fiznat

Ahhh the shotgun approach, eh? Thats a ton of information for a pretty direct and specific question. Nonetheless I'll read and see what I can find. Does anyone else know the answer?

Yea I read them. I didnt see anything about a direct relationship between chemoreceptor perfusion and a resulting variable respiratory rate. We're talking about a scenario where the pCO2 is high and yet respirations are still depressed (presumably 15 is fairly slow for this patient). Whats the pathophysiology? Thanks for referring me to another site (again) though.

Interesting discussion! Just for the sake of argument. If the return of respirations are in fact a compensatory response to a high pCO2 s/p arrest (lol or just status?), wouldnt the resp rate be a little higher than 15? Compensatory rates in live patients tend to be a little higher to that-- are we saying that 15 is pretty much all this poor guy could manage since hes so otherwise compromised? Is there a direct relationship between perfusion of the chemoreceptors and resp. rate? I feel like these types of patients are usually either breathing or not breathing... meaning I've never seen a depressed resp drive in a hypoxic patient-- depressed heart rate, yes-- but resps I usually find to be "on" (tachypnic perhaps) or "off." Is there physiology to back that up?

Yeah Shane youre right, there probably are a few who are capable and actually do this for their patients-- I shouldnt speak so generally. Still you have to agree it is pretty rare to see, even in patients for whom it is indicated. Possibly it has to do with our transport times? LOL alright, haha, I'll run with it: 1. Allergy to PCN 2. Pt takes ASA, an ACE inhibitor, Lasix 40mg, Digoxin, Colace, Ambien, and a MTV 3. hx of HTN and the pt is an ex-smoker (quit 10 yrs ago). There is also a family history ("my father died from a heart attack at age 56") 4. Inferior elevation is all you notice. (I'd like to be able to add more here but I dont have ACLS yet and my 12 lead knowledge is limited) 5. Negative on the abnormal heart sounds 6. Negative again on sounds s/p tx. 7. HTN, A-Fib, CHF 8. None noted, but possible that they are still there. 9. As mentioned, patient is AO to person/place/time/event, but SNF staff say the patient "isnt acting right." 10. Hepato-Jugular Reflux is a little silly to test for given the other S+S of right sided heart failure and the condition of your (unstable) patient, but you decide to to do it anyways cause you are an overachieving showoff and the result is negative. The patient has no JVD before/during/after the test. 11. You notice no JVD at any time, so also negative on the Kussmaul's sign 12. No s+s of any kind of GI dysfunction, the ABD is soft/nontender/no masses, and the patient has no hx of liver disease/failure. From what you see, portal HTN is negative 13. She is a thin, frail old woman. 14. No recent trauma known, no evidence of 15. No signs renal failure/ETOH/hep 16. No caput medusa/spider angioma. I had to look these up, and you already covered this in #12. It was an oppertunity to use an obscure medical term though, jood job. 17. No recent toxic exposures known, no evidence of 18. So far the patient has only recieved the O2 (to which her saturation increased to 90%, negaive MS changes) and the ASA (to which you see no change). 19. No elaborate histories available. 20. You are a paramedic with average protocals. Lets *try* not to get too fancy here, eh? 21. Hospital is just far enough for you to explore a decent amount of treatments. No scoop and run, no 3 hour transport times with crazy drips/med control orders. 22. No MS change so far 23. See #18 24. You ambulance is not equipped with a full lab. Not planning on expanding the scope unless you'd like to copy this thread into some OTHER forum. 25. See #3, #7 26. The patient is unstable in probable cardiogenic shock. The BP/RR/HR are noted. Pt is AOX4 but has a noted MS change by those who are familiar with her baseline. 27. I couldnt possibly

Joshua- EXCELLENT post if I do say so myself! I'm very glad to see that someone else noticed!

Well like I said I wasnt on the call, but ask away. My partner may have mentioned some details that I forgot to post. ...Even if I dont have the details, we could simply make them up so as to present an educational case study.

