OVeractiveBrain

It doesnt matter how its done, NS or water cooling blanket. My point was that induction is not appropriate for field crews. I meant simply as a practical standpoint. Most medical directors are not comfortable with handing out paralyzing medications to every rig. In fact, their misuse and failure of RSI in connecticut has caused some services to have that right pulled. Only small, highly trained and tightly regulated services are allowed to carry those drugs. I agree that the therapy is amazing, but rapid induction with cold saline should be done in the hospitals, not the back of the bus. Ice packs initiate the induction and saline can finish it off. Remember, we cannot cater general policies on the best medics. We have to cater to the mid-range or below. Im not saying that some couldnt handle vec or roc, just that it is not appropriate for the average population of paramedics. On top of that, shivering is not the only complication. Dropping the temperature too low causes hazardous effects (resulting in the abandonment of the therapy in the early 80s). The most effective means of measurement are bladder or esophageal. Two methods medics dont have. To boot, most medics dont even have oral or tympanic thermometers (which are not reliable for the therapy anyway). When ice cold saline can induce some one in under 30 minutes, it is very possible that the medics, with limited assessment tools and manpower, can make something go wrong. I suppose you could argue that since we can intubate we could also place esophageal thermometers, and since monitors are so expensive they could install a temp reader, but to change the system so drastically with yet another severely invasive procedure is challenging. With that, why not teach medics to start central lines, or install transportable X-rays in the back of rigs? Im exaggerating on purpose; field personnel do not have the technique, equipment nor manpower to accurately produce this therapy. Also note seizures, arrythmias, bleeding. Instead, I would much rather see activation of a "code team" much like we have for Strokes, Traumas, and some cardiac issues. That being, there is a code with ROSC that remains comatose, the medics alert the facility so that when the crew arrives, the rapid infuser is set up, the saline is loaded, the ICU has been alerted, and the medications are drawn up. So, like an angiogram or CT scan, the hospital is able to throw in a central line (Which the patient will get anyway being in the ICU), rapidly infused, EEG and ECGs applied, with much better ability to control for bleeding. In fact, Im joinging the "EM" club here at Tulane. I hope to meet some medical directors and give them the presentation fiznat and I gave to the CT North Central EMS. I dont know if we had anything to do with it, but not even a year later, Hartford hospital started using the therapy in house. I hope to get the New Orleans hospitals to start using the therapy (particularly important due to the number of younger codes / would-be codes, mostly from trauma) I am an advocate of the therapy, just not for field personnel inducing in the field. Before we get to that point (if at all) the therapy needs to be applied in hospital with rigorous guidelines with significant manpower. Overactive

