fiznat

lol thats retarded. I cant believe he actually thinks that. ...Then again, in NJ you folks arent even allowed to pump your own gas-- haha so maybe its not too far off to believe that the state wont let you make clinical decisions based on your assessments, either. haha

Ask him WHY he thought the patient was unstable. What in his assessment did he find that led him to believe that risking lives by going pri 1 would have made a difference in this patient's outcome. Dont forget that going priority 1 is DANGEROUS. There should always be a good reason. If he answers you by saying that you "cant be sure" if the patient was unstable or stable, then tell him he needs to learn how to do a better patient assessment, as well as a better evaluation of risks + benefits of risking people's lives on the road.

Absolutely! In my service we hardly ever transport BLS priority 1. It would have to be something pretty major, with no medic available, for that to happen. I wasnt there to see the patient or hear the whole story, but sounds like your partner is waaay in the wrong here. Not only should a pri 1 transport to the hospital be pretty rare, but the s+s you provided do not indicate it (altough it is possible the patient was more unstable than you thought), and being that close to the hospital it seems there really was no need for it. Do you guys routinely transport patients on priority regardless of complaint and presentation?? Thats dangerous! Not only that, but dont you do pri 2 responses in your service area? ...I mean, responding to a 911 call without lights + sirens? We do, I'm pretty sure its very common. If the dispatcher on the other end of the 911 call is able to make a determination hot vs cold response based soley on what the patient tells him over the phone, why cant a trained, experienced EMT make that same determination based on a patient that he has evaluated in person? And even further, in my service usually the provider tech'ing the call makes the transport priority decision. He is the one taking care of the patient, and therefore he is the one most able to make a determination unstable vs. stable. If he didnt tell you to go pri 1, that also is his own fault. No reason you should be yelled at for this at all, by any stretch of the imagination.

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No, thats pretty much what I said the instructor told me. ...That chest compressions were being used not only as CPR, but as an alternative to ABD thrusts as it is done in pregnant women. If we are using chest compressions instead, then, how come ACLS never offers a point to check the airway for dislodged obstructions? I understand that CPR is important, even more important than ventilation for the first few minutes... but with a totally occluded airway (to the point that breaths dont go in), CPR alone with no attention to the airway is going to kill this patient! I just dont get it. It seems ACLS is kindof in an odd spot in medicine here. It's advanced cardiac life support, and yet we're "learning" techniques for the lay person with more focus on simplicity than anything else. Also to answer the question above, there is also NO check for pulse. If the patient is unconscious and not breathing, and the breaths dont go in, we're supposed to go right to CPR. :roll:

I took the ACLS class today (first day out of 2, we test tomorrow), and I wanted to ask you guys what you thought about the new ACLS guidelines for foreign body airway obstruction (FBAO). The guidelines say that for the unconscious patient, the ACLS provider should check for breathing as usual, and of course when no breathing is found, administer 2 slow breaths via BVM or whatever. In this scenario with the FBAO, the breaths do NOT go in. The next step in ACLS is not what what you think. You dont clear the airway. No ABD thrusts, nothing. The next thing to do, apparantly, is deliver CPR. I was blown away. We dont clear the airway before going on to CPR?! I've never even heard of a protocol like this before. Thats the whole point of the sequence of A, B, C. That C doesnt matter if there is no A or B. The instructor pointed out that the alternative for ABD thrusts in the pregnant woman is chest thrusts, but even if this is supposed to be a substitute, ACLS offers no window to check the airway for dislodged obstructions. We're supposed go pump merrirly on with 30 compression cycles. What kind of CPR is that, to circulate blood with no oxygen supply!? I complained about it, as did the rest of the class, but apparantly this is really the way ACLS wants it. The instructor shrugged and said that the AHA wants to make things as "easy as possible" for the lay person. I thought ALCS was supposed to be advanced, and not only that - how advanced is clearing the airway, anyways? I dont understand this, guys. Can anyone find any reason in it?

Nah cause we use sterile water that isnt included with the powder... Its made by a different company entirely.

Guys, guys! I think we're ignoring whats really important here!! LOOK at that ridiculous thing! LOL! We win.

Huh, interesting. I'll have to read the box next time I have a chance. haha nevermind Shane!