I'm currently in medic school (7 months in), and we are the first class at this program to go through with the new guidelines. We did the PALS class a couple weeks ago, which did teach the new stuff. We had to use the older textbooks, but were given the newer flip-books and fold-out charts. The written test appeared to be the same as the old test, except 1 or 2 questions were blanked out. We will be getting the new ACLS as well in about 1 month. The professors at my program have all already been to the new rollout and have access to the new materials. As far as "do you actually use the new stuff in the field," I work as an EMT in a fairly busy urban setting and I havn't seen anyone follow the new protocols completely yet. Granted I've only done 2 codes in the last 4 months, but our AEDs are all still programmed old-style, medics are using 3 stacked shocks, and CPR is continuing at the usual rate. We dont really count out compressions anyways. I think its still a little early to expect to see EMS workers changing their treatments to mirror the new guidelines. Most of the medics/EMTs I work with havnt been presented with the new material yet anyways-- they're just waiting for their current certs to run out before they go back.

What about epi? Good alpha effect, beta 1 for the rate and pressure (chronotropic/inotropic), beta 2 for perhaps some more effective resps, while at the same time getting that dilation of the coronary arteries. ...Of course you cant have your cake and eat it too-- with epi you're increasing myocardial O2 demand so again you get the balacing act. Naturally this is what protocols and on-line medical control are for, but still its nice to think about what we *could* do given the tools we have and the permission to use them.

Atropine was most definitely a consideration here, although in my classes I have been consistently told that the unstable patient should get electricity right away, not meds. Why shy away from pacing? A right sided view was not performed. Truth be told, I cant think of ANY time where my medic partners have taken the time to do extra leads or extra views for a focused, diagnostic ECG. Not that the information wouldnt be valuable, it just seems like this either isnt in the average medic's daily skillset, or lazyness/time constraints get in the way. Another subject for another thread, perhaps.

Your patient: 78 y/o female at a skilled nursing facility (SNF) complaining of nausea, weakness, and 8-10 "chest pressure" radiating down the left arm. Tingling in the fingers, skin cool/pale/diaphoretic. Mental status is AOx4, but the nurses on scene say that the patient is "not acting like herself." Blood pressure is 80/40, resps 20, and on the monitor you see a junctional (narrow complex, retrograde P waves) in the low 40's. Pulse ox is 80% on room air, up to 90% with 15lpm o2 via NRB. In the lungs you can hear some light rales in the bases. A 12 lead ECG reveals huge ST elevations in the inferior leads. I did not have this patient, but my partner did during my day off last week. We were talking about potential treatments for this presentation, and I wanted to hear what you guys think. There is of course the obvious: IV/Monitor/O2, ASA 324mg PO, 12 lead, transport quickly. The NTG is contraindicated (twice) by the presentation, so what else should we do for this patient? I dont think that there is any question about whether this patient is unstable, so in my medic school sparkyness I suggested pacing. The idea was perhaps we can get a little more perfusion with a better rate, and even though I realise that this does nothing to solve the root of the problem (inferior MI), there is still the hope that we can promote some better perfusion with a quicker, better organised rate. My (paramedic) partner was worried about damaging the already weak heart with the electricity, or perhaps sending the patient into a worse rhythm. Whatcha think about that? What about other treatments (Dopamine? Epi? anything else?)

A 70 hour work week plus class/clinical rotations will do that to ya, what can I say. Sorry you've missed me. I guess there really isnt any point in continuing to go back and forth about it. I dont think there is much more I can say to support my position, nor you yours. I'm content to let it drop: perhaps we can bash heads on some other topic instead? Might I suggest: http://www.emtcity.com/phpBB2/viewtopic.php?p=72617#72617

