure) and drive the edema back across the alveolar membrane. You aren't going to pull the pulmonary edema back across by increasing oncotic pressure, but if you decrease hydrostatic pressure, you will decrease the causal problem, then you can fix it.

Now I;m confused :wink:

Actually, D5W although initially is isotonic, once the glucose is taken up at the cellular level (which is quickly), it becomes hypotonic and worsens circulatory volume by drawing water into the vascular compartment due to osmosis and oncotic pressure.

As for the bad evaluation, look at the source. The guy would probably give a bad eval for not giving SL nitro to a RVI too.

I don't think I am confusing it. Correct me If I am wrong, but due to the chronic dyspnea and extreme work of the pt, once they are on the vent, the body says " Cool, I don't have to work anymore, someone is doing the work for me, I think I'll just hang back and kick-it" "Wait, wait, don't take that out, that means I have to work to breath again, I don't like that"!!

Am I wrong, isn't that why CPAP came about?

Ahh, therein lies the connundrom. Typically pt's with CHF in isolation don't suffer chronic dyspnea, this would suggest more of an obstructive component of COPD with the CHF. If a patient gets to the point of requiring intubation, it's not a concern, because they need it in order to live. Weaning from a vent can be a problem, but there are many ways to overcome it. Things like permissive hypercapnea, pressure support (meaning they have to breathe to trigger the vent), etc.

Seldomly have I seen a systemic response to an ingested allergen. Usually it's angioedema.

Assess the tongue, uvula and their voice. Do they sound hoarse or muffled? Can they swallow, breathe through their mouth and nose? Can they stick their tongue out?

Decreased lung sounds is usually a late and ominous sign. If they complain of a sensation of their throat closing and you see evidence of such, believe them.

Historically, our highest success rates are in pulseless patients. Why is that? Could it be the right amount of anesthesia (sedation and analgesia) as well as flaccid paralysis?????