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Sorry, I realised after posting that my comments came across as rude. I'm sure you guys act professionally, and in the best interests of the patient. But, still jealous. My hope is that one day we might treat the UTI in the field. This is already happening in some of the assisted living / long-term care centers locally.

I was expecting something more tricky. It would be quite embarrassing to come into the ER with the blood glucose still so low. Do we have a reason why she became hypoglycemic? She doesn't have a history of DM, Is this just some physiologic stress coupled with beta-blockade and some low glycogen stores? Do you know if there's a name for neurological deficit in the setting of hypoglycemia? I've seen this a lot -- usually it's obvious that they're hypoglycemic because you see a lot of sympathetic response (in this situation elderly + beta-blockade this is blunted). While I would kill my own dead grandmother for a free cup of coffee on any given day (actually, I'm pretty sure she'd kick my ass), I'm not sure what's more concerning, the fact that the ER would provide free coffee to incentivise transport to their site, or that EMS providers would bypass an ER just because it didn't have free coffee. Mostly I feel jealousy. My ERs have a free mop bucket, with complimentary scum.

I don't think it works. http://www.ncbi.nlm.nih.gov/pubmed/21879897 [Link to free .pdf on page] N Engl J Med. 2011 Sep 1;365(9):798-806. doi: 10.1056/NEJMoa1010821. A trial of an impedance threshold device in out-of-hospital cardiac arrest. Aufderheide TP1, Nichol G, Rea TD, Brown SP, Leroux BG, Pepe PE, Kudenchuk PJ, Christenson J, Daya MR, Dorian P, Callaway CW, Idris AH, Andrusiek D, Stephens SW, Hostler D, Davis DP, Dunford JV, Pirrallo RG, Stiell IG, Clement CM, Craig A, Van Ottingham L, Schmidt TA, Wang HE, Weisfeldt ML, Ornato JP, Sopko G; Resuscitation Outcomes Consortium (ROC) Investigators. BACKGROUND: The impedance threshold device (ITD) is designed to enhance venous return and cardiac output during cardiopulmonary resuscitation (CPR) by increasing the degree of negative intrathoracic pressure. Previous studies have suggested that the use of an ITD during CPR may improve survival rates after cardiac arrest. METHODS: We compared the use of an active ITD with that of a sham ITD in patients with out-of-hospital cardiac arrest who underwent standard CPR at 10 sites in the United States and Canada. Patients, investigators, study coordinators, and all care providers were unaware of the treatment assignments. The primary outcome was survival to hospital discharge with satisfactory function (i.e., a score of ≤3 on the modified Rankin scale, which ranges from 0 to 6, with higher scores indicating greater disability). RESULTS: Of 8718 patients included in the analysis, 4345 were randomly assigned to treatment with a sham ITD and 4373 to treatment with an active device. A total of 260 patients (6.0%) in the sham-ITD group and 254 patients (5.8%) in the active-ITD group met the primary outcome (risk difference adjusted for sequential monitoring, -0.1 percentage points; 95% confidence interval, -1.1 to 0.8; P=0.71). There were also no significant differences in the secondary outcomes, including rates of return of spontaneous circulation on arrival at the emergency department, survival to hospital admission, and survival to hospital discharge. CONCLUSIONS: Use of the ITD did not significantly improve survival with satisfactory function among patients with out-of-hospital cardiac arrest receiving standard CPR. (Funded by the National Heart, Lung, and Blood Institute and others; ROC PRIMED ClinicalTrials.gov number, NCT00394706.).

I think this is it. When I look at my peers who have developed PTSD, it's hard to discount their experiences and say, "This couldn't have been me". I think we all have our breaking point. I think that our abilities to cope with the traumatic events we experience are often related to how well our personal lives are. It's easier for me to deal with difficult calls when things are good at home. When they're not, I'm simply more vulnerable. It's easy to judge someone else for having PTSD. If you judge that individual, you don't have to accept that that could have been you. These attitudes prevent us from seeking help, and prevent our peers from seeking help, and ultimately they probably contribute to the suicides that happen. It's a terrible thing to sit back afterwards and wonder, what could we have done to prevent this?

