Two ECGs - which goes to the cath lab?

A recent study suggests that a computer interpretation of the ECG can be extremely specific for diagnosing a STEMI; i.e. if the computer reads 

*** ACUTE MI  ***

you can take that to the bank.

This hasn't fit with my experience, and so I was very interested in Peter Canning's latest post, since it validated my suspicions. He found that the ECGs his system are acquiring show surprisingly poor sensitivity and specificity for STEMI, if you simply rely on the computer to diagnose. 

As an illustration of this point, I submit ECGs from 2 patients. 

(For more pairs of ECGs that show the problem with relying on the computer diagnosis of STEMI, click on the label "Paramedics need to read ECGs..." on the right.)

Case 1
Let's say that this was a middle-aged female, who started having substernal chest pain about 15 minutes ago. The EMS 12-lead shows:

Aside from diagnosing the patient as "borderline," anything else look suspicious?

Case 2
Again, a middle-aged female, this time with pleuritic chest pain and wheezing. An ECG obtained 5 minutes after arrival in the ED shows:

What's an appropriate next step? Call in the (cardiology) cavalry, or do a little sleuthing?

Call for a bat-stent? (source)

Resolution
If you look closely at  few of the leads, especially V3, you can see small spikes preceding the QRS. Since the computer hadn't seemed to notice, I adjusted the settings to recognize pacemakers. A second ECG then showed pretty much the same complexes, but a very different interpretation.

Fixed!

She turned out to have a fairly ordinary case of COPD.

How about case #1?

Evidently the patient was first transported to a non-PCI capable hospital. About 2 hours later she was on her way to a different hospital for an urgent cardiac catheterization. This gave EMS a unique opportunity to capture the evolution of the ECG over a time frame that we don't often find in urban/suburban EMS.

Frankly, I'm inclined to agree with the computer this time! But what did the computer "miss" on the first ECG?

Hyperacute T waves
As Peter found after analysis of his system's STEMIs, computers aren't good at recognizing the earliest sign of an MI on an ECG, the hyperacute T-wave. These are transient features, before the ST segment has had a chance to elevate, and EMS is in a unique position to find these on their initial ECG.

Stephen Smith has some great examples, some of which look very similar to case #2 here. For instance, this ECG was acquired by EMS, and was instrumental in suggesting ACS to the emergency physician:

Dr Smith's ECG Blog - 6/2011

Another case involved an anterior MI that was misdiagnosed as hyperkalemia because of the magnitude of the hyperacute T-waves:

Dr Smith's ECG Blog - 2/2009

Very similar to our patient #2!

The Bottom Line
For more teaching on hyperacute T-waves, follow the links above to the blogs written by Peter Canning or Dr Smith, or check out this review.

And remember - sometimes you have to treat the monitor, not just the patient. Just make sure you're not treating a mistaken computer!

STEMI called from the field - or is it?

As I have remarked before, the computer interpretation of the ECG can only go so far. Occasionally, it mistakes a benign, common finding (e.g. early repolarization) for a STEMI. Other times, it misses an atypical form of a STEMI.

And other times, the computer interpretation has the potential to mislead the clinician in a dangerous direction...

The patient
A mid-thirties male with a history of hypertension had an acute onset of chest pain while at rest. It radiated to his back, and was constant. It was non-pleuritic, constant, and had no associated dyspnea. Interestingly, he had just taken a ever-the-counter "sexual enhancement" pill (such drugs occasionally contain potent - and illegally added - active ingredients).

EMS found him to be bradycardic, and profoundly hypertensive, with a SBP of 230 mm Hg. His ECG was obtained:

Based on the symptoms and the ECG, along with the computer interpretation, EMS alerted the ED that they were bringing in a cath-lab candidate.

ED evaluation
The ED physician met EMS at the door, and called for cath-lab activation immediately. The patient was clearly in severe pain (he would eventually receive a total of 65 mg of morphine in the ED), with waves of sweat rolling off his face and chest. In addition to the severe chest pain, he also described numbness and weakness in his left leg, despite moving it as he writhed in pain on the stretcher.

An ECG was obtained in the ED:

Also a chest x-ray:

The ED physician had a brief conversation with the interventional cardiologist, who asked that the patient be started on the anti-platelet drug prasugrel while he started speeding on his way to the hospital at warp factor 9.  He had viewed an image of the EMS ECG on his smartphone, and thought that a diagnosis of STEMI was likely as well.


