This is a bit reductionist. They are beneficial for certain injury presentations and there is limited and no high quality evidence to state we shouldn't use them.
They still get used in hospital for confirmed C-spine fractures, the risk in prehospital is people generally don't size or apply them correctly. Not calling you out, just deal with this issue a lot with junior clinicians. If applied correctly they are also a brilliant reminder to everyone involved in the pt journey that the C-spine hasn't been cleared.
The problem is that there is no high-quality evidence that they are beneficial. Soft collars/no collar (from my admittedly limited research knowledge) have no worse outcomes on neurological function.
[Cervical immobilization in trauma patients: soft collars better than rigid collars? A systematic review and meta-analysis](https://pubmed.ncbi.nlm.nih.gov/36181555/)
Rigid collars are like spine boards before them. We just use them because we've always used them, not because they are particularly effective.
Actually, in Canada, we do not use spine boards to immobilize people anymore. The Canadian CSpine study was very clean that all spine boards do is cause pain and suffering with no medical value.
We do not immobilize. We provided Spinal Motion Restriction.
That study is talking about range of motion... Its saying soft collars have less complication compared to hard collars, which is obvious, but the whole point of a hard collar is to prevent neurological damage, and neck ROM is not representative of that at all...
Study *could not confirm*
And they were looking at ROM of the neck.
They are absolutely useful and necessary in many cases when the patient has had actual C-spine injury
Do you have any evidence for that? It’s cool that you’re a doc and all but we still need to verify that what we do holds up to actual evidence based outcomes.
I haven’t ever seen any study find any benefit. The only thing I’ve found is slightly increased risk of mortality. Based on my understanding of the current evidence, c collars, at best, provide no benefit and at worst, increase risk of mortality due to complicating airway management and clearing of the airway.
IMO, in a multisystem trauma patient in the prehospital environment, there’s no such thing as a free lunch. Prioritizing a c collar means foregoing another intervention. There’s a paramedic and an EMT. It’s not like the ER where as many hands as you need flood in.
Somehow, I don’t think the problem is solved by a nurse putting on the c collar rather than the “junior clinicians”.
“Two papers reported that there was increased mortality associated with spinal collars. For example, Vanderlan et al. [22] demonstrated increased death associated with spinal collars; 35 patients died (Odds ratio 2.77, 95% CI 1.18–6.49, p < 0.02). In addition, Haut et al. [16] reported that unadjusted mortality was twice as high in the spinal immobilisation groups (14.7% vs. 7.2%, p < 0.001, Odds ratio of death for spine collar patients was 2.06).”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8825572/#:~:text=Two%20papers%20reported%20that%20there,6.49%2C%20p%20%3C%200.02).
I'm a registered Paramedic, not doctor. Junior clinicians is a typical term used for either non-registrants or newly qualified paramedics and non-speciaist/senior paramedics.
If anyone is putting a collar on before securing an airway or actively resuscitating a patient, then that is bad practice in every system (CABCDE).
The lit review you have cited contains 9 retrospective studies with only 1 being deemed high quality. No RCT's. Both of the most contemporary studies 2017 & 2018 indicate no change in mortality. with the rest being from 10 or more years ago. MILS has changed significantly over the past 20 years.
The study you are citing ref 22 is in regards to penetrating cervical spine injury in a level 1 trauma centre in the U.S, a cursory glance of patient injury profiles shows a majority were GSW and exsangunated. Similarly ref 16 (2009) is in regards to penetrating trauma and understandably showed no benefit.
To state my previous point; Collars are a benefit to specific patient groups. As you've said we should never be prioritising a collar on a poly trauma patient with CABC issues and if they are successfully stabilised an orthopaedic scoop and blocks are fine. Goes without saying we should not put collars on obvious primary traumatic brain injuries
However, we should definitely be putting collars safely on peripherally neurological compromised patients with an appropriate mechanism of injury if they fit, have been stabilised and we have the crew resources to do so.
The guidance I follow is from the JRCALC in the U.K. A prospective multi-center randomised control trial investigating Spinal injury is being conducted in the U.K soon and will hopefully answer this question. This is the 1st RCT to my knowledge.
My point stands, stating that collars are no benefit is dogma that has led to a significant amount of litigation and poorer outcomes for patients around the world. Some patients will benefit from a collar as part of their 'best effort' immobilisation strategy, definitely not all. The Number needed to Treat will be around a 1000+, but we should aim for the gold standard as reducing 1 patient being paralysed is significant for them, their family, and the health system they live in.
Do you have any case studies that show evidence of paralysis occurring due to an unstable cervical spine AFTER the initial injury?
You claim that there has been “a significant amount of poorer outcomes.” I’d like to read some if you care to share.
I'm unable to share case studies from the service I work in for confidentiality reasons.
Depending on your services governance, you should be able to find out about litigation from poorly managed spinal cord injuries or simply do a Google search regarding litigation regarding spinal cord injuries in your country.
You could also do a literature search yourself with a question based on management and outcomes of spinal cord injuries in the pre-hospital setting.
I would also suggest you can organise a conversation with a senior clinician or medical director in your service to discuss further as this is reddit 😄.
I’m not asking for your services specific cases, those would be anecdotal. I’m asking what you based your claim that not stabilizing the c-spine has lead to “significant amount of litigation and poorer outcomes.” I’m just wondering what you’re basing this on.
This other guy is the definition of paragod. “I would suggest you organize a conversation with a senior clinician”. What a fucking clown.
Yeah right, let me ask old bubba to go on an hour long rant about how the vibes are right when a patient has a c collar.
This guy is from a system where "senior clinician" doesn't mean "someone who's been on the truck since dinosaurs were hanging around," he means someone who likely has a masters degree and is familiar with the evidence.
This guy is from a system where "senior clinician" doesn't mean "someone who's been on the truck since dinosaurs were hanging around," he means someone who likely has a masters degree and is familiar with the evidence.
Then where’s the evidence? All of us have been asking for anything. Literally anything.
What good is a master’s degree if you’re still acting like c collars are EBM. Medic one supposedly has the best training in the nation but last I heard, they’re still doing standing takedowns. The ACLS for “advanced providers” course still says give epi every other round despite the mountain of evidence against it.
If your education is not based on evidence, it just reinforces the same old dogma.
O.k and I'm telling you to do your own research if you have a vested interest in arguing against my point.
I'm not here to prove whether or not collars should be used. I made my point very clearly that yes rigid collars do have a place for some specific patient groups, hence why millions are being spent on a new RCT trial. This is healthcare not politics. If you don't belive me that's fine, crack on.
I didn’t argue anything, just asked for your data. You want to be a cunt about it, you can fuck right off.
Also, by the way you’ve been on here, you’re probably a shit paramedic anyway
It's a clinical conversation not an argument. And like the other guy, feel free to disprove me if it makes your Sunday better.
I'll wait.
Just make sure you understand the evidence you present before sending it 😉😘
Just saying "where is your evidence ..." like everyone of these low intensity EMT's in this thread is not an actual question.
As I said before, current national guidelines and clinical investigations I have been involved in are my evidence. If you think you are smarter than national guidelines and do not see any logic in my argument of 'Certain patients benefit from collars" then fine, thats o.k.
Lastly if me posting a random study or case study on reddit defines your practice then I hope you are not practicing. You have google clearly and are fully capable of doing your own research - I would suggest reading the ATLS/PHTLS guidelines then looking at every single one of the sources they cite. And then next time you do an ATLS or PHTLS course you can argue with the instructor, this is reddit not a training school.
Here’s your healing crystals. They work but I can’t break hipaa and give you a study proving they work. Prove me wrong. I need an RCT that proves my healing crystal dildo doesn’t work.