Thanks for posting the scenario, by the way. Sorry, 23 mg/dl (US units - hypoglycemic) or 23 mmol/L (International units - hyperglycemic)? If she is hypoglycemic, we should give 12.5 g of dextrose and reassess (a lower dose, d/t the association with badness in neurological injury, and likeliness of intracranial ungoodness). . If she is hypoglycemic, this might explain the right-sided neuro deficits (is there a fancy medical name for this? I know Todd's paresis is focal deficit following seizure? I like to advertise this as much as possible so that I can pretend to be more intelligent than i am). We've got the description earlier that her airway is "patent", even though she's obtunded (GCS 10). Can we get a saturation on her? I assume she's moving good air, and her lungs sounds are ok? No right lower lobe aspiration crackles? The previously fractured pelvis is not obviously fractured again on physical exam? (I appreciate it's a ramus, so it may be difficult to tell). I think from the information I have, I'd be comfortable holding off on advanced airway management, especially if we're going to the community ED 5 minutes away (which in all likelihood would be a good plan if we were going to meet a helicopter or for stabilisation prior to driving 45 minutes). If an emergency medicine staffed ER is willing to take this patient, then I think I'm willing to defer to their greater experience, education and judgment. It would be nice to have a blood pressure. Regarding the ECG, the description we were given is "sinus rhythm". So, the 12-lead shows NSR as well? Thanks! I'm lucky this isn't an issue locally (non-US). The only health economics issue I remember running into is when we first started thrombolysing people, we were run municipally, and the city was losing a couple of thousand dollars on every eligible STEMI for the cost of the tenecteplase. Ultimately the hospitals starting supplying us for free. Now we've changed governance models, and this is no longer an issue. With public medicine though, comes a sort of chronic under-funding and under-staffing. So it's not always a win.

Well, it's beginning to sound like maybe she should have got a CT last night. It sounds like the family has a pretty good explanation for the fall, it's probably a simple trip and fall. This may be partly a result of all the infirmities of age, a prior ortho' injury, and possibly a bit of Parkinson's developing ("shuffling gate"). I think for confounders, any suspicion of elder abuse? Any recent med changes? Any suspicion of sepsis? While we may have other more pressing issues to deal with, it would be nice to point out to the ER if there are any issues in the home to be aware of, e.g. other trip hazards, need for handrails, walking aids, home care, etc. This is beginning to have the smell of a one-way trip. Unfortunately, I think even with this good history, we have to c-spine her. If she was 40 years old with this history I wouldn't. This is going to increase her ICP, decrease her respiratory reserve, increase her risk of aspiration, and make intubation more difficult. But, I can't see the ER being too happy if I don't. ITLS would make this a critical trauma, and we'd be tearing out of there like it's the end of the world. Reality, this has developed over night. Let's get an IV, bG and a set of vitals, and run a 3-lead, and make a decision about where we're going. The 12-lead can probably get done during transport, or as it takes all of two minutes, on scene. I'd pull some blood for an iSTAT en route. It seems unlikely that she's hypoglycemic (although she is old and beta-blocked, which could mask some symptomology) or that this is some sort of atypical seizure activity, but those possibilities should be respected. It's tough here. She's old, probably has a subdural, but may not, probably isn't a good neurosurgical candidate, and has been sympomatic for an unknown period of time. Palliation is a likely pathway. However, it's not really appropriate to speculate on that until a physician has reviewed a CT. On one hand, the local ED with a CT can do this, ease some burden on the trauma center, and rule out some ddx. On the other, if she does have a significant subdural, we're just wasting time, waiting for secondary transfer. In an ideal world, I'd call a physican, respect that they have greater knowledge of this area, and ask their preference. This also avoids me having to take responsibility for a decision where there's good reasons to go both ways. Forced to make the decision myself, I would lean towards transporting to the trauma center.

