Paramagic

I worship daily at the alter of Dave Schriger and Mel Herbet for bringing clarity and common sense to the world of medical literature! You are right about some of the trials having dodgy methodolgy, and it's not just in the IIb/IIIa studies. I can't remember which one off the top of my head, but one of them was comparing plavix AND aspirin against plavix alone and against no treatment and then saying "Wow! look how good plavix is!" Well of course it's better than nothing, that's not really the point! My understanding is simply that on further examination of the data canny clinicans confirmend they had been conned (there's some nice alliteration for this hour of the day!) and simply haven't taken to I haven't read this one yet, but my suspicion is that it is industry funded? In which case it probably read like an advert because it is an advert! It's very common for these sorts of studies to have lots of "slices" of data looked at in an attempt to come up with something that will sell the drugs. Strange endpoints, conclusions that aren't actually drawn from the data: it's all designed to get the product moving. The trouble is, it works. I suspect that most of us (and I am certainly guilty of this) grab a study, read the abstract and conclusion and say "Neato! We should be using this!" Actually burrowing through the data is time consuming and often very difficult, particularly for those of us without much of a mathematical bent (like me) so we take the easy way out. They are certainly interesting outcome measures you mention in relation to that study. I struggle to see how ST segment changes are really a significant measure, given that they are dynamic in STEMI anyway. Does the drug help, or is it merely the natural progression of ST segments trending down (before skyrocketing up again!): a natural regression to the mean? Equally TIMI flow has shown to not necessarily correlate well with survival, so again, not sure how much use that is as a clinical endpoint. May I ask what your background is? I assume sciences or mathematics? It is rare to find a paramedic student who is able to analyse data so effectively, but it is pleasing to see. Maybe there is hope for EMS after all!

The glycoprotein inhibitors studies have produced some excellent sales... oops, there I go again, I mean results! I haven't had a look at them for the last year or so, but there were about 4 studies done, all of them industry sponsored. The patients were all at low risk of bleeding and at high risk from death due to infarct, so these are the patients we would expect to see good results in. There were none. No reduction at all in the re-occurence of MI at 6 months or death at 6 months, yet a reasonably significant (0.8% or about 1 in 115) patients suffered from a significant complication (cerebral haemorrhage or bleeding requiring transfusion) There was a reduction in the need for repeat angioplasty, but as this was separate from and did not effect death or MI, it's really a waste of an endpoint. No benefit, significant harm. No brainer really. Mind you, I'm not aware of any EMS that uses IIb/IIIa inhibitors, so it may be a moot point for us anyway. If there are any studies newer than a year or so old that anyone knows of, please let me know, I haven't been very diligent in keeping up with this lately.

Hi Gumby. I must say that is an excellent post, it has covered exactly the issues there are with plavix, thank you. It is interesting to note that in the CURE study the methodology was actually changed half way through the trial, because the only results they were getting were negative. They moved the parameters to look only at the really high risk patients to try and salvage some sales. Oops, I meant salvage some results... I haven't finished with the COMMIT trail yet, but I haven't really seen anything that we don't already know from it: Small reduction in MI in high risk patients, coupled with reasonable risk of bleeding that pretty much outweighs the benefits. It's also difficult to say how much external validity the study has wth regards to the difference between western and eastern health care systems, in particular with respect to PCI vs. thrombolysis in infarct patients. (The use of PCI is something else that confounds Sabatine's trial as well) The rebound effect from plavix certainly seems to be of concern. There has been a study published in JAMA in 2008 that was very compelling, showing adverse effects out to 90 days post cessation, but the authors recognize that further study is needed. It's certainly something that the cardiothoracic and general surgeons don't like. Given the setting of the back of an ambulance (being on an EMS forum after all) beta-blockers are most definitely a no-go. They are also most likely a no-go after we get them to the hospital. Beta-blockers are a useful drug in patients with coronary artery disease, they have no place in the emergent treatment of evolving ACS, particularly in the back of an ambulance. I think it was the COMMIT trial that had a list of exclusions for patients recieving beta-blockers, one of which was those with a high likelihood of devloping cardiogenic shock (or words to that effect - cardiogenic shock is what we give people when we give them beta-blockers). However one of the recommendations put forward is that beta-blockers should be given to patients with tachycardia. Now, what is a predictor of cardiogenic shock in ACS? That's right, tachycardia! There is far too much evidence of harm and far too few beneficial effects to consider beta-blockers as a standard part of the treatment regimen for ACS.

