Jaymazing

Possibly may never give it. I've always had good relief with a properly done valsalva or spontaneous reversion. Our guidelines are to only give adenosine for SVT only if there is compromise or a hx of SVT responsive to Adenosine. It's specifically differentiated from A.Fib in our guidelines which is treated with Amiodarone. I'm not going to be the person to give Adenosine to someone in A.Fib and then have to explain it in an audit. I can use all the medical research in the world to prove a case that it was worth a try with a funky rhythym, but at the end of the day our guidelines are written by an intensivist and we follow them. We can go outside them provided we can prove we were correct. But as you say, you can't prove you were correct in a pre-hospital setting.

If we revert the SVT with Adenosine we can leave the patient at home provided it's not their first SVT responsive to Adenosine.

That's how I feel about it, too. And I don't advocate going against your medical control or protocols, by any stretch of the imagination. If you want to go against your medical director, become a doctor hahah

I'm also a big fan of BLS before ALS when considering Tx for tachydysrhythmia's

Along that same train of thought, it's really worth remembering that "SVT" is really just a catchall phrase; a supraventricular tachycardia is just that- a tachycardic rhythm with an origin above the ventricles.

A sinus tach...rapid afib...rapid aflutter...multifocal atrial tachycardia...even junctional tachycardia's are all "SVT's."

This isn't to say that adenosine will work on all different types of SVT's, just that people toss the term around without thinking about what it actually means way to often.

This isn't a problem that only happens in New Zealand either.

I couldn't agree more; SVT is a catchall phrase. In many respects, I believe the phrase is used more as a safety blanket than it is a confident diagnosis. I've gone on a few tangents about this topic in this past, myself. I'll spare you my typical SVT lecture (also known as my NCT lecture), as I get the impression we'd agree on most of the key points.

Probably, but not always. Though rare WPW is definetly something to think about when you find someone with new tachy arrhythmia and no history of the same. The higher the rate goes, the more you should be wondering about an accessory pathway. Granted, as you said WPW isn't in and of itself a contraindication, but it's still worth considering as a cause.

Anecdotally they only time in 11 years that I can remember seeing WPW in the field the patient didn't have a clue that they had it...

This basically is repeating my statement made previous, in which I made mention of likelihoods, not certainties.

Speaking strictly statistically, most accessory pathway abnormalities are found early in life (what with advancements in education, understanding of electrophysiology, and newly available telehealth consultation technologies) following previous events. While not being impossible, it's getting more and more rare to both see these phenomenon, but also be the first to discover someone with this phenomenon. However, I digress, because statistics can only take you so far, and I'm pretty sure I'm preaching to the choir here anyways.

Plus it's hard to dissuade from the allure of anecdotal evidence, even among the most knowledgeable practitioners.

I'm a little jealous of anybody who's caught it in person

Very intriguing. Thanks for sharing

Hmmm I'm not sure on that one. We use adenosine ONLY for SVT. You have to be 100% certain it is SVT. Otherwise for all other compromised tachydysrythmia's it's an amiodarone infusion and/or electric cardioversion for significant compromise. I'd be pretty wary of making a guess with any cardiac drug, but adenosine can be pretty nasty so personally I'd err on the side of caution and not go down that line unless certain it was SVT or consulted with clinical and got their view on the rhythm.

Nobody can be 100% certain of a rhythm Dx at that rate in a prehospital setting. End of story. So I guess you're never giving Adenosine. Which is a shame, because it's a good drug for most tachyrhythmias.

If you're going off the rate that the monitor gives, bare in mind that the depicted rate will vary occasionally based on irrelevant artifact (such as patient/vehicle movement), and determination of rate should more likely be based on hands on palpation and R-to-R measurements (use the small box method if it's that fast).

It seems to me that your medical director is opposed to the use of adenosine...Sucks for you, man. The only time I can think of A-FIB being a contraindication for Adeno is if it's in the presence of WPW or LGL syndrome, which are both incredibly rare, and it's likely that if they have either of those conditions that they'll be able to tell you.

Remember though; consider your causes, and is your patient stable....

I'm sold now on the AAA.

STAT to hospital with appropriate surgical options (though the more I think about it, the less likely surgery is for this guy). Consult with OLMC for destination, possible flight options, or maybe blood.

I like the idea of pressors, shooting for a MAP of ~60. And ketamine sounds ideal, too, versus fentanyl.

