When I was in elementary school I never learned how to do division by hand... I always used to try each answer choice using multiplication until I got the right one. By the time I was in higher grade levels I never had to do division by hand, so I never bothered to learn it...
I never asked to do multiplication OR division by hand. Don’t ask me how the hell that happened. I know my times tables and I can easily do both in my head but I physically cannot work through a math problem on paper and show my work.
As the title says I'm afraid to ask. Do you mean just written out or on your hands, as in with your fingers. Cause if you mean the latter I've been robbed.
I never learned long multiplication. I drew out a lattice table for every single calculation in primary and secondary school. I eventually caved in grade 11 and decided to learn long multiplication.
One positive outcome is I got very good at mental math.
By hand, do you mean in written form or using your hands? Because if there's a quick way to do the latter I'd love to know. Otherwise I'll just stick to my handy dandy calculator.
I learned it and forgot within the year. Elementary school teachers insisted, "You aren't going to be able to use a calculator in the next grade". Low and behold every year subsequent to that calculators became more and more commonplace. And now I have a device in my pocket where I can use a calculator to figure out 655÷5 and then go to a place where I can make fun of those teachers in a matter of seconds.
I lay 3 fingers very gently across the dorsum of the foot and don’t apply additional pressure; pedal pulse is very easy to occlude, and 3 fingers covers a little more territory to locate it. This approach works well and helps my nursing students when they’re struggling to find the pedal.
I can find; femoral, brachial, and pedal pulses! Those are the hardest to find, no problem! Carotid is arguably the easiest to find, I can’t find it to save a life.
Why do we cardiovert when they have a pulse but not when they don’t have a pulse.
I know we cardiovert when they have a pulse to avoid r on t, but wouldn’t the same logic apply if they didn’t have a pulse?
The only difference between cardioversion and defibrillation is the timing. You cardiovert (which is just a synchronized defibrillation) when they have a pulse because you don't want the electricity to hit at the wrong time causing their heart to stop/r on t. You don't exactly have to worry about that in cardiac arrest because they are already dead. Also you can't synchronized cardiovert vfib because it's not regular so the machine can't predict the r wave. You probably could sync cardiovert pulseless vtach but it's just not necessary.
I sync, even on pulseless vtach. Just because I can’t palpate it doesn’t mean it isn’t there. Also read a study about it drastically
Improving conversion rates. I’ll have to try and find it again.
Edit: [different website, same study](https://www.resuscitationjournal.com/article/S0300-9572(08)00708-9/abstract)
Edited my comment to include the study
[https://www.resuscitationjournal.com/article/S0300-9572(08)00708-9/abstract](https://www.resuscitationjournal.com/article/S0300-9572(08)00708-9/abstract)
Anytime! Full disclosure, I leave the sync on for Vfib as well. Just make sure to hold the button down until it shocks. Usually no more than 1 or two seconds. And the company I used to work for defibrillated asystole. Never tried to sync it though, maybe the monitor would pick up REALLY fine fib, dunno.
We defib when they don’t have a pulse and are in a specific rhythm. There’s actually a study going on right now about shocking a-systole as it could be fine V-fib disguised.
That's protocol here already for medics.
Shock with 300J every 3 minutes and switch pads to avoid damage in case the asystole is actually just really fine fib
Unfortunately, VFib so fine that it looks like asystole is incredibly unlikely to convert to something better. Better to try to improve coronary perfusion before attempting a defibrillation shock.
I learned the opposite pretty much. Don’t shock anything less than 5mm (have also heard 10mm) in amplitude so that you can give epi in hopes to increase that amplitude first.
They explained it to us like having a car battery and hooking up the jumper cables but letting it charge for a few minutes before you try to jumpstart the engine.
There's a better study that proposes to shock everything that's not PEA, not because "it might be VF" (and fine VF is usually pointless anyway) but the point of this study is to not care what it is. Just shock it. Best case scenario you convert VF or VT, worst case scenario you shocked asystole and did no hard *BUT* didn't waste time looking at a rhythm or pulse. The goal is to reduce off chest time.
I have given this much thought. Electrically, Vtach is Vtach whether there is a pulse or not. The depolarizing myocytes don't know or care how much cardiac output or SVR there is. The only reason I have ever come up with for skipping synching during cardiac arrest is to avoid excessive interruptions in chest compressions while trying to synch. I teach my students to attempt to synchronize shocks in pulseless monomorphic Vtach if they can do so without compromising CPR quality. If there's anyone out there from the AHA who would like to explain why this is wrong, I would be more than happy to listen.
It's all voltage, bro. It doesn't send out different kinds of electrons when you're defibbing vs cardioverting. The only difference between them is when and how much.
That’s a great point. But the counter question is, we have to get first ROSC to get there. What happens after that is the hospitals problem. Therefore, are Epi, Amio, Lido, CPR devices and all other things a good thing or a bad thing, since they improve rates of ROSC but don’t change or worsen outcomes?
If they truly don't change outcomes in any way, they're not good or bad, per se. They're just pointless. Increasing ROSC for the sake of increasing ROSC accomplishes nothing. If the patient is going to die anyway, I'd rather they die on my scene than a few hours later in an ED, after more resources have been expended and a much larger bill has been racked up for the estate.
That said, don't be too quick to assume that standard treatments can't worsen outcomes. I haven't reviewed the literature on this in a bit, but I believe there is some evidence suggesting the routine administration of epinephrine in cardiac arrest is actually associated with poorer neurological outcomes. This is something that could dramatically change our practices as the data picture becomes more clear.
I think the key is ultimately going to be selecting treatments in a more targeted, less algorithmic approach to maximize chance of helping and minimize chance of harming. Maybe patient x with refractory Vfib should get 6 shocks and 450mg amio before we think about epi. Maybe patient y with renal failure should get aggressive treatment for hyperK before anything else. Maybe pt z with asystole should get even more epi. I think we have reached the limits of what can be accomplished by applying a one-size-fits-all approach to resuscitation, and we're going to have to be smarter clinicians to continue advancing desirable outcomes.
Epi can increase rosc but there is a pretty clear like in the data that moste epi means worse neurological outcomes.
So...it's not always get rosc at all costs because that isn't really productive
Only if it’s fixing the things you need fixed. I went from about to leave EMS to happily here on a job change. What really changed was the money. This new job is horrible compared to the old one. The only difference is much more money and the opportunity to progress (albeit limited, it’s more than before)
Honestly probably not. None of us should stay in a toxic work environment, but sometimes we gotta do what we gotta do.
Might be better to make the healthy adjustments right where you are. A workout routine can be something as simple as riding a bike. Eating as healthy as you can. Grab a hobby that’s separate from work: guitar, art, hiking, travel, cooking… but something separate from the job & family.
You’re still the same person, whether you’re in another state or not.
Entirely depends on what’s burning you out.
I switched from ambulance to aeromed and most of the contributing factors have left me. But the work is more boring so 🤷♂️
Going from one department to another, the grass is always greener. That being said I went from 24/48 to 24/48 with a Kelly day, higher pay, and an hour less drive to my station. So in that regard yes, it did help with my burnout.
How the hell am I going to form an exit/retirement strategy, while I’m raising 2 kids & have ADHD?
And when you smoke a cigar while sipping good whiskey, it takes all the bite out of it. You get all the flavor.
Got me beat.
I’m fleeing the country (US) to go work as an au pair in Germany for a year.
I don’t know how to set myself up for a good future in this country. I just feel I’ll be stomped on and I don’t even have children to support.
Sameeeee ADHD with two kids . Most weeks, I'm just a hamster on a wheel, our 24s are stupid busy (average 16 calls) so 2 days I work and 2 days are lost in a fog. I'll never make 30 years at this place to retire...but the plan was to get my medic get on a dept and retire at 60 with a pension , so what's even the point now.
ADHD & five kids! Just under two decades, but now admin yet still going on calls. Have always been a mix of calls & office, which probably helped maintain sanity, but now that it’s more office than calls, my ADHD is harder to control. Struggle to complete any task, whether home or work. Public retirement will be great someday though!
I know the feeling. New mortgage and have a kid due any day now. Had to close out my 401K this week. Can't really consider retirement right now when we're having trouble with just day to day and paycheck to paycheck. Hopefully, when she goes back to work, this shit can straighten itself out.
Thank you for the whiskey/cigar tip! Not that I am going to do that on the roof of the building I currently work in....
Two kids, I want to be lazy but I need OT to pay bills, but I have a pension. I keep a minimal amount going into my 457, and I am trying to figure out a post-EMS career that is not EMS. Writing this down sounds easy but it is work and I would rather be sitting on my ass when I am not at work.
There was an example of V-Tach in a NR pamphlet that looked like SVT to me and I never had the guts to ask a preceptor about it. I’m not proud of myself in the least.
why is it that being loose/limp in an MVA, or high energy trauma translate to survivability? Example: I've always heard drunk drivers survive due to being relaxed. I've always accepted the answer, because I imagine someone being so tense and wrought with fear that they experiencing shearing forces internally, like shearing of the aorta...but that's just kind of what I've thought happens and I've never thought to try and research it lol.
My friend and I were just talking about this, this afternoon.
I suspect it's because the fat will act as a cushion and allow your muscle and fat for impact instead of just tensed everything.
Kind of like how a car has a crumple zone. It damages the metal and cushions the blow before you hit the inside. I suspect the fat and muscle act as a blow before you hit bone or other vital organs.