Actually, it hasn't been proven to be beneficial. Hypothermia post arrest is definitely a good thing, definitely improves neurological outcome. However there is no evidence that starting cooling in the field improves outcomes over starting cooling in the hospital. There needs to be more work done on the exact timing of the cooling. Currently the standard is to cool post-ROSC. However, because we are essentially trying to mitigate reperfusion injury, it may be that we need to start cooling during the arrest to ensure that the first stages of reperfusion injury are blunted before they start. It also needs to be done as part of a high quality post arrest care bundle, maintaining good blood pressures, ventilating appropriately and so on.

Been using post-ROSC hypothermia for some years now and are currently awaiting the green light to trial during arrest hypothermia.

No arguments. The ISIS and GUSTO studies demonstrated clearly the benefit of ASA in ACS. Morphine may worsen outcomes (although I have grave doubts about the conclusions and methodology of the CRUSADE study), Beta-blockers are a definite no go, clopidogrel causes more harm than good (in fact causes no good at all I believe), nitro might be nice for some symptom relief but doesn't alter outcomes and oxygen probably causes more harm than good unless the pt is actually hypoxemic. Aspirin would definitely be my Desert Island Drug.

1) No - with the exception of some rare situations such as profound hypothermia that may theoretically get something in the ER that they won't in the field. 2) No. 3) No benefits. CYA is a redundant argument: if you have done your job properly there is no 'covering' to be done. Dealing with family: likewise, that is part of what we do, if you can't deal with people, why are you in a "people" job? 4) Many and varied. Obvious risk of code 3 transport resulting in MVC (been there, done that, not keen to do it again). There is ample risk to paramedics in terms of potential musculoskeletal injuries or worse even if not involved in MVC, simply due to movement in the vehicle, cornering, being unrestrained. There is risk to the patient: loading takes time, and that is time where effective CPR cannot be done. Effective CPR also cannot be done in a moving vehicle either, so we are taking away the only real chance the patient has of a good outcome for what? We also give the families a false expectation that the ER may somehow magically be able to do something for the body and resurrect them. We also add further burdens to ERs which are typically overburdened anyway, denying care to others that may actually be alive. 5) As in 1, unless there is an actual reason why the patient may somehow get better care in the ER than in the field, no. That includes pediatric arrests.

Yes, the evidence is scarce, but lack of evidence is not necessarily evidence of lacking.

Naloxone reverses hyoptension associated with opioid administration as it is largely centrally mediated (although we still are concerned about the potential [and it is only potential] histamine release): Cohen RA, Coffman JD. 1980. Naloxone reversal of morphine induced perihperal vasodilation. Clinical Pharmacological Therapy Oct;28(4):541- Midazolam has a direct effect on vascular tone through it's effect on inflammatory mediators. The effect can also be profound, much more so than morphine. Nobody is advocating carrying out RSI without sedation. Sedation is indeed a critical part of the process, hence everyone discussing the pros and cons of various combinations. However, intubating with sedation alone is significantly less than ideal. The whole point of sux is to eliminate jaw tone and airway reflexes, giving you the best opportunity to pass the ETT on the first attempt. Yes it relaxes the cardiac sphincter, which is why you have someone apply Sellicks maneuver when giving it. Problem solved. I didn't do many RSI's this year, only 50-60, but I certainly didn't have any problem with regurgitation in any of them. However, to intubate with sedation alone you need very large doses of drugs to eliminate jaw tone and airway relfexes, doses that are then much more likely to cause significant side effects. You are also doing nothing to eliminate the reflexes from messing around in the most innervated structure in the body with a cold steel blade and piece of plastic. In the head injured patient all this is going to achieve is a massive and prolonged increase in ICP, to the eventual detriment of the patient. Whether the patient is breathing or not is largely irrelevant as you de-nitrogenate the patient before attempting intubation, thus allowing ample time of safe apnea to safely pass the ETT before the suxamethonium wears off. There is a good reason why you don't see intubation attempts on patients with sedation alone, as ERDoc's story demonstrates.

See my above post for the reason behind fentanyl being used. It depends on the patient as to whether you use fentanyl/midazolam, fentanyl/ketamine or fentanyl/etomidate. Atropine is a good drug to have drawn up ready to go whenever suxamethonium is used in RSI. Suxamethonium (succinylcholine) is structurly similar to acetylcholine, so it is not unsual to see bradycardia following it's administration, which obviously affects the hemodynamics. It's not something that happens every time, but it is nice to be prepared for it. It used to be recommended that any pediatric patient recieving sux should get 20mcg/kg, under the assumption that you would notice a more profound effect from sux than in adults, but this has proven to not be necessary. I have to ask: if you are carrying out drug assisted intubations, why on earth was this sort of thing not covered in your education?

