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!

Gender, EMS, and STEMI - new study

Does our care of the patient change when the patient is a woman?

If you're like most EMS providers, your response is a strong "no." People who go into EMS generally share strong ideals, and are motivated to provide the best care possible to everyone who needs it. 

With that in mind, though, a recent study found results that are difficult to explain, and ought to prompt us to reflect on our practices. It's not proof, but it deserves discussion.

Is on-scene time longer for women with chest pain?
Time is muscle - you know the drill. With chest pain, and especially in a STEMI, we have the ability to save lives. This is what EMS is for; we identify the sick person, and we get them to the right place, fast.

Too fast! (jk - no injuries.)

With all the emphasis on reducing the door-to-ballon time, we have to identify any reasons that would delay definitive care. What if being female is one of those reasons? 

The authors of Gender differences in scene time, transport time, and total scene to hospital arrival time determined by the use of a prehospital electrocardiogram in patients with complaint of chest pain. (PDF link) looked at the EMS service in San Diego, and analyzed run-forms of chest-pain patients. They looked at two time periods, before & after EMS started obtaining prehospital ECGs. They then looked at the various time intervals, as well as the computer interpretations of STEMI (a required element in their system for field-activation of the cath lab).

They found over 21,000 patients who had been transported for chest pain. About half of the patients were men, but the women were, on average, significantly older (65 vs 59 years of age). Only 3% of the patients (in the later time period) had a STEMI, with most of those being men.

When they looked at the scene times and transport times for chest pain patients, nothing changed between the two time periods overall. In the second period, however, they found that patients with a "STEMI" interpretation on the ECG had shorter scene and transport times.

It gets more interesting, however, when they broke things down by gender. It seems that that women had longer scene times than men, both for those with and without a STEMI. Specifically, women with a STEMI, on average, had scene times about 3 minutes longer than men, while women with chest pain (but no STEMI) had scene times about a 1.5 minutes longer than men. Transport times were the same, roughly, for men and women.

Interpretation
This is a small, but provocative result, and it isn't clear what it demonstrates, let alone proves. 

Did paramedics feel less "urgency" with the female chest-pain patients? This seems unlikely, since the actual transport times were similar. Everyone got driven to the ED at the same speed.

The study design can't answer what accounted for the difference in scene time interval, unfortunately. The generally older age of the female patients could suggest that evaluation was more complex, and accordingly required more time. It's already well-known from other studies that women with ACS generally have more comorbid conditions (such as hypertension and diabetes) than men.And it's also hard to interview older patients quickly; some things are hard to rush.

Lastly, the difference is small in absolute terms. Although the authors suggest that the difference in scene time for STEMI could result in a 0.25% - 1.6% increased mortality, this is based on a questionable extrapolation.

How does this fit with prior studies?
It is still possible that there is bias in the care of female patients that was not captured in the data here. A prior EMS study showed that 7.5% fewer women than men got ECGs for chest pain (Is there gender bias in the prehospital management of patients with acute chest pain?). We don't know if this was the case in the current study, since the authors "assumed that all patients," men or women, got ECGs, since "it was the protocol." Some basic QA about ECG completion rates, by gender, would have strengthened the study.

Another study examined the differences in prehospital intervals  among men & women who ended up being diagnosed with an MI. The authors of Myocardial Infarction: Sex Differences in Symptoms Reported to Emergency Dispatch also found that women had longer on-scene times, by about 1 minute. When they took age into account, whoever, that difference disappeared. Hopefully the next San Diego EMS study will obtain the data to make these sorts of adjustments.

The Bottom Line
Like all studies that are able to "dredge" through a large data-base of run-forms, we end up with more questions than answers. The large number of patients enables researchers to find some statistical results, but the interpretation gets muddy.

Moving forward, the key will probably be in QA; making sure that all the appropriate patients get ECGs, that transport is expedited in STEMI, and that feedback is obtained from the ED and cardiology. I'm hoping that future, and better, studies will demonstrate that EMS is taking acre of everyone to the same high standards. 

