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Maybe you should talk to more gay people? There's quite a lot of them around. Not all of them are the same.

I think the original poster wrote that the patient was 97 years old? Would you be less aggressive with a patient this old? If the swelling is progressing rapidly, how comfortable would you be with a paramedic RSI? Do you think it would be a better strategy to try and get the patient to the ER so someone more experienced can intubate? Just wondering.

Because of the history associated with these words. If straight white people had been systematically oppressed, tortured, killed, enslaved and abused by a mass of gay half mexican half black women then the same stigma would be attached to using the word "cracker". When someone who openly identifies themselves as gay makes a gay joke it's probably not offensive to the gay community at large, because I imagine it's pretty clear there's no evidence of ill intent. These jokes are probably about a shared past, unique to a given community. If you're not part of that community, it's not immediately clear whether you're making light of a painful history or being a modern day bigot. So there's a chance you're going to offend people. One of the few downsides to being straight, white and male.

Munich is a great city! I had a fantastic time when I visited. Germans know beer and good food. Enough said.

I think that's methoxyflurane? It's used a lot in NZ / AUS. Not approved in the US because of a risk of liver CA (I think - or maybe I'm confusing my anesthetics). My preference would be to switch to opiate + antiemetic if that occurs. Ultimately it's the patient's decision. The entonox is essentially self-administered. They hold the mask to their face, breath in as often as they want, and stop when they become somnolent and drop the mask, or when they can no longer tolerate the symptoms. If they want to continue using it despite the nausea, then they can. As I said earlier, I rarely use it as a single agent. It's certainly superior to opiates in managing labour pain, providing it's providing adequate relief. But outside of that setting, it's either for a quick move to the ambulance, if care can be better provided there, or I'm using it with opiates. Obvious caveat: Medical direction determines what treatment modalities are present, and how they should be used.

BLS in the area I used to work was able to use Entonox, and we used to carry it on the ALS trucks as well. However, we didn't use it that often. I think perhaps it was a little underused. A few problems come up with it, as you may have seen: * The pain relief only lasts while the patient's inhaling the nitrous oxide, so once you arrive at a receiving facility, you either have to leave the bottle with the patient (impractical), or take it away (unethical). So usually you end up giving morphine (or another opiate) anyway. * Some people just don't like it. There can be a lot of nausea / dizziness / dysphoria. * There's a risk that the nitrous oxide migrates into air-filled spaces, making it dangerous in bowel obstruction, and you can't really use it in most major trauma, because it can worsen pneumothoraces (or other disease processes involving trapped air). * It just isn't as effective as opiates in most patients. So if the pain is severe, again, you're adding opiates. Now personally, I think that in combination with an opiate, it's a good analgesic for transport / extrication providing none of the issues above apply. It allows you to provide added analgesia to someone while you're moving them around and exposing them to vibration and stress during transport, which can then be d/c'd upon arrival, once these stressors are removed. [For what's it's worth, I also prefer morphine over fentanyl in situations where hemodynamics aren't an issue, as I've had too many experiences where I've got the patient transferred to a bed, given report to an RN, and then had the fentanyl wear off, and been put in a situation where I feel an ethical obligation to provide further pain control, but know that if I do it in the ER, after transferring care, that I'm putting myself in a potentially risky position.]

Well... how much vegemite is in that omelette?

On the pharmacology of ketamine: [Just for general information -- I'm aware that anyone with MD after their name is already aware of the following ] * Ketamine itself is a negative inotrope. * However, ketamine stimulates sympathetic discharge, so administering ketamine may increase CO / MAP, provided, the patient has a functional ability to increase their heart rate and constrict their peripheral vasculature. This may not always be the case, in which case ketamine may cause hypotension. * It is not hemodynamically neutral. It just has less potential for hemodynamic compromise than benzodiazepines, and most opiates. * Part of the hemodynamic effect of ketamine is to raise ICP. However it's also been trialed (unsuccessfully) as a neuroprotective. There is ongoing controvery as to its use in closed head injury. * Ketmaine also has an intrinsic bronchodilator effect, making it beneficial in situations where bronchospasm is an issue, e.g. status asthmaticus. Ketamine is beginning to find its way into prehospital care. For example this system -- which I don't work in, before anyone asks --- (http://www.albertahealthservices.ca/hp/if-hp-ems-mcp.pdf) allows ketamine for RSI or as a sole agent in the intubation of patients presenting with hypotension, airway burns, acute asthma or procedural sedation in hypotensive patients <80mmHg (e.g. pre-cardioversion, or for fracture realignment). I think it's often finding use outside of the US in situations where US providers might opt to use etomidate. As a medic, I'd happily come out to give pain control to anyone. I think it's one of the most tangible benefits of having an ALS response. It's something we actually know we're good at. Personally, I'd never have an issue with coming out to pain control someone. Or, in general, to back up BLS. I'd rather a BLS provider calls me, if they have a concern, and have it be a waste of time than have someone be too afraid to call, and have the patient suffer. But this is going to depend on your system, and the availability of ALS resources. I think that if you're close to the hospital, and can move the patient without undue pain, or you think that a critical life threat is present, then you probably shouldn't wait for ALS. In contrast, if you have someone with previously diagnosed renal colic, having symptoms suggestive of their prior renal colic, and they're a vomiting, diaphoretic mess on their bathroom floor, it might be better just to start an IV (if that's in your scope), and wait for someone who can give opiates.

