Stupid Patient Tricks

I heard about this from a friend of mine.

Dood comes in to the ED with chest pain.  Prior history of cardiac issues including prior stenting.  And a raging drug habit.  Dood gets the million dollar workup showing he’s probably got some new issues with his coronary vasculature and ends up taking a trip to the cath lab.  Lone behold there’s a new blockage and he gets a shiny new stent to fix him up right good.  But here’s where the fun begins.

Claiming he’s having a “reaction” to the Versed he becomes a raging asshole and as soon as the nurse steps out of the room to get supplies he bolts.  With an arterial sheath still in place!

Many times the cath lab sends the patients out to the floor so the sheaths can be pulled on the floor thereby increasing throughput or something like that.  An arterial sheath is a large bore introducer that is used to gain access (in many cath lab cases) to the femoral artery so that diagnostic and interventional catheters can be passed up the femoral into the aorta and then the coronary arteries.

So dood is on the loose outside our facility with a 2-3mm hole in his femoral artery plugged with the introducer which really isn’t built for a whole lot of movement.  If that was to come out, there might be issues…  Security is called, who then call the local PD to find this guy.  They find him (I’m guessing it was at our local watering hole…) and bring him back to the ED where the sheath is pulled.  But the ED docs want him monitored for  any complications post-pull.  Y’know, like bleeding, hematoma, occlusion of the artery.  Minor things.  But dood is still a raging asshole and demands to leave.  And for once, the docs see that to keep him around will only cause issues, they cowboy up and let him roll.  You still have to shake your head and wonder what was so important to get up just after having a stent placed, with a large hole in your femoral artery to decide you wanted out.  Guess we’re adding Versed as an allergy for dood now!

Stents for Mr. Floppy?

UPDATE 1-Medtronic to study stent in erectile dysfunction | Stocks | Reuters.

The study is intended for men who have not responded well to PDE5 inhibitors such as Viagra, Cialis and Levitra.

I figured that was just Nature’s way of saying, “Throw in the towel Rock!”

I can see the PMH now…

65 y/o male, history of coronary artery disease with coronary stents x3 and pelvic stents x2, hyperlipidemia, hypertension, diabetes, erectile dysfunction (resolved)…

or answers on the MRI checklist…

Uh, yeah, I got them stent thingies in my hips or something ’cause I couldn’t get it up no more and Vigara didn’t work…

I mean, really, let’s handle the hard, err..difficult topics in medicine: depression, hair loss and ED.  Got to have your priorities in the right place!

h/t to Dr. Wes

Yikes!

Sphincter-Clenching Case

via ER stories.  It’s pretty damn awesome.

I seem to forget that many times when you have an inferior infarct, odds are pretty good that there is RV involvement.  I remember having an intern literally babysit a patient on the floor one night because she though he was having a RV infarct and was kind of freaked out about it.  She just hung out at the nurses station for hours waiting for the shit to hit the fan, but it never did.  If I remember right, we did a right-sided EKG and it was benign as well.

What bugs me is that during our unit education/skills validation sessions, it’s all LV infarcts.  Which of course means that using nitro is pounded into our heads, but no one stops to ask, “What about RV involvement?”  Sure, it is relatively rare, but it is something that we need to know about.  Granted, LV infarcts are far more common and we need to know how to treat them (at least to keep them alive until they can get cathed…), but I wish the educators would look a little deeper.

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

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.

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

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

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, expecially when considering the patient had endured previous infarctions and had aortic stenosis, but I’m not comletely 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 couldnt’ fix what was wrong.

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

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…