AZCEP

Start documenting right now. Supervisor/administration needs to be made aware of this happening, so maybe they can track it back to when it first happened. I would guess that if it has been there a while the drug in question will be expired. Take it with you to the supervisory staff, so they can see the drug for themselves. Or, on a different ethical level, see if you can convince some "insurgent" employees to take it off your hands.

Where, pray tell, did you find a lower morbidity/mortality with amiodarone over lidocaine? At 12 months, regardless of the agent used, the patient will still be dead. If you are quoting the pre-2000 guidline change AHA research, there are plenty of holes shot through that pile to not even be worthy of further discussion. Amiodarone, supplied in vials, is a soap based medication. When you draw it up too fast, you create soap bubbles in the syringe. This also reduces the available drug, and the amount that has been drawn, and the syringe it is in need to be discarded. Using a large gauge needle, and drawing slowly is the only way to avoid this from happening. The same goes for administration. When pushing it IV, push slowly with a large needle, or it will foam up(tween) and you will not deliver the right dose to the patient.

Higher concentration of total body water. More water, moves through the kidneys faster following the sugar bolus. Can't stop the mechanism in time, resulting in dehydrated kiddoes. It is also less sclerosing to the small veins.

PMHx? What was she doing when it started? Can she localize it? Facial droop?

Sodium bicarbonate does work in the way you describe, but it is also used to provide a greater amount of Na+ to counter the sodium channel blockade that TCA's create. The alkalinizing properties cause the TCA to move more quickly into the urine and be eliminated, while the sodium counteracts the ionic movement limitations.

Not quite. Treating a wide complex tachycardia caused by sodium channel blockade with Lidocaine will have more effect on blunting the sympathetic stimulation, than it will block the sodium channels. Lidocaine is placed in this category due to it's actions, but they are not terribly strong, nor reliable. By steepening phase 3-->phase 4 transition, the lidocaine can, theoretically help to reduce the heart rate. The better choice for treatment is sodium bicarbonate. This will narrow the QRS complexes, and alkalinize the urine to help draw the TCA out of solution. By helping to eliminate the offending agent, the bicarb will do more to mitigate the situation than other possibilities. Treat the underlying cause, instead of the presenting symptom.

Bushy, What you wrote was correct, but you seem to be thinking of them separately. Lidocaine is a class 1b antidysrhythmic, meaning that it is a weak sodium channel blocker. It's primary effect is on phase 4 of the action potential, rather than phase 0-1. It will effectively lengthen the duration of phase 4, allowing for more time between impulse generation. TCA's will block the sodium channels much more effectively than lidocaine, as a side effect of their primary actions. When this happens you will notice a widening of the QRS complex, along with an increased heart rate. The QRS width is caused by the sodium channel blockade, slowing the progression of phase 4-1-0 in the action potential. The increased rate is related to the sympathetic dysfunction that they cause. When you add the two together, the myocardial cell is both less able to generate a normal impulse, and it is being stimulated to create more of them. This leads to the tachydysrhythmias that are common with these agents. They also carry an anticholinergic action that will add to the situation.

Trouble is the real origin has passed into the great beyond of folklore. Here's another version:

This is the very problem of most going into a full paramedic class. They have no earthly concept of what they have signed on for. Even with the warnings, the inexperienced come in thinking it won't be very hard. Then they try to use the analogy of previous standards to the current one. This is great. I applaud you, yet again, Dust for trying to snap some reality into the situation. As a provider that has been around a couple of blocks, I have to know that others on my scenes know what I do. The fact that I'm never far from some reference material aside, if you want to act like a paramedic, then you better know what every other paramedic knows. I don't think the CNA analogy is entirely inappropriate. Many places still force people to be certified as EMT's before allowing them to enter paramedic school. Get your feet wet, come back in a couple years, and we will see what you have learned before we allow you all of the "cool" stuff.

I will echo croaker's sentiment. In Arizona, each transporting provider is issued a Certificate of Necessity. This basically says that a given entity can provide service to a given level with available resources. It also outlines response times based on the size of the geographic area that a service has to cover. Some of the response areas are 3-4 hours across, so telling a provider that they have to have ALS/BLS on scene in 8 minutes would be entirely unrealistic. Most have guidlines based on percentages and times to respond like already mentioned.

