Brandon Oto

I would actually make a controversial recommendation here. Although strictly speaking, using a venous source for your capillary-calibrated glucometer is incorrect, the difference is rarely more than a few points (maybe a little more if they've recently eaten). On the other hand, sick patients will usually have a MORE reliable venous than capillary reading, and this far outweighs that small inaccuracy. In other words, for any patient where it really matters, I would actually prefer a venous reading. I talk about this a bit more here and I can provide sources if anybody wants, but basically, there's plenty of research showing that patients in shock, or sepsis, or cardiac arrest, or really any acute illness inducing a classic stress response (with peripheral vasoconstriction and so forth), your capillary blood is going to be the "last to hear" about any changes in the circulating plasma. Readings can be grossly elevated or depressed -- and yes, it can be either one, so there's no back-of-the-envelope correction you can make. For sick people, venous blood is better. I realize there's a legitimate safety concern regarding needlesticks, to which I'd let everybody make their own reasonable decisions. (It blows me away that anybody is still using non-safety needles.)

Which raises the issue of whether you should give the nitro if circumstances (short transport, limited hands, difficult access) make getting a line or your 12 lead impossible. My feeling is definitely not without the ECG (too great a risk of right ventricular infarct) and, in light of the previous discussion of the marginal benefits of the nitro, probably not without the line. Although if you're comfortable and a gunslinger with something like the EZ-IO this may not come up much.

Thanks DD. I'm just a nerd is all. What's really obnoxious is how hard it is to get access to academic databases once you leave school... Anyway, great post Levi. I guess we can probably agree that nitro is likely worth doing, give it if you've got it, but not something you'd call a high priority, and certainly don't give it in preference to other care (such as ASA). Although now I'm waiting on the emergence of sublingual Viagra...

Thanks for answering, Tom. What I meant is that VT by definition is ventricular, so I was confused when you suggested that 50% of VT might show AV association. I see now that you meant about half of them will demonstrate retrograde conduction, thereby associating P waves and QRS complexes even though the actual rhythm isn't originating supraventricularly. Is that 50% stat a general illustration, by the way, or is that the actual percentage? Do about half of the AV nodes out there have some quality that allows retrograde conduction, and half do not?

My apologies for the outrageous thread resuscitation, but these strip teases seem like they should be lasting resources. If Tom's still reading, I hope he'll be willing to add a little info. Tom, What do you mean by the above? I agree that P-wave association is hard to note in most VT, but by saying it's only present 50% of the time, do you mean that some VT DOES have AV association? Surely that makes no sense unless you're thinking of retrograde conduction.

Maybe I misunderstood your question. If you're specifically referring to the physical assessment only (or physical + hx), then that's a separate story and I may not especially disagree. To me, "assessment" means the entire scope of information-gathering tools available to the provider, from his eyeballs to the machines with dials and lights. There's no particular difference between palpation and blood glucometry, except that some people can get in trouble for doing one of them. All just info and all part of the assessment. And as you say, anyone can either take the information gathered and use it meaningfully, or be without a clue as to its significance. But again, to me, that's not part of assessment; that's part of diagnosis and treatment. I should be able to "assess" a patient and hand you a paper with everything I learned on it; you could then use that data to diagnose and treat, and we've done separate jobs. Obviously the two parts usually go hand-in-hand and should interact. But nevertheless. But maybe this is a digression. Sure. But the significance of the pulse is largely as a way of viewing cardiac activity (the rest of it is probably as a measure of vessel compliance and distal circulation at that extremity, and an indirect look at BP). The medic and the Basic can both take a pulse, and both probably should; but the Basic can't do anything more (except perhaps auscultate for a rhythm, which is of marginal utility to him). The heart's electrical rhythm is a piece of information he will forever lack, no matter how "good" he is at assessment. Likewise, rhythm is something the medic can and will obtain, whether or not he's able to parse its significance. Like I said, getting the information and using it are different skills. Getting it as part of the assessment. Using it (whether to treat, or to inform transport decisions, or to form a working diagnosis, or anything else) is something more and something separate.

