AZCEP

None of the available choices are going to perform very well once the airway is full of fluids inherent to poor intubation technique. The LMA doesn't have a place in the prehospital environment. It is too easy to dislodge, and does a poor job of protecting from aspiration. The King LT is the way to go. Easy to place, simple to replace with an ET tube, no latex. The sizes that are available fit a wide range of patients, so that should not be a concern. Pediatric back up devices are a waste of money in most cases.

Good link jmac. The skin is just a part of the integumentary system. By itself it may not be all that big, but with all the pieces of the system, it is huge.

The maximum recommended loading dose for BZD's is 20 mgs. Any more than that at one time will not give any more of an effect. If a patient needs more medication to control a seizure, consideration should be given to something other than the BZD.

Move her quietly out of the woods. Keep the bite below the level of the heart. Splint the leg.

They are the same class without the depth of administrative requirements. They use the same ECC guidelines that AHA classes use without doing any of the work to achieve them. "Excellent" may be a bit of an over-statement, since the faculty of a given program has more to do with the course utility than the administrative body you get your card from.

Unfortunately, the Hs and Ts memory aid is really on the most simplistic of reminders. Most commonly hypoxia will be the issue, but there are a lot more reasons for a dysrhythmia to show itself. You can use any dose in that range, but you shouldn't expect any great results until you get enough into the system to illicit a response. Half to three-quarters of a milligram/kg will give results, and is recommended for the elderly, hepatic failure, and signs of poor perfusion, but chances are it will take a few more doses to work for you. Most will give two 1-1.5 mg/kg doses prior to changing regimens. Using the half-doses would allow you to use it a bit longer if you felt you needed to. This doesn't happen nearly as often as people would have you believe. Consider the status of the patient in front of you, rather than an outdated nugget from an instructor. Argue away. If you only have one set of information to work from, you will tend to hold fast to it when there may be another way to do things. Willingness to accept a different viewpoint is a sign of a good critically thinking provider. Every new provider, leaving class, feels the same way you do. More is learned in the first two weeks after class ends than in the entirety of the program you graduate from. Luckily, the resources to bolster your confidence are no more than a computer terminal away.

You were smart enough to ask the question, so your status is in serious doubt. A couple of issues here. First, the presence of asymptomatic ventricular ectopy does not absolutely have to be treated. Even with the amount that you are seeing. Chances are it is being caused by something, and you should try to locate that cause. Second, I'm not sure where you got the initial dosing from. Most reference sources use the initial dose of lidocaine at 1-1.5 mg/kg. The follow-up doses are then half of the initial. Even with your dose of 0.5 mg/kg, you would still be several doses from the maximum of 3 mg/kg prior to starting a drip. Your move to "consider" Amiodarone isn't altogether wrong, it just isn't what NREMT wants to hear. You are correct to start thinking of using something else, but you should be sure that the dysrhythmia needs correcting. You wouldn't. After you find out that the full dose of Lidocaine--3 mg/kg--isn't working, you should consider an alternative. You might not need to use it, but it should be considered. They aren't contraindicated, but they CAN increase the risk of AV blocks or refractory bradycardias when used together. The nice thing about Amiodarone is it's ability to manage tachydysrythmias regardless of origin. It also has a 20-25 minute half-life. This allows you to use it without needing to hang a drip if you don't carry enough, which you are correct, most don't. Lidocaine doesn't allow for more options. It is the drug that most are the most comfortable/complacent with. It's easier for people too recall how to use, because it's been around for so long. +5 for asking a question that more should be willing to ask. Maybe if you hadn't been snoozing through class, you could have asked it before your NREMT test, but I can't blame you for that. With the quality of instruction in some programs, a good sleep is the best thing you can accomplish. :roll:

Re-read the previous posts. Sgarbossa's criteria are not particularly useful in ruling in, or out, an acute MI in the presence of LBBB. The question was would this information be useful when given in a report, and said nothing of "dumbing down" anything. The responses already given indicate that those that receive this information from the paramedic will not use it.

Chamber enlargement can give you an idea of other disease progression. Axis Deviation can also provide information related to other disease states. COPD is especially evident from axis deviations. It will also allow for origins of the electrical activity that you see. Bundle Branch Block tends to be overemphasized, but intra-ventricular and intra-nodal conduction delays are useful to specifically look for. Infarct/Ischemia of the acute variety tends to cement a working presentation, but when patients present with evidence of previous events I tend to look deeper. Yes, the 12 lead is a useful tool for many things beside the acute infarct/injury pattern.

As with any ECG data that is gathered, too many patients are not going to show any outward sign that you will be able to use. For those without a LBBB pattern, you have a less than 50% chance the ECG will have the trademark ST deviations. With a LBBB, it is in the same neighborhood. This group of criteria haven't adequately demonstrated they will be any more useful than clinical judgement, yet.