Despite the fact that this back and forth crap is getting fairly ridiculous by this point... I felt that your attitude in that post was condecending. I didnt jump down your throat right away, I only stated that I felt that your tone was a little rude. This part of the argument could have been resolved very quickly with a simple clarification of your meaning. That is, of course, assuming you didnt mean to come across as you did. Of course I'm not. Nor did I ever claim to be. In fact, I went through the effort of posting this whole story so that I could get some insight on this very subject! As impressive as your listing of elaborate (yet redundant) medical terms truly is, in the future you may come off as less arrogant if you were to point out specific errors in an exam rather than dump on the entire thing. Referencing 5000 links to the entire world's history and scientific study on seizures is not what I asked for, nor what any poster on this forum would likely find useful. There is a difference between an ancidotal, friendly conversation about in-the-field observations and a systematic study of internet resources. This forum, and forums in general, generally serve the former. To unload your 10 minutes worth of google searching on this forum says to me that you dont really care to have a conversation about a call, you would rather shove a new user off elsewhere into the depths of data: suggesting that he'd better absorb the minituae of the subject before he is worthy, in your eyes, to come discuss it. Its true, neither my knowledge nor experience are that incredibly deep at this stage in my education- but I know enough to ask the right questions- and I thought that is what I was doing here. Simply because I didnt cover every single detail of what you consider to be an accurate "P/E & H&P" doesnt mean that I cant come in here and ask for ways to make myself better. You pass off all that information you posted as if it were your own, although when it comes down to it I doubt you *truly* do much better than my partner and I did in the feild. Furthermore, the REASON you are able to pick apart details from my assessment as factors which "increase and decrease your index of suspicion" is BECAUSE I POSTED THEM THERE. This was not an accident. You arent seeing things in there that I didnt see, you are simply calling me out for not stating the obvious. OF COURSE the patient's incontinence lowers the index of suspicion, OF COURSE the normal blood pressure and resp rate increase it. I included these details in my post because I KNOW they are necessary for a complete understanding of the patient's condition! What do you think, I mindlessly collect all of this data, remember it, and post it here for you alone to interpret it without any understanding of my own? How arrogant it is of you to assume that! I wrote the post in a manner so that members of this forum could read it, see the presentation, and make a decision on their own. A discussion of those competeting pieces of "evidence," is what I hoped would follow. ...And it did, mostly, except for you. Any EMS worker in the field who does not err on the side of caution for the patient's behalf is a dangerous waste of space. Never once did I suggest that this patient should be recieving any less care than what she got from us. All I was asking for, again, was some ancidotal observations that I could make in order to help me determine the reality of this patient's presentation. In fact, it was YOU who suggested that this patient's treatment should have been altered:

Wow alright, "ace." Are you always this rude and condecending with new people on this forum? I beleive I was VERY respectful, phrasing my challenge to your initial post in the most unoffensive manner possible. It seems you, by comparison, have very few of the same qualms. What an arrogant ass you come across as. Thanks for the tip on scene size up, ace. I specifically mentioned that there was a language barrier between the responders and the people (mom) telling the story. I wrote this portion of the description of the case AS AN EXAMPLE of the questionable nature of the seizure. Food for thought. I did forget to mention it in the post, but did not forget to try this for the patient. She would not tolerate an OPA, and a NPA was impractical given the time we spent on-scene and the effectiveness of the 2nd ativan dose. The patient's airway was patent, and she was at 97%+ on the pulse-ox by the time we got her into the bus. My job after that was to drive the ambulance, so I cannot speak for what happened enroute to the ED. Again, as I stated: I am an EMT in medic school, my partner was the ALS. I did not give *any* ativan to this patient. Not to mention that it is our protocol (as I also stated) to give a 2nd mg of ativan if seizure activity isnt resolved after the 1st dose. Damn straight its hard to say. Your comment on heart rate is totally useless: HR would obviously be elevated regardless of whether she was faking for 45 minutes, or seizing for the same amount of time. Hey, ass. What happened in the ED happened AFTER our oppertunity for intervention had already passed. If she had opened her damn eyes on scene or in our bus, that most certainly would have changed our approach to this patient. Your post-hoc cherry picking BS truly is impressive, though. If only each and every one of us could have the insight to be able to pick apart patients based on their future presentations. Maybe someday I will reach that level. Ace. So I should have picked up on the fact that the patient's "seizure" motion was not equally bilateral? So you believe that this is an accurate indentifier of true seizures? Explain it to me. The rest of the doc's points WERE recoginzed by my partner and me, as I explined them in my original assessment of the patient. Still, the confounding factors of the language barrier and questionable hx are enough to err on the patient's side, no? If I havnt made it clear enough already, it has NOT. Nor do I really beleive you care whether it does or not. How about stop trying to make yourself look good, and simply answer the questions asked. I truly hope that this is a big misunderstanding, because I have been on forums for a very long time (even moderating on a large one), and I very rarely see such arrogance and condecending attitude towards a newer member from an older one. If I am still misunderstanding your tone, I do aplogize- but I quite seriously doubt it.

I posted pretty much the entire assessment of the patient, was there something you see that was missing? I feel I covered most of (if not all, at this level) the pertanant information needed to make this kind of determination. Being that you are the only person that mentioned that my exam may be incomplete maybe you could tell me what else you feel I should have done?

