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Job13_5

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Everything posted by Job13_5

  1. Being bold, I'd not call it AF because it appears regularly irregular. The R-Rs appear consistent for every other beat...ie two different foci working as the pacemaker. So it wouldn't be electrical alternans either. Edit: I should add the caveat that I'm only using a piece of paper to mark the R-Rs from the pic in the phone (no calipers)...but it appears to march out consistently on the running strip.
  2. I've used the Lewis lead quite a bit prehospitally. It's been very useful. For example, the other day I had a patient with a narrow irregularly irregular rhythm in the 150's. A standard set of leads was unhelpful in determining if it was sinus with frequent PACs, MAT, or AF. A Lewis lead helped amplify atrial activity, showing associated p-waves of only two morphologies. I can't think of an instance when it's changed my treatment plan, but by using it, I have been able to be more definitive about rhythms, and I can only imagine that that will eventually lead to a change in course.
  3. The reason for the difference in the two 12-leads appears to be due to a shift in the pacemaker from a supraventricular (or high ventricular) pacemaker, to a lower ventricular one. In the rhythm strip you have a slow, wide, possibly supraventricular focus (maybe high ventricular) pacing the heart at about 60 bpm. This is interrupted by a pause, then an apparent ventricular beat. Afer which the original pacemaker takes over again. In the first 12-lead, the predominant pacemaker is the one we see the most of in the rhythm strip (the supra or high ventricular beat at about 60 bpm). In the second 12-lead, the lower ventricular beat has taken over pacemaking at about 50 bpm. That's why the guy goes from a RBBB to LBBB pattern. He's got some seriously hyperkalemic T-waves and a long QTc with bradycardia, which sure sounds like Hyper-K. But, his history and meds (except for maybe the lisinopril) make me wonder if this is really hyper-k or not. The inferior and lateral ST segments caught my attention and make me worry about ischemia, but they could also be nothing. Lot's of guessing and speculating here. My approach to this patient would be conservative at first. Help treat the things he called for, get his BP up without fluid overloading, do serial 12-leads to monitor for changes (especially watch for continuing axis changes and monitor those ST segments) and send it off to the doc, and not do any initial messing with his heart. If things were to turn south, I'd head straight to his heart. Cool case. I'll be excited to hear what the smarter people have to say. There's a lot more to think about as far as treatment is concerned. But I'll let other people comment before I get myself into hot water
  4. Great information here! Just a quick question, for the potentially spine injured patient that is nauseous and vomiting, in what position are they to be placed/immobilized and how is that patient secured? I admit that though I really like the new evidence based approach to this topic, and the general change in the way we should be thinking about the use of LBBs, I still have it so ingrained in me that it is the best thing for these patients, that there are certain notions that are hard to let go of. With that caveat, I am picturing a retching and vomiting patient not on a LBB (that warranted and got a c-collar) half hanging off the gurney, vs the same patient fully immobilized to a LBB. For the patient on the board, leaning them to the side and allowing them to vomit and assisting them with clearing their vomitus, seems like a more stable "package" in regards to reducing motion of the spine. While the patient that is not restrained onto a board will likely put their spine through much increased ROM. Now, I understand that the patient's who are at high risk are those with unstable fractures, and that these generally produce pain that make the patient limit their own ROM. But vomiting sucks, and to my mind may produce reflexive actions that could compromise even these patient's spines. On a seperate note: Doczilla, are you guys still log-rolling patients?
  5. Point taken. I think some of these instructions are unnecessary because the morphologies described are necessary to even measure a Vi and Vt per the simple criteria. But, I'm going to read the article a few times to make sure I get it...which proves your point.
  6. Now you guys have got me worried that I'm miss understanding the AVR criteria...I thought it was pretty straight forward (except for the last test, but even that one's pretty simple once you get it...unless I've missed something). Are there more intricacies than I know about? For instance, it was posted above that you have to pick the correct QRS when evaluating excursion. I hadn't heard that before.
  7. As for vagaling, I said no because she wasn't bearing down with a BM. That doesn't rule out vagal nerve issues, of course. The doctor worked her as a myxedema coma (spot on DartmouthDave!): hypothyroidism, hypothermic, hypotension, recent infection, waxy skin. From what I read, she fits the bill.
  8. I'll try to answer your questions... I think you misread the first bits. The pt did not have an initial bp per fire, but I felt a weak radial pulse at a rate of 70. Moved the pt to the cot, couldn't get a bp or radial pulse. Meds: vigamox, PCN, phenergan, levothyroxine, maxzide, zestril, flexeril, fioricet, asa, premerin, zocor. Respirations were 14 regular and shallow. GCS was 14 -- opens eyes to voice -- throughout transport GCS was 11 when pt started to decrease in LOC (2,5,4) GCS was 3 when unresponsive. She did not have a vagal episode 2nd to BM because she never made it to the toilet. No lab information. Doc's working diagnosis was before labs, imaging, etc.
  9. I fail to see your point. Isn't this an exercise in examining the 12-lead? The question posted by the OP is "Aberrancy or VT?" My answer is VT. If I'm wrong, I would sure like to know about it so I don't make the mistake when it matters.
  10. No one has mentioned the AVR criteria here yet. According to such this 12-lead would be positive for VT because of the initial R-wave in AVR. Here's a quick article that describes AVR criteria in brief: WCT Algorithms In the article it reports the accuracy of the AVR criteria being at 90.3% with a P of 0.006 vs 84.8% overall for Brugada's. I would feel very confident calling this VT for several of the reasons stated previously, with the addition of the positive AVR criteria.
  11. Can you explain this a little more? I.e. the "proarrhythmic state of the hypothermic heart."
  12. Had a patient yesterday that brought me back to the books and thought I might share. For those that are more learned than me, this will be ridiculously simple, but I had to get the diagnosis from the doc. Called for a 56 YOF "in and out of consciousness." Arrive to find a female on the bathroom floor, average body type for her age in a clean and well taken care of home. Patient is lying left lateral recumbant, breathing quietly about 24 x/min, very pale with "waxy" appearing skin, barely palpable radial pulse at ~70bpm, very cold to the touch, slightly clammy, oriented but responsive only to voice and reluctant to follow commands 2nd to lethargy. Fire can't get a manual pressure. SpO2 is 97% on RA. Lungs are clear. Husband reports a history of HTN, high cholesterol, hypothyroidism, with associated medications and an allergy to Sulfonamides. Husband reports that the patient has been feeling ill for the past several weeks and was recently diagnosed with an infection (doesn't know what) and prescribed PCN, which she has been taking for about two weeks with no ill effect. Husband reports that the patient has been constipated and using stool softeners. Patient was reported to have been heading to the bathroom when she got suddenly weak, laid on the floor, became somnolent, and husband called 911. Moved patient to gurney, placed trendelenburg, no palpable radial pulse, can't auscultate a blood pressure. After two IVs and just 500cc of fluid patient has strong radial pulses and a BP of 142/100. Physical exam reveals no neural deficits and right-sided abdominal tenderness w/ nausea...all else is normal except what's been mentioned above. BG is 140, 12-Lead shows no ST changes or blocks with left atrial enlargement, NSR throughout transport. Delivered the patient to the ED with no changes enroute. (Couldn't get further BPs because the manual cuff went MIA and the automated cuff started throwing faults...figures...however, patient maintained strong radials w/ continuous infusion of NS) ED automated BP was 113/?. IVs were stopped by staff. Patient began to decrease in LOC (over about 10 mins). Manual BP was evaluated at 48 systolic. IVs opened wide. Patient moved to another room, doc called, BP re-evaluated at 135/100, patient is now slightly responsive. Several minutes later patient is unresponsive, and incontinent of feces with a SBP of 66. At this point I had to leave for another call, but the patient evidently remained hypotensive and was admitted. Doc told me his initial diagnosis and I had to go do some reading. Any thoughts? On a side note. There is one aspect of this patient's presentation that I still don't understand: the fluctuating blood pressures. I have my own thoughts, but they're just conjectures...
  13. It works, I've done it. Although, I found that more force needed to be applied than the prescribed "let your fist drop onto pt's chest," making it more of a precordial thump, but aimed just left of the lower end of the sternum. I'd say I used moderate force with my hand 6-8" above pt chest, and it definitely produced perfusing pacing beats. Attached is a snippet of the strip. The difference in beats, seemed to be related to the force used. With percussion pacing, though, I imagine you would have to worry about R on T phenomenon, or commotio cordis...
  14. In the protocols I'm working under right now, these pts would meet inclusionary criteria (meaning there's a higher likelihood of them having a spinal injury), but it doesn't mean we can't still clear c-spine with more assessment. Not being argumentative here, just chiming in with more protocol examples.
  15. Job13_5