That was great advice. I just want to add that when you're faced with this situation there is nothing you can do or say that is going to make it better. It isn't going to be pleasant. The only thing you can do is try and be as professional as possible and not give them false hope.

Another perspective from a someone who's lived and worked in Canada. When I was there, I got: - basic health insurance from the province (think: state) I lived in. Currently this is free (Well, free in that there's no separate tax for it, it just comes out of general revenues). This covered medical treatment with the exception of (i) dentistry / orthodontics, (ii) prescription costs, (iii) ambulance, fixed-wing / rotary wing transport *unless admitted to a given facility [so not ER->ER], (iv) things like crutches, peak flow meters, ambulatory aids, etc. (v) private hospital rooms. Maximum prescription costs are also limited by the province, (vi) driver's medicals, (vii) immigration paperwork / sick notes for work, etc. - additional private insurance through work, covering (i) - (iii) and (v), some of which were capped. So, living in Canada, I never really had to worry about the cost of healthcare. Granted, if I didn't have the private insurance, if my doctor wrote me a script for a $100 antibiotic treatment, I'd be a little out of pocket. Or if I ended up requiring ambulance transport, I'd get a few hundred dollars as a bill. But I'm basically never opening my wallet to pay for healthcare. The tax rate probably is higher than the US. I paid 5% sales tax to the federal government. 0% to the provincial government. The income tax rates might be a little higher. I had to pay city taxes on my house that went towards fire, police, ems, school, public works, etc. But I doubt the quality of life is much different. I'm sure many of you guys have visited Canada. Did you see a big burden being placed on people because of taxation? I never saw it. What are the negatives to the system? - if I need an MRI or a CT or something, especially for a minor joint injury, I'm going to wait. It's going to take a while. If I tear my ACL, it's not getting fixed quickly. As a young person this is inconvenient, and obviously runs the risk of turning a minor injury into some degree of permanent disability. For an elderly person needing a joint replacement, this is disastrous. My understanding is that it's many of these patients that are going to the US for treatment. - experimental drugs often aren't approved by the medical system. So if I develop a rare kind of cancer, and someone develops a new therapy that doesn't have a lot of evidence supporting it, that might reduce morbidity, might reduce mortality a little, it may not be approved. Some of the patients going to the US are going for this sort of treatment, obviously at their own expense. - Dental care can still be quite expensive if you don't have private insurance. I have a relative with bad peridontitis, who has been paying to fly to Mexico and get dental work done. He can pay here, but it's expensive. The insurance company has told him they'll pay to have some teeth removed and get dentures. He wants to get a series of implants instead. They're cheaper in Mexico. I doubt anyone is going to the states for cheaper dental treatment (usually treatment costs are capped -- but obviously as my example illustrates, can be quite expensive). ---------------- The thing with health care is no matter what system you choose for delivery, you have to pay for it. Almost all of the industrialised nations have socialised systems. With the exception of the US. That's a choice you guys have made, and it's not my right to tell you how to design your economy, and run your nation. What I can say, is if you get hurt in Canada, you're still paying for medical care through taxation. You're just not having to worry about getting huge lump sums to pay. You're not worrying about qualifying for medical insurance, and family coverage, etc. Either way you pay. Either through direct taxation and universal coverage, or through partial coverage and direct pay. I couldn't imagine living somewhere where I could get run over by a car, and end up selling my house to pay for it. I wouldn't choose to do that. I'd rather pay the higher taxes.

