AZCEP

Now that would be something I could fully support.

Glucagon is not really effective in someone who has liver damage such as an alcoholic or someone with liver disease...

After you administer the glucagon, go ahead and start your IV and administer the Dextrose. The effects of the Glucagon will not last long at all and the glucose level will drop again pretty soon.

In these groups we need to remember how the drug is working, as to why it isn't giving the response we want.

If the Glucagon gives you a response (read: the patient wakes up, and can follow commands) a better subsequent action is to provide them with something to eat with more nutritional value than a pre-filled syringe of D50 has. The D50 follow up will work, but if the patient can eat something, it will give a longer duration of effect than straight sugar can.

And of course, re-check the BGL every few minutes to trend the changes.

From eMedicine:

Pathophysiology: Oxidation of iron to the ferric state reduces the oxygen-carrying capacity of hemoglobin and produces a functional anemia. In addition, a ferric heme group affects nearby ferrous heme groups. Ferric heme groups impair the release of oxygen from nearby ferrous heme groups on the same hemoglobin tetramer. The result of methemoglobinemia is that oxygen delivery to tissues is impaired and the oxygen hemoglobin dissociation curve shifts to the left.

Organs with high oxygen demands (ie, CNS, cardiovascular system) usually are the first systems to manifest toxicity. Oxygenated blood is red, deoxygenated blood is blue, and blood-containing methemoglobin is a dark reddish brown color. This dark hue imparts clinical cyanosis when methemoglobin levels are at 1.5 g/dL (approximately 10-15% methemoglobin concentration); however, a level of 5 g/dL of deoxygenated blood is required for similar effects. Therefore, when methemoglobin levels are relatively low, cyanosis may be observed without cardiopulmonary symptoms.

Removal of the patient from the offending environment must be attempted by properly trained and equipped personnel

Methylene blue is the first-line antidotal therapy.

Methylene blue accelerates the enzymatic reduction of methemoglobin by NADPH-methemoglobin reductase and also reduces to leucomethylene blue that, in turn, reduces methemoglobin. The initial dose is 1-2 mg/kg IV over 5 min. Its effects should be seen in approximately 20 min to 1 h. Patients who are exposed may require repeated dosing, but high doses of methylene blue may actually induce a paradoxical methemoglobinemia.

Treatment failure may occur in patients with ongoing exposure, patients exposed to sulfhemoglobinemia, and patients who have deficient NADPH-methemoglobin reductase enzymatic pathways. Methylene blue should be avoided in patients with G-6-PD deficiency, if possible, because case reports and in vitro models suggest that this antidote may induce hemolysis in this patient population.

Hyperbaric oxygen and exchange transfusion should be considered for patients who are not candidates for methylene blue treatment or when methylene blue is ineffective.

Because of the disparity of HBO facilities, high concentrations of oxygen should be administered as early as possible.

Methylene blue is also popular at parties. You can readily identify if someone is using your pool as a community urinal with a few drops in their drink.

Don't get your hopes up Eydawn.

NREMT makes these same changes every 5 years, in concert with AHA, and they make the same errors. They use some of the same techniques as other standardized tests, so they can't get all of the blame.

I am curious to see how the computer based testing changes things though.

I did notice that your suggestions missed clean teeth, or is this just a problem in my response area?

My goodness, I think I have found a new career path. "Ambulance readiness assistant," trained to help you to make a better impression when emergency services are required. Now if people will pay funeral homes to fix them up before the lid is closed permanently, don't you suppose they would be willing to fund a little assistance before that happens.

Franchise rights will be going up for bid soon.

I think #8 just made it into my LOC question list.

Speaking only for Arizona.

National Registry is used to test competency for initial certification. You have to fill out a separate state application, but you don't have to take a separate test. This assumes that the course you took is recognized by the state.

If you are coming from somewhere else and currently have a National Registry card, then you will be required to take an ALS refresher course prior to being granted state certification.

I do know that some places require only a state application fee, and copies of your current cards, New Mexico being one. There are also those places that require a fee, your cards, then you have to take either a written, or a practical exam before being granted a state license. Utah and Colorado used to be this way, but I'm not sure of current policy.

The best way to find out is to ask the people in the state/region you want to go. All of the regulatory agencies are happy to give you this information. Just keep in mind, you may get different answers from different people in these agencies.