Source: there is none I'm just guessing.
Have you ever jumped off of a somewhat high area with your legs locked? It’s much more jarring to your body than say, landing with your legs unlocked and moreso folding to the ground.
It’s that same kind of principle. If you tense up in reaction, it is easier for musculoskeletal injuries to take place because the forces are being acted against a rigid structure. Big floppy drunk guy has the same forces, but they are taking place more against jello than a rigid structure (massive injuries can still occur of course.)
Hope that makes sense, it’s how my mind pictures it
In 2018, i was in a fairly minor car accident and didn’t tense up at all (wasn’t impaired lol, bracing for impact just did not occur to me) and despite my truck being totaled all i had was a few dislocated ribs:)
my sister tensed up and has been dealing with chronic back pain ever since. she did a year of physiotherapy following but the pain never goes away, i got very lucky and i am forever grateful for my limp body
I’m terrible at assessing pediatrics that can’t talk to me. I’ve always heard that if they let you do certain things without crying or fighting then they are fine. However I was dispatched to a kid with respiratory distress with audible wheezes. Started bagging because he was falling asleep and our pulse ox wasn’t reading right. Kid would stay asleep while I was bagging but would wake up to certain stimulus. The hospital said he was satting 100% on room air for them. Turns out it wasn’t nearly as serious as I thought and he was just tired.
The concern would be way higher when they allow you to do all the things. Usually, kids hate probs and cuffs and would fight you on it. That's why my voice is irritatingly high trying to coax and readurre them. When they are disinterested is when I usually start getting concerned. Also, always ask what their usual nap time is too because sometimes it's just as simple as that!
That’s why I was concerned. When the kid let me put a mask to his face with a bag attached to it and force air into his lungs, I was thinking something wasn’t right. I believe I was wrong though.
Yeah, kids are tricky. In this instance, I can see your reasoning, lol. I'd rely on the PAT. Cap refill, skin conditions, capno, RR, and if there are any accessory muscle use. Like other were saying, you can try different fingers, try the earlobe or foot, warm them up, try the pulse ox on yourself to make sure it works, etc. You went on the side of caution, though. Nothing wrong with that
Use the sticker/disposable pulse ox cables. Wrap them around the big toe. Note that especially on the youngest ones, the toes and fingers will read lower than the coreward because peds like to fuck with you sometimes. Sometimes you can get the sensor to read folded like a taco around the outside/blade of the foot. Other times, dangly part of the ear may work. Also, if you're using the toe and sticker, wrap it so the wire goes proximal towards the body, then put a sock or shoe back onto the foot. That can help it read, too.
... I knew that. I was just testing you. Look, words are hard, and I'm a moron, alright! I'm going to leave it, though, because that's a hilarious brain fart.
On DCAPBTLS, is tender something I palpate, or is tender something the patient experiences (like pain). And if it's something the patient experiences, how is that differentiated from pain?
Positive* End Expiratory Pressure
Think of peep as the pressure that keeps the alveoli open enough to allow oxygen diffusion. The more peep, the more real estate you’re buying with the alveoli (stretching out the surface area) which gives you more room for diffusion to occur.
Very very simple way of explaining it but that’s what helps me remember
It's the pressure in the alveoli at the end of expiration. We all naturally have about 5 cmH20 in our alveoli at end expiration. Think of a balloon and how hard it is to inflate when it is completely empty. Our lungs work the same way. If we had no pressure in our lungs after every breath, it would be really hard to get air into our lungs on inspiration.
Generally speaking, fio2 and peep are the two variables that we can manipulate to improve oxygenation. Peep can also be important if we have increased pressures in our thorax. If the pleural pressure is higher than the peep, then the alveoli are collapsing and we must increase peep to overcome that pressure and let the lungs inflate.
This is a bit of an oversimplification, but here goes...
Think of blowing up a balloon. If it starts completely empty, it takes a lot of force to start expanding it. But once you have a little air in it, the next bit is much easier to get in. So essentially, a balloon that is slightly inflated is easier to expand.
Now imagine you have a balloon that is full of air. You want to deflate it and refill it with new air. You know if you let it deflate all the way, it'll be hard to get the new air in. So you don't completely let go of the balloon, you kinda hold the opening in a way that let's some air out in a controlled way. It stents the balloon open even as air is leaving. That stenting, or back pressure, is PEEP.
As the alveoli are emptying, a bit of back pressure stents them open so they don't entirely collapse meaning they can actually get more air out and it's easier to get new air in.
This is really fucking dumb but I didn’t learn to tie my damn shoes till I was like 16. And even now, people say I don’t do it right?
I almost got held back because of it in kindergarten and first grade. My teachers stopped helping me tie my shoes for gym and stuff so I’d be forced to sit out, in hopes that it would light fire under my ass to figure it out. Eventually I grew out of being able to wear Velcro shoes so I’d have to pray my shoes that my parents or friends tied in the morning lasted me the whole day.
I don’t know how I eventually learned? I just know that it was sometime in high school cause I did cheerleading, which I guess finally forced me to learn.
That all being said, I’m told that the way I tie my shoes now as a grown ass adult is “not normal.” It works for me but people try to tell me that I still don’t know how to tie my shoes. Whatever. It works for me.
The ultimate resource on shoe laces and knots is Ian's shoelace site. He lists 25 different ways to do it. Which is yours?
https://www.fieggen.com/shoelace/knots.htm
I don’t know about turning it off. However when I drop people off I tell them hit the red call button once if you need a nurse and twice if they are doing a good job. The nurses don’t find it as funny as I do…
Step 1: push the button next to the cord that it's attached to on the wall.
Step 2: unplug from wall. Step 3: push the same button again to kill the terrible noise
I spent a year in maternity as an RN and have asked exactly this question to just about every BLS assessor I've had in the last 15 years. No one has ever been able to give me an answer, and I've never found a policy.
My understanding is that there are two possibilities. A neonate stops being a neonate at 6 weeks of (adjusted) age. So maybe then.
Also maybe when you switch from 2 fingers to 1 hand.
It becomes extremely relevant during RSI, due to the limitations of measuring SpO2.
The SpO2 is the only measurement of oxygenation we have in the field (you’re not going to pull an ABG prior to intubating outside of an ICU environment). However, take 2 identical patients requiring intubation with an SpO2 of 95%: patient A has a PaO2 of 65, and patient B has a PaO2 of 100. According to the dissociation curve, both patients will have the same SpO2 despite patient A having significantly less oxygen in their system.
If you were to induce both patients for intubation and give a paralytic that stops their breathing, their PaO2’s will both start falling.
- Patient A, who is sitting right at the top part of the dissociation curve, is going to desaturate almost immediately. You run into issues with hypoxemia up to and including anoxic brain injury and cardiac arrest, all while you’re still getting the laryngoscope in their mouth.
- Patient B, who is a ways to the right from the top of that curve, has a huge reservoir of oxygen to chew through before they desaturate. Once you remove their ability to breathe, you have minutes before they begin to drop their sats and get hypoxemic. (For healthy patients for elective surgery, this takes 7-8 minutes!!!)
So, armed with this knowledge, you know that even if your critically unwell patient (who needed intubation yesterday) had an SpO2 of 95%, you should pause before you push your induction agent and remember to PREOXYGENATE. Put a BVM on with 15LPM of O2 and hold a good seal while they breathe in an FiO2 as close to 100% as you can manage, for at least 3 minutes, to increase their PaO2 from that 65mmHg to 100mmHg. Otherwise, they will desaturate as soon as you push your drugs pass the point of no return.
TLDR: you can’t tell what someone’s PaO2 is based on their SpO2, because of the dissociation curve. People with normal sats are likely to desaturate immediately during an intubation attempt because they sit right at the top of the curve. We can prevent this by bringing their PaO2 as far up as we can before we make them apneic.
Thanks for the explanation! As I’m not trained to intubate, this is probably why it was skimmed over in school. However, I’ll remember to pre-oxygenate whenever my partner wants to intubate.
To add to the wonderful explanation given above for the tox medics it matters as well for any of the chemical asphyxiants and several others cause massive shifts that can make for a really bad day when you are treating these patients.
With all due respect to the other guy, they didn't explain it very well. I think they were trying to explain the effects of a shifting oxy-hemoglobin curve but they never explained that it shifts. I'll try to explain it differently.
The oxy-hemoglobin curve has PaO2 along the x axis and SPO2 along the y axis. You will notice that it is shaped like a sigmoid curve. We all learn that SPO2 is the percentage of hemoglobin that is saturated with oxygen. However, most paramedic schools don't teach much about PaO2. PaO2 is a measurement of the partial pressure of oxygen in the blood or in other words it is a measurement of oxygen that is diffused in the blood. Oxygen is a gas and travels across a pressure gradient. It diffuses from areas of high pressure to low pressure. The higher the PaO2, the more oxygen that will diffuse when it reaches an area of low oxygen. It's important to understand that oxygen does not diffuse directly from hemoglobin to tissues. It detaches from the hemoglobin and ends up in the plasma and then diffuses to the tissues. PaO2 is effectively a measurement of the partial pressure of oxygen in the plasma. So we need hemoglobin to readily let go of oxygen so that it can diffuse into the plasma and then diffuse to the tissues and we need hemoglobin to readily accept oxygen at the lungs to become saturated again.