Fiznat and I did our capstone project on this very subject. There is no doubt in any of the papers we read that suggests that induced hypothermia upon return of spontaneous circulation in a patient that remains comotose is not a good idea. If you get them back, make them cold. S I can post our abbreviated bibliography if youd like. Most were obtained through Ovid via Yale University, so access may be limited unless you work / know of a place that has fairly loose wallets for subscriptions. Basically, if their dead, you get them back, but they wont wake up, make them cold. I think the best review is in the AHA magazine "Currents" I think it was summer of 06? I cant quite remember which it was, but it was a good review. Since then, talk of inducing hypothermia during the code have arisen. For prehospial providers inducing hypothermia would be ineffective. If we rapidly cooled some body they would shiver, thus increasing metabolic demand and defeating the purpose. To fix that, we would have to RSI them, a technique that most services are not liberal about handing out. Paralysis must be initiated in order to stop shivering. Then there is monitoring for hemmorrhage and seizures. Fully inducing some one on the street or in an ambulance i dont think we will ever see. However, for prehospital providers I like the idea of initating hypothermia. Apply ice packs to central regions (groin, neck, axilla) to start the process. That makes induction by rapid infusion that much easier. Then, if you want to discontinue (which is not recommended because it nearly gaurentees death) you just remove them. The problem is of course when the crews start it, and the hospital doenst follow it up. U Chicago i think was the first to do it here in the states. Hartford hospital on connecticut is utilizing the technique for in-house codes. I think in the next year or two, we are going to see the technique used much more often. This idea comes from the use of hypothermia in other scenarios (such as neurosurgery and some older surgeries in russia). Make the body cold, less bad things happen. So you dont have to read all teh abstracts yourself: Neurologic outcome improves for patients induced to ~90 F for 24 hours and slowly rewarmed. Human study in Melbourne Australia and in Multi-center, multi-nation Europe. It doesnt matter how fast you cool them (sooner the better) but cooling them after too long a time (12 hours) does do any good, and you have to slowly rewarm them. Animal models show this works for trauma, and can be initiated while CPR is in progress (medical and trauma) Risks include bleeding, seizure, vifb (watch for those osborne waves), 1 - Bernard et al, Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia, New England Journal of Medicine. 346(8):557-63, 2002 Feb 21 2 - Bernard, Stephen. Buist, Michael. Monteiro, Orlando. Smith, Karen. Induced hypothermia using large volume, ice-cold intravenous fluid in comatose survivors of out-of-hospital cardiac arrest Resuscitation. 56(1):9-13, 2003 Jan. 3 - Bernard, SA, Outcome from prehospital cardiac arrest in Melbourne Australia; Emergency Medicine 1998; 10:25-9 4 - Bigelow WG, Lindsay WK, Greenwood WF: Hypothermia; its possible role in cardiac surgery: An investigation of factors governing survival in dogs at low body temperatures. Ann Surg 1950; 132:849–866 5 - Hachimi-Idrissi, S. Corne, L. Huyghens, L. The effect of mild hypothermia and induced hypertension on long term survival rate and neurological outcome after asphyxial cardiac arrest in rats. Resuscitation. 49(1):73-82, 2001 Apr. 6 - Holzer, Michael. Efficacy and safety of endovascular cooling after cardiac arrest: cohort study and Bayesian approach. Stroke. 37(7):1792-7, 2006 Jul 7 - Hypothermia after Cardiac Arrest Study Group, Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. New England Journal of Medicine. 346(8):549-56, 2002 Feb 21. 8 - Nordmark, Johanna. Rubertsson, Sten; Induction of mild hypothermia with infusion of cold (4 degrees C) fluid during ongoing experimental CPR. Resuscitation. 66(3):357-65, 2005 Sep 9 - Nozari, et al. Critical time window for intra-arrest cooling with cold saline flush in a dog model of Cardiopulmonary resuscitation, Circulation. 113(23):2690-6, 2006 Jun 13 10 - Vanden Hoek, Terry L. Critical Care Preconditioning and postresuscitation injury. Medicine. 30(4 Suppl):S172-5, 2002 Apr. 11 - de Vreede-Swagemakers, J J. Out-of-hospital cardiac arrest in the 1990's: a population-based study in the Maastricht area on incidence, characteristics and survival. Journal of the American College of Cardiology. 30(6):15 12 - Wu, Xianren. Et al. Induction of profound hypothermia for emergency preservation and resuscitation allows intact survival after cardiac arrest resulting from prolonged lethal hemorrhage and trauma in dogs. Circulation. 113(16):1974-82, 2006 Apr 25. 13 - Zweifler, et al. Rectal temperature reflects tympanic temperature during mild induced hypothermia in nonintubated subjects. Journal of Neurosurgical Anesthesiology. 16(3):232-5, 2004 Jul.

Back to a more interesting physiological point: I dont think that NTG would have benefited the perfusion during cpr. Nitro (as opposed to other nitrates) primarily vasodilates the venous vasculature, and only minorly the coronary vasculature. Though, touche' to the epi, youre probably right. EVen then, epi doesnt work too well on the venous vasculature, mainly on arterial. Anyway, Id still say tremendous foresight, and hey, it worked!

Can i point out that the treatment of asa and ntg fixed the rhythm? Vtach is a sign of transient ischemia. Rapid afib with wide qrs is not. If for some reason you think that this is instead an afib, i suppose you could argue from just the 12 lead. To be honest, i dont see it. Fiznat's S-S anaylisis pretty much proves it. Equal distances between QRSs (in the abscence of ps) x 8 is pretty regular. I think "subtle" variations are either problems with the printer or your eyes. Again, pixels are more certain than your eye, as fiz pointed out. BUT, even if you were absolutely convinced this was a rapid afib, NTG and ASA would not have done anything but made the patient worse. Alleviating the ischemia led to the cessation of runs of VTach. If you dont agree with the 12-lead, look at everything else going on, particularly the treatment, that lends quite the insight to the etiology of the rhythm. Im not saying there couldnt be ischemia of the atria leading to some conduction disorder that some how leads to wide complex atrial fibrillation, but i would be much more likely to believe Vtach. Earliest signs of cardiac ischemia is? PVCs, ventricular irritability, aka, VTach.

My roommate in college began his entrapreneurial conquests with "Speed Lead" the retractable and/or disposable electrocardio gram leads. Yes, ladies and gentleman, retractable. Unfortunately, he left that company to start kiko, before he started Justin.TV (shameless plug for a growing business). I dont know what happened to that company after they started to get incubated. Maybe never panned out? Who knows. Im a big fan of dealing with it. It takes I think 5 seconds do separate them out, and if they are tangled, "here emt partner, fix this please while i start the line with the bag you just spiked." I cant see anything wrong with taping, though I find that rolling them up well, then, while unrolling, pinching the arm leads together and drawing them out. Once you have up and down separated, its pretty easy. Alternatively, if they get really tangled, just do clavicles and abdomen, so it doesnt matter how far apart they are.

