MariB Posted January 23, 2013 Posted January 23, 2013 Alrighty, there is a reason that I am not yet a paramedic yet, I did not think of that. Heh. Yes, I do know our medic would like a line going to have iv access avaliable, however, I am going to now sit back and learn from this, carry on That's interesting. Actually, the ideology that "fluid is always good" has been going out the door for a while now. But I do agree that it's preferred to have a line established in case this patient crashes or needs meds. However, you only want to give them just enough fluid to keep the vein open (TKVO). The reason behind this is that, like all drugs (and yes, saline is a drug), giving too much of it or giving it when it isn't needed can be detrimental to the patients health and worsen outcomes. The days of bolusing every questionable patient are far behind us; you have to have a reason to give it if your going to give it. Some reasons why this patient doesn't need a bolus; his pressure is 114/76, he's not showing signs of hypovolemia, and he is showing signs of cardiac decompensation, which means that he's highly vulnerable to fluid overload, and would likely not benefit from having salt water dumped into his body. However, I would gladly accept that it is appropriate to establish intravenous access on this patient
scubanurse Posted January 24, 2013 Posted January 24, 2013 I would have fluid bolused in preparation for an arrest...500cc isn't going to cause much more damage than already is occurring. Did you ever get a perfusing rhythm back?
Jaymazing Posted January 24, 2013 Author Posted January 24, 2013 (edited) I would have fluid bolused in preparation for an arrest...500cc isn't going to cause much more damage than already is occurring. Did you ever get a perfusing rhythm back? We don't overload the heart to get it ready for an arrest. Not unless he's hypotensive, and even then we only give enough fluid to achieve a perfusing pressure. For one, you don't know that 500cc wont cause more harm, and two, I don't believe you knew he was going to code, or else you should have done a lot more to get ready than just bolus him. Please don't play monday-morning quarterback. We did get him back, 3 times actually. He woke up during CPR post-defib each time. He actually told us on the last one "It's really hard to breathe with that thing in my mouth (referring to the OPA). He had a 90% occlusion of his LMCA, and survived to discharge a week later with 60% EF remaining. And he never developed any significant ST-E, just those giant T-waves of doom and the recipricals in the inferior. With all due respect, arbitrary fluid bolus' are just that. Arbitrary. Alrighty, there is a reason that I am not yet a paramedic yet, I did not think of that. Heh. Yes, I do know our medic would like a line going to have iv access avaliable, however, I am going to now sit back and learn from this, carry on Your participation is both welcome and appreciated! Don't feel like you need to sit out if you get something wrong; what better way to learn! After all, that's what we're all here for Edited January 24, 2013 by Jaymazing
Kiwiology Posted January 24, 2013 Posted January 24, 2013 To have a myocardium that ischaemic/irritable as to have a VF cardiac arrest surprised me as he did not show the classic signs of significant occlusion i.e. ST elevation. Interesting!
craig Posted January 24, 2013 Posted January 24, 2013 To have a myocardium that ischaemic/irritable as to have a VF cardiac arrest surprised me as he did not show the classic signs of significant occlusion i.e. ST elevation. Interesting! Is it a VF arrest....there was no mention of him arresting (but I may have missed it). Ho were it could be TDP.....very slight but could be read that way I assume. Still concur with you on most aspects though Kiwi......and they say "keen interest without intelligence"........might be wrong.
Jaymazing Posted January 24, 2013 Author Posted January 24, 2013 To have a myocardium that ischaemic/irritable as to have a VF cardiac arrest surprised me as he did not show the classic signs of significant occlusion i.e. ST elevation. Interesting! It was very interesting! In fact the only clue that he was going to code was the frequent R-on-T PVC's, which induced the dysthymia. But even if you look at the times on the strips, he arrested just minutes after the last 12-lead. This case was an excellent teaching point for both the significance of hyper acute T-waves in proximal LCA occlusion, as well as the importance of recognizing dangerous PVC's in ACS (both of which lessons I had not learned prior this call). I originally thought hyper-K, but in actuality these T-waves are more blunt and convexed than your typical hyper-K. *** "convexed" was the wrong word. I'm trying to say the t-waves would be an atypical morphology for hyper-K
fakingpatience Posted January 25, 2013 Posted January 25, 2013 I originally thought hyper-K, but in actuality these T-waves are more blunt and convexed than your typical hyper-K. *** "convexed" was the wrong word. I'm trying to say the t-waves would be an atypical morphology for hyper-K I was wondering about hyperkalemia when I saw the T waves in the 12 leads also. Are you saying that the "hyperacute" T waves can be a sign of occlusion, similar to ST segment/ J point elevations? And this pt was indeed having an NSTEMI? Not being a smart ass here, we didn't learn much beyond ST elevations and depressions in my medic class, trying to teach myself the other info now... From looking at the 2 12 leads in comparison with one another, it appears the T waves became much larger in the leads they were elevated in (V2-5) from the first to the second capture. Did you give him any antidysrythmics in addition to electricity?
Jaymazing Posted January 25, 2013 Author Posted January 25, 2013 I was wondering about hyperkalemia when I saw the T waves in the 12 leads also. Are you saying that the "hyperacute" T waves can be a sign of occlusion, similar to ST segment/ J point elevations? And this pt was indeed having an NSTEMI? Not being a smart ass here, we didn't learn much beyond ST elevations and depressions in my medic class, trying to teach myself the other info now... From looking at the 2 12 leads in comparison with one another, it appears the T waves became much larger in the leads they were elevated in (V2-5) from the first to the second capture. Did you give him any antidysrythmics in addition to electricity? Indeed they can be. In a typical MI's evolution, hyperacture T-waves are one of the earliest ECG changes. If the occlusion is big enough and occurs suddenly, the rhythm might bypass having significant ST-Elevation altogether. If you see hyperacute T-waves, and you can't decide if they resemble hyper-K or MI morphologies, the best hint might be in the recipricals! In this case, III and aVF both have depression with a rather ominous down-sloping shape to them. Combined, this equals a very high probability for myocardial infarction. Here is a link to a post about Hyperacute T-waves written by the ECG-guru, Dr. S. Smith And this patient responded very rapidly to defibrillation and CPR; he regained pulses and was telling us to "stop pushing on my chest" before antiarrhythmics could be given (all three times). We handed over care to a heli-crew after that, and I'm not sure what they gave him, honestly.
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