fiznat

What kind of medic program are you looking into? If you can find one that is accredited (maybe at a local community college?), you can apply for scholarships through the school as well as federal aid. You can also apply for student loans. I donno, I would look into those options first before you attempt to portray yourself as some sort of local hero in the making. Medic school isn't THAT expensive, I'm sure there are other avenues you can try before searching out that elusive EMS philanthropist.

I never said that I would have cardioverted, or even given Adenosine to sinus tach. It might help to read back on what has already been posted, over the last 4 pages, and see the discussion that took place about determination of the rhythm and use of the drug - as endorsed by our regular docs here - for a diagnostic purpose. Thank you though, for your grandiose - albit repetitive and late - restatement of all that has already been said. The addition of your point of view was not only vital, but pivotal in the continuation of our discussion here. I was wondering if you could restate again: what is your position on adenosine and sinus tachycardia?

Ugh, this is getting redundant. Sinus tachycardia IS A TYPE OF SVT. Not to mention that this rhythm is not absolutely sinus tach. Sure, it probably is, but there DO exist other possibilities for which Adenosine/Cardioversion could have worked. We've discussed this, maybe 3 pages back. If there is something new you would like to add, then please do.

I'm really surprised to hear that a lot of you guys would take this patient priority 2 (no lights, no sirens). Here is what I was thinking: As far as the width and breadth of my knowledge goes, the hospital essentially has limitless resources that I do not have within my truck. To mention a few are RSI procedures, CT scans, labs for blood works, extra hands, doctors, etc etc etc. I did not clearly know what was going on with this patient, and I am not so arrogant as to assume that the hospital did not have an answer, or a treatment, that I didn't think of or am incapable of providing. Lights + sirens transport shaved maybe 8-10 minutes of travel time for us. I work in a city, and there is a lot of traffic, stop lights etc. I felt that this was a significant amount of a time for this patient. I don't know. Perhaps it is in fact my "inexperience," but while I had some suspicions, I didn't really know exactly what was going on with this critically ill patient, and thought it was prudent to get the patient to the hospital as quickly as possible.

Come on man....

If there is anything that goes without debate in this thread, I imagine it is probably the priority of the transport to the hospital. This patient absolutely was circling the drain, as you say. Hypotensive beyond measure, unresponsive, tachypenic, tachycardic... what else could you ask for? If nothing else, the fact that the patient coded 4 times in the ED should speak volumes as to how critical this patient really was. Priority one, no question about it. Some people don't like to go pri 1 to hospitals with acute MIs because they worry (among other things maybe) that the anxiety of lights + sirens can possibly stress the patient out, increasing cardiac demand and therefore the damage to the heart. Its a matter of opinion, I suppose. This response, however, I don't really think is debatable.

SVT = SupraVentricularTachycardia Supra = above Ventricular = the ventricles Tachycardia = fast heart rate Strictly speaking, a SVT is any tachycardia that originates from above the ventricles. This includes both atrial and junctional foci. People have come to use the term "SVT" more specifically, though, generally referring to reentry tachycardias, ectopic atrial tachycardias, junctional tachycardias, etc. A-fib, A-flutter, sinus tachycardia, etc, although they are technically SVTs, are usually considered to be separate as the treatments are different. Adenosine has a very short half life and a very short duration of action, but that doesn't mean that it's effects dont last longer. Adenosine is a kind of chemical cardioversion-- think of it as defibrillation in a syringe. The goal is break the rhythm into something else, "reset" the heart to a safer rhythm. The drug does it's thing and then goes away very quickly, with the hopes that the heart will do the rest of the work on it's own. That's why Adenosine only works with a few specific tachyarrhythmias: only some rhythms can actually be "broken" back into normal sinus.

lol guys give him a break. He still seems to know a lot more than many EMTs I have seen. I would be careful when you question the medics who ran the code. It seems that you have a few details mixed up and a.....less than complete understanding of ALS resuscitation. Be careful that your tone is more deferential and less accusatory.