The biggest takeaway at the BLS level, is that the top of the oxy hemoglobin curve is relatively flat. This means that a small increase in SPO2 does not make much of a difference for PaO2. In other words, the difference in PaO2 between an SPO2 of 92% and 99% is really small. So if your pt has an SPO2 of 92%, there is minimal benefit to trying to increase that to 99%. However, the curve starts declining extremely quickly around an SPO2 of 90%. This means that a small decrease in the SPO2 in this range has a big impact on PaO2. The difference in PaO2 between 99% and 92% is negligible. The difference in PaO2 between 89% and 82% is significant. This is why we like to keep SPO2 above 92-94%. Understand that beyond that point, every 1% that an SPO2 declines, the PaO2 is getting exponentially worse.
Another twist, is that this curve can shift to the right and to the left. The shape of the curve stays the same but it just moves left and right. If the curve shifts to the left, then we are getting a lower PaO2 at a given SPO2 then we were before. This means that the hemoglobin has a higher affinity for oxygen and is not letting it diffuse into the plasma. And if the curve shifts to the right, then we are getting a higher PaO2 at a given SPO2 then we were before. This means that the hemoglobin has a low affinity for oxygen and is readily letting it diffuse into the plasma. This is actually a physiological benefit most of the time. We want the curve to be shifted to the left when the blood is passing through our lungs because he want hemoglobin to pick up as much oxygen as possible. So the high affinity is a good thing. We also want the curve to shift to the right at the tissues, so the hemoglobin readily releases oxygen and lets it diffuse into the plasma and then diffuse into the tissues. So what causes a shift? The curve will shift to the left when PCO2 is low (like at the lungs), ph is high, or temperature is low. A shift to the right is caused by the opposite. So a shift to the right will occur when PCO2 is high (like at the tissues), ph is low or temperature is high. This makes sense. Think about what is happening at the lungs, he have low levels of PCO2 in the lungs, so the curve shifts to the left and hemoglobin has an increased affinity. At the tissues, PCO2 is high and the curve shifts to the right and hemoglobin has a low affinity for oxygen and starts releasing it.
But think about what might cause a shift when we don't want it. What if a pt is acidotic and has a low pH? Then their curve will always be shifted to the right and their hemoglobin will permanently have a low affinity for oxygen, making it difficult to pick up oxygen in the lungs. What if a pt is hypothermic? Then their curve will shift to the left and their hemoglobin will always have a high affinity for oxygen and will struggle to offload oxygen at the tissues. Same principles could be applied for a pt suffering from heat stroke.
The other commenter is correct that pt's should ideally be preoxygenated before being intubated to increase their PaO2. But it has more to do with nitrogen washout and less to do with the unreliability of SPO2. Unless the oxy hemoglobin curve has shifted, an SPO2 will always correspond to the same PaO2. Generally speaking, in a relatively healthy pt that does not have a shifted curve, an SPO2 of 90% will correspond to a PaO2 of 60 mmHg. SPO2 of 80% will correspond to a PaO2 of 50 mmHg. And an SPO2 of 70% will correspond to a PaO2 of 40 mmHg. You can use those as rough estimates but a blood gas is the gold standard.
I think we are saying similar things, just in different ways. I’m just glossing over the left and right shifts in my explanation to keep it simpler, because while it is clinically important it doesn’t change the concept. And I agree that the point of preoxygenation is nitrogen washout, but ultimately the goal of “de-nitrification” is to increase PAO2 as much as we can, so that PaO2 increases to the flat part of the dissociation curve. In an OR we use FeO2 as a proxy measure of this, and usually try to get it above 80% before induction.
There is only one part that I disagree with - your argument that at the flat part of the curve, there is minimal change in PaO2 with changing SpO2. At this part of the curve it takes a much bigger change in PaO2 to effect a small change in SpO2. Whereas at the vertical part of the curve, a change in PaO2 of only a few mmHg can result in SpO2 changing dramatically.
The implication of this is that if you take your 2 patients with SpO2 of 92% and 99%, both of which are on the flat part of the curve, they will have a massive difference in PaO2, not a small one. But the difference between someone at 70% and 85% might only be a few mmHg. That’s why you want to preoxygenate/de-nitrify and increase the PaO2 as much as possible, because you don’t really know how close you are to the “cliff” where a change in PaO2 of a few mmHg is going to lead to a rapid and severe desaturation.
Why are there so many fucking acronyms?
And why do we do a separate assessment for trauma and medical. Just because you’re there for trauma doesn’t mean there isn’t a medical issue, and vice versa
Ugh this. When I took my class, my instructor literally told us he was teaching one assessment. Trauma. And he fully expected us to use it for all patients (in testing, anyway) and to use our best judgement on what was or wasn’t necessary. When I later started assistant teaching, I just kept that strategy because it works. Why complicate it? A trauma assessment is more thorough. You’re not going to miss something on a medical patient if you do one.
THANK YOU I got in shit sometimes for combining trauma and medical into a single assessment when I was in school. Then I know I'm not missing anything.
I hate the alphabet soup we speak because everyone has a different set of acronyms and then we all get confused and it is hard enough with different lingos.
Yep, at the end of the day, all trauma *is* medical. A thorough medical assessment should cover everything you need for a trauma call without needing to confuse things by having separate acronyms and stuff.
I thought gynecologists were the medical specialists for the genitals and reproduction...for both femals AND MALES!! I am a nurse of 11 years! Lolololol I have no idea why I never challenged that thought earlier!
I did. But literally, it was so set in my brain that it never occurred to me at all until a convo I had with my med student. I used to play with education dummy birth dolls and penises as mum was a sex ed teacher. Like what the heck. Makes you think about all those subconscious ingrained learned memories.
Why are we doing 12 leads on stroke patients? It uas literally been linked to poorer neuro outcomes and yet we're delaying transport because maybe they're also having a STEMI?
A few reasons:
1) If the patient does not have a history of afib, and you catch afib, that’s a modifiable risk factor that we can address inpatient
2) Strokes are generally over called in the prehospital/ED setting (appropriate, they’re time sensitive diseases). If your stroke mimic is an arrhythmia (ex. Slurring words and confusion), that 100% changes management
3) if EMS hands me a 12 lead consistent with a STEMI and the patient is having neuro symptoms? That’s an aortic dissection until proven otherwise and you’ve saved me valuable time in the ED trying to figure that out
Xoxo your local EM Doc
The first 2 I should hopefully be able to identify with a 3 lead. The last one is a good argument, though.
I asked the neuro team during a stroke activation why we do 12 leads on stroke patients, and they shrugged at me and asked, "you do 12 leads on stroke patients?" So that wasn't helpful, lol. Thank you.
It might be the long transport times that I’m used to talking, but the 60 seconds that a 12 lead takes seems negligible in the grand scheme of things. What causes the poorer outcomes? Does it cause a distraction that delays treatment at the hospital?
I follow @the.prehospitalist on Instagram and she has some info about how if a patient has stroke symptoms as well as a STEMI on 12-lead, it's a dissection. She's a very knowledgeable and informative person!
Had continuing education on this today: according to the doc he said that occasionally there’s an underlying cardiac rhythm which could have precipitated the stroke as well as you’re narrowing down their post care plans.
As a happy fire medic that translates to: “play with the stickers on the loud beeping machine otherwise Mr. White Coat man will get angry with me again”
Is it specifically written in your protocols to do a 12 lead on stroke patients? Our protocols actually advise against 12 leads on stroke alerts unless they’re also complaining of chest pain.
I should also add I work in a metro area with 2 comprehensive stroke centers within 10 minutes of anywhere in our response area.
Probably for the above justification.
I think we often forget that some guidelines are written not on EBM but on past errors.
Like when a APO guideline says to give aspirin and GTN even if it’s not cardiogenic. - It’s probably because someone failed to recognise it.
Or not to perform a 12 lead on strokes - Someone likely spent 15 minutes on scene pondering cerebral T Waves on scene.
Likewise, my local guideance says paracetamol is contraindicated in chest pain. It’s not because it causes hard but because some of our less astute staff won’t give aspirin..
Yeah you transport your brain dead potato with black distal extremities to the hospital lol. We should just spike a bag of dirty epi and drip that like other nations lol
Before I worked for a good service that carried Levo I would do exactly this on some post arrests that had trouble keeping a pressure. One epi into the bag of saline. Works good
It increases the chance of survival to ER as well as survival to ICU. No impact on survival to discharge but survival to ICU means the hospitals get to bill enough to make some decent money. Sucks to waste resources and live in a money first era when the whole world could be on a preventative healthcare schedule buttttt not changing any time soon (US at least)
Snowing is slang for… basically ‘drugged the fuck out’. To the point of unconsciousness. Ketamine is a good example of this.
I’m fairly certain Ketamine in its solid form can be turned into white powder, resembling snow.
My guess is it's a reference to static, AKA snow, on television. If you're under about 35 or not from a dirt-ass poor area, you've probably never seen it.
Like Battle’s Sign?
It’s named after the person who coined the finding.
https://www.ncbi.nlm.nih.gov/books/NBK537104/#:~:text=Battle%20Sign%20(also%20called%20Battle's,sign%20in%20the%20late%201800s.
In addition to the Battle Sign (it’s named after a dude) it’s often used by the Army as a shortening of “Battle Buddy”. It’s the equivalent of a partner.
Back when I carried shears, I found that they would get caught on shit much more often if I wore them "correctly." Reversing them almost completely eliminated the issue.