Okay I appreciate the links and all that, but I dont think it is obvious (or even true) at all that I need help with the basic definitions of a seizure. I'm asking specifically about treatment of potentially fake seizures in the field, not about what a seizure IS. I'm not sure if it is meant that way, but you're coming off kinda rude..

I would like to think that I would call their bluff. Obviously there is something seriously wrong with this young patient, be it some sort of medical pathology or be it psychological: the answer would never be to simply let it go and "hope it resolves," as it seems this mother was attempting to do. I do feel sorry for the patient, and I do wonder what exactly is going on with her if it is in fact psychological-- but to get this good at faking seizures requires practice, and practice to me means lots of neglect of this issue by the parents. At this point, I dont feel like the behavior should be reinforced by allowing ourselves to be taken into the act. If she is faking, she needs to cut it out. Coincidently I actually am a psych major. Finished my double major in psych and philosophy at Boston University in 04. Suprise! haha :wink: I was wondering about this as well, and I actually asked the same question of the doc in charge. He basically said that they "just gave it anyways to calm her down," presumably so that she would be easier to deal with for the ED staff. Psychs get ativan too, I suppose. heh

Oh, I'm not really upset that she fooled us-- haha I'm actually pretty impressed. I thought it would be an interesting topic to discuss though, and perhaps there are a few other things we could have done/seen that would have helped us understand what was really going on... Also I'd like to hear what people think about the ED doc's points-- cause some (especially the first one) seem kinda odd to me.

Long post here but it was a good call, so.... My partner (ALS) and I (BLS, in medic school) responded to an "active seizure" yesterday, I'd like to see what you guys would have done differently. On arrival we found a 17 year old female supine in bed in full tonic-clonic generalised seizure activity. The patient was nonresponsive to voice and pain (good, deep sternal rub). We noted the patient was incontinent to urine, frothing at the mouth with eyes in a fixed conjugate gauze to the upward right. PEARRL, not constricted or abnormally dialated. Skin was warm, pink, dry. Family on scene states (through a language barrier/translation) that the patient was in this exact seizing state for a full 45 minutes prior to our arrival. They said that this has happened once before, a month ago, and they assumed this would resolve on its own like it did last time. They denied, however, that the patient had any dx of any kind of seizure disorder. The patient is on no meds, and has no allergies. We placed the patient on 15lpm O2 via a NRB, established an IV (18#, right AC). Blood sugar off of the IV was 108. Per protocol we gave 1mg Ativan IVP with no effect. A 2nd mg of Ativan IVP got the patient to calm down completely. Stair chair'ed the patient to the stretcher, to the ambulance. Got the patient on the monitor: sinus tachy at 137bpm. BP 130/74, RR 24. The patient began to seize again, so we decided to transport right away. Priority 1 to a local children's hospital. Enroute the patient got another mg of Ativan per on-line medical control, which again caused the activity to cease. The patient remained unresponsive for the entire time she was in our care. As we were transferring the patient over to the ED bed, she began to seize again. The ED staff gave her yet another mg of Ativan, which again caused the patient to calm down. The hospital did a search for the patient's history in their own records, which showed that she had been seen at this ED 5 times in the past 2 months for the same presentation. She had a neuro consult a few visits before with no dx. It was written in the history that the seizures were assumed to be "fake." Around this same time, the patient opened her eyes at the request of her mother. She was still not answering questions, but was obviously alert and lethargic. It isnt clear whether the lethargy is part of a postdictal state, or from the 4 mg of Ativan she got over the last half hour. In a converstation with the ED doc after finishing our paperwork, the doctor said that this particular patient was "apparantly very, very good at faking seizures," however there were things in her presentation that led him to believe that she was in fact faking. He claims this was obvious to him before even reading the history. His points were: 1) Her seizure motion was not bliaterally equal. The patient was shaking both arms, but they were seemingly at random and not in sync with eachother at all. The doc stated that "real seizures" generally present with bilaterally equal, or close to bilaterally equal tonic-clonic motion. I have never heard of this before. 2) Her motion was too purposeful. While she never accomplished any sort of task with this motion, according to the doc it was obvious to him that the motion was not genuine seizure motion, but rather a calculated, conscious motion. I dont know how he was able to determine this. She certainly looked like a real seizure to me. 3) Her mother's story didnt add up. A 45 minute seizure doesnt "just resolve" like the mother stated it did last time, and patients who have these seizures dont end up with no dx and no meds - which was the mother's story. So I guess we were fooled. ...But I dont see how we could have avoided it here-- the patient was incontinent to urine, and was COMPLETELY unresponsive to pain. It really blows my mind that the patient could have been conscious and have NO reaction to the sternal rub or IV, nevermind urinate on herself. On top of that, it seems incredible to me that the patient was able to maintain these "fake' symptons for us with 3mg on Ativan on board. Youd think by that time she'd be completely snowed. Anyways, I'd like to hear what experiences you guys have had with seizures. What kind of criteria/tests do you like to use to differentiate between real and fake seizures, and do you think there was anything that my partner and I could have done differently on this call?