First thoughts: * This person is very old. Do they have any documentation limiting what care we can provide? * That looks like a hematoma, not a clear depressed skull fracture. * I like that my fire department uses words like "depressed skull fracture", and am impressed that they're not hitting on the patient's granddaughter. (1) I would like more information about the patient's history, and events surrounding the injury, e.g. fall vs syncope, prodrome, seizure-like activiity, pacemaker / AICD,. anticoagulation (riding the old dagatrabin train?), etc. Are there any bystanders, or obvious findings on scene? (2) ABCDE -- Are they moving all four limbs (particularly the ride side), is there a hx of ambulation since the injury? Aniscoria? We may have to c-spine this person if our history is limited/unreliable and they're comatose. I really don't want to have to do this, especially in an octagenarian I may have to intubate. (3) I have to ask, is it really a depressed skull fracture? Do they smell toast when I push down on it? We should probably avoid the "depressed-skull-fracture by committee" where six different providers push down on the same swollen mass and eventually decide there is a solid structure underneath that seems to be moving. (4) I guess we should do an H&P? (5) I'm not up on what makes a level 3 trauma center. Is this EM stafffed? Does it have a CT scanner? Presumably no neurosurg / neuroICU? [Edit: needed a question mark, probably a couple more beer. And had questions about trauma center designations]

I think this depends a bit on what sort of facility you're transporting to. If I'm 10 minutes from a trauma center, they'll only get intubated if they have no gag or I can't keep their sats > 90%, and they'll end up with an IV or IO. If I'm 10 minutes from a rural ER without EM coverage, I'm probably just going to stop and RSI them now, and either bypass to a bigger ER, or call for a helicopter.

I'm not great at reading labs, but his CO2 is 20, so his HCO3- is probably around 18 mM, right? So, is the metabolic acidosis here just lactic acidosis? Also, why the hypokalemia / hyponatermia? Is there some SIADH here too? On one hand, his crit's 48, but his calculated osmolarity looks to be around 275? Just wondering. I'm trying to get better with this sort of thing since I got access to an iSTAT and started working in the ER a little on the side.

The problem with these case presentations, is we each imagine a slightly different patient. I look at this and see someone hypertensive, with some mildly concerning symptoms; headache, dizziness, proteinuria, and you see the beginnings of hypertensive encephalopathy. We may both be right, but we're just visualising different patients. It's really hard to talk in hypotheticals. I think the analgesia for the headache is a little problematic here, and the best agent probably depends on the severity of the pain. If it is severe and debilitating, some morphine might be a reasonable choice, but runs the risk of obscuring the initial neuro exam, complicating and worsening any change in level of consciousness, and causing a rebound effect. Most headache situations I tend to opt for toradol, but with this hypertension, and the ACE inhibitor, there's got to be some concern about renal function, which means toradol probably isn't the best choice either. I think if you're going to treat, small aliquots of morphine might be the best. If we were to attempt to reduce MAP, labetalol seems like a good option, as you've got some alpha effects there too. I think there's got to be some respect for the history of reactive airway disease in this patient if we're going to give a better blocker, though. In years gone by, we gave nicardipine (adalat), but created some spectacular messes, as it tended to be a little unpredictable. I'm not sure what the best practice is here (hopefully ERDoc can educate us), but based on what I have available on my ambulance, if we treated, I'd expect to get orders for some IV nitroglycerin, maybe with some metoprolol to block any reflex tachycardia.

So, based on the initial description, I wouldn't treat this. Yes, she's hypertensive, and she has a headache and some dizziness, which could be the beginning of a CVA. That being said, she doesn't have any altered mental status, any focal neuro deficitis, any slurred speech, photophobia, nuchal rigidity, ataxia, vertigo, etc. Even if she is having a CVA, this may be the MAP she needs to autoregulate. If, and it's a big if, she's having a CVA, then our target MAP is going to be different based on etiology. I would sit on the patient, reassess, and let the ER work her up. http://www.cfp.ca/content/57/10/1137.short Edited: for grammar, and to add link.

