Levi

I can't pull up the actual study, but are those results statistically significant?

They aren't, not even close. So no reason to suspect even a signal especially when the rest of the data all suggest harm.

^ Agreed. Most importantly for a lawsuit there has to be actual harm to the patient, and the proximal cause of that harm has to be from the provider's negligent act/omission.

I'd be cautious about treating someone's blood pressure before a definitive diagnosis of a hypertensive urgency/emergency, and ruling out alternatives like a hemorrhagic or ischemic stroke. Even then, you are aiming for a 10-20% max reduction in the MAP over the first hour which might be difficult to do outside of an ICU or stepdown environment. I agree with treating the nausea and pain first and then reassessing blood pressure afterwards.

http://www.cardiosource.org/science-and-quality/clinical-trials/a/avoid.aspx?WT.mc_id=Twitter

The link to the slides on the right has most of the actual study in it.

Definetly food for thought; while the people who got O2 had a larger infarct and more adverse events (including another MI), they actually had a LOWER mortality at both discharge, and 6 months. Hmmm...

I'd like to know why they choose 8lpm by facemask instead of 2-4 by nasal cannula. It doesn't make much sense; even the authors admit that what they did isn't a standard therapy.

There was no difference in mortality, just FYI.

The process trial just showed that strict endpoint targets are not important, but recognizing sepsis, giving abx early, giving IV fluids and pressors etc. are what matters. Also you have to realize that the people in the 'placebo' arm of that trial are aware of EGDT and were probably still resuscitating to similar end points.

As to people complaining about getting antibiotics in early, well there is research to support that (8% increase mortality for every hour), but even without research it makes logical sense that it matters. So if your hospital has a policy of getting those antibiotics in early, I'm all for that. If you have trouble doing that because you have sicker patients to attend to, then of course you triage your resources but something should be fixed so that doesn't happen.

I'm sure you were joking about leaving her at home, right?

Junctional rhythm about 75/min

Regular

Axis normal

No acute ST or T wave changes

Don't see any pathologic Q waves

Give her two hardenupacetomol and leave her at home.

mine was 2 years ago. He was a young new Doc though. Maybe he had never done one on a live pt ????

Then again ::: it seems as most of the Docs today are kids.

Maybe I am getting old

New doc should definitely not have been learning about cutdowns....that is very random! Much much better options would be US guided peripheral, central line, or putting in an IO in like 10 seconds.

I've seen a few docs use portable ultrasound to get central lines, and even saw an anesthesiologist use it to get a large bore IV, but it was my understanding that cutdowns were popular in the 90's and then were proven to greatly increase risk of infection so weren't even taught anymore..

Yeah, ultrasound has become the standard of care for safety reasons, when putting in central lines. You will still see tons of people do them by palpation/anatomy/landmarks though, and nothing necessarily wrong with that.

Great information. I'm with you in finding it rather odd this patient was not anticoagulated. Are these criteria not modified based on frequency? For example a particular patient goes into a-fib 1-2 times a year and is succesfully cardioverted each episode within 24 hours. Is that patient really considered the same risk level as an intermitent a-fib patient who is in and out of it every other day?

Both of these patients should likely be anticoagulated, but based on exposure it would seem the higher frequency a-fib episode patient would be at higher stroke risk than the lower frequency a-fib episode patient.

In my own experience these patient's know their INR, and they know how stable their INR is within the accepted range. They might not know why their INR is significant, but all of them seem to notice how interested every doctor they see is in it.

You're probably right that a patient who goes into afib 1-2x/year and is out of it quickly is not at the same risk. In reality though, that type of patient is probably very rare and there's no safe way of identifying those patients. The usual course for afib is that they're in and out of it quite often, and the vast majority of people can't reliably tell you when they're in it. If you've seen 99% of the patients I have, they will be in afib and have absolutely no symptoms of palpitations or other awareness. So the safest option is to assume all patients are the garden variety 'intermittent afib' who have been shown in studies to have the same stroke risk as someone who is permanently in it.

As an example in this same patient we're been talking about, they were probably symptomatic from their respiratory infection, so it's hard to really say how long they've been in afib. There's a good chance the resp infection may have precipitated the episode, but they may have been in and out of it for the past several months and have a big clot that has formed. Another option with these patients if you feel you need to cardiovert now is to do a transesophageal echocardiogram, and take a look at the atrium and a special area called the left atrial appendage where the clots like to form+hide. If there's none there you're pretty safe to go ahead and cardiovert.