No, you took it the way I meant it. It sounds harsh and cold, but you know - EMS is too busy to be all nice and cuddly with every single person we come in contact with. If someone is maliciously abusing the system then as far as I'm concerned- they get what they deserve. I'm not saying we should go out and perform some sort of half-ass vigilante medicine, but I dont see why we shouldnt use a slightly larger bore IV or an uncomfortable KED to gently discourage those who would otherwise further burden our already stressed systems with fake complaints. Maybe I'm a little too cynical, but fake patients kinda get to me. Sure, there are plenty of good reasons to call 911 - even if you dont have a huge medical complaint and would like to talk to a counselor or something. Sure, no problem. ...But people who claim kneck/back pain just so they can sue, or patients who abuse 911 in order to get a ride across town re3ally start to grate on ya after a while... Once again I have to add the caveat that we dont always know what is fake and what is not fake-- so in 99.999% of the time it is of course best to assume the patient's complaints are legitimate.

Correct me if I'm wrong here as I was never a lifeguard, but while the technical skills are similar between the two classifications, I beleive that the EMT level gets a little farther into A+P and the pathophysiology of disease. This comes along with the ability to take vital signs and understand (at least on a basic level) their meaning. The difference may seem small, but I think it would come a little more in handy given the seemingly medical nature of the "call" in this case. As many others said, the laws controlling this kind of scenario do vary from state to state. Working on an ambulance here in CT, we certanly have the right to turn away bystander care- even if it is at a higher level. That said, given this kind of situation it seemed prudent that the lifeguard should try to take advantage of the EMT on scene for the well-bieng of the patient. To deny this, though, was the lifeguard's right and choice.

^^ I donno about you, but I sure didnt take any kind of oath before I started working EMS. You're right though, its probably "mean" and perhaps even abusive- but the fact of the matter is that the "faking" patient is also abusing our system. The way I look at it is, every minute that an ambulance crew/firefighter/police officer/ED staffer spends on the baseless complaints of a faker, another patient who truly needs the attention - goes without it. If we get a little more aggressive with our care in a small effort to discourage this kind of faking, I say the ends justify the means. The tricky part, of course, is deciding exactly who is completely faking and who is a legitimate patient. Best to err on the side of caution here, of course.

Ah I missed it... Guess they're replaying it on Wednesday 11/10c

Man oh man. How do you guys reconcile these points ...With these?

If there are some flight people on here, speak up! I'd like to ask a couple questions as well

While I realize that the differentiation between a very tachy SVT and V-Tach in this patient would be difficult in the field, the question I'm asking is built around the assumption that the patient is indeed in a supraventricular tachy rhythm and has *no* pulse. I'm specifically asking about a PEA SVT, so yes I'm sure its not VT :wink: This is mostly what I am thinking. Fix the rate, THEN go after causes (5 H's, 5 T's). ...Seems like we dont want to treat this like your regular old PEA, as going to epi right away is a bad idea- and jumping right to causes doesnt make sense cause the rate needs to be fixed beforehand. Perhaps this is why my instructor said that "it cant be PEA if the rate is over 150?" ...Because you cant begin following a PEA path of treatment until that rate comes down to something reasonable. So the answer to this question is yes? My understanding is that rates above 150 are NOT compensatory mechanisms. Sinus tach is one thing, a SVT at 170 or more is too quick to compensate for anything- it is it's own problem. Is this why everyone is leaning towards hypovolemia as a cause? Fluids I imagine are still probably a good idea, but why is hypovolemia such the popular choice?