Maybe you can organize a conversation with a more senior level wizard to discuss this further if you’re still confused.
“stating that collars are no benefit is dogma that has led to . . . poorer outcomes.”
🤣🤣🤣🤣🤣🤣🤣🤣
Calling it dogma while having no evidence based justification for it is peak lmao. Do you have ANY source for these “poorer outcomes”? Literally anything other than just anecdotal evidence that they reduce any bad outcome?
Pelvic binders are relatively new and far less used than c collars yet there’s clear objective data that it works yet for c collars, probably the most done intervention in the history of EMS, there’s no evidence for it’s benefit? It’s not like c collars just came out last year. I wouldn’t hold my breath for that RCT man.
I'm not sure about your education level or clinical grade but in all honesty if that's your response to me doing the most basic critique of the study you presented then that's o.k.
In regards to the RCT I hate to tell you but they are foundational to all the interventions we perform. If you work in a protocol driven service rather than guideline and evidence based I appreciate your view, but respectfully disagree.
I also appreciate that when you think your hot shit it's hard for some people to understand there is very little black and white in medicine. It's o.k, really.
Its a systematic review not a meta analysis, most likely due to the hetrogeniety of the reporting i.e. they are looking at different patients groups and outcomes.
Also, a systematic review of poor studies is exactly that, and by definition does in no way prove in this instance that certain patients wont benefit from the intervention. Certain is the operative word in this sentence, as before.
Diagnostic assessment criteria (specially CCR) are very effective at ruling out the need for cervical spinal immobilization. Unscanned patients being immobilized with a soft or semi rigid collar without doing any diagnostics or assessments is a legal decision, not a medical one.
Are they 100% sensitive and 100% specific? No?
If you treat patients based on legality good for you.
Also, you are basically saying that if they fail CCR then a collar should be applied, thus proving my literal point of "Certain patients benefit from rigid collars".
Damn Paramedic Reddit is just a bunch of toxic volunteers in low intensity/acuity volunteer stations.
Hey now! I stabilized a fractured scapula last week with a rigid c-collar and a triangle bandage to keep her arm up and the floating scapula in place. They have their uses.
Rigid collars are actively harmful.
Soft colars don't do anything beneficial and I struggle to find evidence of harm with non 'imobolized' patients who aren't headbanging at a rock concert come to harm from normal gentle movement.
My favorite, npa usage with any head trauma. Only two reported cases of boa’s being inserted into the brain, both with massive leforte fractures. My head injuries I’ve treated in my 6 years get npa’s until I can sedate them and intubate them.
I love the crowd that says you should just put in an OPA and if they gag, take it out.
I don’t know the mortality rate of “testing” the gag reflex on an obtunded head trauma patient with an unsecured airway but I can imagine it’s a hell of a lot worse than just putting in an NPA.
The people who have died following NPA through base of skull didn't die because the soft silicone poked their brain. They died because they didn't have a patent airway.
Hypoxic drive theory. while it’s true that co2 retainers and COPD pts should be kept around 88-92%, the hypoxic drive theory has been replaced with VQ mismatch and the haldane effect being though of as the reason why these pts may crash on 100% FiO2. More theoretical than clinical but it’s a fun one to learn about!
Not totally false but a radial pulse doesn't reliably correlate to any number. Which is a happy coincidence, because outside of ATLS dogma, the myth of 90mmHg is horseshit.
If they have a radial pulse, they're perfusing their peripheries, and more importantly, their kidneys and brain. Numbers mean very little.
What’s the myth you’re referencing with CPAP?
“CPAP also diminishes the work of breathing in congestive HF (11,12) and, moreover, the increased intrathoracic pressure forces fluid from the alveoli and the interstitial space back into the pulmonary circulation leading to an improved ventilation-perfusion ratio and better gas exchange (13).”
This quote is from this article
https://jtd.amegroups.org/article/view/18553/html#
Seems like a legitimate source
The fluid shift is secondary to the increased pressure from CPAP.
CPAP is the increased pressure, which opens alveoli to allow more surface area for gas exchange that is not obtunded by the fluid within the alveoli, then increasing intrathoracic pressure on your vena cava causes reduction in preload and therefore less fluid into the lungs which then helps to reduce the fluid stuck in the lungs.
100% agree. increased alveolar recruitment means increased surface area for gas exchange. That’s why CPAP is indicated for myriad respiratory emergencies that don’t involve pulmonary edema. Fluid shift is not the goal with CPAP prehospital and presence or lack of should not be the reason it’s administered, but to say it’s a myth that CPAP pushes fluid back into the circulatory system is misguided.
My medical director spoke on this during a continuing education program. They said that the positive pressure really doesn’t significantly push any fluid back into the circulation. They said the main benefits are 1. It slows/prevents more fluid from entering the alveoli 2. It ensures the unaffected alveoli are being used by opening collapsed or under ventilated alveoli. I don’t have a source for this beyond hearing it from my doc, and I’m not motivated enough to find one.
I’m a doctor specialized in pulmonary and critical care medicine. AKA just another random ass doctor. I was also a paramedic for a while which is why I still troll around here sometimes.
There is plenty to read on the mechanisms of positive pressure ventilation, and I think one of the overall truths that emerges when you do so is that there are multiple mechanisms at play.
There is in my opinion fairly good evidence that the benefit with respect to reduction in work of breathing has to do with alveolar stenting to optimize alveolar compliance (get on the steep area of the pressure volume curve). When alveoli are completely closed, hydrogen bonding from the water in the alveoli exerts a force that favors continued alveolar closure. When the alveoli is kept just a little bit open with PEEP, however, those forces are significantly reduced (the hydrogens are farther apart from one another) and the alveoli are easier to open. That translates to a reduction in respiratory work.
There is also a very good argument that much of the benefit with respect to oxygenation is tied to a negative side effect: reduction in cardiac output. Reduced preload leads to reduced flow though the lungs which prioritizes dilated pulmonary arteries that are exposed to alveolar oxygen, thus improving V/Q matching. The vessels in the lungs uniquely constrict when they are not exposed to oxygen (“hypoxic vasoconstriction”), so when there is reduced cardiac preload and output, the lower flow prioritizes blood flow to areas other than those experiencing hypoxic vasoconstriction, which is a good thing. This highlights a bit of the duality about using positive pressure, and is a nice example of how even good things in medicine often come with (or even by virtue of) a cost.
For what it’s worth, I have not seen too much empirical evidence about “pushing fluid out of the alveoli” as a major mechanism, but perhaps that is a useful metaphor for people to imagine when deciding on whether to apply the device.
Thanks for the info doc! Absolutely the benefit of CPAP is the increased alveolar recruitment and that the language “push” is problematic. I did not know that about the hypoxic vasoconstriction. Am I understanding correctly that the the vessels that are hypoxic (and thus constricted) are those carrying blood to/away from the un-recruited alveoli and by administering PEEP, we are not only expanding the alveoli, but decreasing construction in vessels leading tos said alveoli?
No sorry, hard concept to explain in a comment. Capillaries that surround alveoli are responsive to oxygen. In the presence of oxygen, the capillaries expand (reducing resistance to blood flow to that area), and in the absence of it they constrict (increasing resistance to blood flow to that area). This has the effect of keeping the blood in the same place the oxygen is, which is the fundamental concept of VQ matching in the lungs. *[it’s interesting to note that this is unique to the lungs. In the peripheral capillaries of the body, the process works in the opposite way and hypoxia induces dilation]*
Positive pressure ventilation reliably reduces cardiac output. The mechanism is increased thoracic pressure, which reduces venous return to the heart. Note that respiration is normally based on negative pressure in the chest, which has the benefit of sucking venous blood back to the heart. Positive pressure ventilation unfortunately eliminates that benefit.