To answer your other Q: the choice to anticoagulate is not based on how often they go into afib (because of the studies showing no difference in stroke risk), but rather on their overall stroke risk. There's a risk calculation tool called CHADS2 that stands for CHF, hypertension, age (>75), diabetes, and prior stroke. Stroke gets 2 points, and all the rest get 1 point. If you have 0 points a daily aspirin is probably okay, if you have 1 point you can go with either ASA or warfarin depending on judgment, and 2+ points they should be on warfarin.

Documented history yes. Constant a-fib not necessarily. Some patients go in and out of a-fib based on any number of things. With this patient it was likely related to both low magnesium levels and a respiratory infection. I did qualify the consideration of CCBs with ensuring the rate was not in fact compensatory (respiratory infection in this case).

All sounds perfectly reasonable to me. Interesting case. Any idea why her magnesium levels were in the toilet?

The reason we worry about afib with a duration of >48 hours, as I'm sure you know, is the risk of post-cardioversion stroke from embolizing a clot out of the left atrium. If somebody has a history of atrial fibrillation their stroke risk is the same regardless of whether they have intermittent or permanent atrial fib. So in someone with intermittent afib, the concept of <48 hours vs >48 hours does not apply to them.

If you have a patient with known afib you should NOT cardiovert them chemically or electrically, unless they have been on anticoagulants for at least 4 weeks. Of course this doesn't apply to a patient who is hemodynamically unstable.

Agreed on the Ventolin/Atrovent.

Anyone else thinking we should consider a beta blocker or a CCB with a 30 minute transport time? Worth giving the Doc a ring and having the discussion anyway. She's already paced so it's lower risk than most patients (a demand pacer considering the ECG findings being shared) and based on her history we're probably looking at an a-fib less than 48 hours old. I'm surprised her medications don't include coumadin or dabigatran. I'm leaning more toward a CCB over a beta blocker in this case with signs of bronchospasm also presenting (I know in Alberta it's metoprolol or metoprolol but a guy can dream).

Not all patients are on anticoagulation for atrial fibrillation, but she probably should be with her medical history. This would not be an afib < 48 hours old though, as she has a documented history of afib. I would consider rate control if you thought her symptoms were related to her atrial fibrillation, but they're more likely due to her respiratory issues.

I didn't see that they were doing it pre-hospitally. IV metoprolol may have some benefit over PO but definitely something should be given within the first 24 hours provided there are no contraindications. The COMMIT trial used some pretty hefty doses of beta blockers so the results weren't all that surprising.

They're pretty much the same. In BC the only extra drugs are naloxone, and possibly benadryl too, as part of your protocols. In Alberta, they are trained on some supraglottic airways like the Combitube and King airways. You also get a crash course in 3-lead ECG interpretation in Alberta programs. I think Alberta EMTs also give D50 instead of D10. Minor differences and your license should be transferrable to either province anyway, so you can choose a school in either province. Hope that helps and good luck.

First off did anyone see the seizures? Can they describe to you what these seizures looked like? People in the public are often not very reliable when it comes to identifying seizures vs. syncope with some post-syncopal clonic activity, or other problems too.

One rule that we are taught to follow when making a differential is to always consider the vasculitides in your diagnosis when there are multiple organ systems involved with an unexplained connection. Has she ever been assessed for a vasculitic condition like lupus? It wouldn't be a bad idea to check for anti nuclear antibodies, as SLE could explain both the seizures and hematuria.

Meperidine can also lead to seizures because of one of its metabolites (normeperidine). There could be some sort of relation to her drug use. Has anything changed with her demerol usage in the past while?

Cool case...let us know if you have any more info!

Hello,

Ok, we are thinking about MSK pain, CVA and a AMI.

So, ALS arrives, and dose an assessment.

The patient is alert and orientated (GCS 15) with no deficits found. His pupils respond to light. Additional findings are the same as the BLS crew. They also place the patient on the monitor and do a 12-lead EKG (see attached....this is not the original...sorry).

So, what other interventions are we thinking of here?

Thank you....

Sorry, did you forget to attach the ECG or do I just not know how to find it?

Without one I would chalk this up probably to an acute coronary syndrome. The BP is a bit concerning. I would consider lowering that a bit because this sounds like the BP could acutely be causing some end organ damage here. Once you head down the ACS pathway you will be giving nitroglycerin and morphine which should help.

Was a neuro exam done? Any focal findings? Any cranial nerve problems? There isn't much that makes me think this is a CVA at the moment, but I'd still do a good exam to make sure there are no findings.

Diaphoresis and a general feeling of discomfort is a bad sign, especially in someone her age. At that age, she is much more likely to have an MI with no chest pain or other specific symptoms. Also she is much less likely to spike a fever if this was an infectious process with sepsis, so do not rule that out. With recent root canal surgery you must also consider bacterial endocarditis and complications associated with that. At any rate, she's earned herself a trip to the hospital to get checked more thoroughly and have some labwork done. I hope she is OK; please let us know how everything turned out, if you can.