A couple of points to make:- PE is definitely a possibility, and is extremely difficult to rule-in/out in the field. With any immobility there's a risk of forming a DVT, and having an embolic event. Also, if the patient is in a situation where they're prone to thrombus formation, it increases the risk of an MI, which could be this patients concern. There remain other issues, with the patient's hypertension. Could this be due to a TAA? Or could we be having a neurologic event, with concurrent MI. The scenario seems to be pushing you towards treating this patient as a stable tachycardia who then decompensates. But that doesn't necessarily follow from the extremely limited information presented. I would have been frustrated and irritated if I had received something like this as an assignment. If there's an altered mental status, and we're cardioverting this patient while their pressure is 130/80, or whatever, then we're saying that cerebral ischemia is happening at a relatively high MAP. This is only going to happen if there's some increase in ICP that's decreasing the cerebral perfusion pressure. This could occur secondary to a tumor, or intracranial hemorrhage. It suggests that something other than a simple tachycardia is occurring and that there's another (or more) disease process(es) ongoing. I'm not sure that's where the author intended you to take this. I suspect it's just badly written. A couple of other points: * Not sure why we'd be using beta-agonists, including dobutamine here? * Beta-2 agonists can cause vasodilation, but I don't think you'd have to worrying about beta-agonism causing a thrombus to move into the CNS. If a thrombus is identified and present, the hospital needs to heparinise and deal with it. With regards to ECG analysis: There's a few good books out there. This one is fantastic for explaining the basic mechanisms, although some of the nomenclature is non-standard (I think): http://www.amazon.com/Rapid-Interpretation-EKGs-Sixth-Dubin/dp/0912912065/ref=sr_1_1?ie=UTF8&qid=1315561310&sr=8-1 This is good for a basic introduction to 12-lead http://www.amazon.com/12-Lead-Coronary-Syndromes-Reference-Package/dp/0323047122/ref=pd_sim_b_3 Both these have a good library of 3-lead strips for basic rhythm identification practice: http://www.amazon.com/Dysrhythrams-Interpretations-Management-Robert-Huszar/dp/0801672031/ref=pd_cp_b_3 http://www.amazon.com/Arrhythmia-Recognition-Interpretation-Tomas-Garcia/dp/0763722464/ref=pd_sim_b_5 This guy makes an excellent pocket reference guide, but is at a reasonable high level of detail. If you're having trouble, this isn't the best to start with. But its a useful tool for all paramedics, in my opinion. http://www.amazon.com/ECG-Pocket-Brain-Guide-Interpretation/dp/1930553145/ref=sr_1_1?s=books&ie=UTF8&qid=1315561563&sr=1-1 I think with a lot of the interpretation you just have to look at lots and lots and lots of strips. Then it becomes easier. Treat it like doing IVs. You don't expect to be good at your 1st, 10th, or even 20th. You need a few hundred. Do the same with ECG analysis. In the beginning it also helps to go through in a systematic approach: (1) is the rhythm regular or irregular? (2) is it fast, slow or normal? (3) is the QRS wide or narrow? (4) are there P waves present? (5) are they present at a constant PR? (5) are there any "extra" beats or "missed" beats? Just work through these systematically with each strip, do a few hundred, and you'll find you improve dramatically. The knowledge required to be a paramedic seems daunting at the beginning, but once you get finished the program, get done the licensing, and work for a couple of years, most of what's taught in medic school will seem very basic, and you're going to spend a lot of time realising how little you actually know, and how little you were taught. Don't worry, it will all come together.

A partial occlusion along the brachial artery would explain the finding, but is somewhat unlikely. A major concern in this situation is the presence of a thoracic aortic aneurysm. If the aneurysm affects flow to the right arm (typically via the right subclavian branching off the brachiocephalic trunk) or to the left arm (via a left subclavian branching directly of the thoracic aorta), then the pulse on the corresponding side will weaken). This is similar to the finding of unilaterally (or bilaterally) diminished pedal or femoral pulses in an abdominal aortic aneurysm. A tumor in the thoracic cavity could cause similar symptoms. If this is an elderly patient, it's possible that their physician is aware that some form of obstruction is present, but surgical repair/treatment may be contraindicated.

No, you didn't. I just wanted to make sure that no-one reading this misunderstood.

12? Wow. I would add to be very very sure that the AICD/pacemaker is functioning inappropriately before you do this. I have had patients complain "my pacemaker's broken, it keeps shocking me!", who were being defibrillated / cardioverted out of VF / VT.

