AZCEP

DC the D5W and replace it with LR. Dextrose containing solutions have no place in resuscitation. Any signs of drug overdose? Trauma? Breath sounds following securing the airway? Pulses generated with compressions? What's his temperature? What's the CO2 on the capnography show?

Actually, the guideline is to use the maximum allowable by the manufacturer of your specific defibrillator. There is to much variation between devices, and the waveforms they use to deliver the energy to set one number as the recommendation. You do not use the adult energy level on children over 8 years. They do not begin being treated as adults until the secondary sexual characteristics are present. This is vague at best, but for most it falls sometime between 11 and 13 years. The 50 kg child should receive 2 joules/kg initially, followed by 4 joules/kg for all subsequent shocks. American Heart and the American Academy of Pediatrics did not change the previous recommendations, due to a lack of evidence.

2 IVs with NS/LR wide open. Secure an airway quickly, and continue compressions. Any other history (medical problems, medications, allergies) on the 42 year old? Have there been any labs drawn?

I had a couple of them when they first came out, and they were more useful to develop a pattern for an assessment than they ever were on an actual scene. Kind of like the check-box style PCR's. As you would go down the page, it would have a box for something you hadn't thought of, and it would remind you. They were very good for daily assessment practice at the station though. I'll see if I can dig them up and scan the pages for posting.

Hey, what happened to the "why do you think this happens" approach?

When SVT is used to describe a rhythm with a clear origin, it shows the provider is not looking closely enough at the information in front of them. The strips you provided show a clear origin for the rhythm. Whether it is ectopic atrial tachycardia, or sinus, the treatment is still not goin to be Adenosine. The argument for using Adenosine as a diagnostic aid is for those times that you can't clearly discern the origin of the rhythm. This patient has a clearly discernible origin. It is not atrial fibrillation, as there are clearly discernible P-waves. Atrial flutter, while being possible, is not a strong possibility due to the absence of the flutter wave moving through the rest of the cardiac cycle. The QRS isn't slurred on the upstroke or at the J-point. That eliminates the possibility of atrial flutter. Yes, you were in a position that you needed to make a choice quickly on how to best manage this patient. Adenosine was not the decision that should have been made, and now you've learned that. Discussing the utility of "priority" transport is immaterial since we aren't familiar with any information that would make a difference in that decision. You got the patient to the hospital alive, and in no worse shape than when you made contact with them. You didn't cause another incident by transporting "priority", so there is really nothing more to argue with the hope of learning something from the incident. Arguing minutae is a complete waste of effort.

The best use I've found for the SAM guide is to create scenarios for students/training. For actual scene use, it is too cumbersome. If you do use one, very quickly you will find that you are following the pattern that is suggested without it. Kind of like the reference field guides. Valuable briefly, then falls quickly into not being used at all.

The Res-Q-Pod prevents the individual that is ventilating the patient from delivering breaths that will exceed a set pressure. The idea being if you can reduce the amount of pressure in the thorax, you will allow better blood return to the heart while compressions are being performed. Think of it as a circulation adjunct instead of a ventilation adjunct.

With the scenario listed, this patient is near unstable. Close enough in fact to consider synchronized cardioversion. Because this rhythm appears to be sinus tachycardia, adenosine is not indicated. Nor is it indicated for atrial flutter. The history combined with the ECG should show us that a rate control medication is not something to consider. Particularly one with the limited usefulness of adenosine. Yes, hindsight is a wonderful thing, but using adenosine when it is not indicated should not be supported.

Shoot, we've probably all watched physicians do things that were worse than this. That's an entirely different discussion though. :roll:

SVT is a default rhythm interpretation when you are unable to isolate any of the other specific narrow-complex tachycardias. If P-waves are present, the rhythm is not SVT. If flutter waves are discernible, again, no SVT. When the rate is so fast that an underlying focus is indiscernible, then it is reasonable to identify the tachycardia as SVT. Any other time, it is the sign of a lazy provider. Adenosine has a half-life of up to 30 seconds, but it's duration of action can last 2-3 minutes depending on the patient's tolerance/sensitivity to it. Patient's on methylxanthines (caffeine, theophylline) have a reduced response to Adenosine. Tegretol (carbamazepine) potentiates the effects.

I'm thinking the patient in this case is moving most of their circulatory volume away from the periphery due to the diaphoresis, and pale skin. This shows the patient's endogenous catecholamines are working as intended, but will make SQ medication administration challenging, and unreliable. Epi-pens are designed to go SQ, which won't be very helpful here. Even deep IM might not be very effective.

What does ectopic atrial tachycardia look like if this is what you think this rhythm could be? It is irregular, and the p-waves have different morphology from beat to beat. Yes, we are making an assumption that this is sinus, but with the strip provided it is the best interpretation you will get. Regular rhythm, identical p-waves in front of each QRS, normal PR interval for each of them. This is sinus. The likelihood of it originating regularly from an ectopic atrial focus is slim, at best. Adenosine was not the indicated treatment for this patient. Second IV or not, using a rate control medication on a patient that is trying to compensate for widespread vasodilation is not recommended anywhere. Your second IV should have been in the biggest vein you could find, including an IO site. This patient needed fluids and pressors.