Question
Now, you might suspect this patient did not end up having a STEMI, or else why would I post the case?

Where, then, did the patient end up? Cath lab? ICU? "Other?"

Subsequent course
The patient's appearance was "sicker than the ECG," and suggested an alternate diagnosis. An echocardiogram suggested widening of the aortic root. An emergent CT angiogram of the chest was performed before the cath lab was ready.

The diagnosis of a type A aortic dissection, extending from the carotid arteries down to the left iliac, was made based on the CT.

Labetalol and nitroprusside were started to control his blood pressure, and the patient was taken to the OR by cardiothoracic surgery.

So, what about the ECG and the "STEMI?"
There is no prior ECG available for comparison, but the ST and T wave abnormalities found on the EMS tracing were stable during the initial hospital course. This suggests that there was no active cardiac ischemia.

Probably, the ST elevation in the anterior leads was likely a repolarization effect, secondary to left ventricular hypertrophy (LVH), a very common STEMI mimic. LVH is typically caused by chronic hypertension, a well-established risk factor for aortic dissection.

Can we use the ECG to diagnose aortic dissection?
Probably not. The diagnostic standard will remain the CT scan, given the excellent visualization.

But are there some ECG findings that could suggest aortic dissection? A recent study provides some answers.

A 2010 study looked at 159 patients with a diagnosis of dissection, and classified the ECGs they found in various ways. Most importantly, they looked at both acute and chronic changes.

Just as seen in our patient, LVH due to long-standing hypertension was fairly common, around 10%. We would expect this ECG finding to be chronic, however, and evident on prior ECGs. Curiously, this patient also had sinus bradycardia, which was seen in 11.3% of the study patients. It isn't clear what this is caused by.

What about the 8.2% of patients that had acute ST elevation? How do we avoid sending these patients to the cath lab, or giving them heparin or other anticoagulants?

First off, aortic dissection is rare, and ST elevation is overwhelmingly more likely to be due to a "true STEMI" than a dissection. Second, a dissection will typically have an abrupt onset, with "ripping" pain radiating through to the back. Since a dissection can propagate up the carotid or vertebral arteries, you can find stroke symptoms along with the chest pain. Similarly, as the dissection can extend into other arteries, there may be ischemia of the arms or legs, along with pulse deficits.

Third, dissection will infrequently cause ST segment elevation due to occlusion of a coronary artery as the dissecting layer spreads towards the aortic root.  The right coronary artery is usually taught as being the one most commonly affected, and the study supports this; over half of the patients with ST elevation had those elevations in the inferior region, supplied by the right coronary. Unfortunately, a number of other patients had left main coronary occlusions, and the ECG findings were much more variable with those.

The Bottom Line
It isn't always a straight-forward STEMI, even if the computer is telling you so!

Two interesting recent EMS calls.

I don't have a deep analysis of a recent study, or a recent change to the protocols, or even my thoughts on some EMS controversy

I do, however, have a gross picture and an interesting EKG! Both of these come from patients brought in by the same long-time medic at American Medical Response in Bridgeport.

First, the EKG.

The patient was an elderly lady, brought in from an nursing home, with a low blood pressure, but not looking "shocky," or at least not yet. Although there was no chest pain or other obvious cardiac complaints, and no arrhythmias, the medic nonetheless (wisely) obtained a 12-lead.

Of course, shooting an EKG, like any other  data point you obtain in the field, has been compared to picking your nose in public - namely, what do you do with the results?

So what would you do with this booger? Extra points if you find the occult STEMI.

The medic, correctly, did not call for cath lab activation.

Now the picture!

Same medic, bringing in a 80-ish year-old women who, because of dementia and multiple strokes, has had her diet restricted to pureed & thickened foods. Unfortunately, her husband, while preparing dinner, turned his back for just a moment while preparing himself a meal. When he turned back she wasn't breathing so well, and was starting to look a little blue-ish.

Not quite this bad.

By the time the patient showed up at the ED, however, she had a mild dry cough, but had her reassuringly pink skin color back!

The paramedic, not sure if we fully appreciated what had happened, held aloft with his MacGill forceps the spoils of the hunt:

Gross.

Nonetheless, a nice save! I have no idea how this lady managed to stuff a piece of meat that size into her mouth, let alone get it down into her epiglottal zone. Definitely a case that required on-scene, definitive, airway management.

Okay, that's it - no deep topics today.

But the next post will be more "meaty," I promise.