In fact, the national registry TEACHES emts to identify "life threatening injuries" and penalizes them for NOT transporting lights and sirens (a critical fail). When I teach EMTs, particularly on the medical assessment stations, I tell them the "national registry" answer and then "my take." It is because, inherently, the EMT education does not teach towards symptomatic / asymptomatic stable / unstable, it teaches possible devastating injuries (which they define as SOB, CP, N/V, etc) and to then activate a medic and transport priority one. Experienced EMTs may still believe in that policy, and others may have adopted a level of confidence (aka, knowledge base beyond the EMT curriculum) to know that the black and white picture of the national registry is not necessarily the street (or correct) way to do it. With experience and advanced education, we, as paramedics, can make more informed decisions. Just as we can make more informed decisions on treatment options (EMTs put on a NRB at 15lpm regardless, only if the patient cannot tolerate an NRB does the EMT curriculum teach NC, whereas paramedics can titrate oxygenation, for example). I do wish that the emt curriculum was stronger in its delineation between symptomatic (no need for urgent transport) and unstable (need for urgent intervention).

I have to admit that was quite impressive foresight. Of course also potentially dangerous. Had the Vtach been an electrical disturbance not induced by an acute ischemia, but caused by an older injury, you might have induced them into a non-perfusing rhythm. What i mean is if the electrical disturbance continued and sustained a tachy-dysrythmia and they have nitrates on board, the decreased venous return and filling time might have tanked their cardiac output. Its the only reason Id be worried about it. However, given the history and story, it sounds like it was likely an acute event. Again, i dont know if I would be so bold to make that step, even with a fairly sure story.

The underlying rhythm remains afib. While i think that an aberrant conduction may produce a whide complex, I would think were looking more towards runs of Vtach. Since HAD chest pain, id be happy to give the ASA. Nitro I wouldnt mind, though if the asa stemmed the pain and bouts of vtach, i wouldnt much bother with it. That being said, this guy has risk factors for ischemia up the wazoo. Even in the abscence of the obvious ST-segment eleveation demonstrative of an MI, runs of Vtach are indicative of ischemic tissue. So the administration of ASA and nitro arent a bad idea. I just dont know if id think to do it (its outside protocol). Id probably be more likely to pull out the Amio, draw it up, and watch for a sustained Vtach. I probably would not give lido or amio in the absence of symptomy, though i would be ready for that irritable heart to move to sustained. I doubt it is an 'abberant conduction disorder.' I mean, if he suffering from runs of Vtach, there is probably some ischemic/necrosed neural tissue that leads to the disorder or the predisposition in the first place. What i mean is that there probably is not any major conduction block / hemiblock that forces the wide complex from what seems to be a fairly narrow complex even at fairly fast rates. In retrospect, since the ASA and NTG ceased the Vtach, it was probably a mild ischemic event that induced a potentially life threatening injury. Id say hell of a job if that was the thought process going in, thats excellent forsight. To be honest, I would not have given the NTG if the patient remains pain free. (Keep in mind im trying to know the outcome, but put myself in the providers position as it is unfolding). I dont think id go along with amio either, unless the runs went into a sustained vtach.

I had not thought of sickle cell, though i would hope that some one who suffers from it would list that amongst "past medical history." I did not ask him specifically though. No history of infections, viral or otherwise. This doesnt look to be a clear case of ACS nor pericarditis (which is probably why the cardiologist activated the cath). I worry, sometimes, though, that Internal Medicine doctors in primary care facilities (this guy was a stress-tester within a Primary Care Office), even when cardiology is their specialty, might be doing exactly what fiznat suggested... passing the buck. Since it wasnt clear cut either way (exertional onset leads towards ACS, global elevation without massive compromise suggests pericarditis) he might have been doing just that. Sometimes I find myself struggling with concepts such as that. I assume that the cardiologist is the end-all of cardiac understanding. The more I think about it, the more I think he just wasnt sure, followed some protocol, and sent him out just in case. I suppose that is a good sign for we paramedics, because sometimes, that is exactly what we do! Treat to the best of our ability,and let some one else take responsibility down the line. I wish I had more information about his cardiac history. It didnt seem to be anything significant, as it was not recent (something in childhood), nor did it cause him any difficulty until the past few weeks. Im sure that could push one way or another. Any of the docs that post on the forums know of any childhood or developmental diseases that predisposes an otherwise healthy young man to suffer from these symptoms. Im sure there are many, but i was thinking along the lines of a congenital defect that predisposes the patient to frequent infections or ACS without plaque development (some sort of spasm or narrowing of the lumen other than the standard processes we discuss)? D