I have to point this out or my head will explode. "Prescription".

Cool. Thanks.

A couple of quick questions for ERDoc:- (1) When you're using a drug like propofol that can cause hypotension, does it create problems if cardioversion fails? Or is the half-life so short that this is rarely a problem? (2) How often do you see patients who have underlying electrolyte issues that need correction prior to successful cardioversion? At what point do you stop if cardioversion is failing to convert?

How do you do this? How many TAAs have you seen? In what percentage of the times that you thought you saw a TAA were you right? In what percentage were you wrong? How many patients have you evaluated who you didn't think had a TAA? How often were you right? How often were you wrong? How do you feel this compares to assessment by a ER fellow? IM / Cardiology? Can you beat U/S or mediastinial changes on CXR? How do you compare to thoracic CT? What makes you think that you can do this better than everyone else? With less education, and less technology? Physicians in the ED with a million times more experience, education and training time, and better technology miss these on a regular basis. Has it? Perhaps it has, I don't know. Or has an increase in education made us more aware of diagnostic uncertainty? Are we better able to understand the limitations and benefits of the technology available to us? I can't. I can identify clear presentations of any of these conditions, but I can't always differentiate them in a complex setting. And perhaps it's because I'm too reliant on technology, and that my physical examination and history taking skills are inferior to yours. Or possibly it's because I know that each of these diseases can occur in the presence of the other. Perhaps I also know that physical exam has limited diagnostic utility for either condition. Perhaps it's because I know that they can look almost identical in early presentations. Or perhaps it's because I know that even far better trained and educated ER physicians routinely misdiagnose CHF and pneumonia patients because even with better technology, e.g. labs, U/S, CXR, cultures, there remains a lot of diagnostic uncertainty. So, just so I understand your position -- you're a paramedic (like me). You've had (maybe) 3 years of education specific to "medicine". You've worked in an ambulance, or perhaps a fixed wing or helicopter for a number of years. And now you feel that you can better diagnose disease states than a physician with a 4-year BSc, 4-year MD, 5 year ER residency, and years of clinical practice. A physician who probably sees more patients in a shift than a medic sees in a tour, who's had extensive rotations through every medical specialty (not just 2 weeks in the OR, 2 weeks in case room, a couple of weeks in CCU, and a couple of days in NICU), and has imaging technology and the ability to get chemistry / microbiology. And you think that you're better than that? Because if you are, we should start collecting money. All of us. And we should send you to Harvard or Yale, or Columbia. you can go talk to the Dean of Medicine there, and show them what they're doing wrong. We can shorten physician training down to 3 years, sell of all the CT machines, get rid of the U/S, put all the RTs on welfare (sorry guys!), close all the medical schools, and you can show them how it's done better. I'm not going to get into the quagmire that is beta-agonists in CHF. Don't have the energy. Am J Emerg Med. 2010 Oct;28(8):862-5. Epub 2010 Mar 25. A multicenter analysis of the ED diagnosis of pneumonia. Chandra A, Nicks B, Maniago E, Nouh A, Limkakeng A. Source Department of Emergency Medicine - Duke University Medical Center Durham, NC 27710, USA. abhinav.chandra@duke.edu Abstract OBJECTIVES: The objective of this study was to describe the prevalence of pneumonia-like signs and symptoms in patients admitted from the emergency department (ED) with a diagnosis of community acquired pneumonia (CAP) but subsequently discharged from the hospital with a nonpneumonia diagnosis. METHODS: A retrospective, structured, chart review of ED patients with CAP at 3 academic hospitals was performed by trained extractors on all adult patients admitted for CAP. Demographic data, Pneumonia Patient Outcomes Research Team scores, and discharge diagnosis data (International Classification of Diseases, Ninth Revision [iCD-9] codes) were extracted using a predetermined case report form. RESULTS: A total of 800 patients were admitted from the ED with a diagnosis of CAP from the 3 hospitals, and 219 (27.3%; 95% confidence interval [CI], 24-31) ultimately had a nonpneumonia diagnosis upon discharge. Characteristics of this group included a mean age of 62.6 years, 50% female, and a history of congestive heart failure (CHF) (14%) or cancer (12%). After excluding patients with missing data, 123 patients (65%) had an abnormal chest x-ray, and 13% had abnormal oxygen saturation. Cough, sputum production, fever, tachypnea, or leukocytosis were present in 91.5% of this cohort, and 63.8% had at least 2 of these findings. Twenty alternate ICD-9s were identified, including non-CAP pulmonary disease (18%; 95% CI, 13-24), renal disease (16%; 95% CI, 13-19), other infections (9%; 95% CI, 7-11), cardiovascular diseases (3%; 95% CI, 2-4), and other miscellaneous diagnosis (28%; 95% CI, 25-31). CONCLUSIONS: Our data suggest that the ED diagnosis of CAP frequently differs from the discharge diagnosis. This may be due to the fact that a diagnosis of CAP relies on a combination of potentially nonspecific clinical and radiographic features. New diagnostic approaches and tools with better specificity are needed to improve ED diagnosis of CAP. Copyright © 2010 Elsevier Inc. All rights reserved. PMID: 20887906 [PubMed - indexed for MEDLINE]