Isn't this akin to saying, "It sure is quiet." ?

We are still waiting for capnography to be mandated, so that we can afford to purchase the equipment. What I have learned about it, makes me wonder why it hasn't gotten into more places sooner. One department I know of spent a significant amount of money for waveform capnography, then didn't bother to educate their personnel on how to use it, other than a full arrest. :roll:

Using etCO[sub:8787094a65]2[/sub:8787094a65], along with a pulse oximeter, will almost allow you to predict what treatment is needed, and how they will respond. If I could only have one, I would go with the capnograph, but we already have the pulse ox, so we might as well use them.

One question for you Rid. Did you mean beta-2 agents? I don't recall capnography relaying as much information about the beta-1's, but I could be mistaken.

I agree with Rid and ak.

If the patient is abnormally large (read: obese), lying flat will make it next to impossible to get good chest expansion. Raise the head of the board 10-15 degrees so the weight is moved a bit, and things should improve. Anxiety states need a calm voice to reassure them that they will be okay.

Re-assess lung sounds and vital signs. Somewhere I remember reading that chest trauma can cause shortness of breath, right? Worse comes to worse, coach their respiratory rate, and maybe assist with a BVM. Doesn't happen often, but it can be useful, if the patient will let you use it.

There is a paramedic that works for University MedFlight(I think that is the name) in Salt Lake City, that had his forearm amputated following a PTO accident on a farm. If I can recall the story he told, he was an paramedic at the time that he lost his arm. Had to relearn how to do the most basic procedures. He now works with the old style clamp/hook on his left arm. Says he invested in a personal laryngoscope so he wouldn't have a problem intubating.

This is only how I remember his story, and I could be waaaayyyyyy off.

Maybe this means that we can carry ourselves like other DOT workers.

You all know the image: One guy doing all the heavy work, four or five others standing around holding shovels, drinking coffee, basically not doing anything to help.

Wait, wait, that just described the last scene I was on. OOOOOOHHH, a perfect fit, methinks. :shock:

If I'm not mistaken, ACLS guidelines recommend ceasing resuscitation attempts after 20 minutes. Personally, I am willing to commit myself to 20 minutes on scene to try to get a response. If none is found, a quick call to medical control follows. The only patients that I'm transporting are able to push their own pulses.

If a patient codes in my ambulance, then efforts are started, otherwise they stay where I found them.

Yeah...I'm going to need a pay raise. :shock:

Look at the pretty colors :roll:

My customer service skills are unmatched... but they are for the customer, my patient, not for bystanders and not for off duty medical personell that don't have there own medical license with which to work under ( nurses still need doctors to work under ).

Anyone and everyone that you come into contact with is a customer. I know, I had a hard time listening through that seminar as well.

Telling anyone something that feels good at the time is usually a bad idea. Without being on scene, I won't second guess what was done, but my own history leans toward making the public less than happy with what I have said. Act like a professional, look like a professional, if you want to be treated like one.

I wish that were true. Since I am in the middle, that would mean we would get Philips, which is ten times better than either Zoll or LP. Unfortunately, I have yet to see one here.

One of our local fire departments recently purchased the Phillips monitor, and have nothing but trouble with it. Simple things like dumping the charge when the rhythm changes from VF-->PEA/Asystole, having cables connected, etc. Like with any piece of equipment, you have to learn all of the ins and outs of what you have sometime before you need to use it. I'll stick with my boat anchor LP12, thank you very much.

DNR status

Depending on that:

O2, probably a little for now

IV, she sounds a bit dehydrated

ECG

last oral intake, and her current meds

That is a good place to start.

Every class that I've been involved with, either as an instructor or preceptor/clinical evaluator, someone has tried to bat their eyes at me. I honestly try to maintain a level of professionalism, but sometimes I truly want to ring their necks. :twisted:

I don't care who you are, or what the setting that I interact with you is. If you don't know what you should know, you will not be granted a passing score. Students will try most anything to pull one over on an instructor. Only the weak ones allow this to happen. Might explain why there are so many piss poor providers fresh from classes.

Of course, I'm also of the opinion that if you have a license/certification and you don't know something that you should, don't expect me to teach it to you while I am fixing your mistakes.

Itku2er: You said 1ml of glycogen IM

I assume that you had meant 1 mg Glucagon IM correct????