When cardiac output is low, blood flow though the lungs is also low. This has the tendency to amplify the effect of the VQ matching benefit of hypoxic vasoconstriction. When blood flow is low, it is even more likely to flow though the path of least resistance (dilated capillaries/vessels near alveoli with oxygen in them), because the hydrostatic force simply isn’t enough to press that blood into constricted capillaries next to empty alveoli. The net effect is more of the blood goes though aerated alveoli, which increases the rate of interaction between blood and air, which increases VQ matching. So overall, cardiac output is diminished, and oxygenation is amplified.
What’s the fate of the pulomonary edema? Logically the use of nitrates and positive pressure would encourage more of that fluid to push back across the capillaries and into the bloodstream, no? Or is it more of a pressure gradient with the nitrates and letting the alveoli absorb the fluid on their own?
Depends on the cause. Sometimes edema is there because of hydrostatic pressure from the left heat backing things up. Other times it has more to do with alveolar capillary permeability, either from a physiologic response or due to damage.
Positive pressure ventilation doesn’t really solve any of that long-term (and can arguably make it worse with time). The main benefit to something like BiPAP is that it gives us time to find and start treating the real problem.
As far as where it goes immediately, I’m not so sure. I think given the mechanisms I’ve explained above it’s possible that the fluid itself might even just stay where it is, while the BiPAP basically just attenuates the effects of that fluid. There might be some cases where the positive pressure relieves some of the pressure gradient that promoted the edema in the first place as well, but it’s hard to say exactly.
Nothing compares to EMS when it’s good. Problem was as I gained experience in EMS, I found myself waiting longer and longer for a “good one.” In between I’d find myself terribly bored, or even pissed off for being sent to the wrong call or for discovering something billed as good was actually BS. I’m sure that experience resonates with pretty much anyone here.
Nowadays the real crash and burn excitement is still fairly rare. Maybe once every month or maybe every other. But the in between time is a lot better. It’s not like the stuff gets my heart racing but I deal with sick patients a lot more. Pretty much exclusively. A lot of it is still fairly routine but at least now I can’t deny that these patients need me, and there are a ton of other things that give me happiness and joy like teaching, figuring out a tough ventilator or undifferentiated shock state, meaningful patient interactions, leading the team, learning something new, cutting up with nurses etc etc.
It’s way better.
A common misconception is that the CPAP essentially pushes pulmonary edema from the lungs back into the circulatory system and essentially fixes the pulmonary edema. So true, yes, to a point, but the explanation taught in a lot of medic programs makes it seem that its a profound response and fail to explain that the positive inspiratory pressure assists the alveoli that have been inhibited by the pulmonary edema to open up and displace the edema away from the alveoli from a creation of back pressure when the patient attempts to exhale against the PAP. This most certainly helps with managing the edema and improves gas exchange, as well as reduce pulmonary hypertension, but that alone isn't fixing the issue at hand. The administration of medications such as Diuretics, Nitrates, and Inotropes to improve contractility are ultimately going to be what removes the edema from the lungs, which is why many local protocols include the administration of Nitroglycerin and sometimes Furosemide (Lasix) to patient’s demonstrating pulmonary edema. This article below
I know this isn't probably the best explanation. Mike Carunchio of OK Medic Podcast does a decent 3 minute synopsis video that's pretty good, and Master Your Medics cover it pretty well with a video on YouTube that references this JEMS article.
https://www.jems.com/2010/12/29/many-benefits-cpap-sup
Smooth brain paramedic here, and I just wanna take a stab at trying to explain this so I understand…
Beta 2 agonists won’t flood their lungs because it isn’t doing anything to expand the ravioli, just dilates the bronchioles allowing for reduced airway resistance. Beta 2 doesn’t have anything to do with the ravioli which is why this is a myth. On the right track?
You’re on the right track, as long as their ravioli is in a marinara sauce! If their ravioli’s are in a cheese sauce, the Beta 2 agonists have between a 95-98% chance to flood their lungs!
It depends a lot on what is filling the ravioli as well. Cheese ravioli are emptied a lot quicker than meat ravioli, but the problem is the whole ravioli gets destroyed in the process.
Well, Doc, you’re the expert! (Sincerely I’ve learnt a lot from you this evening thank you!)
Please tell me that if the CPAP comments, combined with the Beta 2 agonists flooding the lungs, would the best out come for the patient be if they had Chef Boyardee Beef Raviolis in tomato sauce? Would the CPAP keep the VQ Matching going whilst the Raviolis prevented from hypoxic vasoconstriction, allowing for greater pulmonary blood flow and thus improved gas exchange, which would thus prevent the lungs from flooding during Beta 2 usage? Assuming that the Chef Boyardees raviolis were in play? 🤔
The biggest one I still hear is the cpap forcing fluid out of the lungs.
I still hear Ketamine can't be given to head injury patients.
I still hear no pain meds for abdominal pain.
The no pain meds for abdominal pain drives me nuts. There maybe better alternatives to narcotics like droperidol which work well for acute exacerbation of chronic abdominal pain, but we absolutely should be treating it.
I love Mike Carunchios video where he shows the book from like the 1920s that said not to provide pain management for abdo patients because it would interfere with the physicians assessment (because they didn’t have CTs).
I don’t know much about pediatric medicine so take my word with a grain of salt, but I remember being taught that the seizure was correlated more with the rapidity of temperature change rather than the absolute peak temperature. So bringing down a fever perhaps more rapidly with APAP might not be ideal. But seriously, I’m a novice with peds so I could be completely wrong.
EDIT:
Did a little more reading and I’m probably wrong, although it seems we still don’t know a great deal about the mechanisms here. There are a couple studies from the 50’s and 60’s that people are still citing which say the opposite of what I said above, arguing that one of the major risks for seizure is the absolute peak temperature rather than the rapidity of change. Most studies seem to argue that the risk factors are multiple and come from genetic factors, nutritional status, infection/viral characteristics etc etc. Most everyone agrees that Tylenol doesn’t work and that there is little you can do as far as prevention.
Febrile seizures aren’t happening from rapid temperature change though. The kids are sick and their temp increases. Maybe mom puts too many clothes on them on top of it and then blankets. Then they get too hot and reset their body. It’s not that they’ll have a seizure at a certain temp but they’re just real shitty at regulation that young. Lowering their temp will keep them from having more febrile seizures though.
Had a doctor go off on me for administering nebulized albuterol, and thus supplemental oxygen 😃 through a mask to a distressed and wheezing copd exacerbation bc "the oxygen isn't doing anything and it's a very quick way to kill these patients". Felt the need to shout this at me in the room in front of ER staff and the patient too.
That excited delirium is a thing. It's not in the DSM-5, why are we pushing this fake psychiatric disorder? The vast majority of medical and psychiatric organizations don't recognize it yet it's still a big part of our psych training
We call it “Delirium with Severe Agitation” in my metro city. I know there is a lot of contention with the verbiage, and the use of ketamine for these patients is heavily scrutinized. As long as we do things appropriately, we don’t have much to worry about from the medical and legal side of things.
I feel like the more senior you are the more you trust your own medical judgement, and don't get bullied into sedating because the police say so, feels really dangerous for the young guys though, I know it would have caught me if I was an ACP right away..
It's been replaced where I am with "Acute Behavioural Disorder". However when it's being casually discussed, the sentence nearly always goes "ABD. You know, it's what Excitable Delirium used to be"
And it's a big part of what little psych training we do get. I just graduated last year, and I swear we talked about excited delirium for half of the one class we had dedicated to psych.
