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.

click to enlarge

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.

Angiography: Live and In-Person

BBC NEWS | Health | Watch an emergency heart procedure

This is far too cool.  Patient is a 36 year old male, with a blockage of his RCA (according to the cardiologist). Risk factors?  Smoking. I lived in England for 3 months and am sure that smoking was not the only risk factor…but.

I wish they had displayed a copy of the EKG, but I would venture to guess there was some ST-segment elevation for them to rush him back to the cath lab so quickly.  They show a fluoro shot of the dye being injected then stopping, which gives a great visual representation of what is going on.  You can see how it is pretty much totally blocked.  Then they also show a fluoro shot prior to stenting where you can see the narrowed lumen of the artery. Unfortunately, these shots are pretty much fleeting in nature so to get the best view you would have to pause the video, which I highly recommend.

It’s fun, especially when the patient has a bit of a reperfusion arrhythmia!

via Dr. Wes

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.

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.

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!

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:

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…