Dwayne and others, thank you. It is a bit embarrassing sometimes-- especially with cases like this, and the previous one with the other (?wide) tachycardia, where things tend to be much clearer in hindsight. I put this stuff up here because it is extremely valuable to me to hear what you guys have to say, and I hope at the same time that it will be equally valuable to other people as well. Thank you for the compliments (even in the face of my sometimes questionable medicine, haha)-- but I have no doubt that many of you guys would do the same thing. (Post threads, that is :wink:) I did get a chance to follow up on the patient a little bit though today. The doc who had the patient wasn't in, but I got a chance to talk with the nurse. Apparently they did a head CT which was unremarkable, and tried to do some other kind of scan (unsure what he called it) to identify a possible PE but they were unable because the patient's renal function was so low. I guess he couldnt metabolize contrast dye or something? Not sure about that. Anyways, the guy's WBC count was just over 30k-- everyone seemed to be thinking sepsis, as I/we had originally suspected. The patient was sent up to the ICU, extubated, and put on CMO orders with a morphine drip only. The nurse didnt know for sure but he thought the patient had already died. I'll try and get a better, more specific followup next time I run into the doc.

I think you're thinking of multifocal atrial tachycardia (MAT), not simply ectopic atrial tachycardia, which can be from a single focus and therefore maintain a regular rhythm and a single p-wave morphology. You are right, though, that this rhythm is probably fairly rare (although I am unsure of the real statistics), and my patient's rhythm was more likely sinus. You are probably also right that adenosine was not indicated. Given all that, though, at the time I felt that it was worth a try. If the rhythm was truly compensatory, the adenosine would do nothing. If it was ectopic, there is a chance the drug could have helped. I am not putting the patient at risk, but simply attempting a treatment that may or may not work. Will I do it next time? Probably not.

Yeah, and there it is. Like I've said a few times now, I never really thought that this patient had a primary cardiac problem. I used adenocard because I felt strongly that a rate of 180-190 was too fast to be compensatory or singly mediated by infection, and the patient was profoundly hypotensive. I had already done everything else that I could have to help with pressure (fluids wide open, trendelenburg), and I had maybe two minutes to do something else. The choices were (I think we agree): intubate, 2nd IV, or drugs. I went with drugs because I felt intubation would be difficult if not impossible (and the BVM was working nicely), and the patient was a very tough stick-- I didnt think I'd be able to get another line, leaning over the patient to his right arm in the moving, lights + sirens ambulance. Adenosine was diagnostic, yes, but could also have turned out to be an effective treatment. In the unlikely event that this rhythm was originating from an irritated ectopic focus, I might have been able to break the rate and help contribute to a more reasonable blood pressure. Given the amount of time I had, and the complications with my other options, I felt it was the best thing to do at the time.

Wait a minute. Correct me if I am wrong here (I may very well be), but just because there are p waves doesn't mean that the rhythm is coming from the sinus node. All it means is that the rhythm has a single atrial focus. I admit that the morphology of the p waves is pretty consistent, but that would also be true if the rhythm was from a single, irritable ectopic focus. It is simply not true that "there is no other interpretation that this could be." I'm not seeing anything there that tells me that the rhythm is NOT an ectopic atrial tachycardia. In fact, the rate might even suggest it. It could be sinus, too, but I felt that the rate was too fast and I took a shot. Dont worry about the perceived harshness-- its all good. I expect that from you guys, especially if I screwed up! :wink: That would be nice if I had a half hour with the patient. I had 10 minutes, and probably only 5-6 minutes of actual time to run fluids in once I got the line and everything else all set up. The IV was wide open. Theres your bolus.