The largest employer in my region has moved to this design, for all operations; urban / suburban / rural / ALS / BLS / IFT. We are told they are safer, which they probably are, if staff wear the seatbelt as much as possible. Personally, I'm still not convinced that they're much safer --- most ambulance models haven't been crash-tested, and many have hard corners on the cabinetry that are essentially plywood edges covered with a quarter-inch of foam. On the other hand, any move in the direction of safety is long overdue. I fear the bench seat is an endangered species, and will soon be extinct. In terms of negatives, on the models we use, it's impossible to turn the seat 90 degrees to the patient, because your knees/shins will contact the stretcher. In the trucks that do primarily IFT / LDTs, I see most of the seats rotated forward in the direction of travel. In most of the trucks doing 911, I see it facing 45 degrees towards the patient, which is a compromise to allow for patient care while preserving some leg room. On the models I've used, it's not desirable or particularly easy to move the seat while providing patient care. It seems like some of the handles for seat adjustment tend to break off. The positioning of the seat tends to restrict access to the patient somewhat, and make for some awkward IV starts. Removing the bench seat also results in a loss of storage space, causing some supplies to be moved to external cupboards. One of the compromises, in the models I've used, is that the monitor is placed in front of attendants seat, which makes it pretty much impossible to position so that everyone in the truck can see it. It also leads to cables obstructing movement from the seat. So personally, I don't like these designs. I think they take up too much space, are not that usable, but will probably improve. A fair bit of this is not liking change, and may be specific to the implementation my employer has adopted, which didn't have a lot of consultation with front-line staff. My preference is for a bench seat configuration, but, I think these are going to become rarer and eventually vanish.

Hypothesis: "Things I write while mildly intoxicated are not as funny the next day".

I think you're all wrong. Discuss...

So, as I understand the concept, it's not about removing the LSB completely. They still remain in use for intubated patients, combative patients, and those you can't communicate with. The idea, is that conscious, cooperative people will splint their own necks. Further, the application of a traditional LSB/blocks/collar restriction carries some real risks for the patient, with little or no proven benefit. * It takes relatively little time on an LSB to cause pressure ulceration. Most trauma patients are already at increased risk. * Traditional spinal restriction results in a 20% decrease in FRC, which could become a trigger for pre-hospital RSI. * Spinal immobilisation can complicate airway management, and increases ICP. * The LSB is a relatively poor device for spinal "immobiilisation", as you're trying to force a curved structure to conform to a rigid plane. * Healthy volunteers often develop neck pain, and report moderate-to-severe pain when immobilised on an LSB, which can result in unnecessary imaging, which carries costs and risks to the patient. I think the rolls/blocks are primarily there to remind the patient not to move their head. Which is pretty much what they do on an LSB, anyway. I think we're all aware that a patient can generate substantial joint motion while immobilised. There's also the question as to how great the benefit really is with traditional techniques. Only a very small percentage of patients that are immobilised by EMS have c-spine fractures. The vast majority of these are stable fractures. Even most of the radiographicaly "unstable" fractures are not grossly unstable, as in the patient will move their head and displace their c-spine. They're unstable in the sense that it would be unwise to discharge them home, to play soccer or football without addressing the injury. Even when injury does occur in a patient that presents neurologically intact, it's difficult to know whether this is from motion during their care or the natural progression of the initial insult, e.g. cord contusion/concussion. There's a certain argument that the force required to fracture the c-spine is many magnitudes of order greater than any force the patient may apply through voluntary movement of their neck. Also, consider the care provided in the ER, where often the patient is removed from the LSB prior to radiography, and left supine with instruction not to move their head. Even after an injury is identified, it's not like the patient is immediately put back on an LSB and then halo'd. They're basically put on a soft stretcher, and told not to move their head, and log rolled by staff. That's all this really Is. It may be a change in care for EMS, but it's not really a divergence from standard care in the ER. The patients that are combative are still on the LSB --- and these are the patients the ER typically leaves on, right? Because we're using it as a restraint device as much as anything else. The patients that are intubated are still on the LSB -- they can't splint, and tube displacement is a potential disaster. The patients that are significantly altered, or who can't follow instructions due to a cognitive issue or language barrier, they're still on the LSB too. But what's happening, is there's a recognition of the limitations of the LSB, and that "immobilisation", is a fantasy -- what we're doing is restricted motion. This can be accomplished in a number of different ways, which can be tailored to the patient.