24 yo male complaining of mild chest pressure following a chemically induced stress test (dopamine infusion). Patient is an average weight african american male with "heart problems" throughout his life. This is not an occlusion, MI, nor CHF. He states he had not needed to be followed by a cardiologist but recent exertional dyspnea had brought him to one today. Non smoker, Non drinker, No familial History, No Significant Medical History save "heart," No Meds. I dont have the 12-lead to scan, but I can describe it for you. At 15 minutes into the stress test the patient complains of a mild chest pressure and a brief fluttery feeling in his chest. The flutter correlates to a brief (10 second) span of VTach. He is in a sinus tachycardia near 130, that has not been resolved after 20 minutes at rest. He has ST segment elevations in I, II, aVL, V2-6. The st segment elevations have not been alleviated with ASA (325mg PO), Nitro (1.2mg SL), and Lopressor (30mg PO), though his VS WNL (save tachycardia) and GCS:15. His cardiologist activated the cath lab, they only awaited his arrival to the ED. Now, the cardiologist says he needs a cath, and the lab is activated, and im 20 minutes away. Easy one down the main road in town as there was no highway. Im at the limit of my interventions save morphine, but his SYS BP is floating around 100-110, and his pain is not severe. The only treatment i had for him was calming words and talk of the future. Routine ALS of course. Alls well and good. We get to the ER and I go talk to the Doc. I tell him the cath lab has been activated for this patient. Given his low risk (0 Framingham, except for "cardiac history") and global 'ischemia' I asked the Doctor if this wasnt more likely pericarditis. He agreed. Both that it probably is but that the lab was activated, so get him up there. Ok, so you know it wasnt ACS. Pretend you dont for what comes. Cardiologist says ischemia, needs a cath. Im not going to contend with the cardiologist. But it turns out this kid did not have an occlusion and did not need a bypass or a stent. I think he was admitted to a cardiac floor. My only source of followup was with his nurse, who did not follow him very far. I thought the global elevations (and absence of inversions, symptomy and risk factors) were a bit suspicious. Just for a moment, let us suspend our disbelief and instead of a cardiologist handing us a 12 lead, we get it ourselves. Same patient, without PO meds, after he got done with his morning exercises called for chest pressure. I know we already know it wasnt ACS, nor are we sure it was pericarditis. But if youve got a kid with some persistant mild angina with global elevations, despite a framingham of 0, do you activate the lab? We do not yet have the authority to activate the cath lab ourselves, but we sure as hell can initiate the process (i.e. the patient is out of the ER before as his labs come back, usually within 20 minutes). I personally was hesitant with such activation, but since I didnt make the call, it was easy to follow through. Just wondering what your thoughts were on this guy, and on "global ischemia" in the absence of severe clinical findings. Overactive