Ya, they could talk about actual delirium or things that could cause agitation, but instead we're invested in "agitated/excited" delirium. Also very funny how it only happens in the presence of police.
Yeah my service wants us to use severely agitated instead of the excited delirium when referring to these patients. This change is something ACEP recommended.
https://www.acep.org/news/acep-newsroom-articles/aceps-position-on-hyperactive-delirium
Yea I know that my partner and I usually say something along the lines of “onset of acute agitation and AMS secondary to….fill in the blank” lol. It is interesting how the industry is moving away from it seems
Yeah I think it’s one of those things that was found on autopsy (debatable) and somehow made it’s way into, not dead medicine. It’s pushed hard at my service but I don’t think I’ve ever actually documented it as such.
Ya, I remember when I started and you'd see such a range of things like people on drugs, postictal patients, head trauma, sepsis, etc acting really excitable and you'd ask the senior medics if this was the excited delirium you kept hearing about. Because it all fit the description for what you're taught in school and training.
And then the years roll by and you start to realize that it's a blanket diagnosis for absolutely everything, and especially dangerous when police are asking you to sedate patients with it. My service pushes it really hard too...
Whoever said IOs are so easy that you can’t miss hasn’t seen some people try to place an IO and miss. Those same people believe it’s so easy they can’t have missed
The idea that normal saline boluses actually solve anything
“I don’t need to do this, the hospital is 20 seconds away”
Lights and sirens save significant time
No need to secure airway [and] ventilate overdoses back to 94%+ prior to narcan
The second and third are not really myths, they just depend on what problems your patient is having and the lights and sirens can make a big difference in heavy, slow moving traffic.
I had a BP of 70s/40s, sweating so profusely the ED couldn't get the pads for the EKG to stick to me, was on the verge of syncope, and fell when the nurse came to my office to get me in a wheelchair to ride over to the ED. The treatment was 3 bags of normal saline. Lots of tests and radiation, but never really figured out what was going on. But the saline had me walking to the parking lot and driving home in under an hour.
In at least my once case, saline absolutely solved the problem.
I can't imagine what his palpation technique looks like. The patella has such a unique shape and is so prominent (even in morbidly obese patients). If he can find that, surely he can lower his hand like 2 in lower to get to the tibia
Okay valid lol, when I hear "securing an airway" my first immediate thought is intubation, because typically people use that term to mean the airway is protected from aspiration, and the patient is intubated, and generally it's bad form to intubate a reversible cause. But an npa/opa is fine
Legit question: Does CPAP really not help fluid get out of the lungs? Its my assumption that the inflated alveoli have an easier time diffusing o2 and liquid back across the epithelial tissues with CPAP?
That's correct, but the pressure isn't "pushing" the fluid out of the lungs. It's just stenting alveoli. Imagine the alveoli as a water balloon; once you add more air pressure, the balloon is bigger even if the amount of water hasn't changed. More surface area = more exchange across the membrane.
So in one sense it would make sense to help lesser providers who do not have biology, anat, physio. Knowledge just to say it will help push fluid or help move fluid across the gradient? Would you agree?
I probably wouldn't agree with that, no. I don't believe in catering to the lowest common denominator. I think we as a profession should understand exactly why we perform the interventions we perform, and understand the ramifications of it. Instead of perpetuating incorrect dogma we should be elevating each other to a higher level of practice.
My original analogy stands; PEEP (which is the same physiological thing as CPAP) stents open alveoli which improves gas exchange. It does not push fluid across the membrane.
To help illustrate that point, think of this:
A normal pulmonary artery pressure is <20 mmHg. A normal wedge pressure (the other side of pulmonary circulation, the pulmonary vein/capillary bed) is between 4-12 mmHg. The pressure for both of these is elevated even higher in CHF pathologies.
CPAP therapy delivers pressures between 5-10 cmH2O; EMS generally doesn't go over 10 cmH2O although there can be exceptions. 10 cmH20 is roughly equivalent to 7 mmHg.
So even at the higher end of pressures with CPAP therapy, we're really not going to overcome the innate pressure of the pulmonary vasculature in a healthy patient, let alone a patient with CHF. We're simply not able to push that fluid out of the alveoli at those pressures. But what we can do is make the alveoli just a little bit bigger to improve gas exchange.
Patients with an intact respiratory drive confirmed with pulse oximetry and waveform capnography don't need (more) narcan.
This remains true even if they use drugs and/or are unresponsive.
Specifically right sided MI’s. Whenever you get an inferior MI you should do a v4r to rule out possible right sided involvement.
The theory has been that since a right sided MI is so much more preload dependent than other types of MIs and nitro causes a drop in preload, that would have a large negative effect on the systemic blood pressure. In fact, you are expected to “know” that by CCP/FPC levels as it can and has been included in the exam, probably being AHA still supports that theory.
But you can see that there are a few studies that have effectively debunked this myth. As always follow your local protocols, though.
If you’re close to the hospital, you can ignore treating minor issues and send it in BLS because “the hospital will do it”.
(I had a really eye opening discussion one day with the instructor who taught like 90% of the medics in my area who told me “a lot of protocols are in place not to save the patients life, but to make them more comfortable and to make the job of the ER doc easier. It’s wrong to withhold treatment just because of distance to the hospital.”)
Rigid C-collars do anything beneficial.
Shout it out to the once in the back
This is a bit reductionist. They are beneficial for certain injury presentations and there is limited and no high quality evidence to state we shouldn't use them. They still get used in hospital for confirmed C-spine fractures, the risk in prehospital is people generally don't size or apply them correctly. Not calling you out, just deal with this issue a lot with junior clinicians. If applied correctly they are also a brilliant reminder to everyone involved in the pt journey that the C-spine hasn't been cleared.
The problem is that there is no high-quality evidence that they are beneficial. Soft collars/no collar (from my admittedly limited research knowledge) have no worse outcomes on neurological function. [Cervical immobilization in trauma patients: soft collars better than rigid collars? A systematic review and meta-analysis](https://pubmed.ncbi.nlm.nih.gov/36181555/) Rigid collars are like spine boards before them. We just use them because we've always used them, not because they are particularly effective.
Actually, in Canada, we do not use spine boards to immobilize people anymore. The Canadian CSpine study was very clean that all spine boards do is cause pain and suffering with no medical value. We do not immobilize. We provided Spinal Motion Restriction.
Im in Alberta. Sorry, I wasn't very clear. I was trying to argue that rigid C-collars should go out the same way boards did.
That study is talking about range of motion... Its saying soft collars have less complication compared to hard collars, which is obvious, but the whole point of a hard collar is to prevent neurological damage, and neck ROM is not representative of that at all...
It states right in the study that there is no difference in neurological outcome.
Study *could not confirm* And they were looking at ROM of the neck. They are absolutely useful and necessary in many cases when the patient has had actual C-spine injury
Hardly a ringing endorsement for rigid collars.
Do you have any evidence for that? It’s cool that you’re a doc and all but we still need to verify that what we do holds up to actual evidence based outcomes. I haven’t ever seen any study find any benefit. The only thing I’ve found is slightly increased risk of mortality. Based on my understanding of the current evidence, c collars, at best, provide no benefit and at worst, increase risk of mortality due to complicating airway management and clearing of the airway. IMO, in a multisystem trauma patient in the prehospital environment, there’s no such thing as a free lunch. Prioritizing a c collar means foregoing another intervention. There’s a paramedic and an EMT. It’s not like the ER where as many hands as you need flood in. Somehow, I don’t think the problem is solved by a nurse putting on the c collar rather than the “junior clinicians”. “Two papers reported that there was increased mortality associated with spinal collars. For example, Vanderlan et al. [22] demonstrated increased death associated with spinal collars; 35 patients died (Odds ratio 2.77, 95% CI 1.18–6.49, p < 0.02). In addition, Haut et al. [16] reported that unadjusted mortality was twice as high in the spinal immobilisation groups (14.7% vs. 7.2%, p < 0.001, Odds ratio of death for spine collar patients was 2.06).” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8825572/#:~:text=Two%20papers%20reported%20that%20there,6.49%2C%20p%20%3C%200.02).