Importance of the Prehospital ECG

I've talked about the evidence for liberal and frequent ECGs in the field. This, however, is not a literature review, but a "real-world" example.

A patient was brought into the ED recently, treated by Milford Fire. Fortunately for the patient, paramedic Eric Mohr was on duty, and did some nice ALS work.

EMS Course
 An elderly female had developed chest pain, abruptly, while asleep. It wasn't a mystery - she described "squeezing" pain that radiated to the jaw. The first ECG, from onscene, was not exactly a stumper either:

*** THE LP-12 IS VERY EAGER TO TELL YOU SOMETHING ***

Like I said, not subtle.

Transport was intiated, aspirin was given. They were just about to patch in and call for a cath-lab activation, but decoded to grab one more ECG as evidence. (Note the change in time - they switched to an LP-12 that hadn't been adjusted for daylight savings.)

Huh, no more STEMI. Or anything, really.

Furthermore, the patients pain was starting to resolve as well. Aside from brief period of sinus bradycardia that resolved with atropine, the patient's symptoms continued to improve.

In the ED
By the time they reached the ED, she was almost symptom-free. Our ECG was consistent with that of EMS - very, very normal.

More normal than mine. Seriously.

Tell me if you see anything there - I didn't.

Since the patient was now utterly symptom-free, with a normal ECG, I put her in a bed near the desk, and checked in every 10 or so minutes to see if she was feeling anything changes.

About an hour later, she reported the same feeling in her chest and jaw, and I grabbed another series of ECGs:

 

Hmmm. I wasn't sure if the one little change I was seeing was real, so we grabbed V4R (PDF download there). I don't have the actual ECG of that lead (by then there was practically a sheaf of tracings, and it got lost in the pile), but it stuck in my memory. Let me draw it for you:

V4R - According to the courtroom artist

As I described it to the cardiologist, "It's only about 0.25 mm, but that ST segment just wants to come up!"

This ridiculous interpretation of mine made sense to cardiology, and the cath lab was activated, despite the absence of classic STEMI criteria, and a patient whose symptoms had again resolved.

"Classic" STEMI criteria, from Rokos 2010.

Good thing too. She ended up having a 99% occlusion of the RCA.

From this episode, I think there are 2 lessons to take away.

EMS needs to grab ECGs early and often.
If Eric hadn't obtained that initial ECG, this would have been a far more difficult case. It was pretty clear from the onset that she had troubles with her inferior wall. This would have been very difficult to demonstrate solely on the subsequent ECGs, however.

Look at aVL
For this, I give all the credit to Stephan Smith. One of his frequent teaching points is that ST depressions or T-wave inversion in aVL is often the herald, the very first ECG indication of an impending inferior wall STEMI.

He has made this point recently, as well as on numerous prior occasions. Go read those, and look at the tracings, and see how the cases unfolded with EMS and in the ED. Pay special attention to how the emergency physician and cardiology approached the situation. These aren't straightforward cases, and goes beyond "STEMI 101."


The Bottom Line
Yes, it's true that you expect to see reciprocal changes in aVL and perhaps lead I, with an inferior wall MI.

But in a patient with ischemic-type symptoms, and no ECG changes expect for this pattern in aVL, keep your eyes open for ECG evolutions. Run a couple more strips. Grab some right-sided leads. Tell med control to meet you at the door to discuss the situation.

See you at 4 AM!

EMS EKGs Don't Increase Onscene, Transport Time

 Scene times & bumpersticker philosophy
To the guy who came up with the phrase "Golden Hour;" thanks for nuthin'.

"There is a golden hour between life and death. If you are critically injured you have less than 60 minutes to survive. You might not die right then; it may be three days or two weeks later -- but something has happened in your body that is irreparable."    Attributed to Dr. Adam Cowley  Reference

Catchy phrases always seem to win out over nuanced discussion, and we are left in the position of having to justify any increment in pre-hospital time intervals. Given the very real dangers of traveling lights & sirens, we instead should have to justify speeding, running red lights, and other ways of "expediting" transport.

