Learn from each other....

[DrQuinn]

So, I think over the past 6 months or so, the EM forums here have really blossomed into a nice little community. Of course, we still have the "should I take the USMLE Step 2" or "what do I put in my PS," but also there have been quite a few good clinical discussions, which I think are beneficial for all of us as we can all learn from each other.

I thought it would be kinda cool to have one thread dedicated to good experiences we can all learn from. And I think its ok to "toot your own horn" a little bit. We work in the pits and I think we could all use a little support. I'll start.

As you all know I recently graduated and am now at a new EM residency program. Had a 49 yo gentleman, only history of htn, no fam hx of CAD, a retired cop who came in c/o 4/10 substernal chest pain for 20 hours. At triage he told the nurse he didnt' have any chest pain. I see the guy, he looks great. HR in the 70s, doesnt' look like he's in any discomfort, kinda the stoic tough retired cop sort of look. But he's not diaphoretic, and barely complaining. He admits to having 4/10 chest pain now, but, man he doesn't show it.

EKG (I wish I had a copy of it), was done by a new RN. Poor R wave progression, but interestingly in V5 and V6 he's got biphasic T waves, and maybe a smidge (1 mm) of questionable ST segment elevation. I mean, its barely above the T-P segment, but I think its there. And those biphasic T waves. I repeat the EKG, same.

So, here I am, maybe 5 shifts in. I've had one MI that I sent to cath the week before but that was a no brainer. Do I call the cath lab? This guy looks great. Labs are pending (we don't have bedside cardiac markers, believe it or not). All his vitals look good... damn....

Anyways, I called the cath lab, just pulled the trigger. He goes up in 15 minutes.

Cardiologist calls about two hours later. "Hey, you remember that guy you sent up? His pressure is much better now on the IABP. He's got triple vessel disease and is going to the OR now. Thanks for the cath, cool case."

HOLY CRAP.

Lesson for this one is go with your gut. My gut told me this:

This guy was a retired cop, he was in his bathing suit, and was about to head to the beach with his wife. I am sure his wife brought him into the hospital (which saved his life). He's never complained of CP before, so why was he here? Remember the biggest risk factor in chest pain is the fact that they showed up in your ED!

BTW, his first troponin that we sent out in the ED (came back when he was in the cath lab) was 50.

Phew-wee.

Q

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[poloace]

good catch dq. maybe you'll get a 'get out of jail free' card or something!!! haha. that's a good story. i'm sure you'll end up with 100 of those by the end of the year.

 

[southerndoc]

Good catch Quinn. Any ST elevation should concern you and you'd better be completely sure that it's a repolarization variant before you easily dismiss it. Good call.

What was his blood pressure? The cardiologist called saying it was better. Was he hypotensive in the ED?

 

[leviathan]

Good catch Quinn. Any ST elevation should concern you and you'd better be completely sure that it's a repolarization variant before you easily dismiss it. Good call.

What was his blood pressure? The cardiologist called saying it was better. Was he hypotensive in the ED?

I think he said he had normal vitals in the ED...so maybe the cardiologist called assuming he was always hypotensive, but it was a problem that developed later on.

 

[DrQuinn]

Good catch Quinn. Any ST elevation should concern you and you'd better be completely sure that it's a repolarization variant before you easily dismiss it. Good call.

What was his blood pressure? The cardiologist called saying it was better. Was he hypotensive in the ED?

Nyeah, I'm telling you the ST segments were BARELY 1mm, it might have been my imagination. I wish I could get a copy of the EKG, just gotta check the computer to print it out and scan it. I'm guessing it was maybe .8 mm, but it was the weird biphasic T waves and the very poor R wave progression that had me concerned. Interesting thing is he had no reciprocal changes, which would have definately made me feel more secure in calling the cath lab.

His vitals in the ED were HR in the 80s, BP 140s/90s.

Q

 

[Annette]

I had a guy with no impressive EKG changes, negative enzyme, and a atypical story. However, the guy was on the grey side. Triple vessel dz. Went to emergent CABG, which is damned rare in my hospital (~3/yr).

 

[mikecwru]

Nyeah, I'm telling you the ST segments were BARELY 1mm, it might have been my imagination. I wish I could get a copy of the EKG, just gotta check the computer to print it out and scan it. I'm guessing it was maybe .8 mm, but it was the weird biphasic T waves and the very poor R wave progression that had me concerned. Interesting thing is he had no reciprocal changes, which would have definately made me feel more secure in calling the cath lab.

His vitals in the ED were HR in the 80s, BP 140s/90s.