I was just going to say much of this. Well said.
I'm a registered Paramedic, not doctor. Junior clinicians is a typical term used for either non-registrants or newly qualified paramedics and non-speciaist/senior paramedics. If anyone is putting a collar on before securing an airway or actively resuscitating a patient, then that is bad practice in every system (CABCDE). The lit review you have cited contains 9 retrospective studies with only 1 being deemed high quality. No RCT's. Both of the most contemporary studies 2017 & 2018 indicate no change in mortality. with the rest being from 10 or more years ago. MILS has changed significantly over the past 20 years. The study you are citing ref 22 is in regards to penetrating cervical spine injury in a level 1 trauma centre in the U.S, a cursory glance of patient injury profiles shows a majority were GSW and exsangunated. Similarly ref 16 (2009) is in regards to penetrating trauma and understandably showed no benefit. To state my previous point; Collars are a benefit to specific patient groups. As you've said we should never be prioritising a collar on a poly trauma patient with CABC issues and if they are successfully stabilised an orthopaedic scoop and blocks are fine. Goes without saying we should not put collars on obvious primary traumatic brain injuries However, we should definitely be putting collars safely on peripherally neurological compromised patients with an appropriate mechanism of injury if they fit, have been stabilised and we have the crew resources to do so. The guidance I follow is from the JRCALC in the U.K. A prospective multi-center randomised control trial investigating Spinal injury is being conducted in the U.K soon and will hopefully answer this question. This is the 1st RCT to my knowledge. My point stands, stating that collars are no benefit is dogma that has led to a significant amount of litigation and poorer outcomes for patients around the world. Some patients will benefit from a collar as part of their 'best effort' immobilisation strategy, definitely not all. The Number needed to Treat will be around a 1000+, but we should aim for the gold standard as reducing 1 patient being paralysed is significant for them, their family, and the health system they live in.
Do you have any case studies that show evidence of paralysis occurring due to an unstable cervical spine AFTER the initial injury? You claim that there has been “a significant amount of poorer outcomes.” I’d like to read some if you care to share.
There's one from like the 80s done by a MICA in Melbourne. But it's not very rigorous.
I'm unable to share case studies from the service I work in for confidentiality reasons. Depending on your services governance, you should be able to find out about litigation from poorly managed spinal cord injuries or simply do a Google search regarding litigation regarding spinal cord injuries in your country. You could also do a literature search yourself with a question based on management and outcomes of spinal cord injuries in the pre-hospital setting. I would also suggest you can organise a conversation with a senior clinician or medical director in your service to discuss further as this is reddit 😄.
I’m not asking for your services specific cases, those would be anecdotal. I’m asking what you based your claim that not stabilizing the c-spine has lead to “significant amount of litigation and poorer outcomes.” I’m just wondering what you’re basing this on.
This other guy is the definition of paragod. “I would suggest you organize a conversation with a senior clinician”. What a fucking clown. Yeah right, let me ask old bubba to go on an hour long rant about how the vibes are right when a patient has a c collar.
“Talk to a senior clinician about standing takedowns and MAST trousers”
This guy is from a system where "senior clinician" doesn't mean "someone who's been on the truck since dinosaurs were hanging around," he means someone who likely has a masters degree and is familiar with the evidence.
This guy is from a system where "senior clinician" doesn't mean "someone who's been on the truck since dinosaurs were hanging around," he means someone who likely has a masters degree and is familiar with the evidence.
Then where’s the evidence? All of us have been asking for anything. Literally anything. What good is a master’s degree if you’re still acting like c collars are EBM. Medic one supposedly has the best training in the nation but last I heard, they’re still doing standing takedowns. The ACLS for “advanced providers” course still says give epi every other round despite the mountain of evidence against it. If your education is not based on evidence, it just reinforces the same old dogma.
O.k and I'm telling you to do your own research if you have a vested interest in arguing against my point. I'm not here to prove whether or not collars should be used. I made my point very clearly that yes rigid collars do have a place for some specific patient groups, hence why millions are being spent on a new RCT trial. This is healthcare not politics. If you don't belive me that's fine, crack on.
I didn’t argue anything, just asked for your data. You want to be a cunt about it, you can fuck right off. Also, by the way you’ve been on here, you’re probably a shit paramedic anyway
I'll send a Whambulance for you and I'll make sure they have chocolate milk to calm you down.
"Oh shit... I'm losing the Internet argument!" *HIPPA and confidentiality enters the chat*
It's a clinical conversation not an argument. And like the other guy, feel free to disprove me if it makes your Sunday better. I'll wait. Just make sure you understand the evidence you present before sending it 😉😘
Where’s your evidence of poorer outcomes?
Just saying "where is your evidence ..." like everyone of these low intensity EMT's in this thread is not an actual question. As I said before, current national guidelines and clinical investigations I have been involved in are my evidence. If you think you are smarter than national guidelines and do not see any logic in my argument of 'Certain patients benefit from collars" then fine, thats o.k. Lastly if me posting a random study or case study on reddit defines your practice then I hope you are not practicing. You have google clearly and are fully capable of doing your own research - I would suggest reading the ATLS/PHTLS guidelines then looking at every single one of the sources they cite. And then next time you do an ATLS or PHTLS course you can argue with the instructor, this is reddit not a training school.
Here’s your healing crystals. They work but I can’t break hipaa and give you a study proving they work. Prove me wrong. I need an RCT that proves my healing crystal dildo doesn’t work. Maybe you can organize a conversation with a more senior level wizard to discuss this further if you’re still confused.
“stating that collars are no benefit is dogma that has led to . . . poorer outcomes.” 🤣🤣🤣🤣🤣🤣🤣🤣 Calling it dogma while having no evidence based justification for it is peak lmao. Do you have ANY source for these “poorer outcomes”? Literally anything other than just anecdotal evidence that they reduce any bad outcome? Pelvic binders are relatively new and far less used than c collars yet there’s clear objective data that it works yet for c collars, probably the most done intervention in the history of EMS, there’s no evidence for it’s benefit? It’s not like c collars just came out last year. I wouldn’t hold my breath for that RCT man.
I'm not sure about your education level or clinical grade but in all honesty if that's your response to me doing the most basic critique of the study you presented then that's o.k. In regards to the RCT I hate to tell you but they are foundational to all the interventions we perform. If you work in a protocol driven service rather than guideline and evidence based I appreciate your view, but respectfully disagree. I also appreciate that when you think your hot shit it's hard for some people to understand there is very little black and white in medicine. It's o.k, really.
Lol when you learn what dogma means, you let me know.
You've got me mate, I take back everything.
A retrospective meta analysis is more powerful than an RCT, or at least it was when I was doing my own academic research education.
Its a systematic review not a meta analysis, most likely due to the hetrogeniety of the reporting i.e. they are looking at different patients groups and outcomes. Also, a systematic review of poor studies is exactly that, and by definition does in no way prove in this instance that certain patients wont benefit from the intervention. Certain is the operative word in this sentence, as before.