I agree. ...Although at the same time I felt that the rate was possibly a problem in and of itself. Sure, it may be part of some other pathology, but that doesn't make the rate benign. Like I said before, I worried that it was contributing to the hypotension. I couldnt/wouldnt assume that it was the only cause. I agree that cardioversion was indicated considering the patient's condition, but to be honest I sissied out on it a little bit-- mostly because I knew in the back of my mind that the tachycardia was probably not the primary problem. I decided to do a brief trial of medication first and see how that worked out. Meanwhile, I did the fluid boluses and maintained the airway. As far as putting myself out there, thank you. I am new, I admit, and there is a lot I have yet to learn. The same is probably true of many members here. Hopefully we can all learn from these calls.

The assumption is that the rhythm was ectopic. I know that the LP12 printout says "sinus tach" on it, but that readout is often incorrect, and with an unknown rhythm onset I really had very little to distinguish between sinus tach and ectopic SVT. If for nothing else, the adenocard may have helped make that differentiation. Attempting to break the rhythm was not my only treatment. As I mentioned above, I was running fluids as well, along with the airway stuff.

Dispatched: Intercept with BLS crew for shortness of breath. The patient is a 45 y/o male: Hx: "Brain Cysts," HIV+, Unknown other (family not the best reporters) Rx: Family remembers only Morphine and Ativan All: NKDA The patient presents unresponsive, GCS 4 (1 point for occasional moans). Family says (through the BLS crew, I intercepted enroute) that this mental status is baseline x 1 week. I have a hard time believing that, but thats the story. They called 911 "because it looked like he was having troube breathing." VS: RR: 48 HR: 190 BP: Unobtainable. Maybe a radial pulse, hard to tell. SPO2: Wont read (?hypotension/perfusion issue) ETCO2: 10, with good waveform Lung sounds with diffuse rhonchi, no JVD/distal edema. Skin is warm/pink/dry at the core but mottled and somewhat cyanotic to the extremities. Pupils are sluggish to react, 3mm, with a disconjugurate gaze to the upper left (unknown baseline). Rapid trauma assess negative for DCAPBTLS. Blood Glucose is 146. EKG: SVT at 175-190 without ectopy, generalized ischemia. My treatment: I direct assisted vents with BVM+OPA+O2. Reassessment of the lungs finds good expansion on each vent from the BVM, ETCO2 trending upward as the tachypenia is slowed down. IV with NS wide open Trendelenburg position I made a decision here to give Adenosine 6mg. I felt that the heart rate was too fast to be compensatory, and that reduced refilling time could be accounting for at least some of the hypotension. I realized that this patient was probably not having a primary cardiac problem, but I felt that the rate was something that needed to be addressed. 6mg didnt touch the guy-- no changes on the EKG or otherwise. We arrived at the ED before I had time to draw up 12mg. ** In the hospital the patient was intubated with RSI, and promptly coded 4 times, recuscitated each time from the various (VF, VT, PEA, asystole) rhythms. When I turned in my paperwork the patient had a blood pressure in the 70s systolic, and they were mixing up an epi drip in the hopes that it would bump the pressure up. I havnt been able to follow up since, but it didnt look good. Discussion: The crossroads here was really the decision to go with adenosine. I was working with a primary clinical impression of septic shock, but believed that the heart rate was way too fast to be helping. I felt I did what I was able to. I could also have spent my time attempting to intubate, but the patient was biting on the OPA and the BVM vents seemed to be working just fine. I didnt think it would be successful and at the moment, the airway was secure. I suppose I could have also spent the time attempting a 2nd IV. I would like to hear what you guys think.

Not sure what research it comes from, but those are specific numbers right out of our protocol book.