"I wonder if it was worth it to encourage all that risky driving..." Not attributed to Dr. Adam Cowley

Nonetheless, there are medical situations where rapid transport is indicated, and most people agree that a STEMI is one of them. And although prehospital ECG acquisition has been shown improve various outcomes, some people may still harbor the concern that taking the time to do the ECG is delaying definitive treatment.

The study

With that in mind, a study of prehospital time intervals was recently published by the folks out in San Diego. The authors of Pre-Hospital Electrocardiography by Emergency Medical Personnel: Effects on Scene and Transport Times for Chest Pain and ST-Segment Elevation Myocardial Infarction Patients. studied scene time and transport time for patients with chest pain. They used a before & after design to look at the differences in times after EMS implemented prehospital ECG acquistion.

They found a statistically significant increase in scene time and transport time after they started doing ECGs. The increases in times, however, were trivial,  accounting for an additional 14 and 12 seconds, respectively. It just goes to show that, if you have over 20,000 subjects in a study, you are going to find statistical differences that just don't matter.

Interestingly, if they only looked at the subset of patients whose Marquette interpretation was *** ACUTE MI ***, they found that those same time intervals decreased, such that the total scene-to-hospital time was almost 3 minutes faster than in the pre-ECG days. So, it appears that, if anything, EMS care is speeding up the care of the specific patient population in question. In particular, the transport time was almost a minute faster, leading the authors to comment: 

"It is possible that once identified, obvious and suspected STEMI patients were treated with greater urgency resulting in expedited transport to the closest STEMI center."

A note of caution

 While the paramedics likely treated the identified STEMI patients with "greater urgency," as the authors suggest, I am paradoxically concerned about such a large drop in transport time. How was this achieved? The study wasn't designed to answer that question, but another recent study suggests it was unlikely to be because a bunch of new cath labs were built in the area.

Instead, I am concerned that the dramatic reading of *** ACUTE MI *** prompted the drivers of the ambulances to "expedite" transport by driving warp factor 10. The problem is that, when the view through the windshield looks like this:

Pictured: about to bounce too close to a supernova.

... the next view could be something like this:

Aaaannnd, supernova. *

Let's be careful out there. Just getting the ECG is probably saving lives - don't risk them during transport, "golden hour" or not.

*Reference. Note that picture this is used for illustration, but the EMS crew apparently was neither responding nor transporting, and a car ran into them.

STEMI with a twist... and then a second twist!

This would make a lousy case for a EMS 12-Lead-style presentation, because it's a little to difficult to predict the outcome. And I can't really find a new EMS study, or even an old one, to present with this. If there is any lesson to learn from this case, it would have to be: patients will keep you humble.

The Patient
The history was a little iffy, as the patient was elderly and had a history of both CVAs and dementia, and was variably describing either a week of chest pain or "Nothing! I'm fine!"

EMS had called with a STEMI, though, so I met the paramedics at the ED door, and they handed me the ECG:

You know, they say "treat the patient, not the monitor," but when this shows up on the monitor, you treat that.

We grabbed another ECG after cards had been called for the cath lab activation:

By the way,  I know some sharp readers out there are already asking for right-sided leads, but V4R didn't reveal too much. But even without that, one could make a stab at guessing the infarct-related artery - it seems sort of classic. The STE in III versus aVF, the depressions in aVL and I, not to mention V2, all pointed to an RCA lesion. Intern stuff.

And then the cards fellow asks me if I've seen the patients old ECG. Oh, give me a break...

Twist #1
Now, I almost always check the old ECGs before I call cards, but in this case I was wondering how the old ECG could possibly be relevant to this clearly acute ischemia...

Ah. I see.

