Evolution

We don’t often get to see evolving MIs.  Usually they go to cath lab and the ICU so serial EKGs are not available.  In this case, intervention had already been attempted but due to the nature and type of lesion no intervention was possible.  In a case such as this, surgical revascuarlization was the primary modality, but due to multiple co-morbid conditions including age, severe aortic stenosis (valve area in range of 0.55 cm²) and general deconditioning none of our surgeons would touch them.  Notice the subtle changes especially through the precordials.

20:00, Day 1

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So, what do we see? First, Q-waves in leads V1, V2 and V3.  Second, ST-elevation in V1 and V2.  Third, ST-depression in V4 (slight), V5, V6 and flipped T-waves in Leads I and aVL.  Also present is probable left atrial enlargement and  Left Axis Deviation with an axis of around -30°.  Based on this you could theorize that the LAD and Circumflex arteries have some sort of lesion.  The patient is actually hemodynamically stable at the moment.  Previous to this, they had been in atrial flutter with a rate of 110-130’s with some instability.  The cardiologist who was on the floor at the time decided to cardiovert the patient, but as we were prepping to do so they spontaneously converted back to sinus rhythm.  Teetering on the knife edge of stability they enjoyed a nice nap thanks to the Versed we had pushed while prepping for the cardioversion.  It was a reminder to follow the checklist, including ensuring that the patient is still in the rhythm you’re going to shock them out of prior to giving drugs and shocking.  The cardiologist in the last rhythm  check notices that it looks different and at that very moment the tele tech comes running in saying, “They’re in sinus!  They’re back in sinus!”

Next, 24:00 Day 1, patient c/o 5/10 substernal chest pain.

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Nothing too different, although you could say that there is a slight elevation in V3.  The other leads actually look a little better, especially the lateral leads.  No change to axis.  This was after one SL nitro though, so that dilation may have helped, one reason we try to get a 12-Lead prior to giving nitro.

06:00, Day 2

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Now there appears to be ST-elevation in V3.  The lateral leads have calmed down, with just a touch of depression in V5, V6 and I, with flipped T-waves in aVL.

14:00, Day2

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Kind of ugly now, eh?  Now we have questionable Q-waves in V1-V4 (there is a pip right before the wave drops), but fairly significant ST-elevation in the precordials.  Depression and inverted T’s in the lateral leads has returned.  Again this was during an episode of chest pain.

Later that night the patient started to decompensate fairly rapidly.  They had a drop in LOC accompanied by a drop in SPO2 to the low 80’s on 15L non-rebreather.  Lungs we very wet, obviously filling with fluid.  The nurse called the on-call cardiologist who ordered 80mg of Lasix IV, in addition to the 60mg given previously during the day that only got an output of 200ml.  Everything was starting to shut down.  We ended up calling a RRT to get a doc at the bedside, if nothing more than to see if there was anything within the patient’s advanced directive to help.

About a week prior to this, the patient had gone to the cath lab in the failed attempt mentioned above.  Angiography show a 99% occlusion of the left main and distal disease in the RCA, LAD and circumflex arteries.  The left main lesion was so bad that they interventionalist was unable to even pass a wire through, which means it was very, very tight.  They minimal blood flow the heart and absolutely no reserve.  With that in mind, the doc on the RRT realized that we could not fix the underlying problem that was causing the distress.  She spoke with the patient’s family who in the end realized that the patient didn’t have much longer, and made the patient comfort care.  They ended up expiring about an hour later.

Looking at these EKGs one could argue that the ST-elevation is actually LVH with a strain pattern. It certainly fits the criteria, especially when considering the patient had endured previous infarctions and had aortic stenosis, but I’m not completely convinced.  I’m no cardiologist, so I’m going with what I know.  But I am open to other suggestions.  It’s a sad case, especially as the family was still saying how they wanted to talk to the surgeon about open heart surgery the morning of Day 2.  Luckily, we were able to use the means available, notably medication, to give some comfort at the end for the patient, even if we couldn’t’ fix what was wrong.

It’s an Infarct

I was taking care of a patient awhile ago, post-angio.  Currently chest pain free, normal sinus, hemodynamically stable, a good outcome.  But then I took a look at the EKG they shot right after his trip to the cath lab.

anterior_infarct

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So what do we have?  ST-elevation in V1-v4, and flipped T-waves in V5, V6, I and aVL.  Looks nasty, like an anterolateral MI, right?  Maybe some issues with the Left Anterior Descending and Left Circumflex arteries?  Nope.  According to the cath lab report, angiography showed several “hazy” luminal irregularities in the LAD, but nothing stentable.  The patient was kept overnight for aggressive anticoagulation and initiation of statin therapy.