    Oh Poop

    Had a pt the other day who was covered head to toe in her own poop ask "do I have time to put my makeup on before we go to the hospital?" She was a sweet old lady with dementia; obviously didn't know she had been laying in her own filth for two days. It was sad, but her makeup comment sure made the call a little more fun! Ignorance is bliss.
  16. Lol. I've been getting quized a lot lately by my preceptor on cellular physiology, and it's apparent that I could use some refreshing. If you talk, I'll listen. Never mind the haters.
  17. I can't seem to wrap my head around this pt. A 16 YOM tried to OD on 30 Benadryl OTC, and 30 Aleve 12-16hr prior to our arrival. He presented with obvious torticollis (ear turned down to the right, SCM under spasm, jaw deviated and elevated to the left, with left lateral rotation of the neck) that periodically worsened and then relaxed (but didn't go away). He was in the care of a local mental care facility, who had given him Paxil 2 hrs earlier. The nurse then noted the onset of his symptoms 2 minutes after that administration, and eventually called us when the pt complained of having difficulty breathing (laryngeal dystonia?). Pt was lucid, and able to answer questions, although had difficulty speaking. What I don't understand is how this could happen given his recent history. He has never experienced this before; he's on two meds for GERD (hyoscyamin (an anti-cholinergic), and Xifaxan), but his OD included Benadryl. Was this a dystonic reaction? If so, how could it happen with so many anti-cholinergics on board (although Benadryl half life is 2-8hrs)? The only other thing I can think of would be serotonin toxicity from the paxil, but it doesn't fit as well. Luckily we were only a few minutes from the ER. We ended up deferring medication because of the short transport time, although we considered Diazepam to give him a bit of relief. Any help with this one? Thanks all!
  18. Nice, that all makes sense. Now I think I should have figured that out. A few days ago we had another DOA who had just begun to rigor, and her eyes were closed but her jaw was locked and her neck was stiffening...confirming what Herbie said. Thanks for the info folks!
  19. This is a good strip. If I had only seen the second and third pictures, I would have called it a high grade 2nd degree type II. However, it looks to me, in the first picture, that you have p waves falling on the QRS, which makes me think 3rd degree. However, I figured you wouldn't have a narrow QRS with a 3rd degree....Is that not the case?
  20. What can cause a person to die with their eyes open? We had a pt DOA sitting in a recliner with two days of rigor, eyes open, legs crossed, still holding his last meal. No meds found in the house; a healthy looking 55 YOM. What could have happened to this guy? Judging from his position, he seemed to be pretty relaxed when he died. If he asphyxiated I figure he would have uncrossed his legs to change his position. If he blead out, I would think his eyes would close. Any help? Thanks!
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