All the more reason it's important to ask about a patient's medications prior to administering medication if at all possible. Taking a proper and accurate patient history has a tremendous affect on patient outcomes. That's one of the biggest reasons I'm such a proponent for education. If you don't understand what body systems are likely being affected given a patient's signs and symptoms how are you going to know what questions to ask or even what to do with the answers? If you don't have an understanding of pharmacology how are you going to know which medications you can or can't use on a particular patient? Every individual is different making "one size fits all" protocols far from best practice. "Monkey see, monkey do" just isn't good enough anymore. Really, it never was good enough. It was just all we had.

The use of Sildenafil in the treatment of pulmonary hypertension is an interesting development by the way. Do you have access to any research papers that could be shared with the rest of us?

I saw a woman with scleroderma / systemic sclerosis who an attending prescribed it to a few months ago. Here's a NEJM article about it, but there's a lot more out there. http://nejm.highwire.org/cgi/content/abstract/353/20/2148

Thanks DD. I'm just a nerd is all.

What's really obnoxious is how hard it is to get access to academic databases once you leave school...

Anyway, great post Levi. I guess we can probably agree that nitro is likely worth doing, give it if you've got it, but not something you'd call a high priority, and certainly don't give it in preference to other care (such as ASA).

Although now I'm waiting on the emergence of sublingual Viagra...

Yeah I definitely agree that it is worth giving, although with no proven benefit you might want to be cautious with its use under some circumstances. Funny enough, they are actually giving Viagra to people (including women) with pulmonary hypertension!

Actually, I got into a pissing contest with an Aussie (maybe NZ, I can't remember for sure now. (Ak, chicken shit Mike, where was he from?)) doc in Kandahar over this issue. We had one of our drivers begin to react to a new soap that he had showered with. Significant edema where the soap had touched, light headed, slight wheezing. I gained access in the clinic, gave 0.5 epi SQ and was just getting ready to push Benedryl (No oral option) when the doc reached out and stopped me saying, "No! That's for n/v, he needs Phenergan!" Now, I was fortunate that the medics didn't necessarily need to answer to the docs there, as well as having akflightmedic to cover my ass, so I pushed the Benedryl and all was well with the world in a few minutes.

We talked about it after, the doc and some of the rest of us, and it turns out that I was used to using Phenergan as an antiemetic and Benedryll for allergic reactions, yet the Aussies (NZ?) use them exactly opposite. (Perhaps because they're on the upside down side of the planet? Who can say.) I'd not really given any thought up to that point as to why we'd push one instead of the other, and am still not completely sure why. Benedryl and Phenergan were our two options there.

I don't have access to protocols that say that, but that is how it worked there. At this point I'm going to punt to ak as he's still working with the Aussies in that environment.

Dwayne

That's hilarious...in addition to H1 blocking effects, both Benadryl and Phenergan have a lot of antimuscarinic properties. However, on top of THAT, Phenergan also has some alpha blocking properties, so it probably wouldn't be the best to use for someone at risk for developing anaphylactic shock. Only my opinion though; I'm sure the doc had his reasons for wanting promethazine.

There's mixed evidence on nitroglycerin use. It's one of those things that make sense if you understand its pharmacology, but research doesn't show much promise. The most important mechanism for nitroglycerin use is reduction in preload, and not coronary vasodilation. If you have an area of ischemia or infarction, the coronary arteries to that region are already maximally dilated anyway. Because of that, vasodilation of other branches may have two outcomes. One, you may worsen their ischemia by dilating alternate coronaries and allowing blood to travel by the path of least resistance, effectively stealing more blood away from that infarcting area. Alternatively, you may dilate a collateral branch somewhere downstream which does allow slight reperfusion of that region of myocardium.

rock_shoes, I understand the mechanism of both benadryl and zofran, and I understand why zofran is superior to benadryl for n&v. What I am looking for is some evidence of benadryl's antiemetic properties beyond the occasional "diphenhydramine is also a antiemetic" found across the web. I am also looking to see if anyone here has protocols that allow benadryl for nausea in their system.

Hey daedalus,

Diphenhydramine is the exact same chemical as dimenhydrinate. The latter just has an additional substance added to it to prevent (albeit poorly) drowsiness. The mechanism for diphenhydramine/dimenhydrinate is not well understood beyond the presence of some H1 receptors which are found in the vestibular apparatus of your inner ear, which would of course help to prevent motion-sickness. There may be H1 receptors found elsewhere in other parts of the brain, but nothing has been found yet. Zofran (Ondensentran) is a 5HT-3 receptor antagonist which is found directly in the area postrema of the brain (the vomiting centre), so it has a much more direct action.