So what’s the deal?  It could be a couple of things.  First, being a taller, young man, this could be a normal variant on his EKG, unfortunately there was no prior EKG to compare it to.  Second, he could have had a vessel spasm causing acute ischemia, but this would be transient and as several EKGs done over a course of several hours showed this same view , it is not a transient phenomenon.  Finally, this could be an example of microemboli showering from a plaque rupture into the distal circulation served by the LAD.

Microembolic showering highlights some contentious issues in coronary artery disease, the issue of the large vessel versus small vessels.  Too often the distal circulation is overlooked in favor of dealing with the larger supply vessels.  We tend to focus on the big pipes, but where the real perfusion happens in the small distal arterioles that supply the myocardium.  One reason is that why can’t adeuately visualize these small vessels.  We can shoot all the dye we want and still see nothing.  This also delves into the scene where the pipes are clear, but the patient is still experiencing chest pain:  the distal portion is not getting enough blood.

Looking at the tracing, one would expect to have either a complete blockage of at least one artery or a subtotal occlusion, not a minimal irregularity.  Whether or not this gent dodged a bullet remains to be seen, but odds are they’ll be back.  Unfortunately.

*UPDATE*  Thanks to great discussion and several well-informed comments I have learned a great deal.  LVH?  Sure thing.  Not too suprising either considering the patient had a long-standing history of hypertension.  A small caveat though:  I’ve only been taught to identify basics on 12-leads, but I am learning.  Things like his help me learn and increase my skills and knowledge, which is why I share these cases for discussion.

Young MIs

How I survived a heart attack at age 43 – CNN.com

Seen it.  Took care of a patient who had their CABG at 49.  Scary.  Sounds like familial hypercholestemia to me.  This blew my mind:

The oddest thing about the angioplasty was that for six hours they told me not to move my foot, and I didn’t know why.

I know whenI’m taking care of post-angio patients, the whole, “you had a large hole in your femoral artery” is the first thing I bring up when doing post-angio instruction.

ER Follies

“PCU, this is Wanderer, how can I help you?”  I said as I picked up the phone.

“Uh, yeah, this is Nurse FERN-tastic down in the ER, I’d like to call report on Patient So-and-So, going to room such-and-such.”

“Right,” I replied looking at the clock…10 minutes since I gave the bed away, “Let me grab who’s getting them.”

“Hey Nurse Floor-tastic, report’s on #1”  I call across the station.

“Already?” she says, “I thought you just gave the room away?”  as she picks up the receiver.  “Hold on a sec,” she says into the phone, “I’m putting you on speaker so my orientee can hear this too.”

From the desk I hear the muted wah-wah-wah from the ER nurse, kind of like the teacher in Charlie Brown.  “They’re 60 sumthin’,  wahwah-wah-wahwahwah, cardiac history, wahwah-wah, discharged today at 1700,wahwahwahwah.”  I tune out the rest as I go back to charting on my patients.

“Hey Wanderer,” I hear a second later as a phone is hung up, “so, downstairs has no idea why they’re even being admitted at this point,” says Nurse Floor-tastic.  “He just read off the labs and said the ER doc is still in there trying to talk to them.”

“Right, so I just gave the bed away, and they’re not even sure if they’re being admitted?” I ask.  “And they’re calling report?”

“Yep,” she says, “Nurse FERN-tastic said he had a moment to get report out of the way, not that he actually told me anything worthwhile that I couldn’t have gleaned from the chart notes in the system.  He said the rezis haven’t even been notified yet.”

So we wait.  And wait.  And wait.  I keep looking at the screen on the system that shows the ER status.  Then next to the name of the patient where it had said, “Admit PCU” I see, “D/C”.  At that moment the phone rings.  “This is Wanderer.”

“Hey Wanderer, Nursing Supe.”

“Hey.”

“I’m sure you saw already,” she says, “but they’re sending Patient So-and-So home.”

“Right, saw that.  OK, well we still have that room open.  Is the person I assigned to the other bed still coming?” I ask.

“So far.  I haven’t heard otherwise.” the nursing supe says.  “But I’ll try to keep you posted.”

“Thanks.”

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“PCU, this is Wanderer.” as I pick up the phone again.

“Yeah, this in Nurse FERN-tastis Jr.  I’m calling to give report on Chest Pain going to room such-and-such.”

“OK, let me grab Nurse Part-time-tastic.”  I say.  “Nurse Part-time-tastic, report on Chest Pain on 1”

Time slips by.  The clock marches forward.  Midnight.  1am.  I finish my chart checks, finish the staffing report.  2am.

“Hey Nurse Part-time-tastic,” I say as I look over, “Chest Pain here yet?”

“Nope,” she says.  “Still waiting.”

More time.  I have a snack staring at the rack of new charts awaiting the arrival of the patients.  Then from around the corner I hear the dulcet tones of the ungreased wheels of an ER gurney.

“Chest Pain, right?”  I ask the tech as they roll past.