Q

I don't know about the STs, but early precordial leads with biphasic TWs is classic for Wellen's syndrome, a proximal LAD lesion, the "widow maker." So yes, you prob saved his life.

mike

 

[southerndoc]

I don't know about the STs, but early precordial leads with biphasic TWs is classic for Wellen's syndrome, a proximal LAD lesion, the "widow maker." So yes, you prob saved his life.

Wellen's is usually associated with T wave abnormalities in V2-V4 instead of V5-V6.

Type I is characterized by biphasic T waves in leads V2-4, while type II is characterized by deeply inverted T waves in leads V2-4.

Patients must have had a prior episode of chest pain, no Q waves in the precordial leads, and no ST elevations of the precordial leads.

 

[mikecwru]

Wellen's is usually associated with T wave abnormalities in V2-V4 instead of V5-V6.

Type I is characterized by biphasic T waves in leads V2-4, while type II is characterized by deeply inverted T waves in leads V2-4.

Patients must have had a prior episode of chest pain, no Q waves in the precordial leads, and no ST elevations of the precordial leads.

I know. But considering this guy had "weird" biphasic TWs and ended up nearly meeting Jesus (did he infarc a large part of his anterior wall?)--- lead placement can always be off a little bit. And it's just something to keep in the back of your mind. I've had cardiologists who have never heard of this before.

mike

 

[southerndoc]

I've had cardiologists who have never heard of this before.

That's amazing. Anybody who takes care of patients in a chest pain center should definitely know about it. Placing one of these patients on a treadmill may be the ultimate stressor... for the patient and for the physician.

 

[mikecwru]

That's amazing. Anybody who takes care of patients in a chest pain center should definitely know about it. Placing one of these patients on a treadmill may be the ultimate stressor... for the patient and for the physician.

They weren't at my institutions (orimary) but out moonlighting in the community.

mike

 

[DrQuinn]

That's amazing. Anybody who takes care of patients in a chest pain center should definitely know about it. Placing one of these patients on a treadmill may be the ultimate stressor... for the patient and for the physician.

I definately thought about Wellens but it was in the lateral leads, so that just didn't make sense. Plus one shouldn't ever have biphasic T waves in the lateral leads. Something just wasn't right about the guy, so I just pulled the trigger. And "community" cardiologists tend not to know too much about Wellens Syndrome.

Anyone else got some cool cases they picked up and want to discuss?
Q

 

[mikecwru]

I definately thought about Wellens but it was in the lateral leads, so that just didn't make sense. Plus one shouldn't ever have biphasic T waves in the lateral leads. Something just wasn't right about the guy, so I just pulled the trigger. And "community" cardiologists tend not to know too much about Wellens Syndrome.

Anyone else got some cool cases they picked up and want to discuss?
Q

One of my favorite ones from intern year is that I had a lady who was notoriously noncompliant with her dilantin, came in seizing. Ended up getting intubated. Has a prolonged, deep postictal state. Afebrile, fairly low suspicion of meningitis but she had an elevated wbc. So, I was thorough and LP'ed her, she had molasses coming out of the needle. Also had a h/o thyroidl Did a TSH, it was almost 300. She ended up growing group B strep (WTF?) and having myxedema coma.

mike

 

[DrQuinn]

One of my favorite ones from intern year is that I had a lady who was notoriously noncompliant with her dilantin, came in seizing. Ended up getting intubated. Has a prolonged, deep postictal state. Afebrile, fairly low suspicion of meningitis but she had an elevated wbc. So, I was thorough and LP'ed her, she had molasses coming out of the needle. Also had a h/o thyroidl Did a TSH, it was almost 300. She ended up growing group B strep (WTF?) and having myxedema coma.

mike

Dang. What made you do the LP? I bet at most places, she probably would have just been intubated, loaded, and then boarded for an ICU bed. Strong work being thorough! Was it just the WBC and AMS that made you LP her? Honestly, LP'ing an intubated patient isn't that bad if you have help to hold up a patient, but most of us (probably even me) would haven't done it. Oh, was she on a propofol drip or nothing for sedation?

Q

 

[DropkickMurphy]

As Quinn said....nice work. I know you don't value my opinion much Mike, but you do have my respect on this one.

 

[NinerNiner999]

This one is not so common... Had a patient on a night shift a couple of months ago who presented with nonspecific chest pain, no ST elevation on EKG, just vague t-wave flattening. The nurse happened to look at the monitor and said something just "looked different" so she snapped off an EKG, which showed a LBBB. Negative rectal, heparin started, patient was taken to cath three hours later - which revealed two vessel disease. She got stented that night.

 

[doctawife]

Honestly, LP'ing an intubated patient isn't that bad if you have help to hold up a patient, but most of us (probably even me) would haven't done it. Oh, was she on a propofol drip or nothing for sedation?