I really think that you can't gloss over the above. I realize you're trying to emphasize the education gap, as par for the course around here, but the fact remains that a Basic provider could literally be a FACEP in his day job, and a medic could actually be the world's biggest idiot; the first is NOT going to be able to truly assess to the level you're looking for, and the second may very well be able to, even if he's too dense to put it all together. I CANNOT feel a pulse and tell you a patient's underlying cardiac rhythm or abnormalities. It is literally impossible. I can GUESS, depending on regularity, rate, and strength, and correlating with history and other presentation, but even if it's seemingly a gimme (A-fib, say), it will still only be a GUESS. The medic who runs an ECG can, if he is not brain-damaged, tell me what rhythm the patient is in. The fundamental difference between us is that he can use that tool and I cannot. So I grant that the underlying assessment follows the same path, and is looking for the same things; but there is a certain level of clarity that is simply unavailable without the appropriate diagnostic tools, and in some cases that level is the critical one for recognizing conditions or narrowing a differential from meaninglessly large ("sick") to useful.

By and large the difference is that the medic generally has tools that allow him to more directly and precisely assess physiological states that the EMT can only either guess at ("chest pain? could be an MI") or note broadly ("tachycardia" rather than sinus, junctional, SVT, etc.). He can take a blood sugar and say a person is hypoglycemic, where the EMT has to guess based on history and general level of consciousness changes. He can throw on electrodes and tell me that the patient is experiencing acute hyperkalemia where the EMT would just know they're sick. And so on. Both sides are right, but one of them can say much more because he has the resources. Differences based on actual clinical knowledge obviously can exist as well, but are not necessarily part of the roles, IMO. You can have a medic who doesn't understand shit and you can have an EMT with an excellent grasp from cell wall up to hairy chest. Knowledge influences what you do with your assessment; the assessment itself, if done correctly, should simply be data. (The only exception would perhaps be if your clinical impression guides WHICH things you're doing to assess -- e.g. should you be measuring ETCO2 or looking at pupils?)

I was able to get my hands on the fulltext of one of the studies I linked (http://www.ncbi.nlm.nih.gov/pubmed/18347964?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=57). PM or email me (brandon@degreesofclarity.com) if anyone wants a copy; I think this falls within fair use. This one seemed to find from the available evidence that nitro generally improves short-term surrogate endpoints (reduced infarct size, for instance), but the overall long-term mortality rates are either unchanged or very slightly improved. Quote: Some of the research was done with IV nitro but I doubt this matters too much. The evidence does seem to suggest, though, that early nitro is the only nitro that could possibly matter, which tends to mirror our current prehospital usage. (For MI, that is; angina is a separate issue and nobody really disputes its benefit there.)

Just saw an older thread that treated with a similar topic. Some good stuff there. http://www.emtcity.com/index.php/topic/8456-evidence-based-use-of-nitro/

Thanks to those who posted studies. This one seems good, though somewhat dated http://www.ncbi.nlm.nih.gov/pubmed/8087820?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=30 If anyone can drum up research or academic access to these ones http://www.ncbi.nlm.nih.gov/pubmed/19681463?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=11 http://www.ncbi.nlm.nih.gov/pubmed/18347964?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=57 http://www.ncbi.nlm.nih.gov/pubmed/19445779?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=19 http://www.ncbi.nlm.nih.gov/pubmed/19445778?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=20 that would be very helpful I think. I was charmed to see that Viagara might be better than nitro...

Got into a chat recently with another EMT and once everything had shaken out, I realized that I wasn't actually sure whether nitro had been definitely associated with positive outcomes in well-powered research. The gold standard here might be aspirin -- having an MI, take ASA, the data shows more live tissue and better survival to discharge. Does this sort of evidence exist supporting similar use of nitrates? Or is it just "one of those things" that in reality is done mainly as palliative care? I recognize the theoretical mechanism here, but that it makes sense doesn't mean that it works. And this is not an academic issue, since it is potentially important to deciding priorities when rendering care. Anyone know of any studies?

I suppose the theoretical answer is that if a patient is hypoxic without being hypoxemic, their O2 sat will not reveal their true level of cellular distress.

To reinforce that a little, I'm sympathetic to the cries of "better education" and "better training," but until those changes run through the system, folks like me are left to learn on their own. So while I think it's great to complain that Basics et al. should already know this stuff, I'd much rather that you just explained as much of it as possible. I don't want to get in the way of whatever other discussions you guys want to have, but if you really believe in creating more educated providers, well -- we're reading, and that's why we're asking questions.