No answer, but since they’re headed into that room, I guessing it’s them.  Look back at the clock on the wall:  2:40.  3 hours since report was called.  Up date?  Nope.  I guess it really doesn’t matter all that much, they’re still breathing.

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“PCU, this is Wanderer.”

“Yeah, this is FERN-tastic, calling report on Chest Pain 2.”

“Right, they’re mine.  Lay it on me.” I say

“OK, Chest Pain 2, 60 sumthin’, chest pain post-gardening, lower-sternum radiating to neck, called EMS.  VSS since arrival.  Chest pain free.  Took ASA at home and have 1 inch of NTP on.  Just gave them Advil for a headache.  So the labs..”

“It’s OK,” I interrupt, “looked at them already.  Looks like they had something of an event with that troponin of .54.”

“They’ve got an ER special (IV in the antecubital space) for a line.  They’re AOAx3, a real walkie-talkie.  The ER doc wrote holding orders to send them up to ya’.  You ready?”

“Sure,” I say, “Bring it on.”

“See you in about 15.” they say.

Sure enough, as I’m putting the finishing touches on the room, up they roll.

As I dig into the orders, I’m missing something.  In fact I’m missing a whole lot of something.  Labs?  Nope.  Serial enzymes?  Nope.  I have tele orders, nitro, morphine and EKG orders.  No diagnostics, no guidance that maybe, just maybe they’ll be going somewhere, like the cath lab or at least nuke med.  Nothing.  Page the resident.

“Are you following Chest Pain 2?” I ask.

“Who?”

“Chest Pain 2,” I repeat, “let me spell it for ya’.”

“I have no idea who that person is,” she says, “we’re not following.”

“That’s all well and fine, but I need to know who’s going to write orders.” I say, “I have bare bone orders and nothing else.  D’ya’ want to order enzymes?  Maybe an EKG?”

“Oh, wait” after much paper shuffling and a muted conversation in the background, “looks like Cards will follow.”

“Any idea who?  It’s not like I can just call around and ask about it.  Don’t feel right just letting them hang out with nothing.  Sure I can’t persuade you…”

“Sorry, I ain’t crossing them.  If you don’t hear soon, call me back, sorry.”

And the powers that be wonder why weekend survival rates are so dismal.  The right hand and left don’t even know they exist.  Never good.

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Edit: I re-read the post and realize I need to be less trigger happy on the “Publish” button.  I’m going to leave the final summary and wrap-up and assorted ramblings below, but realize that I’m probably just adding fuel to the fire that is ER/Floor relations. It was a bad, bad weekend and this crap burbled out.  I’m not so usually full of vitriol and am able to make sense of what I’m trying to say in a more constructive way. Still wearing flame-proof Attends though! So if you just want to stop reading here and avoid the crap-tastic content of the post, do so now…

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So what’s the point you ask?  First, jumping the gun to give report, just to “get it out of the way” defeats the whole purpose of giving report.  Especially when the patient doesn’t even show up.  You’ve wasted your time and ours.

Second, a hell of a lot can happen in 3 hours.  Shit, it only took 20 minutes for my patient to circle the drain on me the other night.  From the time they started circling to the time we hit the Unit, was less than an hour.  A hell of a lot can change in 3 hours.  How about an update?

Third, that’s the way it should be, except where the docs dropped the ball.  Give report, clear, concise, and then bring the patient in a reasonable amount of time.  None of this lolly-gagging around. Unfortunately though none of the docs are talking to one another so the patient languishes.  Granted, the elevation was not critical, but it is relevant.  A coughing fit ain’t going to cause that. Something’s going on, and when your patient tells you that pretty much everyone in their family has, or had, cardiac issues, alarm bells start going off.  Things need to be done.  And we can only the push the docs so far.

Fourth, FYI Nurse Fern-tastic, there are other sites for IV starts besides the AC.  Really, I swear.  And on a “healthy” person, it’s even easier.  You’re picking that just out of convience.   But c’mon, if you’re going to drop a line in the AC on a Chest Pain-er, shouldn’t at least be a 18 gauge?  Yeah, a 20 guage will work in most situations, but if you’re using the biggest vein in the arm (typically), why not drop a bigger guage IV?  I know you feel like you don’t have anyting to prove anymore, as you told me that yourself once, but if we can get a 20 guage on the demented confused LOL who does not want it, I think getting at least an 18 in a “normal” person shouldn’t be all that far out of your ability.

Now I know that the ED is a different world.  The culture is very different from the floor.  Yes, you have multiple patients.  We do too.  I know that multiple nurses take care of the patients as a way of unloading the nurse in emergent cases, but wouldn’t you at least want to look at the patient before you call report?