Why paramedics need to read EKGs... Part III (Return of the EKG)

In this occasional series (see Part I and Part II) I have presented pairs of EKGs, typically with one that reads

*** *** ACUTE MI *** *** 

from one patient, and one that doesn't, from a second patient. The fun part is figuring out who went to the cath lab, who didn't, and why.

This time, however, while we still have 2 EKGs, there is only one patient.

"What a twist!"

The patient
A young fit man in his early twenties, was brought in by members of the local constabulary, complaining of chest pain. I was told that the symptoms were not typical of ACS, being pleuritic and mostly reproduced with palpation. He did not look particularly intoxicated, and denied any inciting trauma.

An EKG was obtained:

Hmm. I went to see the patient myself, and after a brief re-interview and exam, I requested "an intervention."

Thirty minutes later, a repeat EKG was obtained:

Some labs were obtained, they were fine, and he was released back into custody.

So what did I do?

Lytics, nitro, a bolus of magnesium? A door-to-ballon of 30 minutes? A precordial thump, indicated because... well, just because?

The intervention
I moved around the anterior chest leads, putting them in their proper location. His initial lead placement was disturbingly similar to that pictured here:

Courtesy CBS

My patient had had the V1 and V2 leads placed, not only a few interspaces too high, but also in different interspaces - the 2nd ICS for V1, and a subclavicular placement for V2.

Meanwhile, placement of V3 was optimized, as Brandon Otto has described, to monitor pancreatic function (the MPL3, perhaps?)

The Bottom Line
I don't want to drone on about lead placement, as I've already written at length about it. And sometimes it doesn't matter too much.

Other times, however, it certainly changes the picture!

Why paramedics need to read EKGs, and not just read interpretations - Part II

Why Paramedics Need to Read EKGs - Part II: Interpret Harder

How I picture myself at 2300 hrs in the ED: Dr. McClane.

The interpretation software in modern ECG machines is pretty sophisticated, and often unfairly maligned. However, interpreting signs of ischemia on the ECG relies not only on so-many millimeters of elevation in whichever lead, but also on the appreciation of the subtle changes in morphology of ST and T segments, as well as clinical context. There is a definite role for software in EMS cardiology, but there is also a requirement that an educated prehospital provider interpret it as well.

How others see me at 2300 hrs in the ED: Dr Joe Cooper.

The "Paramedics need to read EKGs" series will highlight the occasional "air ball" that the machines make, especially when there is an interesting, and relevant, clinical context. See Part I for the first in the series.

The ECGs:
Examine the 2 ECGs here, and determine who went to the cath lab, and who was "fixed" in room 4 in the ED. To make this simple, both were middle-aged males with chest pressure starting about 1 hour before calling EMS.

Patient #1:

Patient #2:

The computer seems so darn certain about patient #2, but gets all insecure about committing on patient #1. Discussion just below.











Discussion:
Patient #1 was brought into the Connecticut hospital that "rhymes with ale" by my friend Josh up at the New Haven AMR station. Not content with the computer's waffling, he called it in as a STEMI alert, despite the computer's lack of support!!

Well, good call. Turns out there was a proximal LAD occlusion, and calling the alert in the field shaved off a good chunk of time.

As for patient #2... The ED ECG was:

So, now we have 2 machines telling us *** IN ALL CAPS *** to get this patient to a cath lab. We did not send him there.

We noted that his pressure was low-ish (around 100 systolic) when he hit the door. ALS had given him a fluid bolus (Thanks Jack!), so we tried another 500 ml of NS. Interestingly, the heart rate stayed at 154 the whole time. And then his blood pressure dropped down to the 80s. What to do?

Hint.

This was atrial flutter. There are a few clues in the ECG and clinical course I gave above.  First, it was a regular narrow-complex tachycardia at a rate of about 150. In fact, the rate was so regular that it didn't change with time or with fluid therapy. As Steven Smith points out, this really suggests atrial flutter. I would suggest that you do not look for flutter waves, but instead follow the rule of thumb:

A narrow-complex tachycardia, with a rate somewhere between 135 and 165, that doesn't vary by more than 2-3 beats/minute, is atrial flutter.

Sinus tachycardia will vary depending on activity, fluid therapy, or even breathing. PSVT will usually be a bit faster. AF and MAT will be irregular.

A couple elements of the history that, while not essential to making the ECG diagnosis, are supportive. He had had a recent episode of atrial fibrillation that was apparently provoked by cocaine use, and had been easily treated with diltiazem. He came in this time after some coke adventures as well, as well as some emotional downturns.