Stop touching his abdomen; you're not likely to find a palpating mass in an obese guy. The "ripping" sensation has to be enough to make AAA your primary DDx, and if it ends up being something else, bonus!

Lets also make sure we're all clear on the DNR status of this gentlemen.

I'm with Mobey on prioritizing comfort measures like pain control; his survival chances are getting bleak, let's at least try our best to make sure he's not in complete agony.


Any luck with the pressors?

No more walking him, if I can help it. There's a few things on the DDx, but the one that has me most worried is the potential AAA, which could be perpetuating his organ failure.

Can you describe the pain for me? localize? radiate? quantify?

Any mottling to the extremities?

​As far as I'm concerned, his pressure is low enough to warrent a 20cc/kg bolus. I'd like to get his BP above 80, and I'm titrating to 90. I also want another big bore IV, and I'll position him in trendelenburg.

I feel like correcting the BP will fix the nausea. If not I'd be thinking of Zofran.

Any changes?
Hold off on narcs, I wouldn't want to be chasing my tail fixing his BP.

aw. damn. Now I feel stupid! I use wiki as a starting point for everything (it's the easiest app on my phone to access info). I usually stem off from there and into other resources, but I always start there. It's never steered me wrong (so far). I just thought it'd be a handy starting point for other people, too.

Cooooool. That's two hits for me in one post! haha

http://en.wikipedia.org/wiki/Cauda_equina_syndrome

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3082683/

Hakuna Matata Syndrome! I should have known

Well, hmmmm. Does the pain go away when he lies on the unaffected side?

Does he have an IV still? If not, lets have one.

Also, lets try to keep him from exerting himself or moving too much if possible.

Any N/V/D? Any problems with urinating/BM prior this?


I hope his scooching over didn't aggravate anything...

My partner wants to know if he has any tick bites.

I notice a change! reassess LOC-A-B-C.

Reassure him, "it's okay, that's why we have disposable sheets", and keep him comfortable.
Anything remarkable about the urine? (Blood? strong odor?) ...other than it being a surprise (and adding to the work load of my partner, who will be cleaning)

I want to keep doing repeat neuro's on this gentlemen, to rule-out or rule-in any ascending paralysis/neuropathy or further acute changes.

Is his lumbar pain midline, lateral, or flank?

Was there a diagnosis on his old back injury? any disc herniation or #?

Any family Hx of peripheral neurological disease?

How's his respiratory status? (Rate/quality/Air entry/Sp02)

Circulatory Status? (Heart Rate/BP/ECG/Skin Condition)

What's his temp? Is the temp going up, or coming down? Any rash?

How 'slightly' are the WBC elevated?

Has he ever had chicken pox? Herpes? HIV? Vaccinations?

Any out-of-country travel in past 3 months?

I'm going to initiate infectious precautions (Droplet at the very least)....

Hows the rest of his neuro exam?



This is fun!

I'd just like to say, good luck finding the common ground with the homicidal mental case who's actively baited you into a trap, made you take off your clothes, and is pointing a .357 at your face. "Hey man, do you hate taxes? me too! Down with the man!"

I don't think anybody here is going to "challenge" him for the "alpha dog" role here. Let's be realistic. I don't know about everyone else, but if I'm in this situation, the dude with the gun is calling the shots. No pun intended.

I'm just saying.

I'd take off the rest of my uniform, underwear and all. I've already shit my pants, anyways. Maybe if I act even crazier than he is, he'll let me go. "The government told me I'd get porkchop sandwiches, and applejuice is stealing my thoughts."

In reality, it's gonna depend on who my partner is that day, and if it looks like we're gonna live if we cooperate. I get the vibe already that he's planning a "grand finale", so if calm/collected defusing doesn't work diddly quick, I'm going all in and attempting an aggressive takedown with an attempt at rapidly disarming the psycho. Getting shot in the leg while fighting someone who's gonna murder you is a hell of a lot better than getting shot in the face waiting for the hostage negotiators (which are approx 2-3 hours away, where I work).

That, or the studly facade will collapse in on itself and I'll become a whimpering mass of tears and urine in the corner of the room. Let's roll the dice!

I should also note here that the emergency buttons on the radios where I work were disconnected....so the wait-time just got even longer.

Obviously every student will have their own ideal preceptor. But for me, my dream preceptor is one that will talk through every call, scenario, or discrepancy with thoroughness and patience. Every call ends with a discussion about both the successful and the not-so-successful decisions made, with a conscious point made to note more than one way to accomplish every goal.