Thanks man! I've no idea what a beer summit is, but as long it involves beer, I'm in.

And is your point that because you have a lot of EMS experience you're excused from having to make logical and coherrent arguments? I will agree that TNK and D50W are different drugs, with different indications / contraindications / safety profiles / spellings / pronounciations / scrabble triple-word-score values. Of course there's a world of difference. The point is, I give medications because there's an indication, not because I have a paranoid fantasy that my glucometer is inaccurate. If we just give D50W to patients that are unconscious and sweaty, should I even bother checking the blood sugar in unconscious patients any more? Are we saving the glucometer for identifying HHNC / DKA now? And if I see a high value, am I now going to worry that I'm inappropriately treating the patient because the glucometer was actually inaccurate? The likelihood of the patient being unresponsive due to another etiology seems greater than the probability that today is the day that my glucometer has decided not only not to work, but to report a falsely high value. No, because the sensitivity of the 12-lead ECG for myocardial infarction is approximately 40%, therefore the absence of ST changes has a low negative predicitive value. The patient gets both ASA and NTG. But I'm not going to assume that the 12-lead is giving me a false-negative, push a bunch of enoxaparin and tNK and give the patient plavix. My glucometer is sensitive for hypoglycemia, my 12-lead is relatively insensitive for myocardial infarction. Both machines are quite reliable. The ECG has a low negative-predicitive value, and therefore can't be used to rule out infarction. The glucometer has a high negative predictive value. It's a useful rule-out tool. Sounds like a medication noncompliance issue. ---------------------------------------- [Edit] On a different point, cardiac biomarkers are probably an awesome tool to have for identifying NSTEMI patients who could benefit from transport to a facility capable of PCI, but they have no role in deciding whether a patient is eligible for thrombolysis.

Interesting discussion. I'll admit that pulmonary physiology and ventilator management is an area of weakness for me. What you're suggesting with bagging to maintain pre-intubation ETCO2 seems reasonable, at least for patients that have a high minute volume prior to ETI. But what about the situation where you're patient is in respiratory failure, and their ETCO2 is high? If this is an acute problem, I may be dealing with a simple decompensated respiratory acidosis. Here it would seem like returning ETCO2 to 35-45 would be reasonable. But what would you recommend as a strategy if the patient has pre-existing COPD? If I don't know their baseline PaCO2, I don't know that their current PETCO2 is correlating with PaCO2, and their pre-intubation PaCO2 is likely to be greatly elevated as a result of respiratory failure. If I bag my patient aggressively to 35-45, I'm going to generate an iatrogenic metabolic alkalosis. If I don't bag my patient aggressively enough they may remain acidemic. What would be a reasonable strategy here?

Well, there's no question that vec alone will get you intubating conditions. But it's a little committing. If you can't intubate you're left with a paralysed patient with a rescue airway device that may not be that great for preventing aspiration. Midazolam as a sedative is going to be dangerous / contraindicated in hypotensive patients. And it's probably going to make some of your normotensive patients quite hypotensive, depending on the dose. Which might not be good for them. Not having analgesia is going to produce a stress response and sympathetic output that won't be good for your patients with elevated ICP. It seems like adding fentanyl to the protocol would be a good idea. It would also allow the midazolam dose to be decreased.

* Using a low dose of vecuronium as a defasciculating agent only makes sense if you're then going to give succinylcholine. From what you described earlier it sounds like you're using vecuronium as a paralytic instead of succinylcholine? * I agree that you need pain medication. Midazolam is not an analgesic. * The King sounds like a good idea. Hopefully you also have waveform capnography and the option to do a surgical airway. All the best.