This ECG was recorded a number of months prior. The patient, at that time, had been brought to the hospital for another medical emergency, and was incidentally found to have an apparent STEMI. The catheterization revealed a totally occluded RCA, likely chronic.

"What a twist!"

Sooo, no cath then?

Despite the vague history the patient provided, it seemed consistent enough with AMI. There was also some concern that the collaterals that were serving her right ventricle might have acutely occluded.On top of all that, the deep drop in her blood pressure (thankfully transient) after I gave her nitroglycerin seemed to confirm the ECG. Off to the cath lab she went, leaving me feeling only somewhat less sheepish.

Twist #2
And the infarct related artery was...

"Ta-da!"

The LAD.

A "hazy appearing" lesion was visualized fairly proximally in the LAD, just before the first diagonal. Just to be sure, they used the intravascular ultrasound to confirm the freshly-ulcerated plaque, and put in a few stents. All better!

Follow-up
Well, not really. Our patient suffers from "multiple comorbidities," and did not tolerate the procedure so well. A ballon-pump was placed to support her hypotension during the procedure, and during her subsequent hospital stay any number of issues have popped up; bleeding, sepsis, renal stuff.

And her current ECG, a month later?

Huh.

Bottom line
Stay humble. I like to think that I've gotten pretty good at guessing the culprit artery in STEMI, but I was out of my depth on this one!

Cath lab cancelation after EMS activation

In the last 2 posts, I reviewed recent studies that looked at the decision to obtain a prehospital ECG, and a novel method to teach STEMI identification to novice ECG readers. This leads to the last installment in this trilogy: How often does EMS mistakenly activate the cath lab? For that matter, how good are emergency physicians?

Reference

(Side note: This is the second paper I have reviewed that has Jon Studnek as an author. He's a paramedic who also has a PhD, and is faculty at Carolinas Medical Center. He writes a lot, and I probably could fill all of my posts with reviews of his publications.)

AKA "Dr. Medic"

This study uses data from the Reperfusion of Acute Myocardial Infarction in Carolina Emergency Departments (RACE) program in North Carolina. This program has already been shown to improve time to PCI or lytics for patients with a STEMI,  as well as other process measures. While recent data on actual patient outcomes is mixed, there is no doubt that this ambitious collaboration has brought some order to the notoriously fragmented emergency health care system in the U.S.!

The investigators used data from the 14 hospitals in North Carolina that acted as the receiving centers for STEMI patients transferred for emergent percutaneous coronary intervention (PCI).They looked at  sub-groups of patients, broken down in three different ways:

• Patients who first presented to a PCI center, or to a non-PCI center;
• Patients who had the cath lab activated by EMS, or in the ED; and
• Patients who used EMS, or those who "walked in" to the ED.

Because of the size of the program, they were able to look at a total of almost 4000 catheterization lab activations. That's one of the main strengths of this study - they have a lot of data.

Another aspect of the study that gives it some "real-world" applicability is how they defined an "inappropriate" activation of the cath lab. While other authors have described a "clean cath" as an inappropriate activation, the authors acknowledge that there are many scenarios where PCI for presumed STEMI is appropriate, despite the 20/20 hindsight of a negative cath. Takotsubo cardiomyopathy, for example, often requires an emergent angiogram to clarify the diagnosis.

So, instead they defined an inappropriate cath lab activation "If catheterization was canceled because of ECG reinterpretation or if the patient was deemed not to be a candidate" for PCI. Clinical factors, such as age or DNR status, were used to determine candidacy.

The overall results, comparing paramedics and ED physicians were that 15% of activations were inappropriate:

They analyze the results further, breaking down the data into the subgroups described above. The group of interest is all the patients who were transported by EMS, and had their initial activation by EMS. In other words, none of these patients were "walk-ins," but it included both patients who were brought to PCI and to non-PCI centers (initially).

They compare these activations against all the patients who had cath lab activation performed by the ED physicians (both at PCI centers and non-PCI centers), with patients who either came in by EMS or car.