So, instead of diltiazem, he got propofol and 50 joules (synchronized).  His next ECG was this:

The blood pressure also came up, thankfully. In case you were feeling unsatisfied by the lack of an obvious sawtooth pattern, he had an episode the next day of 4:1 atrial flutter.

Aaah, closure

Bottom line:
You need to read the ECG. While it is prudent to consider the computer interpretation, it is a sign of true wisdom to judge the interpretation against your own reading. One small, interesting study highlights this element.

In one study, medical residents, both emergency and internal medicine, were shown this ECG.

(The actual patient who had this ECG was sent to the cath lab from the ED, and had the computer interpretation shown. She had clean arteries, and was determined to have pericarditis.)

Some of the ECGs had no computer interpretation attached, while others had an  ** ** ACUTE MI  ** ** alert attached. The residents who were given the ECG with the ** MI ** interpretation were more likely to send the patient to the cath lab. They conclude that:

The presence of CI reading affected the aggressiveness of the recommended action, even though this was not reflected in the interpretation of the ECG. In other words, the computer reading did not affect the residents’ ECG interpretation; it affected what the residents believed they would do about the ECG reading.

So, the computer interpretation will affect your interpretation - anticipate this, and incorporate this into your own thinking. Don't discard the information, but don't let it run roughshod over your judgment.

When in doubt, call med control to discuss the context, and we'll meet you in room 5!

Why paramedics need to read EKGs, and not just read interpretations.

Two patients, 2 EKGs, and 2 very different stories! Both these patients came into the Bridgeport ED, 1 of them by EMS. One of them went to the cath lab, while the other got some tests and a sandwich.

So, here's the EKG for pt #1, a 40 y.o. male who was complaining of some brief, transient, and sharp chest pains:

And for Pt #2, a 60 y.o. male who had drank a 12-pack by himself, vomited, and now complained of chest pain:

So, who got the expensive metal in their coronary artery, and who got the expensive sandwich? Which one would you have called in as a PAMI?


One of the prominent roles for EMS is in identifying the ST-elevation myocardial infarction. The basic idea is simple ("time is myocardium"), but trying to decrease the time from symptom onset to balloon inflation is pretty complex, and involves multiple decisions, actions, and environments.

Now, the role for EMS is seemingly straightforward - give the aspirin, get an EKG, and call up the ED early if you have a potential cath lab activation. Heck, the protocol seems fairly black and white.

But our patients were not put on Earth to follow the protocol, were they?

Now, pt #1 would seem like an easy cath lab activation, but a close look at the ECG suggest benign early repolarization, or perhaps pericarditis, as the most likely culprit. He had a mess o' ECGs and troponins over the next few hours, and nothing came up funky. He appreciated the sandwich!

Pt #2 had the not-so-helpful computer interpretation; "Cannot rule out Anterior infarct." Logically, you can put that on every ECG you record, since you rule out an MI with sequential troponins, over many hours! But despite the patient's intoxication, this ECG is actually classic for a bad problem, an occlusion in the proximal LAD. When we got this ECG right after he rolled into room 5, I immediately activated the cath lab. The interventionalist found a complete occlusion of the LAD just proximal to the first diagonal.

D1 = First diagonal. Lotta real estate downstream from there!

If you take another look at EKG #2, there are impressive ST-segment depressions in multiple leads, and multiple regions. Up until now, the conventional wisdom had been that this was an NSTEMI, and did not require emergent intervention.

Research over the past 10 years has changed our perspective, however. The key is in aVR, the "forgotten lead." The definite ST-segment elevation in that lead suggests an occlusion of the proximal LAD, perhaps even the left main coronary artery. If you look at the picture above, you see that the Left Main segment is responsible for >75% of the blood supply to the left ventricle. Widow-maker, indeed.

This isn't in the guidelines - yet. In one recent article, a group of cardiologists and emergency physicians suggested additions to the currently accepted cath-lab activation criteria.

Let's focus in on that last one...

So, this is all proposed stuff for now - what do you do tomorrow when you're bringing in a guy with this EKG?

Hint: Not just drunk.

Well, follow the rest of the SHCGB guidelines - ASA, IV, O2, monitor, and grab some more ECGs during transport, especially if the symptoms change. Talk to triage about bring this this patient to room 5; they may not end up going to the cath lab, but I would prefer to see that patient sooner than later!