Opinions.... First thing, if you're really interested in "researching" RSI, then you need to look for some better resources than the opinions of a bunch of anonymous paramedics on-line. I'm not saying this to be rude, but check out the text paramedicmike referenced, it's fantastic, and go on over to www.pubmed.com, and throw in a few search terms like "paramedic", "EMS", "EMT", "prehospital" and "intubation". Take a look at the limited amount of real data that's out there. Learn the pharmacology of the different agents, and how to do a thorough airway assessment (if this wasn't already taught in your medic program). Having pointed out that empirical research should trump personal opinion, I'll now proceed to give you a whole ton of my personal inexpert opinion Regarding trends in RSI in the future:- (1) I think poorly-run systems are going to continue being poorly-run. Many places aren't going to change their practices. Many providers aren't going to act responsibly. Many medical directors are going to continue to collect a pay-cheque without doing their jobs. Their patients will suffer. These systems may have RSI, they may not. They'll continue to do a bad job. (2) A lot of systems are going to question the value of paramedic RSI, and other forms of pharmacologic intubation. This is going to result in fewer systems providing RSI, fewer providers within individual systems performing RSI, hopefully greater oversight, and more restrictive indications for out-of-hospital intubation. The latter is potentially problematic, as we risk turning every prehospital intubation into a crash airway, if we refuse to allow providers to intubate until the patient is moribund. (3) More widespread adoption of new technology. As of several years ago, any system placing as much as a combitube, let alone an ETT, regardless of whether they're using pharmacologic intubation should have access to waveform capnography. This may not be the case, but should be. I think any service even contemplating RSI should have a back-up airway, e.g. King, LMA, Combitube. This should also have been the gold standard for years. I think we'll see more use of technologies like the Glidescope, and I hope adjuncts like the Gum Elastic Bougie or Eschermann will see more widespread use. (4) Better oversight in good systems. Hopefully some form of oversight in poor ones. Better recording and reporting of data, hopefully to a standardised template, so we can identify the effect of new technology, new guidelines, and ongoing education. (5) Better pharmacology, and a greater percentage of intubations occurring without paralysis, e.g. ketamine + fentanyl +/- lidospray. Regarding succinylcholine, there are indeed a number of contraindications, relative and absolute to its use. The most potentially problematic in EMS are going to be when intubating patients with unidentified hyperkalemia, e.g. acute renal failure, or if we end up inducing malignant hyperthermia in a susceptible individual. The bigger issue with any RSI is getting into a can't-intubate-can't-ventilate scenario. This is also a possibility when using other agents to facilitate intubation. If we generate apnea, we need to be able to ventilate at least as well as the patient was doing before we elected to intubate. There's also the ever-present risk of insult from hypoxia / hypercapnia / hypotension / ICP from repetitive, prolonged or unskilled laryngoscopy, and the risk of aspiration. Using midazolam alone as an agent for induction is problematic due to the relatively large doses required as a single-agent, and the hypotension it can cause. This renders it unsuitable for intubating hypotensive patients. Benzodiazepines also rarely relieve trismus completely (and often have negligible impact) in patients with increased ICP. This presents the very real scenario of (1) generating a hypotensive, apneic / hypoventilating mess, without having generated intubating conditions --- i.e. having made the situation much worse, or (2) underdosing the patients sedation, so that when you do paralyse they exert a physiologic response to a painful, noxious process, and potentially remember the procedure. The long duration of action of vecuronium relative to succinylcholine would scare me, if I was using it as a paralytic for induction. On the other hand, many of the patients we intubate prehospitally will exhibit critical hypoxia before the succinylcholine wears off in a critical RSI. Sux may be slightly safer if the intubation attempt goes south. It's difficult to tell from the post you've written, but it seems possible that by "low-dose vecuronium" you may be talking about using a defasciculating dose prior to succinylcholine? I don't have any experience with this, but was told by several EPs that it was largely unnecessary (I recognise this isn't a decent answer). This site is quite useful, too: http://crashingpatient.com/resuscitation/001-airway.htm

How do you feel about patellar dislocations? Or if the patient has a history of repeated anterior shoulder dislocations? I just ask because I've dealt with a few situations where I've been filling people full of fentanyl / morphine +/- benzos, and felt like I've just created a bigger problem for the ER once they reduce it, and end up with a somnolent patient.