One of the more commone trade names for glucagon is Glucagen. Neat little way of mashing the two together and confusing the [bleep] out of the uninitiated.

From the sound of things, the patient didn't have much GLYCOGEN stored in the first place. Or maybe had some competing medications blunting it's response. Anyhow, I wouldn't expect much of a response to glucagon in this patient, given the initial vitals. Peripheral perfusion is probably terrible, so the response will take an extremely long time.

Carry on.

Definitely keep your description as simple as possible.

If you only see one hole, well that must be the entry. If you see two, describe them as penetrating injuries and where they are located.

If they have a hole, plug it. If they need a hole, make it.

Every drug that you will ever be exposed to will cause nausea/vomiting, so I won't spend a lot of time on that one.

For the hypotension/tachycardia, you might look at the indicated use for glucagon. Also delve into how the body will naturally respond to this indication.

Now, when the body becomes hypoglycemic, one of the first things that happens is the cardiac output will increase as a response to be able to get some food. The sympathetic nervous system is stimulated, and glucagon is released from the pancreas to use some of the stored liver glycogen.

So, with the SNS stimulation you will get tachycardia, and typically hypertension, as the body tries to provide nutrients to the brain while they are still available. The hypotension can result from the smooth muscle relaxant properties of the glucagon, but it is fairly uncommon.

First, keep in mind that a capillary sample for your BGL will probably be inaccurate in a cardiac arrest. The blood stops moving so it can't deliver the sugar to the tissues.

The frequent DKA patient that finally arrests needs a couple of things to bring them back. First would be fluid volume. DKA will cause a level of dehydration unlike most other causes. That might justify early central access, if there were difficulties getting peripheral lines.

The acidosis that is associated will skew the level of K+ to the high side as well. It is not uncommon to treat the hyperkalemia in a code, but remember that once the blood sugar returns to normal your treatment will cause a degree of hypokalemia. Typically the presenting rhythm will be tachycardic, due to the hypovolemia. Without seeing the strip, Epi/Atropine are reasonable PEA drugs. I would have gone with the Bicarb/Calcium before the Insulin, because it will have a more direct effect on the myocardium.

Now for the calcium. Calcium gluconate or chloride will stabilize the transmembrane potential in the myocardium. When there is an excess amount of potassium outside the cell, the sodium and calcium won't want to move out as easily. This creates a situation that does not allow the muscle cells to contract/relax as they are supposed to. Your doc was trying to stabilize a suspected hyperkalemia with the Bicarb/Calcium/Insulin/D50. Although, if the patient is already hyperglycemic, there isn't really a reason to through more sugar into the equation.

What you saw was pretty standard. Was there any change in the patient's status following all of this? Otherwise good practice.

Everybody has anectdotal evidence that a particular treatment will "cure" autism. I've yet to see any of them backed up scientifically. Hey now, if it works for your kid great, but my wife and I have bought into too many ad-hoc plans of treatment that amounted to nothing more than snake oil.

As you said, every autistic patient is different. Makes it tough to say that any one treatment will work better than any other now doesn't it?

As it stands right now, there are plenty of tools in the box. The problem is more a matter of having enough providers that know how/when to use them.

As an example, only using capnography on a cardiac arrest patient. Why not use this device to prevent the arrest in the first place?

I agree with Rid. We have to get past the appearance that we are minimally educated, and shouldn't be expected to know too much. Whether you like it or not, we are practicing a very specialized form of medicine. It just so happens to have some fairly significant restrictions because of size and weight of the equipment that we must use. There are very few people with higher levels of education-supposedly-that would be able to function in our environment, with the equipment that we have.

Many times an autistic patient will react to the approach of the care giver. If you act like something is bothering you, then the patient will act bothered by it as well.

I also have an autistic daughter, and one of the greatest challenges is convincing her that things will be alright, eventually. Autistic disorders tend to be rooted in routine. Mealtimes, medications, baths, waking up usually occur at, or near, the same times. When an event throws the routine off, the patient often will have a difficult time coping with the change.

Keep everything calm, try to build some degree of trust, maybe use a blanket wrap to help restrain, if needed. Good luck getting vascular access, consider nasal versed/ativan as a last resort. Unless they are critically injured, most of our treatment will only agitate them further, and make the situation worse.