That's great, Vent. And I do appreciate the complexities involved with everyone's favorite little diatomic inhalant. But pending my training as an RT, if you hand me a patient, I still have to either give them oxygen or not; the pathophysiology involved may be largely over my head, but there's still only two options available to me. Can't we reduce these things to a somewhat easier set of principles or rules of thumb based on the brief time the patient will be under my care -- i.e. in the 8-15 minutes it's going to take me to back into the ER, I'd like to help some, but I probably don't need to work any miracles... just palliate a little. Or are you advocating the old everyone-gets-it strategem as the safest scheme for a low-level prehospital provider with a limited period of patient contact?

This is awesome and informative, guys, but I'm still interested mainly in the original question. I guess we've all agreed that there can be a strong placebo effect attached to any use of O2; that said, there will still be cases where it's also physiologically beneficial, and those where it's not. My treatment for anemia is a bolus of definitive care

There's a fair amount of back-and-forth recently about the status of supplementary oxygen for a few high-profile conditions, such as stroke and cardiac arrest. It'll be nice to see how that eventually cashes out, but my personal interest is in the less-discussed fronts. A lot of prehospital providers -- particularly the poor BLS buggers who can't do much else -- tend to use O2 as a panacea, on the somewhat religious assumption that it'll help with almost any ailment. But when will it actually help? I'm curious in two things -- 1. For a given condition, in your PERSONAL EXPERIENCE, have you witnessed either ALLEVIATION OF SYMPTOMS or IMPROVED OUTCOMES following the administration of oxygen? This is obviously just anecdotal, but it's the best we're going to do in many cases. 2. For a given condition, have you seen any rigorous research that supports or denies either of the above? I'm interested in this to better inform us all about the true indications for supplementary oxygen. It probably goes without saying that someone with dyspnea and trouble oxygenating will improve with high-concentration O2, but it is far from obvious whether the guy with the broken leg will hurt any less, the guy with appendicitis will live any longer, or the woman with nausea/vomiting will feel any better. "Throw on a cannula" may not be all that harmful but we'd probably all rather avoid unnecessary treatment when possible. So -- any thoughts? I'm interested in everything from AAA to Zebras. I will say for my own small contribution that I've had mixed results giving patients with anxiety and similar psych states low-flow O2 by cannula; sometimes seems to help, sometimes not at all.

I used quick clips (X across the chest, straight across hips, straight across legs) at my last agency, and while it's fast and good for BS C-spining, ghetto-splinting, and "just to making carrying easy" jobs, I don't really trust it for serious immobilization. If you're going to be cartwheeling people through hallways or the like I think you need much better superior-inferior immobilization. I vaguely remember something about looping around the feet from back in school, but we use 9-foot straps here and that works for me -- you can still go straight across if you want (just have lots of slack), but you can also do a Grady strapping which IMO is very secure due to the hips being "harnessed" in. Pad voids if possible and you're golden. Just make sure to tighten down reasonably well, too many people just kinda tug on the straps like they would on the stretcher, which I don't think is good enough... I do prefer the stick-on plastic headbeds to the ginormous blocks though. I suppose security is debatable either way but I'd rather not carry around the damned things.

Here's a source for the Cushing's that sort of covers all the bases: "The triad refers to three signs caused by Cushing's reflex: 1. Bradycardia 2. Hypertension (with widened pulse pressure) 3. Bradypnea (often irregular)" (http://books.google.com/books?id=0nDvZP8qnigC&pg=PA26&lpg=PA26&dq=source=bl&ots=n2tsb2aoql&sig=91t0v__evYsM7hIuZevbcwotk-U&hl=en&ei=CvHySrPFD4bAlAfTkt22Aw&sa=X&oi=book_result&ct=result&resnum=6&ved=0CBMQ6AEwBTge#v=onepage&q=&f=false) Fair enough. To be honest, in my rough understanding of Cushing's reflex, it's not clear to me why a widened pulse pressure would become evident. Correct me if I'm wrong, but the hypertension here is mainly a product of peripheral vasoconstriction -- right? Surely it CAN'T be a product of increased cardiac output, because we know that one of the other signs is BRADYcardia! But HTN due to vasoconstriction would seem to imply a rise in both systolic and diastolic pressures, at least in my mind. Am I missing something?