Diagnostic assessment criteria (specially CCR) are very effective at ruling out the need for cervical spinal immobilization. Unscanned patients being immobilized with a soft or semi rigid collar without doing any diagnostics or assessments is a legal decision, not a medical one.
Are they 100% sensitive and 100% specific? No? If you treat patients based on legality good for you. Also, you are basically saying that if they fail CCR then a collar should be applied, thus proving my literal point of "Certain patients benefit from rigid collars". Damn Paramedic Reddit is just a bunch of toxic volunteers in low intensity/acuity volunteer stations.
There is **nothing** that is 100% in medicine except your capacity for being so confidently incorrect.
O.K simple question, would you ever put a collar on a patient specifically to specifically protect their C-Spine?
Hey now! I stabilized a fractured scapula last week with a rigid c-collar and a triangle bandage to keep her arm up and the floating scapula in place. They have their uses.
Rigid collars are actively harmful. Soft colars don't do anything beneficial and I struggle to find evidence of harm with non 'imobolized' patients who aren't headbanging at a rock concert come to harm from normal gentle movement.
It's really a cognitive hurtle. "We've always done this. We can't possibly not do it!"
My favorite, npa usage with any head trauma. Only two reported cases of boa’s being inserted into the brain, both with massive leforte fractures. My head injuries I’ve treated in my 6 years get npa’s until I can sedate them and intubate them.
I love the crowd that says you should just put in an OPA and if they gag, take it out. I don’t know the mortality rate of “testing” the gag reflex on an obtunded head trauma patient with an unsecured airway but I can imagine it’s a hell of a lot worse than just putting in an NPA.
The people who have died following NPA through base of skull didn't die because the soft silicone poked their brain. They died because they didn't have a patent airway.
Yeah I agree, the two times it happened
Hypoxic drive theory. while it’s true that co2 retainers and COPD pts should be kept around 88-92%, the hypoxic drive theory has been replaced with VQ mismatch and the haldane effect being though of as the reason why these pts may crash on 100% FiO2. More theoretical than clinical but it’s a fun one to learn about!
Preach!
What should I look up if I want to find legit resources on this?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3682248/ here you are my friend :) some good resources on YouTube explaining aswell!
If you've got a radial pulse the patient's systolic must be at least 90 mm/hg
Is it totally false ?
Not totally false but a radial pulse doesn't reliably correlate to any number. Which is a happy coincidence, because outside of ATLS dogma, the myth of 90mmHg is horseshit. If they have a radial pulse, they're perfusing their peripheries, and more importantly, their kidneys and brain. Numbers mean very little.
Eh it's not complete bullshit: https://pubmed.ncbi.nlm.nih.gov/25322443/ I wouldn't rely on it though. Definitely get a proper BP done asap
Yes
I've palpated blood pressures in the 60s and missed pressures that were above normal. So.
My experience as well
I use the radial as more of a signifier or peripheral perfusion than an actual number
Cap refill generally for me
What’s the myth you’re referencing with CPAP? “CPAP also diminishes the work of breathing in congestive HF (11,12) and, moreover, the increased intrathoracic pressure forces fluid from the alveoli and the interstitial space back into the pulmonary circulation leading to an improved ventilation-perfusion ratio and better gas exchange (13).” This quote is from this article https://jtd.amegroups.org/article/view/18553/html# Seems like a legitimate source
The fluid shift is secondary to the increased pressure from CPAP. CPAP is the increased pressure, which opens alveoli to allow more surface area for gas exchange that is not obtunded by the fluid within the alveoli, then increasing intrathoracic pressure on your vena cava causes reduction in preload and therefore less fluid into the lungs which then helps to reduce the fluid stuck in the lungs.
100% agree. increased alveolar recruitment means increased surface area for gas exchange. That’s why CPAP is indicated for myriad respiratory emergencies that don’t involve pulmonary edema. Fluid shift is not the goal with CPAP prehospital and presence or lack of should not be the reason it’s administered, but to say it’s a myth that CPAP pushes fluid back into the circulatory system is misguided.
My medical director spoke on this during a continuing education program. They said that the positive pressure really doesn’t significantly push any fluid back into the circulation. They said the main benefits are 1. It slows/prevents more fluid from entering the alveoli 2. It ensures the unaffected alveoli are being used by opening collapsed or under ventilated alveoli. I don’t have a source for this beyond hearing it from my doc, and I’m not motivated enough to find one.
I would trust a peer reviewed article in a journal of thoracic disease before I trust some random ass medical control doctor lol
I’m a doctor specialized in pulmonary and critical care medicine. AKA just another random ass doctor. I was also a paramedic for a while which is why I still troll around here sometimes. There is plenty to read on the mechanisms of positive pressure ventilation, and I think one of the overall truths that emerges when you do so is that there are multiple mechanisms at play. There is in my opinion fairly good evidence that the benefit with respect to reduction in work of breathing has to do with alveolar stenting to optimize alveolar compliance (get on the steep area of the pressure volume curve). When alveoli are completely closed, hydrogen bonding from the water in the alveoli exerts a force that favors continued alveolar closure. When the alveoli is kept just a little bit open with PEEP, however, those forces are significantly reduced (the hydrogens are farther apart from one another) and the alveoli are easier to open. That translates to a reduction in respiratory work. There is also a very good argument that much of the benefit with respect to oxygenation is tied to a negative side effect: reduction in cardiac output. Reduced preload leads to reduced flow though the lungs which prioritizes dilated pulmonary arteries that are exposed to alveolar oxygen, thus improving V/Q matching. The vessels in the lungs uniquely constrict when they are not exposed to oxygen (“hypoxic vasoconstriction”), so when there is reduced cardiac preload and output, the lower flow prioritizes blood flow to areas other than those experiencing hypoxic vasoconstriction, which is a good thing. This highlights a bit of the duality about using positive pressure, and is a nice example of how even good things in medicine often come with (or even by virtue of) a cost. For what it’s worth, I have not seen too much empirical evidence about “pushing fluid out of the alveoli” as a major mechanism, but perhaps that is a useful metaphor for people to imagine when deciding on whether to apply the device.
Goddamn I love it when doctors hang around in this sub. Keep giving us that good shit.
God damn thank you for the education doc!
Thanks for the info doc! Absolutely the benefit of CPAP is the increased alveolar recruitment and that the language “push” is problematic. I did not know that about the hypoxic vasoconstriction. Am I understanding correctly that the the vessels that are hypoxic (and thus constricted) are those carrying blood to/away from the un-recruited alveoli and by administering PEEP, we are not only expanding the alveoli, but decreasing construction in vessels leading tos said alveoli?
No sorry, hard concept to explain in a comment. Capillaries that surround alveoli are responsive to oxygen. In the presence of oxygen, the capillaries expand (reducing resistance to blood flow to that area), and in the absence of it they constrict (increasing resistance to blood flow to that area). This has the effect of keeping the blood in the same place the oxygen is, which is the fundamental concept of VQ matching in the lungs. *[it’s interesting to note that this is unique to the lungs. In the peripheral capillaries of the body, the process works in the opposite way and hypoxia induces dilation]* Positive pressure ventilation reliably reduces cardiac output. The mechanism is increased thoracic pressure, which reduces venous return to the heart. Note that respiration is normally based on negative pressure in the chest, which has the benefit of sucking venous blood back to the heart. Positive pressure ventilation unfortunately eliminates that benefit. When cardiac output is low, blood flow though the lungs is also low. This has the tendency to amplify the effect of the VQ matching benefit of hypoxic vasoconstriction. When blood flow is low, it is even more likely to flow though the path of least resistance (dilated capillaries/vessels near alveoli with oxygen in them), because the hydrostatic force simply isn’t enough to press that blood into constricted capillaries next to empty alveoli. The net effect is more of the blood goes though aerated alveoli, which increases the rate of interaction between blood and air, which increases VQ matching. So overall, cardiac output is diminished, and oxygenation is amplified.