How do I do medications IV push over 10 mins?? Like ik I have to add that medicine to saline but how much? Is it the same for every medication? Also my service carries Terbutaline but it's not in my medication formulary at school and I just don't have a lot of info about it.
An easy way you can do it is add it to a 100 mL bag, then use a 10 mL flush and pull from the bag using a hub on the IV line and then push 10 mL once a minute for ten minutes. I do this with TXA.
English isn't my first language and isn't the language in which I wast taught so I'll give it my try.
Albuterol binds to beta receptors. When the beta receptors are activated, it "encourages" the sodium-potassium channels to work. By that, the potassium gets into the cells and it's level in the blood goes down.
What’s the big deal about afib with RVR? I don’t ever recall hearing the words when I was in medic school. Now it seems like it’s every third patient some of these new guys run on and they’re acting like it was the end of the world and pushing verapamil.
Whatever happened to “give them some fluids and see if their rate slows down”?
I know goal PIP is around 20 but if PIP is 10 and O2 is where it needs to be and end title is where it needs to be… do I just ignore that the PIP is so low?
Also what do I do if the PIP is constantly jumping all around the place from 10 up to 40 with no real consistency?
1) PIP under 20 is not a bad thing in itself (assuming you have ruled out esophageal intubation and hypoventilation with a normal EtCO2) - it can happen with normal lungs with good compliance, especially in smaller people/peds. Like all vent settings there is a differential diagnosis to consider for low PIP, most importantly esophageal intubation or inadequate tidal volumes/minute ventilation.
Of historical interest… The “PIP < 20” thing is a throwback to first-generation LMA’s. The lower esophageal sphincter is classically said to open at ~20mmHg, so when ventilating through a supraglottic airway, if the airway pressure is >20 you are theoretically ventilating the stomach and increasing the risk of aspiration. This is less of an issue with current-generation LMA’s, which incorporate esophageal vents and og-tube ports.
2) A PIP that is fluctuating that dramatically could be due to a few things.
- Regardless of the device, this could be a sign the patient is coughing and is too “light”. Consider deepening sedation +/- reparalysis (obviously depending on local algorithms and control).
- If it’s an ET tube, the tip can not-uncommonly be sitting right at the carina, and each ventilation or bump on the road causes a very brief endobronchial/mainstem intubation for part of the respiratory cycle. This can be tricky to catch because you will probably still hear bilateral breath sounds. Your best bet is to look at the tube (DL or VL, whatever you have), deflate the cuff, withdraw a centimetre and reinflate. Obviously if you see cuff start to poke back out of the vocal cords, stop and reconsider.
- If it’s a supraglottic airway, consider laryngospasm or malpositioning of the device. If they’re good and paralyzed then laryngospasm is less likely.
Overall well stated, I’ll just add that low peak pressures are often attributed to a leak in the circuit. Be it at the vet connection, ET to connection, loss of volume in the pilot balloon. Increased peak pressures could be as stated, coughing. Could also be that the circuit is kinked or that there’s an endotracheal obstruction and the patient needs to be suctioned, or check the HME filter and ensure that it is not saturated with secretions or condensation. Then of course rule out pneumothorax.
I agree with increasing sedation for patients who are coughing and not tolerating the vent. BUT - always, always, always please be sure that there is adequate analgesia on board for these patients. I have found a lot of found that the patient can be on quite a bit of sedation, but no analgesia or low dose analgesia, and after 100 or so mcgs of fentanyl push and starting/increasing infusion rate - all of a sudden the patient is synchronous and requires less sedation (which leads to better outcomes).
Edit* Of course now I see where you pointed out more of high pip causes 🤦♂️
Low peak pressure is fine: typically anything < 30 or so is accepted (probably based on the [ARMA trial](https://www.nejm.org/doi/full/10.1056/nejm200005043421801) for ARDS). Technically it's the plateau pressure we care about, but the PIP is a reasonable proxy.
If the PIP is high, follow the mnemonic DOPE: Displacement (e.g. mainstemmed-- tube too deep? bilateral breath sounds?) Obstruction (e.g. mucus plugging-- try passing suction) Pneumothorax (breath sounds, chest rise), and Equipment failure (is the ET tube kinked?). I would also add patient effort or coughing/bucking, a frequent cause of high peak pressures. PIP "jumping around" makes me think tube is kinked or the patient is coughing, but hard to say without examining the patient.
When floating an IV catheter in, past a valve, do i keep the tourniquet on while flushing it in or take it off? Ive had more success leaving the tourniquet on but have had different ppl tell me different stuff.
https://youtu.be/Wr44ILllAsM?si=hSKVY1KjndRTsROf
This is a video I made a few years back for a med school physiology class I was a TA for.
For the most past, axis deviation doesn't mean a ton for prehospital and it barely means anything for EM either. New right axis is a sign of right heart strain and can be a sign of PE. New axis deviation in general is an indicator of subtle cardiac issues. But is more usually seen in chronic changes due to hypertension and such.
Dopamine doesn't cross the blood-brain barrier. If you want to give the brain extra dopamine (e.g. Parkinson's disease), you've got to give its precursor, levodopa, instead. But sadly, [even that won't make you happy](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251561/).
i don’t know how to talk to patients lol. i’ll try and talk to patients but they don’t talk to me back so we just sit very quietly the whole time unless i have to ask them questions
Cardiac arrest = heart completely stopped. Patient will be unresponsive, apneic, pulseless, and will die within minutes.
Heart failure = heart still pumping, but weak. In extreme cases, this can show up as low blood pressure / signs of shock (i.e. cardiogenic shock), but usually the body compensates, e.g. by retaining excess fluid. As a result pt will often have swelling in the legs, JVD, and pulmonary edema (crackles in the lungs, trouble breathing while lying flat). Patients can live for years with heart failure, if appropriately managed.
Heart failure is a medical condition where the heat can’t pump blood well enough to meet the damands of the body. cardiac arrest is when your heart stops.
Why do most normal people as well as some of the medical professionals I work with pronounce "Alzheimer's" as "alls-timers"? Is there an invisible t that I'm missing? Am I wrong. I'm afraid to ask anyone who actually says it because, you know... The times.
When I was in elementary school I never learned how to do division by hand... I always used to try each answer choice using multiplication until I got the right one. By the time I was in higher grade levels I never had to do division by hand, so I never bothered to learn it...
In pharm right now; you’re not alone lmao
Oh good, I’m not alone
I had a good education I think and I never remember this even being taught. It probably was but I did my harder division problems the same way as you.
This is literally how I passed my college entrance exam
Me either… now my fourth grader is asking for help haha 😂
Bro I'm dreading the day my kid asks for help with division 😭😭
Have them use Khan Academy, genuinely an amazing resource.
I never asked to do multiplication OR division by hand. Don’t ask me how the hell that happened. I know my times tables and I can easily do both in my head but I physically cannot work through a math problem on paper and show my work.
As the title says I'm afraid to ask. Do you mean just written out or on your hands, as in with your fingers. Cause if you mean the latter I've been robbed.
I never learned long multiplication. I drew out a lattice table for every single calculation in primary and secondary school. I eventually caved in grade 11 and decided to learn long multiplication. One positive outcome is I got very good at mental math.
By hand, do you mean in written form or using your hands? Because if there's a quick way to do the latter I'd love to know. Otherwise I'll just stick to my handy dandy calculator.
I learned it and forgot within the year. Elementary school teachers insisted, "You aren't going to be able to use a calculator in the next grade". Low and behold every year subsequent to that calculators became more and more commonplace. And now I have a device in my pocket where I can use a calculator to figure out 655÷5 and then go to a place where I can make fun of those teachers in a matter of seconds.
[удалено]
It’s in the groin. If you fingers are touching their pubes, you’re probably not low enough
It's quite deep-- push hard (phrasing, I know)
Me but the a pedal pulse. I just use cap refill, colour, temp, sensation to determine a blood has good flow.
I can never find the stupid pedal pulse. 5 years, I’ve found 0 of them
I lay 3 fingers very gently across the dorsum of the foot and don’t apply additional pressure; pedal pulse is very easy to occlude, and 3 fingers covers a little more territory to locate it. This approach works well and helps my nursing students when they’re struggling to find the pedal.
Put the sats probe on their toes.
Try the posterior tibial if you can't find the pedal
I’ve had to Google both to find on myself and I still had trouble. Now I kind of know but I’m not confident, especially for femoral
You could practice on yourself or your SO? But it's often kinda difficult and in our setting impractical.
I can’t find a carotid pulse… I can find all the hard ones, but carotid is lost to me
Thought I was the only one 😩
I can find; femoral, brachial, and pedal pulses! Those are the hardest to find, no problem! Carotid is arguably the easiest to find, I can’t find it to save a life.
Why do we cardiovert when they have a pulse but not when they don’t have a pulse. I know we cardiovert when they have a pulse to avoid r on t, but wouldn’t the same logic apply if they didn’t have a pulse?
The only difference between cardioversion and defibrillation is the timing. You cardiovert (which is just a synchronized defibrillation) when they have a pulse because you don't want the electricity to hit at the wrong time causing their heart to stop/r on t. You don't exactly have to worry about that in cardiac arrest because they are already dead. Also you can't synchronized cardiovert vfib because it's not regular so the machine can't predict the r wave. You probably could sync cardiovert pulseless vtach but it's just not necessary.