In fact, dustdevil, i think this is quite an appropriate forum. ALS providers are expected to make more severe decisions in care, including transport. If i asked in an EMT forum, I would get a different answer. If i posted in a rural forum, that would get one, whereas an urban would get another. In fact, this issue is a source of major contention amongst ALS providers (even within some of our posts here). It is sometimes viewed as "old versus new" or "inexperienced vs experienced." Im trying to a)get the subject out and discussed, dissuade providers from giving in to these misrepresented assumptions and c) find out what individuals would do in their own situations. For example, I do not transport priority for a stroke unless Ive defined them as a candidate for fibrinolytics (normal baseline, <65 yo, new onset [protocol says <6. i stick with <4], obvious deficit in speech, hemiparesis, or any change in cranial nerves / mental status with 3+risk factors, and inclusion/exclusion criteria) while another provider may choose to transport anyone exhibiting the signs and symptoms of stroke. The difference in choosing a medication for an arrhythmia and a priority for a transport is very small; they are both part of a clinical impression and decision making. (By the way, my decision for stroke patients was based on a recent CME where I learned that most Stroke Patients get a hospital course of "wait and see what happens and hope we can take care of them after", that cath procedures for cardiac patients are not available for stroke patients, and that 6% of patients that receive fibrinolytics suffer hemmorage and worsening symptoms, and thus facilities are hesitant in the administration of the drug despite "time is tissue"). One impetus for this post was that I often listen in to priority patches, to see what people are bringing in. Sometimes its an ALS provider throwing out BLS decisions, "difficulty breathing on oxygen." Great, why are you on a 1? Obviously this may be a result of poor patching, not poor decision making, but i find it interesting how and why people choose priority patches over flow of traffic. It also happens to be a hot topic in EMS education, one particular facet of this website that I enjoy. The learning. Another important topic is that different providers have different criteria for what constitutes "hemodynamically unstable." As fiz pointed out, we do have limited knowledge and tools for the formulation of a diagnosis. TO be honest, if some one is hemodynamically unstable, I keep it simple: electrical, pump, tank. When dumbed down so simply. the problems become easier to fix. If I am to transport a medical case priority 1 its because the cause is unfixable (ACS with compromise) or I cannot discern the underlying problem. That usually involves fluid, ascertaining the electrical system, and checking for hemorrhage. Only after a failure to improve patient condition to stable (though often still symptomatic) do i then upgrade to a one. Other providers may find that the patient deserves a priority one, and they will get done what they can enroute, and allow a more sophisticated clinician make decisions based on data obtained by the medic. Neither is wrong, and Id like to understand the motivation of both. That is to say, I make my transport decisions after formulating an impression, a plan, and see what the response is to my treatment. That being said I have hustled the fire department to get a patient out of her room and into my truck. I often allow the FD to assume control of the scene (since they are first responding paramedics in their territory). This girl was 24 years old, renal insufficiency (though still able to maintain urinary output), supposed to be on dialysis but has skipped it for a month, now complaining of N/V, Dizziness, and intense anxiety when seated upright. She has no palpable radial or brachial pulse, and auscultation reveals a heart rate near 150. I dont get acutely emotional, so when I stress urgency, my partner knows it means now. Getting her into my bus, on a monitor with some fluids, was when I could calm down (sinus tach with poor PO intake and vaginal bleeding for 3 days). My initial urgency was fear of an electrolyte imbalance and the start of some ventricular dysrhythmia (yes i did not have my monitor, and the FD had taken theirs down without putting her on it...) You could say I was "on a one" until further data changed my mind; we were 5 minutes away and I was able to get her stable without the use of the hospital. Her crit was 20, by the way. Thats when I was taught to use the conjunctiva as an indication for low H&H (the whiter the conjunctiva of the eye, the lower their value). Had I been 20 minutes away at 5pm driving through the 91-95 interchange (literally 30 minutes to go 1 mile) I probably would have taken her in on a one, despite her stability. Thats why I want to discuss the topic here. Flush out the grey area. This is somewhat in contention to fiznat's advocacy: I dont need special equipment or knowledge to diagnose the problem. In fact, i dont even have to diagnose at all. In unstable patients, its my job to stabilize them. In my mind, some one who remains with a reduced GCS but maintains perfusion, color, sp02/ETc02, is symptomatic, but stable. I am very lenient when it comes to what is considered unstable (That is, the level of symptomy that is the cut off for unstable is probably more symptomatic than many others would allow). Obviously, I had my own beliefs on priority transport ion generating the post. I had hoped for a little more discussion (thanks Foster) or for some one to take an alternative stance. Im pretty sure no one is going to say "Priority Transport for every ALS patient" nor will some one say "Priority Transport is NEVER indicated." Especially for reasons already discussed about safety. Again, Im looking to fill in the cloud of that grey area, get people's own thoughts or simple protocols about the subject.