Woah, weird. My service used to get the fluid and powder in a box together for reconstitution, but now all we get is the powder. Medics have been using sterile water (not NS) to mix the drug. The quote above seems to say that what we're doing is incorrect? I wonder what the PH of the sterile water we have is... Shane, do you know?

I understand where youre coming from, I'm just saying that it is probably just as incorrect to assume that your alcutated blood pressure is accurate within +-2mmHg as it is to say "I heard the first thump when the needle was about halfway between 120 and 130." Lets not kid ourselves. Theres plenty of fudge room and variablity in blood pressure measurement-- who is to say that a reading of 124 is correct while a reading of 125 is not. Just because there isnt a tick between two slashes on the gauge doesnt mean that that isnt where the first thump was heard. How is it more accurate to round up or round down in these cases? In between 124 and 126 will always be 125... As long as someone knows how to count, I dont see how this could be a problem. There are better way to judge peoples credibility... all I'm sayin...

I dont really undrestand this attitude with blood pressures. I understand that the sphygmamonometer (yeah I used the big word haha) is usually demarkated with ticks at every 2 mmHg, but arent we going a little far when we think BPs measured with a cuff + scope are actually accurate to the point of +- 2 mmHg? True blood pressures are measured by wedge pressures, swan catheters and A-lines, not indirect tamponade and korotkoff sounds. What we hear with our scopes are, and will always be, approximations of the blood pressure. Therefore, if I hear the first thump when the needle is halfway-ish between 120 and 130mmHg, why not call the systolic 125? Not that 1-2mmHg is gonna make one bit of difference for treatment anyways.

Its finally that time! I just finished my 2nd semester of medic school and, after a few more weeks of lecture, will be starting ride time!! I'm freakin pumped... after 9 months of sitting in classrooms, clinical sessions, and labs, I am itching to get out into the ambulances and start applying this to the real world. I wanted to ask you guys, what advice do you have for me for ride time? Is anyone here an instructor? How can I best prepare? How should I present myself? How aggressive should I get on calls? What kinds of things can I expect to be quizzed on? Etc etc etc. Any advice you guys can give me will be appreciated. I feel pretty confident with my skills and knowledge to this point, but ride time has a reputation for shaking that confidence so I hear. Help me out!

Agreed, what did he say you couldnt do? ...And why is this in the ALS section?

Huh, a suction port on an ET! Sounds like a cool idea-- does it work well?

haha I know that it really goes "treat the patient, not the monitor." Just commenting on the seemingly opposite approach necessary for this patient. I used to think the NC was a waste of time also, but I've been using it more and more often with similar effects to the NRB. It helps to avoid setting off already anxious patients (and possibly increasing O2 demand through stress... hey, it happens), and also makes it easier to ask questions (and have them answered). Not to say the NRB doesnt have its place of course...

haha I like that! Man, scary case though. As I was reading, I have to admit my eyebows were raising a little bit with your choice of the NRB. I probably would have just given her a cannula at 3-4lpm. ...Mostly cause of the restrictive/stressful nature of the NRB and the apparant lack of necessity here. Big surpise to find out this one was actually something real-- very nice catch. Kinda scary to see that. I know LOTS of medics who would have jumped at the chance to downgrade this one. By the way. I'll add this in cause I'm still a medic student and I like asking questions. Is this a true case of "treat the monitor, not the patient?" ...Cause while the EKG obviously did change drastically enroute, it seems that the patient's complaints and presentation did not.

Good case! My question is, with the patient's presentation (pretty much stable although the tachyness and SOB complaint is a little worrysome), why do anything at all about that rhythm? Sure its funky and wide and could be SVT/VT whatever, but if the patient is presenting okay, I think I would hesitate to go after an unknown rhythm and potentially upset this otherwise fairly stable patient. Isnt this one of those "treat the patient, not the monitor," IV/O2/Monit. patients they keep telling us about in class? Also as far as the SVT/VT rhythm, could you start off with some vagal maneuvers and see what that does for ya first? Amio would be nice, but you guys are just like my service. Too expensive a drug or something, I guess. With the drugs that you had on hand, assuming you would do anything at all, I think you were correct with the lido. You have to assume that it is VT in this situation anyways, bieng that it is probably potentially the more dangerous rhythm.