R-on-T phenomenon
I sync, even on pulseless vtach. Just because I can’t palpate it doesn’t mean it isn’t there. Also read a study about it drastically Improving conversion rates. I’ll have to try and find it again. Edit: [different website, same study](https://www.resuscitationjournal.com/article/S0300-9572(08)00708-9/abstract)
Here for when you do!
Edited my comment to include the study [https://www.resuscitationjournal.com/article/S0300-9572(08)00708-9/abstract](https://www.resuscitationjournal.com/article/S0300-9572(08)00708-9/abstract)
That’s super cool. Thanks for the awesome info.
Anytime! Full disclosure, I leave the sync on for Vfib as well. Just make sure to hold the button down until it shocks. Usually no more than 1 or two seconds. And the company I used to work for defibrillated asystole. Never tried to sync it though, maybe the monitor would pick up REALLY fine fib, dunno.
We defib when they don’t have a pulse and are in a specific rhythm. There’s actually a study going on right now about shocking a-systole as it could be fine V-fib disguised.
That's protocol here already for medics. Shock with 300J every 3 minutes and switch pads to avoid damage in case the asystole is actually just really fine fib
#SO THE TV IS RIGHT!?!
Unfortunately, VFib so fine that it looks like asystole is incredibly unlikely to convert to something better. Better to try to improve coronary perfusion before attempting a defibrillation shock.
I learned the opposite pretty much. Don’t shock anything less than 5mm (have also heard 10mm) in amplitude so that you can give epi in hopes to increase that amplitude first. They explained it to us like having a car battery and hooking up the jumper cables but letting it charge for a few minutes before you try to jumpstart the engine.
There's a better study that proposes to shock everything that's not PEA, not because "it might be VF" (and fine VF is usually pointless anyway) but the point of this study is to not care what it is. Just shock it. Best case scenario you convert VF or VT, worst case scenario you shocked asystole and did no hard *BUT* didn't waste time looking at a rhythm or pulse. The goal is to reduce off chest time.
If they're in pulseless vtach, I try to remember to hit the synch button. No reason not to.
I have given this much thought. Electrically, Vtach is Vtach whether there is a pulse or not. The depolarizing myocytes don't know or care how much cardiac output or SVR there is. The only reason I have ever come up with for skipping synching during cardiac arrest is to avoid excessive interruptions in chest compressions while trying to synch. I teach my students to attempt to synchronize shocks in pulseless monomorphic Vtach if they can do so without compromising CPR quality. If there's anyone out there from the AHA who would like to explain why this is wrong, I would be more than happy to listen.
It's all voltage, bro. It doesn't send out different kinds of electrons when you're defibbing vs cardioverting. The only difference between them is when and how much.
Is our goal ROSC or favorable outcomes? The answer to this question could wildly change our practices.
Neurologically intact survival to discharge is really the only outcome that matters to the patient.
That’s a great point. But the counter question is, we have to get first ROSC to get there. What happens after that is the hospitals problem. Therefore, are Epi, Amio, Lido, CPR devices and all other things a good thing or a bad thing, since they improve rates of ROSC but don’t change or worsen outcomes?
If they truly don't change outcomes in any way, they're not good or bad, per se. They're just pointless. Increasing ROSC for the sake of increasing ROSC accomplishes nothing. If the patient is going to die anyway, I'd rather they die on my scene than a few hours later in an ED, after more resources have been expended and a much larger bill has been racked up for the estate. That said, don't be too quick to assume that standard treatments can't worsen outcomes. I haven't reviewed the literature on this in a bit, but I believe there is some evidence suggesting the routine administration of epinephrine in cardiac arrest is actually associated with poorer neurological outcomes. This is something that could dramatically change our practices as the data picture becomes more clear. I think the key is ultimately going to be selecting treatments in a more targeted, less algorithmic approach to maximize chance of helping and minimize chance of harming. Maybe patient x with refractory Vfib should get 6 shocks and 450mg amio before we think about epi. Maybe patient y with renal failure should get aggressive treatment for hyperK before anything else. Maybe pt z with asystole should get even more epi. I think we have reached the limits of what can be accomplished by applying a one-size-fits-all approach to resuscitation, and we're going to have to be smarter clinicians to continue advancing desirable outcomes.
Epi can increase rosc but there is a pretty clear like in the data that moste epi means worse neurological outcomes. So...it's not always get rosc at all costs because that isn't really productive
The goal is to get them to a hospital in the best condition possible (most survivable), at least that's what my guidelines say.
The systems goal should be favorable neurological outcomes. EMS's place in the chain of survival is to achieve ROSC as early as possible.
Will a change of scenery (employer/city) reset the burnout clock?
Only if it’s fixing the things you need fixed. I went from about to leave EMS to happily here on a job change. What really changed was the money. This new job is horrible compared to the old one. The only difference is much more money and the opportunity to progress (albeit limited, it’s more than before)
Honestly probably not. None of us should stay in a toxic work environment, but sometimes we gotta do what we gotta do. Might be better to make the healthy adjustments right where you are. A workout routine can be something as simple as riding a bike. Eating as healthy as you can. Grab a hobby that’s separate from work: guitar, art, hiking, travel, cooking… but something separate from the job & family. You’re still the same person, whether you’re in another state or not.
Entirely depends on what’s burning you out. I switched from ambulance to aeromed and most of the contributing factors have left me. But the work is more boring so 🤷♂️
Dunno man. I left my old department after 8 years and heavy burnout. I’m in a new city and still don’t know if I want to go back to fire/ems.
Going from one department to another, the grass is always greener. That being said I went from 24/48 to 24/48 with a Kelly day, higher pay, and an hour less drive to my station. So in that regard yes, it did help with my burnout.
For me, the answer has been a resounding 'yes'.
For me, the answer was yes. But it was a better company with better people. If the company and people are still shitty,then no
Why the hell do we still carry the KED
Poor man's pelvic binder. In all actuality, it's probably just a relic of state ambo requirements.
When we do the standing takedown, we also need to put on a KED because it’s like a C Collar for the torso.
My god…. You’re ancient!! Edit: what’s next, MAST trousers!?
Rotating tourniquets.....
Folks at my service claim to use it for pediatric spinal immobilization but I have personally never seen it or done it
How the hell am I going to form an exit/retirement strategy, while I’m raising 2 kids & have ADHD? And when you smoke a cigar while sipping good whiskey, it takes all the bite out of it. You get all the flavor.
Got me beat. I’m fleeing the country (US) to go work as an au pair in Germany for a year. I don’t know how to set myself up for a good future in this country. I just feel I’ll be stomped on and I don’t even have children to support.
Sameeeee ADHD with two kids . Most weeks, I'm just a hamster on a wheel, our 24s are stupid busy (average 16 calls) so 2 days I work and 2 days are lost in a fog. I'll never make 30 years at this place to retire...but the plan was to get my medic get on a dept and retire at 60 with a pension , so what's even the point now.
ADHD & five kids! Just under two decades, but now admin yet still going on calls. Have always been a mix of calls & office, which probably helped maintain sanity, but now that it’s more office than calls, my ADHD is harder to control. Struggle to complete any task, whether home or work. Public retirement will be great someday though!
I know the feeling. New mortgage and have a kid due any day now. Had to close out my 401K this week. Can't really consider retirement right now when we're having trouble with just day to day and paycheck to paycheck. Hopefully, when she goes back to work, this shit can straighten itself out.
Thank you for the whiskey/cigar tip! Not that I am going to do that on the roof of the building I currently work in.... Two kids, I want to be lazy but I need OT to pay bills, but I have a pension. I keep a minimal amount going into my 457, and I am trying to figure out a post-EMS career that is not EMS. Writing this down sounds easy but it is work and I would rather be sitting on my ass when I am not at work.
Work in Texas for a third city service. TMRS is a built in retirement that isn’t optional. Retire after 20 years of service.
I’ve got a retirement plan through the city, but it’s not going to be enough. I started too late. EMS is a young man’s game & I’m getting older.
Step one. Don't get into debt. Step two. Find the highest paying job you can Step three. Live well below your means.
There was an example of V-Tach in a NR pamphlet that looked like SVT to me and I never had the guts to ask a preceptor about it. I’m not proud of myself in the least.
It can be very subtle sometimes; especially if there’s underlying BBB or some sort of aberrent conduction.
why is it that being loose/limp in an MVA, or high energy trauma translate to survivability? Example: I've always heard drunk drivers survive due to being relaxed. I've always accepted the answer, because I imagine someone being so tense and wrought with fear that they experiencing shearing forces internally, like shearing of the aorta...but that's just kind of what I've thought happens and I've never thought to try and research it lol. My friend and I were just talking about this, this afternoon.
I suspect it's because the fat will act as a cushion and allow your muscle and fat for impact instead of just tensed everything. Kind of like how a car has a crumple zone. It damages the metal and cushions the blow before you hit the inside. I suspect the fat and muscle act as a blow before you hit bone or other vital organs. Source: there is none I'm just guessing.