There are a couple different ways to analyze these results, but overall the physicans performed better that the medics. Well, 7+ years of training ought to pay off somewhere, and and incremental accuracy in ECG interpretation is a reasonable expectation.

However, you can't even conclude this from the data presented, since an activation may have been deemed "inappropriate" because of a patient's DNR code status, say, or severe comorbidities (e.g. sepsis, or terminal disease). Specifically, we don't have the break-down for ECG accuracy versus judging cath lab candidacy for the 2 groups - it may well be the case that medics are just as good as emergency physicians at reading ECGs, but the physicians are better at judging which patients actually warrant an emergent catheterization.

The last table emphasizes the point that, while this sort of study is great at generating statistically-significant results, there is a lot of "granularity" that is not accessible to us.

Clearly, not all EMS agencies or EDs are equal - some systems are better than others. In this table, note the range of appropriate activations:

There are few EMS agencies and EDs who are evidently did not generate a single inappropriate activation! However, a 100% appropriate activation rate may also suggest a system that is too restrictive, and is missing too many STEMIs.

On the other hand, it is concerning that some EDs, even at the big hospitals with cath labs, have a "false-positive" rate of 25%. Similarly, some EMS agency inappropriately activates the cath lab 1/3 of the time!

The Bottom Line

This isn't a study that you can use to change your clinical practice in the next shift. It isn't even very useful at changing practice at your EMS agency or ED. However, it points the way to doing the more practical research, by highlighting important aspects.

For example, how do paramedics at different agencies decide to activate the cath lab, and how do these methods correlate with accuracy? Could a closer look at the 65% - 100% range in appropriate activations suggest a "best practice" for EMS? Should we rely more on intensive continuing education for paramedics? Alternatively, should there be more emphasis on computerized and/or human algorithms for ECG interpretation?

Furthermore, since the "Not Cath Lab Candidate"group accounted for such a large proportion of the inappropriate activations (4.3%), might their be a better way to anticipate this exclusion? To a large degree, the cardiologist is the individual who is deciding the patient's candidacy for the cath lab, and it is often difficult for the emergency physician, let alone the paramedic, to anticipate their decision. I'm not sure that the accuracy of prehospital STEMI activation should be judged using such "soft criteria."

So, more research is called for, as usual. But this paper serves as a very useful guide for the future.

An Alternative Method of ECG Interpretation

Just when a paramedic student has started to feel somewhat confident about rhythm interpretation, she is introduced to the other 11 leads.

First off, the leads are organized even worse than the QWERTY keyboard. Inferior leads are the left of anterior, the lateral leads are in two different places, and aVR sits there all by itself, like a chump.

Then there are all the depressions and elevations, T waves flipping around, ischemia vs infarct. And then someone shows you how to pick up on a posterior MI by flipping the paper over. Madness, I tell you.

In particular, identifying a STEMI can be difficult, even if ST segment elevation is clearly seen. For example, the following ECGs all show ST segment elevation, but...

1. Not a STEMI

2. Not a STEMI either

3. Nope.

 But with a fairly undramatic ECG like:

4. Bingo - Occlusion of the proximal LAD

The first first three ECGs demonstrate 3 common cause of ST elevation that we see in EMS or the ED, so-called "mimics" of STEMI. Now, there are a host of rules and criteria to help you diagnose each of these mimics, but it's hard to learn all of these, and to feel confident about them.

Is there a simpler way to achieve ECG excellence? Some short-cut to Jedi-level ECG mastery other than slogging through hundreds of tracings?

Perhaps a training montage?

Well, no.

But there are a few different ways to develop pattern recognition, and switching up the methods can put things in perspective. Hartman and colleagues have helped the novice ECG student tremendously with a new, focused approach to ECG interpretation. While this does not replace experience, practice, and feedback on interpretations, it's a good alternative way to tackle ECGs.