This is a common theme amongst prehospital providers, and is a recent source of debate. In particular, the call for non-emergent transport for patients manageable prehospitally (most of them) has been strong, especially in Connecticut. I hope to give some insight into reasoning and leave this open for discussion. Note: "hot", "code 3", "priority 1", and "lights and sirens" are synonymous Note: "cold", "priority 2", "flow of traffic", and "no lights or sirens" are synonymous Priority responses both to and from the hospital are reminiscent of an older EMS system; the so-called "grab'n'go" era. Many providers, even new ones, maintain the need for priority transport to the hospital. Still, other systems attempt to activate only the necessary resources via EMD (for example, dispatching the medical engine hot, and the transporting ambulance cold until advised by the engine). I unfortunately have no actual data on the efficacy of systems. I know that at one of my services, a project of electronic data acquisition is to demonstrate that the central medical dispatching unit SHOULD be dispatching us priority 1, where they do not, since we are often upgraded by the FD. If anyone has preliminary data on response times and outcomes, Id love to see it. Since there are so many variables, I find it difficult to rely on any one source. Personally, I lean towards the side of priority to the call, flow of traffic from the call. In my system we have a wealth of resources including an engine and an ambulance, sometimes another first responding paramedic, and the PD if we need it. I practice in an urban and suburban environment. We have the resources should we need them, we have the interventions and authority to use them via standing order, and the greatest response time is approximately 20 minutes. Unless there are some extenuating circumstances of the day or traffic, its not hard to get to any of our hospitals. I believe that I have the skill and diagnosing prowess to define a problem and fix it. Thusly, patients I can manage (nearly all of them) I take in flow of traffic. Until I cannot manage a patient, that is. The exception to this rule is clear-cut CVA and trauma. In my service area we have both stroke alerts and trauma alerts. If I think some one is a candidate for fibrinolytics, I’m on a one. If I know the hospital will, trauma-team some one, I’m on a one. The only other cases are point by point; an ACS with hypotension (difficult to manage), pre-activated cath lab per MD order (even that im on the edge with), ROSC s/p Cardiac Arrest with complications, the patient is borderline stable and traffic is bad, etc. This is my own personal view on my patients, not a rule I suggest everyone follow. A brief digression I feel is warranted. People sometimes associate "priority 1" with "blow through stop lights and annihilate anyone in their path." Priority responses merely ask for the right of way. My EMT partners are aware that priority means "drive the way you usually do, except now you can go around cars and through intersections." At American Medical Response (one of my services) we are required to stop at all red lights (including on priority) and the FOB limits dramatic forces on the vehicle. Priority 1 for me and my partners is not an insane bounce-a-thon to the hospital; rather it is an acceleration of the patient to the hospital. A 20 minute trans time can be reduced to a 10 minute trans time, or a 15 to a 10, or even a 5 to a 2, and safely. There is NO CIRCUMSTANCE which I can justify putting myself, the patient or my partner at risk by driving crazy. While lights and sirens may induce a heightened state of anxiety, a trained professional driver need not succumb to that anxiety. I note an anecdotal story of one of my friends, looking for me in every ambulance that passed, stating “all I saw was two guys not you, lights and sirens, looking so bored”. I consider that crew, experienced. That said, there are obvious risks associated with priority transports. Even a hypervigilant driver puts the crew at a greater risk priority 1 over priority 2 responses. While a good driver can reduce the risk, it is ever present. I have seen minor MVAs be caused as a result of cars obeying the law and pulling to the right and stopping (into each other) or as a result of crossing the double yellow lines. The major reason to NOT go priority 1 is the risk of safety, or the inability to manage a patient as a result of being thrown around. Different systems can influence decisions made. In a rural setting, with few cars in opposing traffic and usual long distance transports, priority one can be made without much risk. The access to a helicopter may not always be available, and speed is necessity. The counter argument is, however, that in a rural setting priority one may not be necessary if there are so few obstructions. A rural setting provides more obstacles: frequent traffic lights, heavy traffic, limited access to large or multi-laned roads, etc. This increases the risk of and need for priority transport. Id like to hear people’s opinion on the subject, in particular their own personal beliefs towards priority transport. Im sure there will be many debates over the individual points ive made. Since they aren’t backed by anything but anecdotal evidence, they aren’t terribly believeable. In addition to people’s own view on priority transport (and why they feel that way), if anyone has any data on patient improvement or crew/public safety, id also love to see that as well. Discuss. Overactive

http://foster.adams.justgotowned.com/ sorry, you were pwnt Overactive

we recently conducted a study of 100 paramedics to see if (A) they can properly identify an STEMI and ( whether they make the correct judgement call to activate a cath lab. There are 4 major hospitals in connecticut with the option for percutaneous coronary intervention, and transport (via helicopter or ground ambulance is not far off from any satelite/cumminty hospital). While there are horror stories of doctors "sitting" on an ACS patient waiting for labs / etc, most hospital courses are discharge to a PCI suite within an hour (usually with Integrilin and Heparin). The problem is that too seldomly is there a patient having "the big one." And not the big one as any medic would see it, but the pale cool diaphoretic patient with a pressure of 70/P with STsegment elevation of 5mm in II III and aVFwith reciprocal chanes in the anterior leads. So most of the time the care is routine, medics administer ASA NItro and Morphine (or fix the cause), hospital grabs labs, starts clot-buster cocktails if there is no PCI available, or sends them up to the cath lab if the suite is present in house. While the need for PCI is present in our system, it is not recommended to divert to a PCI hospital 30 minutes away, especially if they are a clot-buster (and i use that to refer to any of the medications allowable for the job) candidate, an uncertain MI (new/old LBBB?) or stable to take the ride. So yes, we recognize the need to go to a hospital with PCI, but it is recommended to go to the nearest hospital for initiation of care and transport out.