And people are always wondering why the floors make life hard on the ED.  Really, it’s because we’re too busy hiding beds, playing canasta, taking our breaks and eating lunch.  Far be it from us to actually work.  I can’t speak for others, but on my floor unless we’re in the middle of some shit, like someone’s crumping, or we’re up to our armpits in poop ensconced in an isolation room, we take report when it’s called.  And when we can’t take report we offer to call them back.  Do we get snarky?  Sure, when you sit on a patient for over 2 hours to flush them at 0645 right as you change shift and just before we do, we get a little snarky.  It’s not you, it’s us, we know that the expectation of the day shift is that all the admit stuff will be done and if it’s not we’ll just get a bunch of flak, makes the last little bit of the shift oh so wonderful.  If we were to work together, there might not be such animosity.

And don’t get me started on the residents that admit these folks.  They’re starting to piss me off.

Any thoughts?  Don’t worry, I’ve got my flame-proof Attends on.

Fun with EKGs

Yes, I admit: I am an EKG nerd. There’s nothing more “fun” to me than poring over a weird strip trying to figure out what exactly is going on with the particular patient. Maybe it’s just and exercise in academia, but i have found it to be useful. I just stick that little nugget of electrical conductance deep into my brain and ever so often it will pop out with an, “A-ha!” moment. What I love more though is putting the pieces together into the whole clinical picture.

So tonight I figured I would let y’all into my archive of nerdiness. Or at least show off the most recent additions.

1. Ride the Lighting.

No, not the Metallica song, (although I’m listening to it just to set the mood…), but an elective cardioversion. Just suppose a patient presents to the ED feeling, “weak.” According to the Cardiology resident, they’re in sinus tachycardia. But if you look closely, you can see the wonderful F-waves that are the hallmark of atrial flutter. The attending Cardiologist realizes this is new-onset, so a cardioversion can be done. Anticoagulation is prescribed as are beta-blockers. In the morning they do a TEE and see nothing to worry about. Then comes the fun. Nothing sounds as much fun as DC electricity coursing across your chest. So, here’s the first shock.

cv_ekg1.jpg

Starting out in atrial flutter (see those nice F-waves…) a shock of 150 joules is applied, reseting them to atrial fibrillation. That’s still no good, we’re looking for a fix. Hit ’em again!

cv_ekg2.jpg

200 joules later and a beautiful sinus rhythm is restored. Ain’t modern medicine (and a little electricity) great?

2. Why Door-to-Balloon time is actually important.

Suppose you were out ambling along in your back 40 when you start to feel this vague feeling of pressure come creeping over your chest. It soon transforms into badass substernal chest pain. Full-blown, elephant on the chest, clutching your left pec chest pain. Now think and remember that your father, bless his soul, died of a massive heart attack when he was 50. You’re over 50. Don’t panic, head for home. Get home, tell the wife and head down the road to the fire department. They see it and go, “OK, let’s head to town.” Along the way they tell you they are going to take you to Hospital V. Before they get there they hook you up to a 12-lead EKG. After reading it, the paramedic tells his partner, “Head to whatever’s closest and don’t spare the lights and sirens.” You arrive at the ED, they fuss all over you, drawing blood, hooking you up to a cardiac monitor, starting IVs, the full-monty. They shoot another 12-lead and get this:

12_lead_hpyeracutemi3.jpg

You also over hear them talking about how your troponin is only 0.05, but nonetheless you’re whisked off into the cath lab to inflate a balloon in our heart, therefore reperfusing your heart and saving your life.

Now of course, this is hypothetical. It would also be hypothetical to say that post-intervention, your troponin level was 180.6. Yes, 180.6. That is high. In fact, I’ve never seen it that high. Looking at the EKG, besides the computer diagnostic screaming ‘ACUTE MI’ at you, what do you see?

I’ll wait.

OK. See those T waves in V1-V4, they look kind of funny right? Really wide and peaked. Not narrow and peaked like hyperkalemia, but wide and peaked. Look closer, see the J-point? Right, it’s kind of off the baseline isn’t it? Hmmm…what do we have?

Any guesses?

Right then.  You’re looking at an antero-septal MI in the hyperacute phase.  By looking at the J-point, you can see that ST segment elevations are beginning to start, but no other signs.  Rarely do we get to see this, so seeing one is a great learning opportunity.  I admit, I had to look it up to see exactly what was going on.  The hypothetical patient had a 90-95% occlusion of his proximal LAD and got stented for it.  The really cool thing was the timing.  Joint Commission goals are a door-to-balloon time of under 90 minutes.  This particular hypothetical patient had a pain onset-to-balloon time of just under 2 hours.  45 minutes to the ED and about 65 minutes to the cath lab.  But check out those troponin levels, pretty spectacular.  Sometimes knowing when to come in and not wait makes all the difference in the world.  Oh, the hypothetical patient?  Hypothetically, they had no loss of LVEF or other signs of myocardial damage.

Hope this was as fun for you as it is for me…