Sorry. I hate it when people introduce new abbreviations without defining them. Spinal Motion Restriction. Just another way of saying "take c-spine". Implicit to the term is the idea that you can't immobilise the c-spine short of surgical fixation, just that you're trying to reduce movement, i.e. not everyone needs to be on a long board, not everyone needs to be supine, and a collar isn't a halo. Interesting discussion. I don't see the need to take this person to a center with cathlab, CT-angio, neuro-ICU or trauma services. It would be a good idea to aim towards a site with inpatient beds and a CT. There's not much information available here to guide this decision. Common things being more likely, I wonder if, in the end, our fellow might not have a touch of the pneumonia, and be a little dehydrated, weak and/or orthostatic.

Re: the above; it's a gestalt, you take all available information, formulate a list of DDx, and find a working diagnosis. It's not treat the X, not the Y. It's treat both. This is a great attitude, so we should keep this discussion constructive. I think there are two questions here: (1) Was SMR indicated? and (2) How should SMR be performed? On one hand, you have a ground level fall in a 58 year old man. He's moving all four limbs without gross motor weakness. There's no obvious deformity to the c-spine. On the other hand, it's not clear how alert he is, and whether he would be able to report any paresthesia or sensory deficits that he might be experiencing. For c-spine rule-out, the first question is whether there's a potential mechanism., I would submit that a ground level fall in a 58 year old, probably isn't. But this is a matter of debate, and how you interpret this probably dependings on practice in your area. If you do feel that a potential mechanism exists, then, as indicated by ErDoc who's much smarter than me, then SMR is mandated. As to how SMR should be performed, I think the best choice would be to place the patient supine, with a C-collar on, and instructions not to move their head. If he is hypoxic, and becomes distressed while supine, they he could be placed semi-Fowlers, with the same. If he needs to be spinalled, and can't follow instructions, then you have to decide if he can tolerate being supine. If he can, a scoop or long board might be in order. My opinion, and it's just that, is that none of the ECGs attached show a.fib. I didn't see this patient, but my opinion is that I'd be unlike to placed oxygen on someone who didn't appear hypoxic, just because they have a few PVCs, and I can't get an SpO2. The question here is, are these PVCs acute or chronic? I don't see anything here that really pushes towards acute hypoxia as a cause. It seems more likely that this is a chronic exam finding for this patient. So, as others have mentioned, your ECG has a lot of artifact. Reading through it, and making my best attempt to fill in the gaps, I see a sinus rhythm with probable LAFB, with frequent PVCs (probably from high on the posterior wall of the RV), and Q waves with some very modest ST elevation in V1, V2 (and maybe V3, V4). There's also voltage criteria for LVH. I think this represents prior cardiac disease that either the patient is unaware of, or the staff are unaware of. It may or may not have been seen by a healthcare worker before (you'd need old ECGs for comparison). As this ST elevation is modest (much < 25% of the preceding Q wave), I'd suggest it's probably persistent elevation from an old infarction, versus a new acute event. Serial ECGs and troponins will be necessary to know for sure. In any case, there's no criteria for diagnosing STEMI in a background of LVH. I'm sure there's cardiologist who can do it, but I don't think it's an EMS thing. I don't see the lateral ST depression, and just want to point out that you really don't see reciprocal ST depression in V5-V6. Especially not to anterior elevation, which typically only produces reciprocal change inferiorly in the presence of lateral involvement. If it is there, another possibility is LV strain, but like I said, I don't see it. I don't think I would have put on oxygen, or attempted SMR. My primary concern here would probably be the risk of traumatic brain injury from the impact, especially if the patient is anticoagulated, and I expect they would get wound closure and maybe a CT. Then there's the question of whether there was a medical reason for the injury. It's unclear from the history whether this was a true syncopal event. If there has been a progressive functional decline, sepsis and medical change/interaction have to be high up the list of differentials. It's possible he's NSTEMI'd, or having a TIA/CVA, but I don't think there's anything definitive in the story here. Just opinions from another paramedic.