The asthmatic wheeze is caused by alveolar mucus plugging, often described as a "one way valve" or a "trap door" that generally lets air in, but constricts air out- which causes the telltale expiratory wheeze. Still though, this is just a general common presentation of these patients. The fact of the matter is she has a serious, chronic asthma and lots of mucus in her lungs. I dont see why she couldnt wheeze in OR out, provided there is lots of mucus everywhere anyways. It is the mucus that defines asthma, not the times at which that mucus produces wheezes. If her albuterol makes her nausious, has she considered asking the doc for a change in medication? No reason for her to suffer when there is such a plethora of bronchiodialators available for asthma patients. I'm sure there is something else out there that she can use with more comfort. Like others have said, LISTEN TO HER LUNGS! As long as your friend is fine with it, definitely take the opportunity both as a chance to learn/experience the sound, and also to find out what her baseline is in case you are with her during a true emergency.

Also a new medic (medic student, actually) here, but I was under the impression that at least as benzos go, versed is a fairly weak muscle relaxant and therefore only minimal precautions for hypotension are necessary? I understand that hypotension is still a precaution and a relative contraindication, but am I correct in understanding that we need to worry a little less about those kinds of effects with this drug? Obviously - as always - this is a "how does your patient present" kind of situation, but am I correct in understanding that versed in particular is less likely to worsen hypotension (as compared to other benzos like Valium, or an opiate analgesic like Morphine) for this already unstable patient?

My understanding is that it is national standard that EMTs can give ASA to chest pain patients. I think it is mostly a medical control/local issue that stops some EMTs from this line of treatment. In my system some people say EMTs can give ASA, other people say they cannot. As an EMT almost done with medic school and someone who knows the doctors at our local hosptials, I can say that I DO give ASA to chest pain patients and I've never had a problem with it. Since you must be also just about done with medic school I doubt it is of much concern to you, but I'd check with your local medcon and see what they say about BLS ASA. I bet theyd have no problem with it at all. BLS nitro is another story alltogether though. Most good medics I know really try to avoid giving NTG without an IV line established in case the pressure begins to tank. I really doubt any medical control would be willing to give standing order NTG to BLS providers who are unable to start IVs and give fluids. Maaaaybe for EMT-Is, but even then I beleive (although I'm not sure) that these providers lack the A+P background necessary to understand the indications and contraindications of fluid bolus treatment for hypotensive patients. Correct me if I'm wrong there.

Very good information about benadryl here. Some good study material, for sure. Still, this isnt exactly what I'm asking. I used benadryl as an example simply because it is the drug that led me to the question, which is: why does antagonism of the parasympathetic system cause sedation, when logically it seems as if it should not? I understand about the blood brain barrier, and how some "older" antihistimines can behave in an anticholonergic manner, but what I am not getting is how an anticholonergic causes sedation, when you would think that an anti-parasympathetic would also be anti-sedative. (Anti "feed and breed") Maybe Im not asking the question right?

The bit about H1 receptors causing "wakefulness" is interesting, I didnt know that. Hmm. Still, This is the mechanism that I am specifically asking about. It seems like it should go the other way, doesnt it? I mean- if parasympathetic tone causes the "feed and breed" (and sedate?) response, why wouldnt antagonising that system cause the opposite (or, at least, less sedation- not more)?

I was doing some light research the other day after assisting my medic in giving diphenhydramine (benadryl) and hearing his warnings about the potential side effects of the drug, one of which is sedation. I understand that the drug works primairly as a H1 receptor antagonist, but also that it is quite non-selective and has some potent anticholinergic effects as well. Supposedly it is this effect that is the cause of the sedation (and many of the drug's other side effects also). What I dont understand is why inhibition of the cholinergic (parasympathetic) response through acetylcholine reduction produces sedative effects. It is my understanding that the parasympathetic response IS the relaxed, "feed and breed" sedate kind of response. It seems to me that inhibition of this system would serve to rather excite the patient, not sedate. ...Like Atropine will cause an increased heart rate, not decrease it. Can anyone explain to me what mechanism is working here? RE: diphenhydramine: http://en.wikipedia.org/wiki/Diphenhydramine anticholinergic: http://en.wikipedia.org/wiki/Anticholinergic

While I'm reading, care to offer a synoposis on your understanding of the pathophysiology in question?