Abstract. If you want a pdf, message me at Facebook.

The rule has 4 steps, and we'll tackle them in that order

1. Is there ST elevation in at least 2 related leads?

The first rule specifies a minimum amount of elevation: 1-2 mm in two anatomically related leads.

It doesn't take long before a paramedic student identifies their first patient with ST elevation. Okay, granted, it's usually not an actual STEMI that they find, since the majority of ST elevation found in the ED or by EMS is not a STEMI. Typically, ST elevation will be due to any number of "mimics," such as left bundle branch block (LBBB), left ventricular hypertrophy (LVH), early repolarization (ER), as well as a number of other conditions. Surprisingly, if you look at all the patients who come into the ED with ST elevation, only about 1 in 7 patients have a true STEMI!

On the other hand, if you don't have some ST elevation, the patient probably doesn't have a STEMI. (Yeah, we're going to miss a true posterior or a proximal left main. This rule is for the novice reader, okay?)

No ST elevation, so not a STEMI.

2. Is the QRS a normal height?

The heart, over a period of years, responds to hypertension by bulking up and adding muscle mass. This process results in LVH, which, in the long run, isn't good. It shows up on the ECG as deep S-waves in V1 and V2, and high R-waves in V5 and V6.

In the short term, though, it mainly serves to distract us, as it can produce ECG findings that can look a lot like a STEMI. If we look at ECG #1 above, we see ST elevations in leads V2 and V3. Could these represent a STEMI?

Likely no, for several reasons. Now, a lot of the reasons involve interpretation of subtle, qualitative signs - the morphology of the ST segments and T waves, "notching" of the J-point,  reciprocal changes, etc. it just doesn't "look" like a STEMI, but you need to read hundreds of ECGs to feel comfortable with those.

It is far simpler to count the big boxes. Rule #2 boils down 3 sub-steps:

• First, look at the S-waves in V1 and V2. Pick the deepest one, and count the big boxes.
• Next, look at the R-waves in V5 and V6. Pick the highest one, and count the big boxes.
• Last, add those two numbers. If it is over 7 big boxes, the ST elevation is probably due to LVH

7 big boxes equals 35 little boxes, or 35 mm. Count the small boxes if you prefer, or if the you're near the cutoff. Looking at ECG #1 as an example, and counting the little boxes, we find:

So, about 40 mm, or 8 big boxes, so likely not a STEMI.

3. Is the QRS a normal width?

Rule #3 is simple -  If the QRS is over 0.12 seconds long, don't call a STEMI.

Probably the most common cause of dramatic ST elevation is the LBBB, as in ECG #3 above. You can also see the same pattern if the the patient has a pacemaker.

Now, the experienced and sophisticated paramedic knows that there is a way to interpret the LBBB for signs of STEMI, but even the "simplified" rules for determining STEMI in LBBB are somewhat complicated. Many paramedics are familiar with the rule, but the new paramedic shouldn't be expected to make this call. If the patient has a pacemaker, it's even more unreliable to interpret the ECG.

4. Is there ST depression in at least 1 lead?


Rule #4 - if there is no ST depression, do not call a STEMI.

Most students have learned that you should look for reciprocal ST depression in a STEMI. Unfortunately, because of the non-intuitive, non-anatomic way that the ECG is arranged, it isn't clear which leads are "opposite" each other. And the patterns of depression can vary a lot, depending on which coronary artery is occluded. For example, an "inferior" STEMI may or may not have depressions in I and aVL; it depend on whether the culprit artery is the RCA or the obtuse marginal.

A much simpler criterion for reciprocal depression is any ST depression on the ECG. This would eliminate, for example, ECG #2 above. Although the computer interpretation was STEMI, it is a classic example of early repolarization, or possibly pericarditis (less likely, as the ECG did not evolve). Another example from my ED is this ECG:

27 y.o., prior dx of pericarditis

Just like ECG #2, there is diffuse ST elevation without any ST depression. Not a STEMI.