Yeah it's tough. I talked to one of the KCM1 medical directors at a conference earlier in the year, and it sounds like they're doing continuous asynchronous compressions with an OPA, then intubating at the 10 minute mark, in most of their patients. And when they're intubating, they're doing it without pausing compressions. And it's working for them, clearly. It's hard to expect them to turn around and go to standard ACLS, and attempt to capture the airway in the first few minutes of the code, or to use an SGA when they have a high intubation success rate and a strong QI/QA program. The problem almost becomes, with services like that contributing large numbers of patients to ROC, is does their data really resemble the average system, with less motivated medical control, less experienced providers, weaker QI/QA, etc. At a certain point, you start wondering, can I really generalise this to other centers, because they don't have these things? It's the same situation with some of the ETI versus SGA versus OPA resulsts, is do they reflect data from services with optimised resuscitation care? Because if there's clear basic steps that need to be taken for these services to start approaching Seattle rates, then these are the obvious first steps that should be taken. Then again, how much of Seattle is demographics, PAD, citizen CPR training, and how much is targeted ALS -- because no one's really shown a benefit for ALS in an RCT environment yet. [Edit: spelling, grammar, etc. -- got some, missed some.]

It seems like anesthesia occasionally uses the LMA for neurosurgical procedures, so you'd think if it decreased CPP, they'd noticed pretty quickly in someone with bolted with an a-line. Of course the corresponding pressures are much lower during CPR, and hardly resemble normal physiology. The newer devices, e.g. King, EGTA, iGel, etc. obviously have a smaller weight of evidence behind them, although I'm sure much of it is probably generalisable. I said earlier the Hasegawa study had n = 65,000. It appears I was wrong, it was n= 650,000 : http://www.ncbi.nlm.nih.gov/pubmed/23321764 There's a good discussion of the relevant issues here: http://www.ncbi.nlm.nih.gov/pubmed/23519082 The problem here, is no one has run the RCT yet (for airway management in out of hospital cardiac arrest). There's a fair amount of retrospective data, but when you start seeing papers like Bobrow et al., where there's a survival benefit to apneic oxygenation (http://www.ncbi.nlm.nih.gov/pubmed/19660833), or this huge Hasegawa paper, it's clear that it needs to be done. This is being looked at currently, although it's probably more of a 2020 guidelines issue: http://www.clinicaltrials.gov/ct2/show/NCT02090218?term=cardiac+arrest+airway+management&rank=1 http://bmjopen.bmj.com/content/3/2/e002467.abstract http://www.clinicaltrials.gov/ct2/show/NCT01718795?term=cardiac+arrest+airway+management&rank=8 (Looking at effectiveness versus survival)