The potency of morphine versus fentanyl is not really relevant: you simply need to give an equivalant dose of morphine to achieve the same effect as the dose of fentanyl you would normally give. However fentanyl has a quicker onset and is indeed less likely to cause hypotension as it does not have the propensity to cause histamine release that morphine has. An opioid is a vital part of the induction process for drug assisted intubation. Laryngoscopy and intubation causes a rise in ICP due to sympathetic stimulation. This is exactly what we want to avoid when we are intubating someone whom we believe to have issues with their ICP already (TBI, intra-cranial bleed and so on) Fentanyl (as the usual dug of choice) blunts sympathetic response to the procedure and at high enough doses will completely eliminate any sympathetic response. It seems bizarre that you would premedicate with lidocaine which has no proven role in the management of ICP during RSI, yet not give a drug that does have an accepted role. Midazolam most certainly does have a significant effect on vasomotor tone and is well known to cause (usually transient) hypotension following bolus doses, probably through it's effect on the synthesis of prostanoids. Loss of cardiac output secondary to this and the loss of the thoracic pump secondary to positive pressure ventilation are always anticipated and very easily managed with appropriate preparation and judicious use of fluid loading to avoid them becoming problematic. If you are siginificantly concerned about the patient's blood pressure and don't want to preload with crystalloids, then the sensible option is to use fentanyl and ketamine along with suxamethonium (or a short acting NDNMBA like rocuronium or atracurium) To be honest I haven't heard of anyone attempting intubation with sedation alone for a long time. I'm aware of a few services that still have it on hte books for respiratory collapse with the rationale being that the patient would not be able to adequately de-nitrogenated prior to intubation being attempted and thus sedation alone would allow continual respirations. However to use sedation alone, especially with a single agent, on patients with a neurological problem is scary and barbaric.

Are you happy with ambos having amiodarone, adrenaline, adenosine, lidocaine, morphine, fentanyl, NDNMBAs, oxygen, aspirin or any of the other poisons we carry? There is nothing inherently more dangerous about propofol or etomidate compared to any of these other medicaitons. They can all be harmful if used incorrectly and useful if used correctly.

With regards to IM naloxone having a slower uptake: this is not necessarily a bad thing. So long as adequate ventilation is ongoing there is all the time in the world to administer narcan. In fact I personally feel that this is a better route to take. Oxygenate well, let the narcan work slowly and you have a much happier patient at the end of it all. In 13 years I have never had an overdose come up angry or swinging. All the angry/swinging/puking ones I have seen or heard of seem to be a result of having a hypoxic head and a sudden blast of IV narcan to ruin their day. I like to take my time, utilize the opportunity to give my student or BLS crew some time to do some manual airway management (which is difficult and often poorly done) and bring them up slowly. That and treating the patient with respect by not cutting up their best (only?) clothes means that the overdoses I wake up tend to shake my hand and thank me for saving them.

Sorry, I misundertood. So V4R, V5R and V6R are all elevated. Obviously that changes the game somewhat, now that we have a proximal RCA occlusion. Aspirin and plavix PO. No O2 unless he becomes hypoxic or starts to really look awful. IV access x 2, large bore with crytalloids hanging on both TKVO at this stage, ready to start squeezing. No LMWH for me unfortunately. Fentanyl for pain relief, as much is necessary. I'd have my atropine drawn up, along with my inotropes/pressors. Now, what I would not do is give nitrates. We are all aware that this patient is, or will become, very much preload dependant to maintain his cardiac output. I very much disagree with the idea of trying desparately to maintain preload with fluids, only to take it away with nitrates. The primary reason we give nitrates is to reduce preload and thus myocardial workload. They have a variable effect on coronary vasculature and this is also impeded by the fact that we are dealing with sclerosed and occluded vessels. There is also no compelling evidence that nitrates reduce mortality in ACS. So the risk is I obliterate his blood pressure compared to the benefit of.... nothing. Not a very good Risk/Benefit comparison there. I'm not an advocate of helicopters whizzing around all over the show, but with that kind of transport time and an evolving infarct this patient would benefit greatly from primary PCI in as short a time frame as possible, so that would be my first choice. I do not carry thrombolytics, but I have several 24/7 cath labs available within a 30 minute or so transport. This patient could feasibly benefit from thrombolysis if it is available.