Applying the rule

Let's take another look at ECG #4:

Okay, going through the rules:

• Rule #1 - Over 1 mm of ST elevation is seen in both V1 and V2, which are anatomically contiguous.
• Rule #2 - The S-wave in V1 is about 1 big box deep, while the R-wave in V5 is 3 big boxes high. That's a total of 4, so the QRS height is normal.
• Rule #3 - The QRS looks narrow, about 0.100 seconds wide.
• Rule #4 - There are ST depressions in the lateral leads, most notably in V5.

So we see that this simple 4-step rule, intended to assist the novice paramedic, actually picks up a STEMI that the computer missed!

The Bottom Line

This elegant method of ECG interpretation, although intended for the student, can be very useful for the experienced paramedic as well.

The IMMEDIATE trial: Should EMS give Glucose-Insulin-Potassium?

The results of the IMMEDIATE trial have been popping up repeatedly today on Facebook, partly because I "like" a few EMS FB pages, and also because one of the authors (Hi Carin!) is a FB friend (IRL too!).

Here's an example of the way the trial is being described:

"Cut the risk of death in half." Sounds great!

The result they are describing, to be specific, is that 8.7% of the people getting the placebo had a cardiac arrest, or died while they were hospitalized, while only 4.4% of the patients getting the study drug did. That's either an (absolute) difference of 4.3%, or about a (relative) 50% decline.

Such an effect would be stunning.  In the years after thrombolytics and aspirin were introduced, the incremental benefits of new therapies for AMI have been getting smaller and smaller. This result here would blow the others out of the water.

For instance, back in 1988, it was shown that either the use of aspirin or of thrombolytics reduced the risk of death in MI by about 2-3% over placebo. The combination was better of course.

After that, it's been harder to show that the more complicated and expensive therapies save that many more lives. When we send a patient to the cath lab for an AMI (instead of giving a thrombolytic in the ED), for example, there isn't that huge a benefit. One recent analysis suggested that, overall, you could only find a 0.7% difference in mortality (6.6% vs 5.9%) between lysed patients, and those that went for PCI. A lot of money for not much gain.

So, if this combination of glucose, insulin, and potassium (GIK) could cut mortality in AMI from 6.6% to, say, 3.3%, it would be freakin' amazing.

"I bet there's a catch. There's always a catch."

Well, I don't mean to be an Eeyore, but the perhaps we should wait for, yes, "further study." I offer three reasons why:

1. They weren't studying mortality.

The principle outcome they were studying was whether the initial presentation of ACS would progress to an MI, or it would be an "aborted" MI. This is the outcome that they believed had the most biochemical and clinical justification, and they clearly thought that it had a reasonable chance of being demonstrated.

It turns out there was no difference in the percent of people who progressed to completed MI - the GIK infusion did not help, at least not here. So the trial is negative for the real primary outcome.

2. There were 12 secondary outcomes.

Look at the table of the results:

Remember: the outcome they staked the success of the trial on was the one at the top: "Progression to MI," for all participants.  The rest are a bunch of secondary outcomes, and they don't count to the same degree as the primary outcome.

Analogy: A friend is flipping a coin, and you call heads. That's your primary outcome of interest. But if you also say to your friend "Okay, I call heads, but I also call it if you drop the coin, if it flips over 5 times in the air, if your phone rings in the next 30 seconds, or if your nose starts to itch in the next 10 seconds.

Now, you may be wrong about heads, but say your friend's nose does indeed start to itch in the next 10 seconds? Will he concede defeat? What will he say?

"No pick! NO PICK!" 

Most likely your friend will point out that the most relevant and important prediction you made was heads vs tails. Furthermore, you called out such a long list of other items that you were almost certain to come up with a positive result. He will insistent on another coin toss, where the primary outcome is now nose-itching, not heads or tails.