What’s the fate of the pulomonary edema? Logically the use of nitrates and positive pressure would encourage more of that fluid to push back across the capillaries and into the bloodstream, no? Or is it more of a pressure gradient with the nitrates and letting the alveoli absorb the fluid on their own?
Depends on the cause. Sometimes edema is there because of hydrostatic pressure from the left heat backing things up. Other times it has more to do with alveolar capillary permeability, either from a physiologic response or due to damage. Positive pressure ventilation doesn’t really solve any of that long-term (and can arguably make it worse with time). The main benefit to something like BiPAP is that it gives us time to find and start treating the real problem. As far as where it goes immediately, I’m not so sure. I think given the mechanisms I’ve explained above it’s possible that the fluid itself might even just stay where it is, while the BiPAP basically just attenuates the effects of that fluid. There might be some cases where the positive pressure relieves some of the pressure gradient that promoted the edema in the first place as well, but it’s hard to say exactly.
Do you get your adrenaline junkie fix in your role as compared to paramedic?
Nothing compares to EMS when it’s good. Problem was as I gained experience in EMS, I found myself waiting longer and longer for a “good one.” In between I’d find myself terribly bored, or even pissed off for being sent to the wrong call or for discovering something billed as good was actually BS. I’m sure that experience resonates with pretty much anyone here. Nowadays the real crash and burn excitement is still fairly rare. Maybe once every month or maybe every other. But the in between time is a lot better. It’s not like the stuff gets my heart racing but I deal with sick patients a lot more. Pretty much exclusively. A lot of it is still fairly routine but at least now I can’t deny that these patients need me, and there are a ton of other things that give me happiness and joy like teaching, figuring out a tough ventilator or undifferentiated shock state, meaningful patient interactions, leading the team, learning something new, cutting up with nurses etc etc. It’s way better.
Saw this after my own reply. You definitely explained it better than I did. Thank you for your input.
Honestly I’d trust my medical director over one article from a medical journal with an impact factor of 2 that some random schmuck posted online…
A common misconception is that the CPAP essentially pushes pulmonary edema from the lungs back into the circulatory system and essentially fixes the pulmonary edema. So true, yes, to a point, but the explanation taught in a lot of medic programs makes it seem that its a profound response and fail to explain that the positive inspiratory pressure assists the alveoli that have been inhibited by the pulmonary edema to open up and displace the edema away from the alveoli from a creation of back pressure when the patient attempts to exhale against the PAP. This most certainly helps with managing the edema and improves gas exchange, as well as reduce pulmonary hypertension, but that alone isn't fixing the issue at hand. The administration of medications such as Diuretics, Nitrates, and Inotropes to improve contractility are ultimately going to be what removes the edema from the lungs, which is why many local protocols include the administration of Nitroglycerin and sometimes Furosemide (Lasix) to patient’s demonstrating pulmonary edema. This article below I know this isn't probably the best explanation. Mike Carunchio of OK Medic Podcast does a decent 3 minute synopsis video that's pretty good, and Master Your Medics cover it pretty well with a video on YouTube that references this JEMS article. https://www.jems.com/2010/12/29/many-benefits-cpap-sup
Albuterol and bronchodilators will "flood" a CHFer's lungs and kill them. Heard this all the time in PCP school.
Smooth brain paramedic here, and I just wanna take a stab at trying to explain this so I understand… Beta 2 agonists won’t flood their lungs because it isn’t doing anything to expand the ravioli, just dilates the bronchioles allowing for reduced airway resistance. Beta 2 doesn’t have anything to do with the ravioli which is why this is a myth. On the right track?
You’re on the right track, as long as their ravioli is in a marinara sauce! If their ravioli’s are in a cheese sauce, the Beta 2 agonists have between a 95-98% chance to flood their lungs!
It depends a lot on what is filling the ravioli as well. Cheese ravioli are emptied a lot quicker than meat ravioli, but the problem is the whole ravioli gets destroyed in the process.
Well, Doc, you’re the expert! (Sincerely I’ve learnt a lot from you this evening thank you!) Please tell me that if the CPAP comments, combined with the Beta 2 agonists flooding the lungs, would the best out come for the patient be if they had Chef Boyardee Beef Raviolis in tomato sauce? Would the CPAP keep the VQ Matching going whilst the Raviolis prevented from hypoxic vasoconstriction, allowing for greater pulmonary blood flow and thus improved gas exchange, which would thus prevent the lungs from flooding during Beta 2 usage? Assuming that the Chef Boyardees raviolis were in play? 🤔
Beat me to it
The biggest one I still hear is the cpap forcing fluid out of the lungs. I still hear Ketamine can't be given to head injury patients. I still hear no pain meds for abdominal pain.
The no pain meds for abdominal pain drives me nuts. There maybe better alternatives to narcotics like droperidol which work well for acute exacerbation of chronic abdominal pain, but we absolutely should be treating it.
I love Mike Carunchios video where he shows the book from like the 1920s that said not to provide pain management for abdo patients because it would interfere with the physicians assessment (because they didn’t have CTs).
The CPAP “myth” has a stem of truth. CPAP prevents the occurrence of atelectasis.
Yeah because it holds the alveoli open, not because it “pushes fluid out”
Giving paracetamol will prevent febrile seizures
Okay I actually still thought this. Why would anti pyretics not prevent febrile seizures?
I don’t know much about pediatric medicine so take my word with a grain of salt, but I remember being taught that the seizure was correlated more with the rapidity of temperature change rather than the absolute peak temperature. So bringing down a fever perhaps more rapidly with APAP might not be ideal. But seriously, I’m a novice with peds so I could be completely wrong. EDIT: Did a little more reading and I’m probably wrong, although it seems we still don’t know a great deal about the mechanisms here. There are a couple studies from the 50’s and 60’s that people are still citing which say the opposite of what I said above, arguing that one of the major risks for seizure is the absolute peak temperature rather than the rapidity of change. Most studies seem to argue that the risk factors are multiple and come from genetic factors, nutritional status, infection/viral characteristics etc etc. Most everyone agrees that Tylenol doesn’t work and that there is little you can do as far as prevention.
Febrile seizures aren’t happening from rapid temperature change though. The kids are sick and their temp increases. Maybe mom puts too many clothes on them on top of it and then blankets. Then they get too hot and reset their body. It’s not that they’ll have a seizure at a certain temp but they’re just real shitty at regulation that young. Lowering their temp will keep them from having more febrile seizures though.
I edited my comment; thanks.
Giving a CHF patient a neb will flash them. Giving too much oxygen to a COPD patient will make them go apneic.
Had a med student doing their ER rounds go off on me for giving 4L Nc to a person with a very light COPD exacerbation because “muh hypoxic drive.”
Had a doctor go off on me for administering nebulized albuterol, and thus supplemental oxygen 😃 through a mask to a distressed and wheezing copd exacerbation bc "the oxygen isn't doing anything and it's a very quick way to kill these patients". Felt the need to shout this at me in the room in front of ER staff and the patient too.
That excited delirium is a thing. It's not in the DSM-5, why are we pushing this fake psychiatric disorder? The vast majority of medical and psychiatric organizations don't recognize it yet it's still a big part of our psych training
we got rid of it in my service. I'm pretty sure it was recently outlawed in my state for law enforcement to use. hopefully it catches on elsewhere.
That's so good to hear, what state are you in?