I think they want you to be really careful with these patients because when the body gets that cold, the heart - if it is not already there - is VERY likely to go into VF. ACLS reminded us to treat these patients as carefully as possible- meaning even avoiding excess jostling and movement. Second, very bradycardic or hypotensive patients with cold, hardened skin may not have a detectable pulse, even if one does in fact exist. Starting CPR in this situation could instigate VF out of a (semi) perfusing rhythm, which is obviously not the thing to do. Honestly I would not want to ever mess with one of these patients without a monitor so I could actually see what was going on, but I suppose as an EMT I would like to put the AED on first to find out if the rhythm is shockable-- if it is, then shock away and do CPR (30-40 compressions/min), but otherwise... I donno... Be REALLY sure about pulselessness (check carotid/femorally, and anywhere else you can think of, use your scope for heart sounds, anything) before I started CPR. I forget if they said to shock only once or to continue shocking. Pretty sure they said continue shocking as normal. I do remember though that you are supposed to give only one round of meds, if at all, because the metabolism of the compounds is so much slower when the body is that cold. Our protocols specifically offer the advice that successful resuscitation without CNS complications has been accomplished in patients with a core temperature less than 70*F, so "once you have CPR - do not give up!"

Rookies in Cromwell, CT! Hahaha come on by, good times will be had by all! :wink: EDIT: hahaha I just looked at their online schedule and guess what the show is for Saturday night haha... I'll just copy and paste: MINI KISS is a full costumed Kiss Tribute Show with 4 little men. wooooooooooooo sounds like a great time! hahahahaha

Thats right fellas! Button up your houses and keep your family members close: I'm out on my own as a fully licenced/registered/medical-controlled paramedic! I had my last ride yesterday with the Cheif Paramedic, and at the end of the shift he shook my hand, congragulated me, and requested that I kill as few people as possible. My first shift is on Friday-- I'm stoked!! :wink: :!:

I got into this because my roomate in college was working as an EMT-B part-time to pay the bills while we were in school. He would come back from work every once in the while with such great stories, making the job sound exciting, purposeful, important. I thought it would be a good time and needed the cash anyways, so I signed up for class. It was my introduction to medicine as much as EMS, and I've been working to better myself in those fields ever since. I got cut loose as a paramedic this week ( ), and I will be applying to medical school in about a year.

I'm hoping for a restraint protocol involving Succinylcholine, or perhaps Adenosine drip? Anyone got anything like that?

Yeah doc, thanks for the benefit of the doubt, but it isnt your computer screen. The more I look at it, the less wide it seems to me-- the rhythm did change quite a bit, but to be perfectly - painfully - honest here I think i got a bit carried away thinking this was wide complex after seeing a few runs that appeared wide either because of apparant ST elevations (in the 3 lead only), or possibly from some other abbarancy. There were a lot of runs like this, too: But even those are probably not truly wide-- it almost looks like there are pacer spikes there though the LP12 didnt pick them up. I dont know. I was on the fence about it, so I chose a medication that worked to cover both. I should have done a 12 lead first (shame on me), but I was eager to help with this guy's pain and (initally) skipped a necessary step. Especially with a questionable rhythm like this. I didnt get called out in the ED or anything, the doc actually said I did a good job, but on closer inspection I really think I probably could have done better. Dustyn-- we have buritrols and 250 cc bags, but it so happens that our buritrol was broken on this call. We went to use it and found out the chamber had a crack right down the side of it. Instead, we just took a 250 cc bag and let out all but 100 cc from it, then mixed in that. It doesnt have to be exact, just some NS to dilute the mixture and drip in. She had crap veins and I only got a #22 gauge, but even still we had no problem dripping the mixture in within 10 mins.