Forget it. Let's just work on shining a little light on a confusing world. John, is CPR for brady an ACLS thing? I've never run into hide nor hair of it on the basic side and I suspect numerous layers of people above me would have kittens if I pulled that one on scene.

On the suctioning point, here was that bit of the AHA recs: "Aspiration of meconium before delivery, during birth, or during resuscitation can cause severe aspiration pneumonia. One obstetrical technique to try to decrease aspiration has been to suction meconium from the infant’s airway after delivery of the head but before delivery of the shoulders (intrapartum suctioning). Although some studies suggested that intrapartum suctioning might be effective for decreasing the risk of aspiration syndrome, subsequent evidence from a large multicenter randomized trial did not show such an effect. Therefore, current recommendations no longer advise routine intrapartum oropharyngeal and nasopharyngeal suctioning for infants born to mothers with meconium staining of amniotic fluid (Class I)." (http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-188) The main study cited in support notes: "No significant difference between treatment groups was seen in the incidence of MAS, need for mechanical ventilation for MAS, or in the duration of ventilation, oxygen treatment, and hospital care. INTERPRETATION: Routine intrapartum oropharyngeal and nasopharyngeal suctioning of term-gestation infants born through MSAF does not prevent MAS. Consideration should be given to revision of present recommendations." (http://www.ncbi.nlm.nih.gov/pubmed/15313360?dopt=Abstract) This was nearly five years ago, so I don't know if there has been any more recent data. Nevertheless, my EMT text still teaches the suctioning and I believe it's required in most state testing. And my protocols state: "10. Suction mouth, then nose of the infant as soon as possible." (pg. 82, http://www.mass.gov/Eeohhs2/docs/dph/emergency_services/treatment_protocols_704.pdf)

I guess this has been moved into the Students forum. I have to admit that I find that vaguely offensive, since I'm not a student (except in the loose sense that we're all students...), and since in my opinion these are "questions" not because I haven't flipped to the right book but because the books don't seem to agree. Maybe these are all obvious issues to whoever moved this, but if so I'd appreciate them sharing with the rest of us, because they are non-obvious to me; and yes, I am a working EMT.

I've bumped into a few little oddities or inconsistencies recently, and I figured I'd roll them all together and ask for input on them. Interested in any thoughts. 1. I was originally taught that during a field birth, you suction the neonate's mouth and nose as soon as the head becomes available. This is to prevent aspiration of meconium once the little bugger starts breathing. However, I've been flipping through the 2005 AHA recommendations and I note that they actually do not recommend this practice, called "intrapartum suctioning"; according to their review of the literature it shows no benefit to either decreased infant mortality or decreased aspiration. Some poking around on my own seems to confirm this. What do you guys think? My service still stocks little bulb syringes for exactly this. I'm not 100% clear, however, on whether the AHA et al. are contrasting intrapartum suctioning with NO suctioning, or with suctioning after completion of the second stage of labor. 2. CPR and PALS guidelines recommend chest compressions on an infant with signs of inadequate perfusion and a HR below 60. This is because, well -- that's not good enough. My question -- why isn't this an option for profound, symptomatic bradycardia in ADULTS? You medics can go to town with pacing or meds, but if you're BLS and presented with a patient showing shock and a very slow pulse (I'm thinking, for instance, a drug overdose or a hypothermia case), why can't we use the above logic to begin compressions and increase circulation manually? I've never seen this recommended but it's not clear to me why it wouldn't work, except maybe minor paranoia about commotio cordis. 3. Just what on earth is Cushing's triad really supposed to be? I thought I knew, but I've seen three versions: hypertension + bradycardia + irregular respirations; hypertension + bradycardia + widening pulse pressure; widening pulse pressure + bradycardia + irregular respirations. The second is the one I knew but apparently everyone has their own version. Try a quick Google -- it's kinda funny. Thoughts?

I was assuming BLS since that's my bailiwick, so the idiot box isn't going to shock asystole unless you jiggle it just right. But the medics have more options available anyway. Great input guys. You're probably right that no matter how you squint at it, the "right" answer is going to involve bringing medical control into the huddle.

Uh... that's from my website, but is not current. I'm off in Boston now. Why?