WOOTZ WOOTZ. Congratz. Care to celebrate? Youve got my digits

It may be just the uneven sketch, but doesint it look like fibrillation between the waves in particular in II and aVF? Also the rhtyhm is irregularly irregular. You really think its a reentrant rhythm?

its an organophosphate

I hear in Uzbekastan they have intranasal parathion

You know, it never occured to me that you could let some of the fluid of a 250 cc bag BEFORE adding the medication to concentrate the drug. What a brilliant idea! BRILLIANT (cheers guiness) Overactive

We in New Haven are not fortunate enough to have haldol. Its up to 2mg Ativan or 5mg of Versed IV/IM. Its standing order for patients that are a threat to themselves, online permission required for sedation of combative or violent patients. We can also use at will for anxiety Man does this stuff work well. Overactive

Im going with erdoc on this one. Lead III on the 3 lead looks scary. Compare it to II and aVF and they look narrow to me, with some tracings BETWEEN the QRS complexes, not within them. Lead III jumped out at me, and at first i assumed worst-case and went with wide-complex tach as well, though the irregularity as well makes me hesitate. With close inspection and a twelve lead (always get a twelve lead, especially in a stable patient, SHAME ON YOU!) I would have gone rapid afib and given 10mg of cardizem (our protocol) since he isnt already on a beta blocker (which is suprising). If he were, its 5mg of Lopressor q 5 min max 15mg for rate control. Of course the amio wasnt a bad decision in this case. You werent trying to treat an arrythmia for necessity of perfusion, you were treating him for his pain. He wasnt symptomatic nor had any complaints (except that he was being shocked). The perfusion and half life of amio I guess couldnt hurt - youre slowing the rhythm so he doesnt get shocked anymore, and it will last. Amio is the wonder drug for rapid arrythmias, so its not a bad catchall, especially if you have even an inkling of wide-tach. I still would have gone with rapid afib, taken it on a two, and given him some cardizem/diltiazem. I dont know if those are actually ST segment elevations. V1-v3 i think youre talking about, Doc. There arent any reciprocal changes that I can see, and life pack 12s (especailly in a moving ambulance) are notoriously unreliable for subtle changes (especially with the tracing bounching around so much). While it may be, I wouldnt go cardioverting or activating the cath lab. Amio is given over 10 minutes. You can stand there and push it, or you can buratrol or smalll bag it and just let it drip in. One frees you to do other things, one is a bit more engaging. We unfortunately have only 250 cc bags as our smallest, and no buretrols to speak of, so were SOL for convenient drips as well (the 250 is bad, i know). Overactive

Im just happy all our touting about ROSC hyporthermia is actually paying off! Did Turbiak mention anything about in the ER? Or is it just an ICU protocol now? Im trying to get Midstate to do it, maybe even Yale, but I think its hot that anywhere is actually taking the step! I heard youre officially cleared now? Overactive

As I understand it, a chest X-ray 'positive for plerual effusion' without further evaluation of the fluid is quite useless. All it says is "yes, you have fluid in your pleural space." Using it to differentiate a worsening CHF or a new pneumonia is useless. Often times the nurse (as in always) will not know whether the fluid is determined as Transudate or Exudate, let alone whether it has been confirmed as serum plasma or gram positive. Can we use the information of "has a pleural effusion" or "has had pleural effusions" without further information of the effusion to form a clinical impression in the field? I understand that all differentials come from a combination of sources, but i am looking for a useful (or be told its not) way to use the information of plueral effusion in forming a clinical impression and choosing a therapy. OveractiveBrain