Q

The big trick to LPing intubated people is to NOT lay them on the right side, 'cause that will buy you a nifty desaturation due to right mainstemming the ETT. It's a fairly obvious point if ya think about it, but I didn't think about it once in the EC 'cause the room set up made rolling to the right look so much easier...

Anywhoo, the patient pinked back up nicely, was rolled to the other side and CSF obtained. (Paralytics make the LP so so much easier!) But it's not a point I'll forget anytime soon.

 

[southerndoc]

The big trick to LPing intubated people is to NOT lay them on the right side, 'cause that will buy you a nifty desaturation due to right mainstemming the ETT. It's a fairly obvious point if ya think about it, but I didn't think about it once in the EC 'cause the room set up made rolling to the right look so much easier...

I'm a little confused. Most right main stem intubations occur because the tube is advanced too far and the right main stem is more straight (in line) with the trachea. The left has a steeper angle from the trachea.

So by turning a patient onto their right side, it should be less likely for gravity to pull it into the right mainstem as it would be if the patient were on the left side. With a steeper angle, gravity is more likely to pull the tube.

Nonetheless, I think it's more of advancing the tube and not really gravity pulling it down. If you turn the patient and the ET tube gets pushed in during the process, it doesn't matter if the patient is on his left or right side, you will have a resultant mainstem intubation. If you avoid pushing the ET tube in, things should be ok.

I've LP'd a couple intubated people in the right lateral decubitus without any problems.

 

[DropkickMurphy]

As the "staff RT" on this forum, I'd be inclined (no pun intended) to agree with SouthernDoc....so long as whomever has the head and therefore the ET tube (RT anyone?) holds the tube as you roll them, tube displacement shouldn't be an issue. That is of course assuming that the tube is properly secured- if it's properly taped or secured using one of the commercial holders, I can't see gravity having much influence on it. Also checking for displacement after moving the patient regardless of anything else should be the order of the day.

 

[Arch Guillotti]

The big trick to LPing intubated people is to NOT lay them on the right side, 'cause that will buy you a nifty desaturation due to right mainstemming the ETT. It's a fairly obvious point if ya think about it, but I didn't think about it once in the EC 'cause the room set up made rolling to the right look so much easier...

Anywhoo, the patient pinked back up nicely, was rolled to the other side and CSF obtained. (Paralytics make the LP so so much easier!) But it's not a point I'll forget anytime soon.

I've rolled a bunch of kids on their right side to do a caudal in the OR and never had this problem.

 

[Apollyon]

I think I mentioned this before, but, about 4 or 5 months ago:

70ish female, had poorly described "syncopal episode" that lasted about 20 seconds and resolved spontaneously. No cardiac hx, no HTN, (+) DM.

Pt with no chest pain, no short of breath, normal mentation (but a weird affect), and normal VS (BP unremarkable, HR ~80, afebrile, not tachypneic).

EKG laterally had minimal elevations (like, less than 1mm) in V5 and V6. It just wasn't coming together.

I called the CCU fellow (a raging dingus) who came down and saw the patient. This was Sunday afternoon at 5pm. Something clicked in his mind, and he called the interventional fellow (who happened to be in-house for another case). The Duke Interventional chief was the attending with him, and they came down and saw the patient. Since they were "nice people", the attending said they were taking her to the lab.

As she is on the table, the first markers come back - MB of 75, trop T of 2.5. The pt had a 100% LCx, but LV function was retain, so it was acute. She did very well.

So, no chest pain, no short of breath, (+) markers and 100% lesion. It's a LOT better to pull the trigger and fire a blank than to miss the killer.

 

[beyond all hope]

50s female, history of severe EtOH abuse and psych, came to the ED drunk.

I saw the patient and what was strange was that she wasn't just intoxicated, but she was actually aphasic. She would start a sentence and then just twist up her face like she was unable to finish it. Called Neuro, who decided that they wouldn't evaluate a drunk person until her alcohol level was zero. Scanned her head.

Of course, the CT showed a ginormous mass. Gave decadron and dilantin and called Neurosurgery. Who knows how long this had been brewing written off as EtOH.

20s female comes to the ED in status epilepticus for at least 20 minutes. Psych history but only on Geodon. No TCAs in the house. Monitor shows wide complex. I start pushing bicarb. Lots of bicarb. The attending looks at me funny (still a resident then) but he lets me run with it. 6 amps later the complex narrows and she's not seizing. Three days later she's on the floor, neurologically intact. Turns out she had stolen her brother's Ellavil and ODed.