We were dispached to a SNF for an older male at a nursing home who's AICD has been discharging every few minutes. On arrival we find our patient jumping in his bed about once a minute as the AICD shocks. He says this has been happening all day- he is a DNR/DNI/Do Not Hospitalize, but he would like us to treat him today because "I just cant stand this damn thing shocking me." The man is without complaint except for the constant shocking. In between and right before shocks he denies pain, SOB, weak, dizzy, n/v, palpitations, and anything else I could think of. 82 y/o Male in apparant discomfort only during shocks Hx: s/p CABG x 4, CAD, AICD (duh), CHF, Hypocalcemia Rx: Lasix, Percoset, Klonopin, Wellbutrin, Risperdol, Ambien NKDA I wont list my whole assessment here but he was largely unremarkable. Lung sounds clear, no JVD, no distal edema, PEARRL, skin warm/pink/diaphoretic, no complaints, etc etc. Vital Signs: BP- 132/111 HR- varies RR- 22 SPO2- 99% on RA GCS- 15 On the monitor we see a lot of this: In between AICD shocks, the rhythm would alternate quite a bit. This strip is pretty tachy still, but he did slow down to about 140 or so in between AICD discharges. I called the underlying rhythm a-fib with various, multifocal ectopy (the ectopy is more apparant in other strips). I simply called the faster rhythm a "wide complex tachycardia of unknown origin." About once a minute the rhythm would widen and speed up to about 180-190, and the AICD would shock. I gave the pt 4lpm O2 via n/c, started a line of NS @KVO. I then administered 150mg Amiodorone, mixed in 100cc NS and dripped over 10 minutes. Transport priority 1 to the ED. Enroute I get a 12 lead. This is about 5-6 minutes into drug administration. link to a bigger version: http://i62.photobucket.com/albums/h99/fizn...CT12leadbig.jpg (might need to copy/paste that to avoid frames) The last AICD shock was observed about 2 minutes into drug administration, and we never saw another - even after writing paperwork in the ED. The rate remained tachy, but not AS tachy I suppose. This 12 lead was at about as fast as it ever got. The complexes also seemed to narrow quite a bit. The patient said he felt the same but was greatful the AICD had stopped shocking. In the ED the patient was given Lopressor for rate control, which in about 30-40 mins brought the rate down to about 100. The patient remained without complaint. I wanted to discuss this call a little bit with you guys, especially my choice to administer Amiodorone when clearly I could have gone with a calcium channel blocker for the a-fib. I chose Amio because the rhythm appeared wide to me, and while I admit I probably should have done the 12 lead first, I knew that this drug is indicated for both atrial and ventricular rhythms so I beleived I had my bases covered. Rookie mistake not getting the 12 lead done first, I know. I understand that abbarancy on the a-fib could have explained the width, but that wouldnt quite explain how the width appeared to increase along with the rate, right before the AICD would discharge. As usual, things seem much clearer after the fact. Looking at everything again the rhythm doesnt seem nearly as wide as it did on the call, although there is still some there. Id like to hear what you guys have to say.

I work with both Shane and Code 8 Paramedic, and share that same 5 Haldol, 2 Ativan protocol. I am a new paramedic and have actually only used this combination once so far, but I have seen it done a few times. It is my experience that the drugs dont take much effect until about 10-15 mins after administration which, for us, usually means just about the time we are arriving at the hospital. They are nice to have, I suppose, but I feel the effectiveness of this protocol for seriously combative/dangerous patients is hampered quite a bit by such a long time of onset. Usually the things that really get these patients calmed down (or at least neutralized) are lots of people and physical restraints.

I figured someone would really call me on this sooner or later. To be completely honest, I screwed it up. I didnt look at the 12 lead for rhythm at all, I just examined for infarct and injury and moved on. That was (obviously) a mistake. In something of a defense, though, I didnt simply go by the machine's interpretation: I never do that. I couldnt have, in this case anyways, since even the LP12 calls the rhythm "undetermined." I was working under the loose impression that the rhythm was junctional, as the rhythm does appear to be for at least a significant portion of the time. A critical mistake I made was to remain loosly interested in the rhythm itself, not looking specifically for blocks (even when giving lidocane), and chalking up a lot of irregularity to simply "an irritable post-arrest heart." Looking back, though, the rhythm does seem to change several times, with varying degrees of AV dissociation throughout our transport. The 12 lead was done almost last, though, so I think it is probably fair to say that the heart did finally settle into a consistent 3rd degree block. I should have cut off the lidocane at that point. When I get home tonight (I'm at work till 1730 today), I'll try and post up a few of the actual 3 leads so that we can get a better idea of how the rhythm changed throughout the call. I guess there isnt much more that I can say. It was a mistake, and I agree a potentially bad one at that. I'm lucky that things ended up so well. Next time I will NOT miss something like this.