Also, no down time allowed (if you're not running 24 hr shifts, like some of us). If there's no calls, be running scenarios or writing essays, but always be learning. My preceptors only wanted to watch mountain-biking videos. Needless to say, I didn't benefit from those times...

I think this topic is spinning into the ditch.

The Lewis lead is a hand tool, if used correctly and in the right circumstances, to acquire an extra piece to the puzzle when met with an interesting case. What I think people are trying to suggest here isn't that it's pointless to broaden your knowledge of ECG's, cardiology, or patient care, but are instead suggesting that there is in fact a delicate balance that must be maintained when applying these non-standard practices to standard-care.

What Kiwi and Craig are saying is a valid and reasonable response to the concept of modifying chest leads in the prehospital setting, and I do not believe that their remarks were meant to shut you down. While no, you did not suggest the act using this configuration on unstable patients, we should remember that many tachycardic rhythm's in which atrial activity cannot be accurately defined are statistically unstable by their very nature, and current studies suggest that recognizing distinguishable, organized atrial complexes is an act that often times delay's treatment (even if it wouldn't delay your treatment).

I have't had any clinical use for the Lewis lead in my career, but I look forward to the day it helps me diagnose a tricky rhythm so that I can show off to my partner. I fear I've yet to impress her...

Every May, during EMS week, the division in which I work participates in fundraising and BBQ's in order to raise money for different things (eg; public AED's, Capsule of Life, etc). This year, there's been question about what "cause" we should support, and I've decided to put forth the idea of raising awareness for EMS, 9-1-1, and prehospital/community health. We're an ALS service in a very rural community full of farmers and country folk, and many of the residents in this jurisdiction are of the belief that an ambulance is just a big expensive taxi to the hospital. Part of the problem is that the ambulance service that formerly operated in this region was BLS, and quite frankly did VERY little to show any presence in the community, or educate the public.

What I'm looking for are ideas, suggestions, and advice for accomplishing a vague and generalized goal. I'd like to raise awareness about when to call 9-1-1, what we do in the back of the ambulance, what to do when you see lights & sirens, and begin spreading the concept of paramedics being "Prehospital providers" as opposed to strictly being "Emergency personnel/ambulance drivers".

An example of an idea that I've had is to put on a free first-aid/CPR course for the community, during which we will include some of the teaching points mentioned above.

If you have any ideas, or related past-experience in public awareness that you can share, I would love to hear it!

What do you think?

Our service is lined up to switch over all our monitors to the Zoll X Series within the next week or so. I've heard lots of hype, and I'm hoping it's better than the M Series.

I've yet to even touch one, but I've heard the print out format isn't the standard 3-row 4-column layout that you typically get 12-leads in. Which makes me uneasy. But I have no idea if there's any truth to that.

I'd love to hear about somebody's ACTUAL experience with these monitors!

There's so much to learn on this one! I need to work more shifts where you work, sir

I was wondering about hyperkalemia when I saw the T waves in the 12 leads also. Are you saying that the "hyperacute" T waves can be a sign of occlusion, similar to ST segment/ J point elevations? And this pt was indeed having an NSTEMI? Not being a smart ass here, we didn't learn much beyond ST elevations and depressions in my medic class, trying to teach myself the other info now... From looking at the 2 12 leads in comparison with one another, it appears the T waves became much larger in the leads they were elevated in (V2-5) from the first to the second capture.

Did you give him any antidysrythmics in addition to electricity?

Indeed they can be. In a typical MI's evolution, hyperacture T-waves are one of the earliest ECG changes. If the occlusion is big enough and occurs suddenly, the rhythm might bypass having significant ST-Elevation altogether.

If you see hyperacute T-waves, and you can't decide if they resemble hyper-K or MI morphologies, the best hint might be in the recipricals! In this case, III and aVF both have depression with a rather ominous down-sloping shape to them. Combined, this equals a very high probability for myocardial infarction.

Here is a link to a post about Hyperacute T-waves written by the ECG-guru, Dr. S. Smith

And this patient responded very rapidly to defibrillation and CPR; he regained pulses and was telling us to "stop pushing on my chest" before antiarrhythmics could be given (all three times). We handed over care to a heli-crew after that, and I'm not sure what they gave him, honestly.

I would acquire an ecg and 12-lead, then promptly share it with the good folks of EMTcity.