The same holds in statistics and study design, and is also why the authors state in their conclusion (my emphasis):

"The primary end point was not significantly different between groups, and the observed favorable results of GIK were based on prespecified but secondary end points, although biologically plausible and consistent with preclinical studies. The study tested one primary hypothesis, 3 major secondary, and 6 other secondary hypotheses. All were prespecified and no adjustment for multiple comparisons among the secondary end points was made; thus, reported significance levels should be considered approximate. Accordingly, given the lack of complete consistency of the findings, and the modest P values for most of the statistically significant findings, it would be appropriate to describe the observed favorable effects on the secondary outcomes as generating clinically testable hypotheses for evaluation in larger cohorts."

3. 30 day mortality seems pretty important too...

Ok, say you can take the "cardiac arrest or in-hospital mortality" results at face value. What, then, shall we make of the 30-day mortality? It was shown to be basically the same in both groups.

We just saw this discussion take place last month. A study from Japan showed that giving epinephrine in cardiac arrest got people to the hospital with ROSC more often, but the 30-day mortality was no different (We'll leave the neuro results alone for now.).

It would be nice if epi put all the dots on the right side of the graph. But it doesn't.

So, say the results are right - people don't die or arrest in the hospital as often, but they still die in the first 30 days just as often. Now, maybe everyone's hospital stay was over 30 days, but I doubt it.

Still feel excited?

Bottom line:

I believe that EMS has an essential role in managing ACS, of course. But, as it stands, giving this mixture to your ACS patients is not yet ready to be added to your drug box.

Just a little burning... and a ton of bricks.

To get back in the flow after the holidays, I got a small one. No big mysteries either - it's an MI, and there's some atrial fibrillation. But it's a nice example of ALS gettin 'er done. Thanks to Tyler, from AMR, for taking care of this lady.

So this 60-ish woman with an "extensive cardiac history" calls 911 for a little burning in her epigastrium, and a feeling of palpitations. Upon further questioning, she admits that she also feels like she has a "ton of bricks" on her chest.
First ECG:

Okay, got some work to do here. A bit of diltizem, get the aspirin on board, and a little nitro. This all brings down the load her chest to just a few bricks. Time for another ECG!

Hey, where did the  *** ACUTE MI SUSPECTED *** label go? To me, the ECGs look pretty similar, but some element in the interpretation algorithm - the depression in aVL? The STE in aVF? - changed enough such that the computer didn't want to make the call. Now, on a gut level, the ST segments in the inferior leads "feel" the same as before, but it sure looks like we have lost the strict "1mm of elevation" criteria that's been drilled into our heads.


We got an ECG in the ED which looked basically the same as the EMS tracing.

 Hmmm.

This is a tough one. It looks like we just fixed a potential cath lab patient, but you should be dubious. You can change a lot of ST depression with NTG and diltiazem, maybe even re-flip some inverted T-waves. But not too many things (at least until we get tenectaplase in the protocols) "fix" ST elevations.

So, the answer to confusion about new ECGs is usually an old ECG. Tough to do at 75 mph, but somewhat easier in room 5.

Our lady's ECG from the recent past:

About 4 months ago

Tyler and I compared the two, and agreed on our interpretation - activate the cath lab. After a brief conversation with one of the great cardiologists at Cardiac Specialists, our patient was whisked up to the cath lab.

Good thing too. Turns out she had thrombosed a stent that had been placed some years back in her RCA. Real bad luck for her, despite being on Coumadin for her a fib, as well as aspirin!

So what is the larger point here? 

If the paramedic had just looked at the rhythm strip and (correctly) treated the rapid a fib, the less-prominent ST elevations might not have been noticed in the field. Heck, it might have slipped past me in the ED! On the other hand, a second ECG may have shown growing elevations - you never know. That's why in some regions EMS is now obtaining up to 3 ECGs in the field as a matter of protocol, and they are catching more STEMIs as a result.

By the way, when I talked to the cardiologist during the cath report, he had one request - that we send the patient up with the prehospital ECGs!