My question is why you have called it right sided? You don't have V4R to confirm it, and haven't mentioned the degree of elevation in II as compared to III. Further, if the patient has elevation in V4, V5, V6 and II, III and aVF this would suggest a left dominant circulation with a reasonably proximal LCX occlusion, which would make right sided involvement highly unlikely. I'll leave the discussion of giving with one hand and taking away with the other by giving fluid and nitrates for another time; at this stage treat as per your ACS protocol, this is an inferolateral infarct.

Hypothermia and particularly cardiac arrest managment in hyopthermia is actually a very poorly studied field (for obvious reasons) What little science there is on hypothermia suggests that CPR until such time as active rewarming is instituted (either extracorporeal or passive) is the way to go. There are case studies of VF resolving on rewarming with no further intervention. The things to remember with hypothermic patients is that 1) they are very fragile. If they aren't in arrest now, any insult, however slight, will cause them to arrest. and 2) they are essentially hibernating. Their basal metabolic rate is so low that they don't require the same "numbers" that they would normally require to maintain cellular function. The biggest mistake people can make is seeing a low BP, heart rate or resp rate and thinking they need to do something about it. Now, as to a patient being hypoglycaemic to the point where thermoregulation is impaired, I would suggest that they are in far more dire straights than we are going to be able to rescue them from. Hypoglycemic patients do get cold, mostly because they sweat like a madman, but this is not the same as the actual hypo causing loss of heat regulation. When you think about it, you are saying that the patient has become so hypoglycemic that their brainstem has stopped working. Not a good sign! So, to cut a long story short... no I would not give D50 to the hypothermic patient. They do not need large amounts of energy as they are in a low energy state and all I would be doing is introducing a thick, hypertonic solution into a bloodstream and body that isn't really going to cope with it and doesn't really need it.

Very well put Dwayne.

It's an interesting question, and not, I would think, one that is going to be answered anytime soon due to the massive numbers of confounding variables that come in to play in pre-hospital cardiac arrest. Personally, I do not routinely push fluids during the arrest unless I have reason to suspect that volume depletion is an underyling cause of the arrest (eg PEA as presenting rhythm), but I will allow it to run TKVO and to use as a flush following drug boluses. However we have been inducing hypothermia for several years now with 2 litres of ice cold normal saline given as rapidly as possible, and our experience has been that there has not been the problems with pulmonary edema that many were expecting. Now, part of the rationale behind using ice-cold fluid as opposed to other methods is that we are mounting a three pronged attack in the post-arrest patient: Hypothermia (which we should all be conversant with now), Hypertension (to maintain adequate cerebral perfusion - hypertension being a relative term, we are looking for 'normal' BP/MAP rather than just accepting any kind of perfusion as adequate) and finally, Hemodilution. The main cause of further neurolgical injury in the post-arrest patient is reperfusion injury. Following the arrest there are large amounts of nasty stuff like calcium, glutamate and so on that is suddenly being moved around the brain to areas that may not have initally been as ischaemic or injured. The principle in managing this is to dilute these factors to minimize their impact: in essence 'flushing them out' before they can cause further injury. As a result of our aggressive management of the post-arrest patient (as well as public education, co-response from fire, and a tiered system with well trained EMTs) we have a survival to neurologically intact discharge rate from bystander witnessed VF/VT of about 30% We are soon to start a trial of cold saline induced hypothermia during the arrest, in effect managing the reperfusion injury before the reperfusion injury takes place, so it will be interesting to see how this pans out. It will take a number of years to complete however.

Hmmm... volatile agents in an ambulance, curious. Lungs will kill him before the kidneys will, so it may be worth a shot. IV morphine, IM fentanyl, no IV fentanyl? Odd. Can you get on to OLMC and get permission for some IV fentanyl?

Mechanism (in relatoin to motor vechicle collisions) is a poor predictor of injury. Mechanism alone is not sufficient to warrant the risk of running emergent to a trauma center. Mechanism should be used as a cue to alert you to look for specific patterns of injuries, not as a reason to not treat appropriately.