Did the abdomen become less distended following NG/OG tube placement? Were you able to ventilate with BLS adjuncts?

Yes, pull the ET tube and ventilate with a BLS airway for a minute. Consider an NG/OG tube to decompress, and perhaps place a Combi-tube in the interim. Re-assess lung sounds, throw the EDD in the trash, shake your head at a provider that should have known better. :roll:

Management of the stable patient tends to be a bit more complex than the unstable. With stability comes the decision of treating or not, gathering more information or going with what you have. When the patient turns unstable, the decision becomes much easier.

I can't seem to find the one that I had. I'm thinking I must have given it to someone that was struggling to find a pattern to their assessment.

By measuring to different points on the QRS you are proving my point. There is a subtle irregularity there. Measure again to the same point of the QRS, and you will see it.

You do realize that the rhythm is irregular, right? It is subtle, but it is definitely there.

I'd probably consider holding off on the ASA, just because the patient is already on it daily. It might be reasonable to use a lower dose even. The ECG is pretty interesting, just because you don't often get to see this mechanism in action. On the three lead, continuous strip, it appears that when the rate speeds up the QRS complexes narrow, and when it slows down, they widen. Much more common to see the reverse happen (ie, faster-wider, slower-narrower). This looks like a rate control issue more than an irritable foci. With the history, it could be any number of things, but it might be useful to consider rate control of the atrial fibrillation. The patient being asymptomatic leads me to think that it would be acceptable to just watch things as they happen, and not jump to any specific, possibly detrimental, actions.

Tough to judge without seeing the patient while this was happening. Some of the subtle findings get lost in the translation. That young, without risk factors as you describe, I'd probably forgo the cath lab also. I'm sure there is something in the history that would have suggested something other than an ischemic event, but can't really say so from this information. You've described the situation very well, but there is always something left out that may well swing the decision another direction. Luckily, an angiogram is not a terribly difficult procedure to perform, and once it is done the cardiology team will have good information to work from. It doesn't sound like this patient absolutely needed one, but that's for someone else to determine.

Shall we say it's a good thing he is non-ambulatory, on Plavix and a beta blocker, and quite used to people taking care of him? Over 45 with a complaint above the waist gets a twelve lead. You just can't trust people to tell you what is going on.

Blood glucose? ECG? Is it possible the patient got a double dose of his atenolol?

Rapid IV push KCl then? Did she put the potassium into the bag, or into the injection port? Where in blue blazes is the dialysis team? Let's take a moment to think about the scenario so far. A dehydrated middle aged male that is nauseated. IV running and sent to radiology to take a picture of the abdomen. Patient arrests following a mistake from someone and the patient's potassium is now off the charts. So there is evidence of some lactic acid building up, probably due to the dehydration leading to nausea. This will elevate the potassium level by itself, although it is not a true elevation. More of a misappropriation of the amount that is present. The dextrose containing IV solution is not going to help with the potassium level, or the fluid imbalance. Switching to a volume expander will be much more useful. This patient probably had some compromise of his renal function to start, we don't have IV fluids to maintain them as is, and then we add in the contrast dye. Any one of these things could have influenced the direction this is going, but in combination, obviously less than beneficial. The NaHCO3/CaCl/Albuterol/Insulin (I forgot that one before ) will temporize the problem, but we desperately need to get the offending electrolyte out of the system.

Yes, I took that into account scottymedic, and thank you for pointing it out. I'm sure someone will use the information you provided as a reference point for their own mismanagement.

Just something to keep in mind. Phenergan can cause a retention of potassium which would elevate the level artificially, leading to some pretty significant problems. Adding some potassium to the IV might have been a good idea, but was it done in a way that was going to be easy to control? By that I mean, did they hang it in a separate bag that was not being used for fluid resuscitation, or was it just mixed in the one bag? Obviously we want to stop the infusion of the potassium for now, and try to normalize/stablize the situation. Was emergent dialysis available?

Bingo!! Sodium bicarb/CaCl/Albuterol ASAP. Do we have any electrical activity on the monitor, or is it still asystole? Might consider emergent dialysis, if it's available. Blasted phenothiazines anyway.

We need a potassium level immediately. Also consider switching from epinephrine to vasopressin. Hypoxia = managed with the intubation/BVM Hypovolemia = two large IVs with NS/LR Hypothermia = negative Hypo-/Hyper electrolytes = definite possibility Hypo-/Hyper metabolic = Not at present Tamponade = unlikely Tension pneumo = negative Tablets = aside from the effects of the phenergan, nope Thrombus, pulmonary = not likely Thrombus, cardiac = not likely