The conduction system defect is unlikely to cause the TCP to be unable to capture. The pacer isn't relying on the intrinsic conduction system too much anyway. It would be likely that the events played out as you suspected, but instead of the damage to the conduction system, perhaps the ischemic/injured myocardium was unable to accept the stimulus. When a degree of acidosis presents, the tissue just doesn't want to respond like we expect it too. Patient factors aside, it may be time to take the pacer to your bio-med person to give it a good going over.

Do we know what his normal blood sugar is? 60 mg% is pretty low. Most places will consider treating it with this presentation. I will be glad to help Asys with the duct taping. Might even provide a UPS label for the trip. Now is not the time for my EMT partner to question my thinking. Later will be fine, but not while I'm trying to figure this situation out. What are his pupil's size? Sinus brady would be expected with the beta blocker. The blood pressure isn't horribly low, and should be plenty to give us a better response than what is there. Atropine won't be much help anyway. It will only remove the restriction on the heart rate from the PNS. With this presentation, vitals where they are, there probably isn't much vagal stimulus present. Pacing Sinus brady doesn't strike me as a good idea either. Figure out a cause of the altered mentation, and try to keep your EMT's hands out of the drug box.

Why would you not be able to diagnose an inferior MI with these changes? Two contiguous leads--check Diagnostic spectrum--check MI identified Would it be good to have the other 10 leads, 9 if you discount aVR as you should? Yes, but you could still use the information you have.

Depending on the equipment you are using, diagnostic and monitor quality usually refers to the electrical spectrum that the monitor views in. Some are adjustable to work in diagnostic mode when utilizing limb leads, some will only do so when analyzing a twelve lead. Monitor quality is a range of 1-30 MHz, while diagnostic is 0.5-45 MHz. The wider range that is allowed in diagnostic mode, allows a better picture of the electrical events.

This argument is carried by the NREMT testing process. Does it really happen in practice, let's hope not. If you want to focus on one aspect of care, perhaps it would be better directed to think in terms of the invasive nature of the treatment you are wanting to perform. Start simple, less invasive, and work to more complex/invasive modalities. There's a reason paramedic students become hermits for 2 years of their lives. Hopefully, it is in a pursuit of understanding why this testing station mantra doesn't apply to actual people they will have to treat.

Hold the blade in the right hand, face the patient, tube in the left hand. Everything is turned opposite of the norm. Some people actually find it easier to intubate in this position.

When DE-polarization is abnormal, RE-polarization will be abnormal

Active cooling has it's place, but I'm not sure it is prehospital. The need to keep the temperature between 90 and 92 degrees Farenheit is troublesome at best, under closely monitored circumstances. In a moving ambulance, it will be next to impossible. There was some discussion a few years ago that most resuscitations are mildly hypothermic through passive mechanisms, so the need to actively cool them wasn't being supported. Reducing the metabolic demand is a great idea, but doing it through cooling carries many questions on methodology. Very interesting how the EMS system has influenced the hospitals to continue the treatment.

It all depends on what your school tells you, you can, and can't do. There is usually a working agreement with the facilities in question, prior to clinicals starting. You will probably be given a list of places you can do your time.

Fair enough. Just looking for an explanation that I might have missed. I would also expect Vtach to be faster, but a rate of 126/min would not typically be fast enough to cause a rate related aberrancy either.

And your reasoning behind Afib RVR with aberrancy?

Most of the treatment suggestions are based on best evidence. Beta 2's, steroids, IV fluid replacement, and considerations of PPV are all backed with EBM. Magnesium hasn't been supported with great research, but when it is used, the pharmacology of it, can be justified.

Ventricular origin, rate greater than 100/minute = Vtach

I'd like to see a continuous strip, and get a patient's history. What does the patient look like? Can't use the information from a single ECG in a vacuum of information. Have to know what else is happening. With the information provided, I'm calling this Vtach, treating with Amiodarone, and preparing to cardiovert.

Leads I, II, and III are bipolar limb leads. They use a positive and negative pole to view the activity. Leads aVR, aVL, and aVF are unipolar limb leads. They use a single positive pole to view activity. The ECG calculates the location of little to no electrical activity and uses this site as the negative electrode. Electrical activity(EA) in lead I + EA lead III = EA lead II, or (lead I + III) - II = 0 The precordial leads use the same central terminal(CT) for their negative electrode. If you want more information than this, look for Einthoven's law.