The trouble with these studies, is they're retrospective -- none were randomised to control for confounders. They weren't intended to compare ETI versus SGA versus OPA versus ApOx, for example. Instead, someone took a bunch of registry data (CARES, Hasegawa et al. -- the Japanese study wit 65K participants), or reanalysed data from a trial designed to look at another intervention (ROC-PRIMED). So, we see a significant association between OPA use and survival -- but this could simply be that patients who are resuscitated in the first few minutes of a cardiac arrest are more likely to survive and less likely to have been intubated -- so they end up biasing the basic airway group towards survival. Likewise the Japanese study showed OPA >> ETI > SGA, but this could simply be a result of longer cardiac arrests being less likely to survive and more likely to get some form of advanced airway, and the patients with multiple failed intubations, or less skilled providers, more likely to end up in the SGA group with more interruptions in CPR. This is a fundamental limitation of this sort of study design, you can only find associations. To infer causation, you need a RCT -- I believe there's one ongoing in the UK (http://bmjopen.bmj.com/content/3/2/e002467.abstract), where you set out to randomly either intubate, place an SGA, or use an OPA (or potentially use ApOx), and then you group the patients by intent-to-treat, so if the patient gets ROSC before airway placement they're analysed as if they had been intubated, or had an SGA placed, etc. It remains possible that the SGAs are affecting cerebral blood flow -- this seems to be the case in pigs (http://www.ncbi.nlm.nih.gov/pubmed/?term=LMA+carotid+compression) , but it's difficult to know if this happens in humans. There are two small studies showing compression of the carotids with LMA use (http://www.ncbi.nlm.nih.gov/pubmed/9466022), http://www.ncbi.nlm.nih.gov/pubmed/9303289 . But it's difficult to know if this has a clinical effect, at this point. It will be interesting to see how this plays out.

Hi mobey! When I wrote "anecdotally", I was referring to my having better luck getting good capnographs with an ETT versus a King, more than to the utility of CO2 in predicting outcome, and assessing the effectiveness of CPR. All the best.

I agree that it's unacceptable to stop CPR to place an ET tube on a cardiac arrest, outside of a few select situations, e.g. copious amounts of blood in the airway, inability to ventilate by other means. I do think that it's possible to intubate (+/- a bougie) a lot of people without stopping compressions, and have done this on the last few arrests I've worked. At the same time, I think there's no shame in throwing in a King, either as a primary airway, or after taking a look and realising that this is not the airway that's going to be captured easily during CPR. Anecdotally, I like having a good capnograph, and have had some problems with getting consistent readings on a King. In terms of a comparison between supraglottic airways and ET tubes, I think you're got a couple of issues: 1. A supraglottic airway can fail due to glottic edema, e.g. anaphylaxis, caustic ingestion injury, inhalation burn, angioedema 2. The cuff on most supraglottic airways typically fails at fairly low pressures versus an ETT. So this might not be the best airway to use on someone who requires high peak pressures to ventilate. 3. Not everyone is going to be easy to ventilate using a supraglottic airway. Granted, these will work for the vast majority patients. I'm looking forward to seeing some data published from studies comparing primary ETI versus primary SGA versus primary BVM. This should resolve some of the issues over which approach is best.

Thanks for posting this. I embarrassed myself very early in my career as a paramedic by withholding analgesia from a 20 year old woman who called from a very divey motel, asking for morphine for her cholecystitis. I told the staff that she seemed like she was med-seeking, because she had a vague abdominal complaint, requesting analgesia within seconds of my entering her room, had a psych history, and was unkempt and living in a dum, oh, an her heart rate was 70 and her blood pressure was normal. A resident took me aside, and instead of telling me exactly what an ignorant fool I was, took the time to explain to me that pain, especially from hollow organ injury, often comes with a vagal component, and that heart rate and blood pressure changes are insensitive and nonspecific. Some years later, I've formed the opinion that there will always be medseekers and drug addicts. Many of them will be very manipulative, and very convincing actors. And this leaves me with two choices; (1) I can try investigate all complaints of pain, and see if they qualify to meet my subjective standards for what acute pain should look like, and withhold analgesia from people with questionable histories. This comes with accepting that I will inevitably withhold analgesia from some people in acute pain. (2) I can stop judging people, and accept that pain is what the patient says it is. This comes with the risk of giving opiates/opiods to someone who is drug seeking, and potentially encouraging further system abuse. But, given the fairly trivial amounts of analgesia that I'm giving, it's unlikely anyone is getting too euphoric from 5-10mg of morphine, given that a lot of the addicts I meet are using over 200 morphine equivalent milligrams of diverted prescription opiod per day. I'm probably just easing their withdrawal symptoms. This comes with the benefit that I no longer have to be as judgmental towards my patients, and no longer run the risk of failing to provide analgesia to someone in severe pain, and giving them a label that will likely follow them through the ER, and probably into other areas of the healthcare system, all because theiir presentation doesn't meet my entirely subjective, culturally-biased and ill-educated opinion of what acute pain should look like. As a paramedic I am always appalled when I see articles like these being published: http://www.ncbi.nlm.nih.gov/pubmed/23478179 http://www.ncbi.nlm.nih.gov/pubmed/17920974 http://www.ncbi.nlm.nih.gov/pubmed/16036826 http://www.ncbi.nlm.nih.gov/pubmed/12385607 http://www.ncbi.nlm.nih.gov/pubmed/16036825