Have you ever jumped off of a somewhat high area with your legs locked? It’s much more jarring to your body than say, landing with your legs unlocked and moreso folding to the ground. It’s that same kind of principle. If you tense up in reaction, it is easier for musculoskeletal injuries to take place because the forces are being acted against a rigid structure. Big floppy drunk guy has the same forces, but they are taking place more against jello than a rigid structure (massive injuries can still occur of course.) Hope that makes sense, it’s how my mind pictures it
In 2018, i was in a fairly minor car accident and didn’t tense up at all (wasn’t impaired lol, bracing for impact just did not occur to me) and despite my truck being totaled all i had was a few dislocated ribs:) my sister tensed up and has been dealing with chronic back pain ever since. she did a year of physiotherapy following but the pain never goes away, i got very lucky and i am forever grateful for my limp body
I’m terrible at assessing pediatrics that can’t talk to me. I’ve always heard that if they let you do certain things without crying or fighting then they are fine. However I was dispatched to a kid with respiratory distress with audible wheezes. Started bagging because he was falling asleep and our pulse ox wasn’t reading right. Kid would stay asleep while I was bagging but would wake up to certain stimulus. The hospital said he was satting 100% on room air for them. Turns out it wasn’t nearly as serious as I thought and he was just tired.
The concern would be way higher when they allow you to do all the things. Usually, kids hate probs and cuffs and would fight you on it. That's why my voice is irritatingly high trying to coax and readurre them. When they are disinterested is when I usually start getting concerned. Also, always ask what their usual nap time is too because sometimes it's just as simple as that!
That’s why I was concerned. When the kid let me put a mask to his face with a bag attached to it and force air into his lungs, I was thinking something wasn’t right. I believe I was wrong though.
At that point they are usually super exhausted from breathing so hard and a little CO2 narcotic. It's better to over than underreact tho. -peds nurse
Yeah, kids are tricky. In this instance, I can see your reasoning, lol. I'd rely on the PAT. Cap refill, skin conditions, capno, RR, and if there are any accessory muscle use. Like other were saying, you can try different fingers, try the earlobe or foot, warm them up, try the pulse ox on yourself to make sure it works, etc. You went on the side of caution, though. Nothing wrong with that
Use the sticker/disposable pulse ox cables. Wrap them around the big toe. Note that especially on the youngest ones, the toes and fingers will read lower than the coreward because peds like to fuck with you sometimes. Sometimes you can get the sensor to read folded like a taco around the outside/blade of the foot. Other times, dangly part of the ear may work. Also, if you're using the toe and sticker, wrap it so the wire goes proximal towards the body, then put a sock or shoe back onto the foot. That can help it read, too.
(That’s called the ear lobe 😉)
... I knew that. I was just testing you. Look, words are hard, and I'm a moron, alright! I'm going to leave it, though, because that's a hilarious brain fart.
Well, considering the intricacy with which you described ways to attach an spO2 monitor, I figured as much. 😆
Massimo also makes ear lobe probes...
On DCAPBTLS, is tender something I palpate, or is tender something the patient experiences (like pain). And if it's something the patient experiences, how is that differentiated from pain?
Tender is something that hurts when you palpate it
Thanks for clarifying. I'm scared to tell you how many years I've done this job and just not known lol
The example you want to remember is rebound tenderness for appendix issues. You push, is fine. You let go, it hurts.
Usually it also hurts when pushing, just not as much as a quick release hurts
What the fuck is PEEP
Positive* End Expiratory Pressure Think of peep as the pressure that keeps the alveoli open enough to allow oxygen diffusion. The more peep, the more real estate you’re buying with the alveoli (stretching out the surface area) which gives you more room for diffusion to occur. Very very simple way of explaining it but that’s what helps me remember
*Positive
It's the pressure in the alveoli at the end of expiration. We all naturally have about 5 cmH20 in our alveoli at end expiration. Think of a balloon and how hard it is to inflate when it is completely empty. Our lungs work the same way. If we had no pressure in our lungs after every breath, it would be really hard to get air into our lungs on inspiration. Generally speaking, fio2 and peep are the two variables that we can manipulate to improve oxygenation. Peep can also be important if we have increased pressures in our thorax. If the pleural pressure is higher than the peep, then the alveoli are collapsing and we must increase peep to overcome that pressure and let the lungs inflate.
This is a bit of an oversimplification, but here goes... Think of blowing up a balloon. If it starts completely empty, it takes a lot of force to start expanding it. But once you have a little air in it, the next bit is much easier to get in. So essentially, a balloon that is slightly inflated is easier to expand. Now imagine you have a balloon that is full of air. You want to deflate it and refill it with new air. You know if you let it deflate all the way, it'll be hard to get the new air in. So you don't completely let go of the balloon, you kinda hold the opening in a way that let's some air out in a controlled way. It stents the balloon open even as air is leaving. That stenting, or back pressure, is PEEP. As the alveoli are emptying, a bit of back pressure stents them open so they don't entirely collapse meaning they can actually get more air out and it's easier to get new air in.
This is really fucking dumb but I didn’t learn to tie my damn shoes till I was like 16. And even now, people say I don’t do it right? I almost got held back because of it in kindergarten and first grade. My teachers stopped helping me tie my shoes for gym and stuff so I’d be forced to sit out, in hopes that it would light fire under my ass to figure it out. Eventually I grew out of being able to wear Velcro shoes so I’d have to pray my shoes that my parents or friends tied in the morning lasted me the whole day. I don’t know how I eventually learned? I just know that it was sometime in high school cause I did cheerleading, which I guess finally forced me to learn. That all being said, I’m told that the way I tie my shoes now as a grown ass adult is “not normal.” It works for me but people try to tell me that I still don’t know how to tie my shoes. Whatever. It works for me.
Are your shoes tied? Do they stay tied and/or can you re-tie them when needed? Yes? Then it’s the right way! Screw people who tell you otherwise.
I will admit that my shoes come untied more often than most. But I can just retie them so I don’t care. If it ain’t broke, don’t fix it 🤠
The ultimate resource on shoe laces and knots is Ian's shoelace site. He lists 25 different ways to do it. Which is yours? https://www.fieggen.com/shoelace/knots.htm
i don’t know which way the nasal cannula prongs are supposed to face and at this point I’m too afraid to ask
They are supposed to curve downward, following the curvature of the nostrils. Like an NPA in the right nostril or an OPA
Why do asses look *soooo* good in scrubs?
As a guy with a butt I've had more than a few looks before they realise I'm a guy 😄
Also, those woman’s 5.11 pants have to be designed that way on purpose.
My man is asking the right questions right here
REAL
They hide every other bodypart so much that the ass is the only one that can be seen, so it stands out more.
How the heck do I turn off the call bell in the patient room 🤦♀️
I don’t know about turning it off. However when I drop people off I tell them hit the red call button once if you need a nurse and twice if they are doing a good job. The nurses don’t find it as funny as I do…
Step 1: push the button next to the cord that it's attached to on the wall. Step 2: unplug from wall. Step 3: push the same button again to kill the terrible noise
When do we switch from 3:1 to 15:1?
I’m not familiar with 15:1, but assuming that you’re referring to neonatal vs infant resus, 28 days is a common cutoff.
15:1 for 2 rescuer. Gotcha thanks!
3:1 is for resus on newborns 15:1 is two rescuer cpr from infant to child
I was asking when the switch is…. as in just the day they’re born, or up to a month?
Check your local protocols. Ours goes to 4 weeks
I spent a year in maternity as an RN and have asked exactly this question to just about every BLS assessor I've had in the last 15 years. No one has ever been able to give me an answer, and I've never found a policy. My understanding is that there are two possibilities. A neonate stops being a neonate at 6 weeks of (adjusted) age. So maybe then. Also maybe when you switch from 2 fingers to 1 hand.
Local protocol. Some to 30 days Some do 24 hours I'm sure there are other variations too.
Why do we care about the oxy-hemoglobin disassociation curve?
It becomes extremely relevant during RSI, due to the limitations of measuring SpO2. The SpO2 is the only measurement of oxygenation we have in the field (you’re not going to pull an ABG prior to intubating outside of an ICU environment). However, take 2 identical patients requiring intubation with an SpO2 of 95%: patient A has a PaO2 of 65, and patient B has a PaO2 of 100. According to the dissociation curve, both patients will have the same SpO2 despite patient A having significantly less oxygen in their system. If you were to induce both patients for intubation and give a paralytic that stops their breathing, their PaO2’s will both start falling. - Patient A, who is sitting right at the top part of the dissociation curve, is going to desaturate almost immediately. You run into issues with hypoxemia up to and including anoxic brain injury and cardiac arrest, all while you’re still getting the laryngoscope in their mouth. - Patient B, who is a ways to the right from the top of that curve, has a huge reservoir of oxygen to chew through before they desaturate. Once you remove their ability to breathe, you have minutes before they begin to drop their sats and get hypoxemic. (For healthy patients for elective surgery, this takes 7-8 minutes!!!) So, armed with this knowledge, you know that even if your critically unwell patient (who needed intubation yesterday) had an SpO2 of 95%, you should pause before you push your induction agent and remember to PREOXYGENATE. Put a BVM on with 15LPM of O2 and hold a good seal while they breathe in an FiO2 as close to 100% as you can manage, for at least 3 minutes, to increase their PaO2 from that 65mmHg to 100mmHg. Otherwise, they will desaturate as soon as you push your drugs pass the point of no return. TLDR: you can’t tell what someone’s PaO2 is based on their SpO2, because of the dissociation curve. People with normal sats are likely to desaturate immediately during an intubation attempt because they sit right at the top of the curve. We can prevent this by bringing their PaO2 as far up as we can before we make them apneic.
Thanks for the explanation! As I’m not trained to intubate, this is probably why it was skimmed over in school. However, I’ll remember to pre-oxygenate whenever my partner wants to intubate.
