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.

Did the machine miss something big?

I'm going out on a limb here, since I don't have the cath report yet. But I'm getting it soon, so we will have some closure on this!

The case:
A 68 year old male called 911 for "10/10" chest pain, and took aspirin before EMS arrival. Nitroglycerin was given by the medic, but it dropped the BP. Some normal saline took care of that, and transport was expedited.

The first ECG:

Computer interpretation: "Widespread ST-T abnormality suggests myocardial injury/ischemia"

Literally seconds later, the monitor showed a burst of activity:

A repeat ECG then showed:

No further events enlivened transport to the tertiary-level, primary-PCI facility.

So what does the first ECG show?
This ECG suggests a proximal LAD occlusion in two different ways, and justifies cath-lab activation, in my view.

The first pattern is likely familiar to astute 12-lead ECG readers. There is widespread depression throughout the ECG (II, III, aVF, and V3-V6), and ST elevation in aVR. Such a pattern indicates either severe 3-vessel disease or severe occlusion of the left main artery.

The second indication of LAD occlusion is not as well-known. Note the upsloping pattern of ST depression in the precordial leads.  This is distinct from the horizontal or downsloping pattern that you often find with a posterior AMI.

For example, this posterior MI demonstrates horizontal ST depression:

Source

Another example of a posterior MI shows a downsloping pattern of the ST segment:

Source

By contrast, in our ECG we have a sharply upsloping ST segment. Furthermore, it terminates in a tall, fairly sharp, T-wave.

DeWinter "waves"
Back in 2008, de Winter and a few other authors described a ECG pattern that they had seen in 2% of anterior AMIs. Interesting, all of the patients with this pattern had occlusions of the LAD in the proximal region - a very serious blockage that could infarct a good chunk of myocardium.

[T]he ST segment showed a 1- to 3-mm upsloping ST-segment depression at the J point in leads V₁ to V₆ that continued into tall, positive symmetrical T waves. The QRS complexes were usually not widened or were only slightly widened, and in some there was a loss of precordial R-wave progression. In most patients there was a 1- to 2-mm ST-elevation in lead aVR

They offered 8 examples of the precordial ST-T pattern:

Interesting looking ST segments and T-waves! Comparing these examples to our patient, looking at a blow-up of the precordial leads:

Upsloping ST-segment depression? Check.
Tall, positive, symmetrical T waves? Check.
Loss of R-wave progression? Check.
Normal-width T-wave? Check.
ST-elevation in aVR? Check.

So even without the 20/20 hindsight that blogging affords me, I'm anticipating a proximal LAD occlusion.

The final ECG
It appears the ST segments have normalized - both the ST elevation in aVR, and the ST depressions in multiple leads have returned to baseline. Even though this spontaneous reperfusion is an encouraging development, the patient still requires emergent angiography in my opinion, given the high likelihood of a dangerous, unstable lesion.

The Bottom Line
There - you know what I know now. Do you see anything that points to an alternative diagnosis, another concomitant problem, or different management?

I'll dig up the final results, and and them in the comments in a few days.

Why do paramedics not want to treat pain in kids?

Forgive me for my provocative title.

Of course, most paramedics do want to treat pain in kids. It's been shown, however, that EMS (like many areas of medicine) doesn't do a great job treating it. Why is that?

Quantitative versus qualitative research

Studying many questions in EMS is relatively straightforward, as you can always look at the numbers.

Does prehospital CPAP prevent intubations? Just count how many people get tubed in the ED! Does use of a CPR-machine save lives? Well, count up how many patients get ROSC!

These sorts of studies, where we look at numerical comparisons, rates, and statistical differences are all quantitative - these rely on obtaining and comparing numbers. To answer this question (about what keeps medics from providing analgesia to pediatric patients), however, EMS researchers in Rochester NY used a qualitative method. 

So this study didn't involve measuring or testing, and collecting a bunch of numbers. Instead, the authors went out and, essentially, listened to what paramedics had to say on this topic!

PubMed link

How they did they do the study?
Getting a paramedic to open up and share their experiences is not exactly the hardest thing in the world...

Pictured: A whole book about medics talking.

 Far from just writing down a bunch of "war stories," however, the authors followed a few steps to ensure they obtained useful and credible information. 