Did atropine/epi+pacing+bolus have any benefit? This is a tough scenario to play out without seeing what we're dealing with. *hint hint*

*****i see now that it says asystole. I missed that at first.

*************apparently I should pay more attention

To have a myocardium that ischaemic/irritable as to have a VF cardiac arrest surprised me as he did not show the classic signs of significant occlusion i.e. ST elevation.

Interesting!

It was very interesting! In fact the only clue that he was going to code was the frequent R-on-T PVC's, which induced the dysthymia. But even if you look at the times on the strips, he arrested just minutes after the last 12-lead.

This case was an excellent teaching point for both the significance of hyper acute T-waves in proximal LCA occlusion, as well as the importance of recognizing dangerous PVC's in ACS (both of which lessons I had not learned prior this call).

I originally thought hyper-K, but in actuality these T-waves are more blunt and convexed than your typical hyper-K.

*** "convexed" was the wrong word. I'm trying to say the t-waves would be an atypical morphology for hyper-K

I would have fluid bolused in preparation for an arrest...500cc isn't going to cause much more damage than already is occurring.

Did you ever get a perfusing rhythm back?

We don't overload the heart to get it ready for an arrest. Not unless he's hypotensive, and even then we only give enough fluid to achieve a perfusing pressure. For one, you don't know that 500cc wont cause more harm, and two, I don't believe you knew he was going to code, or else you should have done a lot more to get ready than just bolus him. Please don't play monday-morning quarterback.

We did get him back, 3 times actually. He woke up during CPR post-defib each time. He actually told us on the last one "It's really hard to breathe with that thing in my mouth (referring to the OPA). He had a 90% occlusion of his LMCA, and survived to discharge a week later with 60% EF remaining. And he never developed any significant ST-E, just those giant T-waves of doom and the recipricals in the inferior.

With all due respect, arbitrary fluid bolus' are just that. Arbitrary.

Alrighty, there is a reason that I am not yet a paramedic yet, I did not think of that. Heh. Yes, I do know our medic would like a line going to have iv access avaliable, however, I am going to now sit back and learn from this, carry on

Your participation is both welcome and appreciated! Don't feel like you need to sit out if you get something wrong; what better way to learn! After all, that's what we're all here for

Well I don't know if there's anywhere else to go with this scenario. In real life, this was his next ECG:
http://sphotos-a.ak.fbcdn.net/hphotos-ak-snc6/166588_10152477195835026_1562051472_n.jpg

Get him off the non rebreather mask; put him on a nasal cannula. Like fluid, oxygen is not always "good to have" and appears to make mortality in patients with acute coronary syndrome / myocardial infarction worse.

You put him on the NC, and he tolerates it quite well. His Sp02 remains at 94%, and he denies any shortness of breath.

Does his chest pain get significantly better / go away and/or does his ST depression resolve with GTN administration? If either of these are the case, and then they come back, I would give him more GTN but if neither of these are the case then I would not give any further GTN.

Upon administering nitro twice, his discomfort and condition remain unchanged. The 12 lead is repeated, and it remains identical.

The ECG looks like some ST depression in the inferior leads with reciprocal ST elevation in V4 and V5? The rhythm strip shows quadrageminal PVC.

Would you say that these are R-on-T PVC's?

No further treatment apart from GTN if appropriate and some analgesia as required. If his chest pain significantly improved with GTN then he has no immediate life threat and is not time critical (status 3) however if not then he is time sensitive (but not time critical) and has a possible threat to his life (status 2). Normal transport.

He refuses all narcotic pain killers. He states "I don't want to get addicted, like those people on TV"

Fluid always good, plus you have a line in for future possible need.

Im not a paramedic, but know many that like to get fluid running and a line in for any high suspicion cases

That's interesting. Actually, the ideology that "fluid is always good" has been going out the door for a while now. But I do agree that it's preferred to have a line established in case this patient crashes or needs meds. However, you only want to give them just enough fluid to keep the vein open (TKVO).

The reason behind this is that, like all drugs (and yes, saline is a drug), giving too much of it or giving it when it isn't needed can be detrimental to the patients health and worsen outcomes. The days of bolusing every questionable patient are far behind us; you have to have a reason to give it if your going to give it.

Some reasons why this patient doesn't need a bolus; his pressure is 114/76, he's not showing signs of hypovolemia, and he is showing signs of cardiac decompensation, which means that he's highly vulnerable to fluid overload, and would likely not benefit from having salt water dumped into his body.

However, I would gladly accept that it is appropriate to establish intravenous access on this patient