<br /><br /><br /> That's a good question. They certainly have been used to deal with the fluid shift, but on the erroneous assumption that there is an overload of fluid. The key term is 'fluid shift'. Eliminating the fluid in the system does not necessarily correct the fluid shift (it's not systemic overload we are usually worried about with ACPE - it's fluid in the wrong place, not too much fluid) and can lead to further problems with electrolytes (K+ in particular of course) and long term poor outcomes. Nitrates and ACEI's all serve to better correct the imbalance between hydrostatic and colloid oncotic forces that are the main problem to allow the fluid to shift back (or rather be taken up by the lymphatic system) and CPAP splints alveoli open to improve oxygenation and the problems that come from the V/Q mismatch (and shunt if really bad) (hopefully someone else can explain that better than me) Regarding long term CHF patients with an exacerbation, there are two schools of thought. One is that diuretics are appropriate as this may at least in part be a problem that has overload as a contributing factor. The other is that in the face of the sometimes quite substantial amounts of furosemide that these patients are taking alreadsy, a small amount may just be peeing into the wind and not achieving anything. To be honest, I am not sure how much data there is or isn't to support either of these positions. I currently am coming down in favor of giving the frusemide to these patients, but really, I'm not sure whether that is to make them feel better or me feel better... And it is only in cases of documented fluid overload that I consider it. I certainly would like to think that the potential to do harm with furosemide that we have in the true acute cases is not there for the acute on chronic cases. I stand to be corrected on this though, so if anyone else has a position, or better some data to support one way or another I would love to see it. That probably doesn't help a great deal though does it? I'll have a fossick around tomorrow and dig up some studies to support my ramblings. Paramagic

Thanks, long time lurker, first time poster.... At this stage, generally speaking, I would be in favour of removing lasix from the drug box, at least for the setting of suspected pulmonary edema - nitrates, CPAP and ACE Inhibitors are first line treatment for this, and irrespective of the difficulties with differentiating ACPE from pneumonia, it probably leads to worse outcomes. However, while there seems to be less and less of a role for it in the setting of ACPE, that is not to say that it does not have uses elswhere in pre-hospital care (hyperkalemia for example) although these instances may be rare, and a cost/benefit analysis should probably be undertaken. I am, however, firmly against protocolisation (is that a word?) of emergency medicine as the sole form of clinical risk management. The first line of clinical risk management should always be education. In some cases further protocolisation may be required, but it shoud be a last resort. Something else we need to be careful of is being against losing 'skills' or drugs for reasons other than patient care (ie. ego). There often seems to be an attitude that removal of a particular drug or procedure somehow reflects badly on us as paramedics (not that I am trying to imply that this is your stance; this is just a general observation) Now, if this has occured because, say we have been unable to differentiate between the decapitated/non-decapitated patient, then fair enough, we should be ashamed. However if it has occured because the best available evidence demonstrated no benefit, or even harm from using it, then we should happily wave it goodbye and maybe give it a Viking Burial at sea. We need to practice emergency medicine, not massive egotism. The studies quoted earlier in the thread seem to me to relate to a systemic problem in the diagnosis and management of a particular cohort of patients in a particular service. One needs to be careful with making generalisations regarding our own practice or service from these kinds of studies without having read and understood the study in it's entirety, including any methodological errors before making decisions regarding it's applicability to our own specific circumstances. When we just read abstracts we end up with blanket statements being made like "RSI is bad, mmmmkay" that may not be appropriate depending on ones circumstances.

There is more to the removal of furosemide than purely the risks involved in misdagnosing pneumonia. Patients with acute cardiogenic pulmonary edema (ACPE) have traditionally been treated for having too much fluid - after all, there is fluid in the lungs, so they must have too much fluid everywhere. Hence the use of diuretics in the acute setting. However we know that this is not actually the case. ACPE occurs not because there is too much fluid, but because there is fluid in the wrong place. It is at it's heart a problem with pressure - innappropriate systemic vascular resistance leads to a redistribution in fluid and the subsequent vicious circle of decreased oxygenation, increased sympathetic response aggravating SVR, decreased contractility aggravating back-flow, leading to further decreased oxygenation. Eventually the right heart gets in on the action too, with a RV afterload mismatch caused by hypoxic shunt from increased pulmonary cascular resistance. Bad news. Most ACPE patients are not in fact fluid overloaded, but euvolemic and in many cases they are actually dry, so diuresis is not going to provide anything beneficial. Whilst some may argue that there is a degree of vasodilation that occurs due to furosemide administration (and this is true) the degree of dilation and the time it takes to happen is extremely variable and not clinically relevant when superior agents such as nitrates are available to achieve the same ends. THere may be some call for furosemide in certain cohorts of patients, such as those with a history of fluid overload, however it should be used with caution if at all. Now, on top of all of that, there may actually be a place for the use of furosemide in the setting of a patient with pulmonary edema, just not in the acute or pre-hospital setting. It seems that patients who recieve positive pressure ventilation for more than about 24s have a subsequent inappropriate production of anti-diuretic hormone and their fluid balance and CVP and so forht needs to be monitored carefully (which of course will be done in the ICU, not the ambulance) There are a number of good papers and text books out there that discuss this issue that are not too hard to find if you look for them. Paramagic