They recruited medics from a variety of agencies in western NY state, with differing levels of experience, and varying levels of comfort dealing with kids. They also brought in a paramedic to actually conduct the interviews, figuring that this would be less intimidating than a physician or PhD. They also tried to figure out a useful way to guide the interviews, designing a set of provocative questions, but also planned to let the medics talk freely and widely on the topic.

So what did the medics say?

Some surprising things!

Now, this sort of research isn't designed to produce statistics or predictions, but I want to highlight some of the results that were felt by the authors to be new and significant, as well as direct quotations from the interviews.

The authors found that "the majority [of medics] viewed relieving pain as unimportant and not part of their job."

They also saw that the medics, in general, "were also concerned that the patients might have an unknown allergy to morphine ... [and had] a similar concern for causing respiratory depression"

Lastly, they found that paramedics "reported receiving generally no response or a negative response from hospital pediatric ED staff."

There are a number of other results and quotations in the article, but I think that these 3 selections convey the general point. Analgesia for pediatric patients is seen as fraught with risks, and is not emphasized as a priority.

As the medics see it, there are few ways to win, and many ways to lose!

Given the inconsistent support from supervisors and ED staff, there is every incentive to shove the issue off, and let the ED handle analgesia.

So, what can be done?

Paramedics are known for their aggressive attitudes in the field, and they don't shy away from challenges. Drilling needles into bone, cardioverting VT with a pulse, or even giving tPA in the ambulance - medics get into the field so that they can tackle the tough problems, not avoid them!

So it's not too hard to figure out where the medics acquired these perceptions about pediatric analgesia. They got these ideas from their supervisors, from their EMS educators, from their rotations in the ED, and in discussions with ED nurses and medical control doctors every day. I agree wholeheartedly with the authors when they conclude that

... the onus of responsibility to change the belief structure regarding pediatric pain management lies not with the paramedic, but with physicians, hospital staff, and paramedic supervisors.

The Bottom Line...

Medics, like all of us, like to engage in a modest amount of medically-appropriate bragging.

"Modest bragging" source

Whether it's sinking a tight ET tube, reversing a bad CHF with aggressive CPAP and nitro, or cardioverting VT in a patient's living room - it's all good material for illustrating your medical prowess. So why not with analgesia?

Perhaps in the future, we'll have quotations from medics that read a little different from those in this study. So, if medical control physicians all do our job right, we'll hear medics bragging about how many mg/kg of morphine they gave, or how quickly they medicated the kid with a femur fracture!

With that in mind, I made my own EMS meme. If we do our jobs right, maybe this will be less of a joke, and more of a reality in the future.

I can getz artsy on Cheezburger!

Should we increase the duration of CPR before "calling it?"

If you have worked in EMS for longer than one shift, you know how most codes will end up.

True story: During my tech/medic days, I got to tie a few toe tags myself.

This is old news - if EMS doesn't get a pulse back by the time the patient is moved onto the longboard, the prognosis is grim.

That's why the authors of the ACLS guidelines support appropriate field termination-of-resuscitation, writing in the 2010 Ethics portion of the ACLS guidelines:

Field termination reduces unnecessary transport to the hospital ... , reducing associated road hazards that put the provider, patient, and public at risk. In addition field termination reduces inadvertent paramedic exposure to potential biohazards and the higher cost of ED pronouncement. More importantly the quality of CPR is compromised during transport, and survival is linked to optimizing scene care rather than rushing to hospital.

They provide a suggested algorithim for field termination by paramedics, based on the most recent evidence:

The protocols for the Sponsor Hospital Council of Greater Bridgeport reflect this evidence. 

The relevant section, 3.16,  provides criteria for termination, which are, in part:

Most EMS systems around the country have similar protocols, and comfort with "calling it" onscene has been increasing in the EMS community.

And then this happens...

You can always trust what you read on Twitter!

Oh boy - are we going to go back to transporting them all to the ED?

So what's this new study?

Link

This study used data from a retrospective registry, collecting data from 435 hospitals over a 9-year period (2000-2008). They ended up with about 65,000 patients who had had a cardiac arrest while in the hospital.

First, they looked at how long patients received resuscitative efforts, and calculated the average duration of CPR at each hospital for patients who did not have ROSC. 

That last part is key - when the news reports talk about "how long patients got CPR," what they really mean is "the average duration of CPR at each hospital for nonsurvivors." Subtle, but important difference.