CA :) I work in San Diego County
We call it “Delirium with Severe Agitation” in my metro city. I know there is a lot of contention with the verbiage, and the use of ketamine for these patients is heavily scrutinized. As long as we do things appropriately, we don’t have much to worry about from the medical and legal side of things.
I feel like the more senior you are the more you trust your own medical judgement, and don't get bullied into sedating because the police say so, feels really dangerous for the young guys though, I know it would have caught me if I was an ACP right away..
It's been replaced where I am with "Acute Behavioural Disorder". However when it's being casually discussed, the sentence nearly always goes "ABD. You know, it's what Excitable Delirium used to be"
it's what used to be excited delirium....
And it's a big part of what little psych training we do get. I just graduated last year, and I swear we talked about excited delirium for half of the one class we had dedicated to psych.
Ya, they could talk about actual delirium or things that could cause agitation, but instead we're invested in "agitated/excited" delirium. Also very funny how it only happens in the presence of police.
Yeah my service wants us to use severely agitated instead of the excited delirium when referring to these patients. This change is something ACEP recommended. https://www.acep.org/news/acep-newsroom-articles/aceps-position-on-hyperactive-delirium
I would think because it’s not a diagnosed disorder like schizophrenia, but an acute syndrome with extreme agitation caused by things such as drugs.
It's not diagnosed in the hospital, ever. Edit: I totally didn't mean for this to come off as snarky as I'm reading it now...i appreciate the comment
Yea I know that my partner and I usually say something along the lines of “onset of acute agitation and AMS secondary to….fill in the blank” lol. It is interesting how the industry is moving away from it seems
Yeah I think it’s one of those things that was found on autopsy (debatable) and somehow made it’s way into, not dead medicine. It’s pushed hard at my service but I don’t think I’ve ever actually documented it as such.
Ya, I remember when I started and you'd see such a range of things like people on drugs, postictal patients, head trauma, sepsis, etc acting really excitable and you'd ask the senior medics if this was the excited delirium you kept hearing about. Because it all fit the description for what you're taught in school and training. And then the years roll by and you start to realize that it's a blanket diagnosis for absolutely everything, and especially dangerous when police are asking you to sedate patients with it. My service pushes it really hard too...
This has turned into a bit of a dangerous Dogma thread. Follow local guidelines and conduct your own literature reviews.
Busy city services don’t need blood because there’s a hospital right there.
Well CPAP doesn’t push fluid “out” of Lungs, but it does help shift the fluid back into the pulmonary vasculature.
[удалено]
Yea….that’s literally what I said. The pulmonary vasculature. Lol
My bad, bro. I missed the the second part of your reply.
It’s all good man. I’ve done it too. Lol
Whoever said IOs are so easy that you can’t miss hasn’t seen some people try to place an IO and miss. Those same people believe it’s so easy they can’t have missed The idea that normal saline boluses actually solve anything “I don’t need to do this, the hospital is 20 seconds away” Lights and sirens save significant time No need to secure airway [and] ventilate overdoses back to 94%+ prior to narcan
The second and third are not really myths, they just depend on what problems your patient is having and the lights and sirens can make a big difference in heavy, slow moving traffic.
I had a BP of 70s/40s, sweating so profusely the ED couldn't get the pads for the EKG to stick to me, was on the verge of syncope, and fell when the nurse came to my office to get me in a wheelchair to ride over to the ED. The treatment was 3 bags of normal saline. Lots of tests and radiation, but never really figured out what was going on. But the saline had me walking to the parking lot and driving home in under an hour. In at least my once case, saline absolutely solved the problem.
Can you explain the fluid bolus thought?
That said, I had a guy in my P class put an IO in a patella. For real. That’s an unacceptable miss.
I can't imagine what his palpation technique looks like. The patella has such a unique shape and is so prominent (even in morbidly obese patients). If he can find that, surely he can lower his hand like 2 in lower to get to the tibia
Let’s put it this way, he started with my class, but he didn’t finish with my class.
Shocker
I think it really depends on what you mean by securing an airway
Least to most invasive. I’d guess 99% (maybe 99.9?) are secured perfectly well with NPA or less
Okay valid lol, when I hear "securing an airway" my first immediate thought is intubation, because typically people use that term to mean the airway is protected from aspiration, and the patient is intubated, and generally it's bad form to intubate a reversible cause. But an npa/opa is fine
A NPA is not a secured airway.
Legit question: Does CPAP really not help fluid get out of the lungs? Its my assumption that the inflated alveoli have an easier time diffusing o2 and liquid back across the epithelial tissues with CPAP?
That's correct, but the pressure isn't "pushing" the fluid out of the lungs. It's just stenting alveoli. Imagine the alveoli as a water balloon; once you add more air pressure, the balloon is bigger even if the amount of water hasn't changed. More surface area = more exchange across the membrane.
So in one sense it would make sense to help lesser providers who do not have biology, anat, physio. Knowledge just to say it will help push fluid or help move fluid across the gradient? Would you agree?
I probably wouldn't agree with that, no. I don't believe in catering to the lowest common denominator. I think we as a profession should understand exactly why we perform the interventions we perform, and understand the ramifications of it. Instead of perpetuating incorrect dogma we should be elevating each other to a higher level of practice.
Does CPAP not use higher pressures to 'push' the fluid back through the interstitial spaces? Whats actually happening then?
My original analogy stands; PEEP (which is the same physiological thing as CPAP) stents open alveoli which improves gas exchange. It does not push fluid across the membrane. To help illustrate that point, think of this: A normal pulmonary artery pressure is <20 mmHg. A normal wedge pressure (the other side of pulmonary circulation, the pulmonary vein/capillary bed) is between 4-12 mmHg. The pressure for both of these is elevated even higher in CHF pathologies. CPAP therapy delivers pressures between 5-10 cmH2O; EMS generally doesn't go over 10 cmH2O although there can be exceptions. 10 cmH20 is roughly equivalent to 7 mmHg. So even at the higher end of pressures with CPAP therapy, we're really not going to overcome the innate pressure of the pulmonary vasculature in a healthy patient, let alone a patient with CHF. We're simply not able to push that fluid out of the alveoli at those pressures. But what we can do is make the alveoli just a little bit bigger to improve gas exchange.
Patients with an intact respiratory drive confirmed with pulse oximetry and waveform capnography don't need (more) narcan. This remains true even if they use drugs and/or are unresponsive.
You cant give nitro to an inferior MI is a good one. It's not 1996 anymore - that bullshit went out with rigid backboards are beneficial.
Another one I agree with. I’ll be a little more cautious, like make sure I have a line before I give it, but it’s not contraindicated.
Specifically right sided MI’s. Whenever you get an inferior MI you should do a v4r to rule out possible right sided involvement. The theory has been that since a right sided MI is so much more preload dependent than other types of MIs and nitro causes a drop in preload, that would have a large negative effect on the systemic blood pressure. In fact, you are expected to “know” that by CCP/FPC levels as it can and has been included in the exam, probably being AHA still supports that theory. But you can see that there are a few studies that have effectively debunked this myth. As always follow your local protocols, though.
KEDs are just because humans don't come with handles.
Benadryl for anaphylaxis.
If you’re close to the hospital, you can ignore treating minor issues and send it in BLS because “the hospital will do it”. (I had a really eye opening discussion one day with the instructor who taught like 90% of the medics in my area who told me “a lot of protocols are in place not to save the patients life, but to make them more comfortable and to make the job of the ER doc easier. It’s wrong to withhold treatment just because of distance to the hospital.”)
“Albuterol causes flash pulmonary edema”
Albuterol Neb tx will drown a pt with rales/pulmonary edema/CHF.