Judging from the flow of the post im probably going to get flak, but im putting in my two cents. The 12-lead is just ONE piece of information that can either help you rule in our rule out ACS. However, regardless of EKG changes, interventions can be performed if the presenting symptoms are indicative of ACS. Of course it always depends, and anyone who says otherwise is a cookie cutter, but personally, id rather have the line than the 12lead if i had to choose. This is in the instance of HAVING TO CHOOSE. Of course i would like a preliminary 12-lead prior to intervention, but I would also like to give a spray of NTG or some aspiring to initiate therapy over diagnostics. This of course leads into many more discussions (do you need a line for NTG, of which I also think no, but lets leave that for another time). Just as you can obtain an IV enroute, you can obtain a 12-lead enroute. The hospital is going to draw labs and get a 12-lead regardless so I assume this is a hypothetical arguement where both are required. Getting the line first or getting the 12-lead first? Probably provider preference (20 seconds for a line, 30 seconds for a 12-lead). While its useful to think "12 lead for every call" if you dont have time, screw it. It is nice to say "look at this 12-lead before, after intervention 1, after intervention 2, and now" but I dont think the topic of the post is that at all. I assume the initial author was questioning priority of the IV or the 12-lead, or, if only possible (for whatever reason) to only get one, which do you get? Id say the IV is more important as a portal to initiate therapy, resucitate of the patient decompensates or sufferes an undesired side effect, whereas the 12lead is only a piece of data. A piece of data that is also inconclusive given the abscence of enzymes. If you get a 12-lead that shows STEMI, they might go to the Cath or they might wait on labs. If you DONT have STEMI/NSTEMI theyll still get labs. If you have STEMI (but dont get a 12lead) and one preemptive spray of NTG alleviates the STEMI, youll still see lasting enzymes, have treated the patient, improved their condition, and have enough diagnostic information to initate this patient as a cardiac patient. The point im making is that there are multiple tools you can use to draw a clinical impression of ACS, of which a 12-lead is just one. The IV is the portal to treat the ACS or other maladies should you move in a different direction. Personally, with practice and lucidity you will be able to obtain (as one of the previous posters has said) all your ALS and transport in a short amount of time (i believe 2 minutes to 12lead and 10 minutes to trans, with additional ALS enroute). It doesnt matter how you do it, or what order you do it, really, so long as it all gets done. Enroute or not. I think an item to stress the most is that even if your transport time to the hospital is 5 minutes, your immediate interventions can save tissue. If trans times are longer you better do everything. If trans times are short, I am of the nature of therapy prior to diagnostics. But if you cannot conclude which illness and therefore which therapy, do another diagnostic. So if youre pretty sure its ACS, go therapy, if you arent, go diagnostic. In short: it depends. Because i hate that answer: IV. Overactive

So, Im pretty sure the incidence of prehospital return of spontaneous circulation in a non-traumatic arrest is about 50%. How many of those end up going home is another story. Medical codes, particularly ones in dense metropolitan services where response times are short, and even more so in areas where bystander education and intervention is great (i.e. seattle) have a pretty good chance of resuscitation. Personally, I have worked 5 prehospital codes (2 BLS 3 ALS) and EVERY one has had a return of spontaneous circulation. Strictly anecdotal, and I am awesome, so maybe not representative of the EMS field (also more modest than most). But seriously, joking aside, prehospital management of a cardiac arrest mirrors hospital intervention and can be fairly successful. If you think about it, the parallels are quite apparent. In the ER you have a documenting RN, a med RN, an intubating/code-running doc, a nurse/tech x2 for compressions and maybe an extra hand. In the field, the paramedic assumes the role of doc, another medic may have control of the meds (obtaining access and administration of meds), FD EMT/MRTs for compressions, and your BLS partner to bag after the tube is in. AZCEP is right, the management in both cases is quite similar. As for you, ERDoc, you can take your higher education and superior knowledge/skill/experience right out the door with you! TVP! HA! ILL TVP YOU! In any case, it is true that the structure and rigor of ACLS isnt really there. That is why medics (at least I hope) go through the rigor they do in class. Personally, when I went into ACLS we had already covered mostly everything, to the point of absolute memorization, prior to the ACLS cert. ACLS for prehospital providers I feel is more along the lines of updating changes, refreshing knowledge, and generating a certification for what we do anyway. For others, such as nurses and physicians, is more along the lines of familiarizing these practicioners so they arent caught totally off guard when they are asked to use those skills. For Docs in the ER, it is not their ACLS certification, but rather their knowledge and experience beyond the cert, that allows them to control a code. The cert defines an obvious, known baseline; a minimum that all providers expect from those who have completed the course. Does the RN assisting the doctor need to know the difference between an SVT with aberrancy and Vtach to push the Amiodarone? No. But if the doctor calls from 450mg Amio, she can say, "isnt that too much?" If everyone on the code CAN differentiate, so much the better, but it is not necessary (too many chefs spoiling the meal kind of thing). Just because the certification isnt rigorous does not mean there is less emphasis on the field or the expectations of the providers is any less. We paramedics are expected to perform at a level higher than that of our certification. That is what excellence is all about. Knowing that we, as well as our fellow providers, at least meet the minimum standard and are made aware of the practice is useful in the field. I also thin tnuiqs hit it on the head. In order to disseminate information to a vast number of people it is necessary to dumb down the information and make it easy to remember. For we paramedics, ACLS is our life-blood. Its 50% of what we do. Its pretty much all that matters from a medical standpoint. The monitor and our drug bag are designed for the interpretation and treatment of cardiac emergencies. But to another provider who has more concerns than just ABCs should be familiar with cardiac care, but also must save room for other information that pertains to them. So, our liscencing bodies decides the quality of knowledge while the AHA can educate and produce information quickly and easily to as many people as possible. Overactive