Of course, for every story I have here, there are twenty episodes when I treated/called a consult/done a test that wasn't necessary. The misses rarely count. It's the hits that make all the difference.

 

[Hard24Get]

To help my fellow med students study up on beyond all hope's second case:

"The list of cardiotoxic overdoses for which bicarbonate is effective is growing. Sodium bicarbonate should be considered for any toxic wide-complex tachycardia. Sodium bicarbonate reverses the membrane stabilizing effects of various toxins and counteracts QRS widening as well as AV block and hypotension. The goal is an arterial pH of 7.50 to 7.55. Bicarbonate should be considered in the following overdoses: TCA's, cyclobenzaprine, orphenadrine, procainamide, disopyramide, quinidine, quinine, chloroquine, encainide, flecainide, propafenone, mexiletine, amantadine, thioridazine, mesoridazine, carbamazepine, cocaine, bupivacaine, propoxyphene, diphenhydramine, chlorpheniramine, pyrilamine, arsenic, and taxine (yew plant ingestion). Another antidysrythmic drug to consider in toxin-induced VT or VF is magnesium sulfate, especially when QT prolongation is present. The dose is 2 grams in adults and 25 mg/kg in children, administered over 2 minutes."
above quote from: http://www.iowapoison.com/index.asp?pageID=143
more info:
http://www.uic.edu/com/er/toxikon/cases/case11t.htm

Also, I will mention the case that my outpatient medicine attending took the time to tell in my evaluation. I did the rotation at the VA, and it felt like the ED because everyone was pretty sick and the pace was hectic. A 40-something year old smoker/alcoholic came in with labored breathing, but when we did the O2 SAT, he read 99%. Something made me argue that the machine was wrong, and we eventually got a new one where he came in at 85%. I examined his head and neck and felt cancer for the first time (one of those things you know it when you feel it, I guess). Turned out it was Stage III laryngeal cx. He had gotten a full workup in the ED 1 week ago and was released as a "COPD exacerbation", and had also seen the attending recently, but I caught the cx because I was looking for JVD and lymph nodes (you know, full MS3 exam ). First time I felt truly useful in clinics.

50s female, history of severe EtOH abuse and psych, came to the ED drunk.

I saw the patient and what was strange was that she wasn't just intoxicated, but she was actually aphasic. She would start a sentence and then just twist up her face like she was unable to finish it. Called Neuro, who decided that they wouldn't evaluate a drunk person until her alcohol level was zero. Scanned her head.

Of course, the CT showed a ginormous mass. Gave decadron and dilantin and called Neurosurgery. Who knows how long this had been brewing written off as EtOH.

20s female comes to the ED in status epilepticus for at least 20 minutes. Psych history but only on Geodon. No TCAs in the house. Monitor shows wide complex. I start pushing bicarb. Lots of bicarb. The attending looks at me funny (still a resident then) but he lets me run with it. 6 amps later the complex narrows and she's not seizing. Three days later she's on the floor, neurologically intact. Turns out she had stolen her brother's Ellavil and ODed.

Of course, for every story I have here, there are twenty episodes when I treated/called a consult/done a test that wasn't necessary. The misses rarely count. It's the hits that make all the difference.

 

[southerndoc]

To help my fellow med students study up on beyond all hope's second case:

"The list of cardiotoxic overdoses for which bicarbonate is effective is growing. Sodium bicarbonate should be considered for any toxic wide-complex tachycardia. Sodium bicarbonate reverses the membrane stabilizing effects of various toxins and counteracts QRS widening as well as AV block and hypotension. The goal is an arterial pH of 7.50 to 7.55. Bicarbonate should be considered in the following overdoses: TCA's, cyclobenzaprine, orphenadrine, procainamide, disopyramide, quinidine, quinine, chloroquine, encainide, flecainide, propafenone, mexiletine, amantadine, thioridazine, mesoridazine, carbamazepine, cocaine, bupivacaine, propoxyphene, diphenhydramine, chlorpheniramine, pyrilamine, arsenic, and taxine (yew plant ingestion). Another antidysrythmic drug to consider in toxin-induced VT or VF is magnesium sulfate, especially when QT prolongation is present. The dose is 2 grams in adults and 25 mg/kg in children, administered over 2 minutes."
above quote from:

Although correct, the above is actually misleading. It's not the bicarbonate or change in pH that overcomes TCA's, bupivacaine, etc., but is in fact the sodium. TCA's have sodium blockade properties, which is why there is widening of the QRS and terminal delays in aVR. Sodium bicarbonate has a large amount of sodium in it and can be given quickly. The sodium is the antidote, and one can argue that hypertonic saline will do the same thing as sodium bicarb.