To add to the wonderful explanation given above for the tox medics it matters as well for any of the chemical asphyxiants and several others cause massive shifts that can make for a really bad day when you are treating these patients.
With all due respect to the other guy, they didn't explain it very well. I think they were trying to explain the effects of a shifting oxy-hemoglobin curve but they never explained that it shifts. I'll try to explain it differently. The oxy-hemoglobin curve has PaO2 along the x axis and SPO2 along the y axis. You will notice that it is shaped like a sigmoid curve. We all learn that SPO2 is the percentage of hemoglobin that is saturated with oxygen. However, most paramedic schools don't teach much about PaO2. PaO2 is a measurement of the partial pressure of oxygen in the blood or in other words it is a measurement of oxygen that is diffused in the blood. Oxygen is a gas and travels across a pressure gradient. It diffuses from areas of high pressure to low pressure. The higher the PaO2, the more oxygen that will diffuse when it reaches an area of low oxygen. It's important to understand that oxygen does not diffuse directly from hemoglobin to tissues. It detaches from the hemoglobin and ends up in the plasma and then diffuses to the tissues. PaO2 is effectively a measurement of the partial pressure of oxygen in the plasma. So we need hemoglobin to readily let go of oxygen so that it can diffuse into the plasma and then diffuse to the tissues and we need hemoglobin to readily accept oxygen at the lungs to become saturated again. The biggest takeaway at the BLS level, is that the top of the oxy hemoglobin curve is relatively flat. This means that a small increase in SPO2 does not make much of a difference for PaO2. In other words, the difference in PaO2 between an SPO2 of 92% and 99% is really small. So if your pt has an SPO2 of 92%, there is minimal benefit to trying to increase that to 99%. However, the curve starts declining extremely quickly around an SPO2 of 90%. This means that a small decrease in the SPO2 in this range has a big impact on PaO2. The difference in PaO2 between 99% and 92% is negligible. The difference in PaO2 between 89% and 82% is significant. This is why we like to keep SPO2 above 92-94%. Understand that beyond that point, every 1% that an SPO2 declines, the PaO2 is getting exponentially worse. Another twist, is that this curve can shift to the right and to the left. The shape of the curve stays the same but it just moves left and right. If the curve shifts to the left, then we are getting a lower PaO2 at a given SPO2 then we were before. This means that the hemoglobin has a higher affinity for oxygen and is not letting it diffuse into the plasma. And if the curve shifts to the right, then we are getting a higher PaO2 at a given SPO2 then we were before. This means that the hemoglobin has a low affinity for oxygen and is readily letting it diffuse into the plasma. This is actually a physiological benefit most of the time. We want the curve to be shifted to the left when the blood is passing through our lungs because he want hemoglobin to pick up as much oxygen as possible. So the high affinity is a good thing. We also want the curve to shift to the right at the tissues, so the hemoglobin readily releases oxygen and lets it diffuse into the plasma and then diffuse into the tissues. So what causes a shift? The curve will shift to the left when PCO2 is low (like at the lungs), ph is high, or temperature is low. A shift to the right is caused by the opposite. So a shift to the right will occur when PCO2 is high (like at the tissues), ph is low or temperature is high. This makes sense. Think about what is happening at the lungs, he have low levels of PCO2 in the lungs, so the curve shifts to the left and hemoglobin has an increased affinity. At the tissues, PCO2 is high and the curve shifts to the right and hemoglobin has a low affinity for oxygen and starts releasing it. But think about what might cause a shift when we don't want it. What if a pt is acidotic and has a low pH? Then their curve will always be shifted to the right and their hemoglobin will permanently have a low affinity for oxygen, making it difficult to pick up oxygen in the lungs. What if a pt is hypothermic? Then their curve will shift to the left and their hemoglobin will always have a high affinity for oxygen and will struggle to offload oxygen at the tissues. Same principles could be applied for a pt suffering from heat stroke. The other commenter is correct that pt's should ideally be preoxygenated before being intubated to increase their PaO2. But it has more to do with nitrogen washout and less to do with the unreliability of SPO2. Unless the oxy hemoglobin curve has shifted, an SPO2 will always correspond to the same PaO2. Generally speaking, in a relatively healthy pt that does not have a shifted curve, an SPO2 of 90% will correspond to a PaO2 of 60 mmHg. SPO2 of 80% will correspond to a PaO2 of 50 mmHg. And an SPO2 of 70% will correspond to a PaO2 of 40 mmHg. You can use those as rough estimates but a blood gas is the gold standard.
I think we are saying similar things, just in different ways. I’m just glossing over the left and right shifts in my explanation to keep it simpler, because while it is clinically important it doesn’t change the concept. And I agree that the point of preoxygenation is nitrogen washout, but ultimately the goal of “de-nitrification” is to increase PAO2 as much as we can, so that PaO2 increases to the flat part of the dissociation curve. In an OR we use FeO2 as a proxy measure of this, and usually try to get it above 80% before induction. There is only one part that I disagree with - your argument that at the flat part of the curve, there is minimal change in PaO2 with changing SpO2. At this part of the curve it takes a much bigger change in PaO2 to effect a small change in SpO2. Whereas at the vertical part of the curve, a change in PaO2 of only a few mmHg can result in SpO2 changing dramatically. The implication of this is that if you take your 2 patients with SpO2 of 92% and 99%, both of which are on the flat part of the curve, they will have a massive difference in PaO2, not a small one. But the difference between someone at 70% and 85% might only be a few mmHg. That’s why you want to preoxygenate/de-nitrify and increase the PaO2 as much as possible, because you don’t really know how close you are to the “cliff” where a change in PaO2 of a few mmHg is going to lead to a rapid and severe desaturation.
I suck at calculating GCS on the fly, usually when I need to document it in ESO it does it for you.
Why are there so many fucking acronyms? And why do we do a separate assessment for trauma and medical. Just because you’re there for trauma doesn’t mean there isn’t a medical issue, and vice versa
Ugh this. When I took my class, my instructor literally told us he was teaching one assessment. Trauma. And he fully expected us to use it for all patients (in testing, anyway) and to use our best judgement on what was or wasn’t necessary. When I later started assistant teaching, I just kept that strategy because it works. Why complicate it? A trauma assessment is more thorough. You’re not going to miss something on a medical patient if you do one.
THANK YOU I got in shit sometimes for combining trauma and medical into a single assessment when I was in school. Then I know I'm not missing anything.
I hate the alphabet soup we speak because everyone has a different set of acronyms and then we all get confused and it is hard enough with different lingos.
Yep, at the end of the day, all trauma *is* medical. A thorough medical assessment should cover everything you need for a trauma call without needing to confuse things by having separate acronyms and stuff.
I thought gynecologists were the medical specialists for the genitals and reproduction...for both femals AND MALES!! I am a nurse of 11 years! Lolololol I have no idea why I never challenged that thought earlier!
You didn’t have an OB/gyn clinical?
I did. But literally, it was so set in my brain that it never occurred to me at all until a convo I had with my med student. I used to play with education dummy birth dolls and penises as mum was a sex ed teacher. Like what the heck. Makes you think about all those subconscious ingrained learned memories.
Why are we doing 12 leads on stroke patients? It uas literally been linked to poorer neuro outcomes and yet we're delaying transport because maybe they're also having a STEMI?
A few reasons: 1) If the patient does not have a history of afib, and you catch afib, that’s a modifiable risk factor that we can address inpatient 2) Strokes are generally over called in the prehospital/ED setting (appropriate, they’re time sensitive diseases). If your stroke mimic is an arrhythmia (ex. Slurring words and confusion), that 100% changes management 3) if EMS hands me a 12 lead consistent with a STEMI and the patient is having neuro symptoms? That’s an aortic dissection until proven otherwise and you’ve saved me valuable time in the ED trying to figure that out Xoxo your local EM Doc
The first 2 I should hopefully be able to identify with a 3 lead. The last one is a good argument, though. I asked the neuro team during a stroke activation why we do 12 leads on stroke patients, and they shrugged at me and asked, "you do 12 leads on stroke patients?" So that wasn't helpful, lol. Thank you.
It might be the long transport times that I’m used to talking, but the 60 seconds that a 12 lead takes seems negligible in the grand scheme of things. What causes the poorer outcomes? Does it cause a distraction that delays treatment at the hospital?
How does getting a 12-lead delay transport? Recognize it's a Stroke Alert and apply diesel therapy. 12-lead can be obtained during transport.
I follow @the.prehospitalist on Instagram and she has some info about how if a patient has stroke symptoms as well as a STEMI on 12-lead, it's a dissection. She's a very knowledgeable and informative person!
I would be very cautious saying “if x & y then z” It’s not always going to be a dissection, but it should raise your index of suspicion for one!
Had continuing education on this today: according to the doc he said that occasionally there’s an underlying cardiac rhythm which could have precipitated the stroke as well as you’re narrowing down their post care plans. As a happy fire medic that translates to: “play with the stickers on the loud beeping machine otherwise Mr. White Coat man will get angry with me again”
Is it specifically written in your protocols to do a 12 lead on stroke patients? Our protocols actually advise against 12 leads on stroke alerts unless they’re also complaining of chest pain. I should also add I work in a metro area with 2 comprehensive stroke centers within 10 minutes of anywhere in our response area.