Next, they figured out a way (regression analysis) to make all the patients and hospitals "equal." For example, patients who came in to the hospital with CHF were clearly at higher risk of cardiac arrest than those who had cellulitis, so they figured out the difference, and calculated it in mix.

Last step - they looked at the "average" cardiac arrest patient at the hospitals with the longest average duration of resuscitation, and compared the survival rate with patients at the hospitals with the shortest average durations.

What did they find?

First, they found a some variation in how long hospitals would attempt to resuscitate patients. The hospitals that "coded" non-survivors for the shortest time did so for about 16 minutes, while those hospitals in the more persistent group ran resuscitations for an average of 25 minutes. These averages hide, of course, a lot of individual variation.

So how did the patients at the 16-minute hospitals (quartile 1 in the figure below) fare compared to those at the 25-minute (quartile 4) hospitals?

There was a 12% difference. 

Put another way, for every 100 patients that survived a code at the 16-minute hospital, the 25-minute hospitals (on average) would have 112 survivors.

So, does this apply to my patients in the field?

First, keep in mind that this study only looked at in-hospital cardiac arrest. Importantly, they excluded arrests that occurred in the ED, and EMS codes were not included either. We already know that in-hospital cardiac arrest patients are different from those in in the pre-hospital realm, so the results are not immediately applicable.

Second, the results are modest, and may be as small as only a 2% survival advantage if you look at the confidence intervals (95% CI) in the figure.

But probably the biggest reason to not let this study change your practice is that it wasn't comparing patients - it was comparing hospitals. And those hospitals were likely doing more than just doing CPR for longer periods of time. They may have been employing better CPR, getting people and resources to the patient faster, or using better post-resuscitation care. We don't know anything else about the hospitals except that they tended to do CPR for longer on the non-survivors!

The Bottom Line
Data from retrospective, registry trials like this is provocative, not least because it can generate statistical results from the large numbers of patients included. It's impossible, however, to explain those results, or show cause and effect. For that we need prospective trials. 

I don't see anything in the current study that could justify changing our current approach, so keep following the current protocols for termination, provide quality CPR, and if you do have a reason to transport while continuing resuscitative efforts, do so safely!

New Guidelines for Anaphylaxis

The ALS guidelines for managing anaphylaxis have just been updated. It's a good time to both describe the changes, as well as explain why they were changed.

What Changed?
First, what was changed?

The ALS treatment for anaphylaxis has been changed from subcutaneous epinephrine to intramuscular, as well specifying injection in the thigh.

Let me show you the exact changes:

In addition, the guideline for allergic reaction was also changed:

Of course, the pediatric guidelines were changed as well, simplifying the dosing, and changing the route:

Okay, but why were the guidelines changed?
Fair question.

The use of SQ epi for anaphylaxis has been around for a while, and had previously been seen as the standard of care. EMT-Basics could use the Epi-Pen, and it may have been assumed that this was solely because they had to use a simpler, "fool-proof" system, while the ALS providers were trained to administer the standard treatment.

Ironically, though, the EMT-Basics have been the ones who have been providing the "state-of-the-art" therapy, while ALS providers have been held back!

Epi needs to go IM, in the thigh.
The best evidence shows that epinephrine is best given IM, in the thigh.

For example, in this study the researchers compared the levels of epinephrine in the blood after giving it either subcutaneously or intramuscularly, and either in the thigh or deltoid area.

This graph explains it all. The orange and yellow lines represent epinephrine given IM, in the thigh. The serum concentrations are clearly more elevated than the other methods. By contrast, SQ epi in the arm (green line) doesn't bump epinephrine levels much higher than the placebo injections!

What about Benadryl & Solu-Medrol?
There are no changes in the guidelines regarding these medications.

In fact, it's worth re-emphasizing that these medications are just adjunct treatments for anaphylaxis, and some experts do not consider them essential. I reviewed in a recent post ("Anaphylaxis Knowledge Among Paramedics") the misunderstandings that some paramedics have about this, and also about the contraindications for epinephrine in anaphylaxis.

(Spoiler: There are no contraindication to epinephrine in anaphylaxis.)

The Bottom Line
Paramedics, starting now, need to treat anaphylaxis with intramuscular epinephrine, in the thigh.

For the full Paramedic Treatment Guidelines, go to the website to download the updated  protocols (pdf).  EMT-Basics, on the other hand, can just keep using their "old" protocols.

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!