So, opinions were asked for, so here are mine: For: ==== Arming paramedics might help some patients in areas where police response times are slow. Currently, most systems have some form of "staging" policy, where paramedics won't go into a potentially unsafe situation, and will wait for cops. In some areas, response times may be over an hour, and some systems may even hold these calls until the police department indicates that they are ready to respond. For severely traumatised patients, this delay in care, could result in additional morbidity or mortality. This would also preserve police resources. It's not always possible to anticipate every violent situation. Many acts of violence against paramedics are committed by individuals under the influence of drugs, including alcohol, patients with acute mental health crises, those that are postictal, or hypoglycemic, and people that just simply aren't nice and don't play well with others. The information that dispatch is able to obtain is often severely limited, and sometimes violence erupts unpredictably. Having an armed paramedic might mitigate some of this risk. Occasionally paramedics come across crimes in progress. In a paranoid right-wing fantasy world, it's always remotely possible that you could stumble upon an active shooter situation and intervene. Against ====== Firearms laws vary greatly from country to country, and indeed, between regions within the same country. I don't live in the US, but my understanding is that many laws regarding concealed or open carry and which weapons may be purchased vary from state to state? If your paramedics are working in an area that doesn't allow concealed or open carry, then they may need to either (1) become police officers, or (2) have the appropriate statutes changed, in order to carry a firearm. This carries a logistical burden. There's an obvious training requirement for anyone carrying firearms in professional capacity. This would be expensive, and could detract from the time and resources devoted to other areas of training, including clinical care and driver training. A firearm alone is unlikely to be sufficient to meet the challenges facing an EMT or Paramedic. So you probably need to add some form of impact weapon, and possibly a taser, or pepper spray. These all carry additional training burdens. Focusing on firearm retention while providing patient care is an additional distraction, and being armed presents the risk of losing your weapon to a potential assailant. It's difficult to imagine what the rules for firearm discharge would be. Are your paramedics going to be encouraged to intervene if they witness a spousal assault? Is this putting them further in harm way? Are the relevant legal statutes present to permit intervention? What's the personal and employer liability in the event of an accidental discharge or injury to a bystander? How often do you expect your paramedics to use these weapons in exchange for the training required? Is there a measurable benefit to your paramedics, your EMS or healthcare system(s), and your patients or bystanders? Are you existing staff fit enough to be expected to handle impact weapons? What will you do for staff who fail to quality? ================================== So, my opinion is that it's not worth arming EMS, because there's too large a training demand, too low a likelihood of needing to use the weapons, too high a risk of injuring bystanders or a patient who is disoriented, and that by doing this, you're essentially duplicating the efforts of another government agency, and encouraging mission creep. I think that there's very little benefit, and that there's a far simpler answer in continuing to encourage paramedics to follow existing staging policies. My job is complicated enough already, and it's difficult enough to meet my training needs to provide decent clinical care without having another set of training requirements. I certainly wouldn't want to be placed in more dangerous situations with inadequate training, which I think would be a recipe for disaster. =================================== I also agree that you seem to be begging the question. By titling your work, "Why aren't EMTs and paramedics armed", you've already taken a position, i.e. that they should be armed, before you've even outlined the problem and the merits of the different sides.

Edit: There's also this, on-line. It has the trappings of a journal article but isn't indexed on pubmed. It also deal with a lot of low quality data. http://ispub.com/IJRDM/1/2/12892