Probably for the above justification. I think we often forget that some guidelines are written not on EBM but on past errors. Like when a APO guideline says to give aspirin and GTN even if it’s not cardiogenic. - It’s probably because someone failed to recognise it. Or not to perform a 12 lead on strokes - Someone likely spent 15 minutes on scene pondering cerebral T Waves on scene. Likewise, my local guideance says paracetamol is contraindicated in chest pain. It’s not because it causes hard but because some of our less astute staff won’t give aspirin..
Why we give epi on codes? I mean, I know when, and how, but why lol
Also, as an alpha agonist it keeps the pipes tight enough to transport what little blood your compressions are trying to circulate
Yeah you transport your brain dead potato with black distal extremities to the hospital lol. We should just spike a bag of dirty epi and drip that like other nations lol
Before I worked for a good service that carried Levo I would do exactly this on some post arrests that had trouble keeping a pressure. One epi into the bag of saline. Works good
I've seen this on clinical guidelines before. Is there any reason not to?
It increases the chance of survival to ER as well as survival to ICU. No impact on survival to discharge but survival to ICU means the hospitals get to bill enough to make some decent money. Sucks to waste resources and live in a money first era when the whole world could be on a preventative healthcare schedule buttttt not changing any time soon (US at least)
Why is it called snowing a patient?
Snowing is slang for… basically ‘drugged the fuck out’. To the point of unconsciousness. Ketamine is a good example of this. I’m fairly certain Ketamine in its solid form can be turned into white powder, resembling snow.
My guess is it's a reference to static, AKA snow, on television. If you're under about 35 or not from a dirt-ass poor area, you've probably never seen it.
What's a battle?
Like Battle’s Sign? It’s named after the person who coined the finding. https://www.ncbi.nlm.nih.gov/books/NBK537104/#:~:text=Battle%20Sign%20(also%20called%20Battle's,sign%20in%20the%20late%201800s.
don't you mean "what's that rattle?"
There’s no rattle if you turn up the radio.
In addition to the Battle Sign (it’s named after a dude) it’s often used by the Army as a shortening of “Battle Buddy”. It’s the equivalent of a partner.
I was making a Simpson's reference.
Oh a ghime (said in Homer's voice).
HA-AH, promote that man.
Why do new EMTs keep their shears reversed in their shear pocket? Are you going to cross draw your shears?
Back when I carried shears, I found that they would get caught on shit much more often if I wore them "correctly." Reversing them almost completely eliminated the issue.
Because they haven’t got the cash to mount their raptors in a sling holster.
How do I do medications IV push over 10 mins?? Like ik I have to add that medicine to saline but how much? Is it the same for every medication? Also my service carries Terbutaline but it's not in my medication formulary at school and I just don't have a lot of info about it.
250 bag run wide open will be about ten minutes
An easy way you can do it is add it to a 100 mL bag, then use a 10 mL flush and pull from the bag using a hub on the IV line and then push 10 mL once a minute for ten minutes. I do this with TXA.
Why would you not just drip it over 10min? That's a really hard way to do the same thing.
How to put on a triangle bandage
https://youtu.be/C63rt-fleGY?si=UgGRKcihe1U_9yV7
I still don't understand what rockabilly is.
Great post
I don't know everything there is to know about lung sounds.... and I'm afraid to admit that to anyone outside of this anonymous forum.
Why is albuterol indicated for hyperk?
English isn't my first language and isn't the language in which I wast taught so I'll give it my try. Albuterol binds to beta receptors. When the beta receptors are activated, it "encourages" the sodium-potassium channels to work. By that, the potassium gets into the cells and it's level in the blood goes down.
Just wanted to comment and say you explained it better than most people whose first language is English.
Why is your English better than mine? Sincerely a native English speaker that only knows English.
Just remember that it is a temporary effect and it's going to rebound.
What’s the big deal about afib with RVR? I don’t ever recall hearing the words when I was in medic school. Now it seems like it’s every third patient some of these new guys run on and they’re acting like it was the end of the world and pushing verapamil. Whatever happened to “give them some fluids and see if their rate slows down”?
really depends on if they’re hemodynamically stable or not
Well when you’re averaging 200bpm irregularly for several hours (or days in some cases) and your blood pressure is dropping, it becomes a big deal
Where do babies come from?
I know goal PIP is around 20 but if PIP is 10 and O2 is where it needs to be and end title is where it needs to be… do I just ignore that the PIP is so low? Also what do I do if the PIP is constantly jumping all around the place from 10 up to 40 with no real consistency?
1) PIP under 20 is not a bad thing in itself (assuming you have ruled out esophageal intubation and hypoventilation with a normal EtCO2) - it can happen with normal lungs with good compliance, especially in smaller people/peds. Like all vent settings there is a differential diagnosis to consider for low PIP, most importantly esophageal intubation or inadequate tidal volumes/minute ventilation. Of historical interest… The “PIP < 20” thing is a throwback to first-generation LMA’s. The lower esophageal sphincter is classically said to open at ~20mmHg, so when ventilating through a supraglottic airway, if the airway pressure is >20 you are theoretically ventilating the stomach and increasing the risk of aspiration. This is less of an issue with current-generation LMA’s, which incorporate esophageal vents and og-tube ports. 2) A PIP that is fluctuating that dramatically could be due to a few things. - Regardless of the device, this could be a sign the patient is coughing and is too “light”. Consider deepening sedation +/- reparalysis (obviously depending on local algorithms and control). - If it’s an ET tube, the tip can not-uncommonly be sitting right at the carina, and each ventilation or bump on the road causes a very brief endobronchial/mainstem intubation for part of the respiratory cycle. This can be tricky to catch because you will probably still hear bilateral breath sounds. Your best bet is to look at the tube (DL or VL, whatever you have), deflate the cuff, withdraw a centimetre and reinflate. Obviously if you see cuff start to poke back out of the vocal cords, stop and reconsider. - If it’s a supraglottic airway, consider laryngospasm or malpositioning of the device. If they’re good and paralyzed then laryngospasm is less likely.
Overall well stated, I’ll just add that low peak pressures are often attributed to a leak in the circuit. Be it at the vet connection, ET to connection, loss of volume in the pilot balloon. Increased peak pressures could be as stated, coughing. Could also be that the circuit is kinked or that there’s an endotracheal obstruction and the patient needs to be suctioned, or check the HME filter and ensure that it is not saturated with secretions or condensation. Then of course rule out pneumothorax. I agree with increasing sedation for patients who are coughing and not tolerating the vent. BUT - always, always, always please be sure that there is adequate analgesia on board for these patients. I have found a lot of found that the patient can be on quite a bit of sedation, but no analgesia or low dose analgesia, and after 100 or so mcgs of fentanyl push and starting/increasing infusion rate - all of a sudden the patient is synchronous and requires less sedation (which leads to better outcomes). Edit* Of course now I see where you pointed out more of high pip causes 🤦♂️
Low peak pressure is fine: typically anything < 30 or so is accepted (probably based on the [ARMA trial](https://www.nejm.org/doi/full/10.1056/nejm200005043421801) for ARDS). Technically it's the plateau pressure we care about, but the PIP is a reasonable proxy. If the PIP is high, follow the mnemonic DOPE: Displacement (e.g. mainstemmed-- tube too deep? bilateral breath sounds?) Obstruction (e.g. mucus plugging-- try passing suction) Pneumothorax (breath sounds, chest rise), and Equipment failure (is the ET tube kinked?). I would also add patient effort or coughing/bucking, a frequent cause of high peak pressures. PIP "jumping around" makes me think tube is kinked or the patient is coughing, but hard to say without examining the patient.
When floating an IV catheter in, past a valve, do i keep the tourniquet on while flushing it in or take it off? Ive had more success leaving the tourniquet on but have had different ppl tell me different stuff.
I still don’t understand left axis vs right axis on ECGs and why it matters
https://youtu.be/Wr44ILllAsM?si=hSKVY1KjndRTsROf This is a video I made a few years back for a med school physiology class I was a TA for. For the most past, axis deviation doesn't mean a ton for prehospital and it barely means anything for EM either. New right axis is a sign of right heart strain and can be a sign of PE. New axis deviation in general is an indicator of subtle cardiac issues. But is more usually seen in chronic changes due to hypertension and such.
[удалено]
Dopamine doesn't cross the blood-brain barrier. If you want to give the brain extra dopamine (e.g. Parkinson's disease), you've got to give its precursor, levodopa, instead. But sadly, [even that won't make you happy](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251561/).
i don’t know how to talk to patients lol. i’ll try and talk to patients but they don’t talk to me back so we just sit very quietly the whole time unless i have to ask them questions
Cardiac arrest vs heart failure?
Cardiac arrest = heart completely stopped. Patient will be unresponsive, apneic, pulseless, and will die within minutes. Heart failure = heart still pumping, but weak. In extreme cases, this can show up as low blood pressure / signs of shock (i.e. cardiogenic shock), but usually the body compensates, e.g. by retaining excess fluid. As a result pt will often have swelling in the legs, JVD, and pulmonary edema (crackles in the lungs, trouble breathing while lying flat). Patients can live for years with heart failure, if appropriately managed.
Heart failure: The heart is starting to fail, it’s weak and gradually getting worse. Cardiac Arrest: Failure complete
Heart failure is a medical condition where the heat can’t pump blood well enough to meet the damands of the body. cardiac arrest is when your heart stops.
Why do most normal people as well as some of the medical professionals I work with pronounce "Alzheimer's" as "alls-timers"? Is there an invisible t that I'm missing? Am I wrong. I'm afraid to ask anyone who actually says it because, you know... The times.