You have a patient with a clearly discernible sinus tachycardia. Even if you do not use the machine's interpretation, which is a good move, your own eyes should tell you that there are P-waves preceding each QRS complex. There is no other interpretation that this could be. It is sinus, the rate is due to a compensatory mechanism. Adenosine is not indicated for this situation. Pressors and enormous amounts of fluid replacement are needed. Not rate control. I apologize for the harshness that is probably coming out of this post, but I've had to run through this same progression a number of times recently. :roll: It would seem that some providers are missing a couple of days of class.

One correction kristo, solumedrol does not work quickly. It has an onset following an IV dose of 2-4 hours, patient depending of course. The "tier" failed the OP in this case. He recognized the need for ALS early on, and tried to have them meet much sooner. Using the epi-pen probably would have been moderately to completely ineffective. This patient was shut down peripheraly. Unless they were able to put the standard dose deep into a large muscle group, the response would have been a bit haphazard. Instead of having EMT's picking up extra skills, let's send them to school to better learn the why's and when's of using medications.

What is her "normal" blood glucose level? 132 mg/dL could very well be hypoglycemic for this patient. ECG? Pupillary response? She seems to be protecting her airway adequately for now. Move to the transport unit.

A tough situation for sure, but it beautifully illustrates why you should go to paramedic school. Do you understand why the albuterol wasn't working for this patient? From your description you might want to look a little closer at what epinephrine does for asthmatics, and anaphylactic patients. Sounds like you've oversimplified things. This patient needed an ALS provider from the outset. The fact that only BLS was available is a system issue, not one to slap the band-aid of add on BLS skills onto. Get this patient a paramedic that can provide the treatment(s) she needs more quickly, and the "respiratory arrest" probably doesn't happen. Medical control may well give you the order to use your epi-pen in this case. The dose is going to be the same as the IM dose the medic used. Unfortunately, if they give you an order outside of your protocol, you are responsible for knowing if it is acceptable or not. The epi-pen usually goes SQ, rather than IM, so the absorption will be less predictable. It may be worth trying, but if it's not approved you will have other problems later. It's good you are asking the questions now. Get enrolled in a paramedic class and find out how you are woefully unprepared for these types of situations.

This is actually the AHA's definition of long term survival. It is also the standard they use to determine an intervention's effectiveness.

Emergency departments using "un-licensed" staff are doing so for the dollar. They are typically unable to recruit enough nursing staff to manage the patient load, and the nurses they have need help. Nursing students are their to continue their education, and as a recruiting tool, as Dust mentioned. A basic EMT is done with their education, and can't be expected to reduce any of the workload for the licensed staff.

Beta 2 receptors are not exclusive to the bronchi. They are found in all smooth muscle, with a predominance in the bronchi and coronary/cerebral vasculature. They are also in uterine smooth muscle, but that doesn't really apply to pulmonary edema very often. When we combine the alpha response of peripheral vasoconstriction, with the beta 2 response of central vasodilation the result is a restriction of fluid movement out of the central circulation. This causes the failing heart to receive an increased workload without giving it someplace to move the fluid volume. Result: pulmonary edema worsens.

Epinephrine's alpha effects are a good place to start with why you wouldn't want to use it for the patient with pulmonary edema, but they are just the start. Epinephrine is a potent beta agonist as well. The problem is you can't decide which beta effect you will get from it. Beta one effects will make the failing heart work harder, and worsen the MVO2. Beta two effects will create bronchodilation but it will also cause the coronary vessels to dilate. Combine the beta two response with the alpha (peripheral vasoconstriction), and you will cause the pulmonary edema to become worse. Nitrates/diuresis/NIPPV are the hallmark treatments for pulmonary edema. Epinephrine should be left until all other options have proven ineffective.

If it was a septal rupture, perhaps the slow rate and low blood pressure happened for long enough to allow some scar tissue to form, sealing the hole. Definitely an unusual progression.

There is no one with a higher licensure, or more education at this "Stroke center" than a basic EMT? Your training as an EMT is not sufficient to be able to assess anyone with a reason for going to a "Stroke center". To say you are the only one allowed to assess patients is a bit obtuse.

The heart is dependent on preload to generate the myocardial stretch for an effective contraction. The preload is created by the diastolic filling of the right and left ventricles. The systolic contraction remains fairly constant up to rates greater than 250 beats per minute. Your answer is diastolic, not systolic.

As an insulin dependent diabetic, you should recognize that no two individuals will present the same. I too, am a type I diabetic. My normal BGL is 64 mg/dL, and it can drop into the teens with no significant loss of function. How this has anything to do with the question at hand is escaping me. :roll: No matter what his current BGL is, if he presents as hypoglycemic, treat it. The patient's body becomes reliant on a given level of sugar. Once that level drops below the norm, they will present as there isn't enough of it. If they are hypoglycemic, the last thing you want to deal with is the continuous infusion of any insulin. Even the low basal rate will give them more than they need. Turn off the pump, and give the dextrose.