I “over-diagnosed” an ECG. Maybe you should too.

It’s important to be wrong now and then. Not just for the usual blather about being humble, understanding cognitive biases, or even nailing the Kobayashi-Maru test.

Don't do it...

Don’t do it Saavik…

No, it’s important to be wrong in the right sort of way, a willingness to be humble in the interest of patient care. Let me explain!

Case #1: I was sooo right.

EMS brought in a middle-aged male who was “found on the floor,” having been their for an unknown period of time. Their medical history and medications were also unknown, and his altered mental status didn’t help. Vital signs were okay, although the heart rate was unexpectedly low for someone who looked sick and dehydrated. While my resident was examining the patient, I talked with Sara, the paramedic, about the ECG.

EMS pseudo hyper k

“Huh,” I said to Sara, “funny it’s so slow, since he looks dry as dust. T-waves also look a bit funky – I wonder about hyperkalemia. Hey, don’t be afraid to empirically treat if the history and ECG make you suspicious.”

We grabbed our own ECG in the ED:

pseudo hyper k 2

ACUTE MI? Wat R U doin computer stahp

This was also supportive of hyperkalemia, and so I pushed calcium before waiting for the lab results. The potassium turned out to be 6.3.  #JediECGskillz   #AmIGoodOrWhat

Case #2:   #OrWhat

An elderly female with no prior ECGs, or records of any sort, was brought in by EMS with a report of “altered mental status.” She actually seemed mostly okay to me, but the veteran paramedic, Chris Lovell from Norwalk, showed me the ECG:

paced rhythm t slope

Now, I know what you’re thinking…” Yeah, it was paced, so some of you might say “you can’t tell anything from the ECG.” Probably should have listened to you! Two points in my defense however:

First, there are a number of case reports of hyperkalemia manifesting in paced rhythms. See here, here, and here, for example.

TL;DR? You might see loss of pacer capture, or significant QRS widening compared with an old ECG. Some of the better examples:


Second, did I mention I have Jedi-like skills in detecting hyperkalemia?


I proceeded to personally push 3 grams of calcium gluconate, and rechecked the ECG to document my “win.”


PRESS THIS NOW for the musical accompaniment.

No changes whatsoever. The potassium was completely normal.

Okay, so I was wrong. But was it a capital-F “Fail?” (Of course, my short answer is “No.”)

Here’s the longer answer why this was NOT a fail.

If an ER doctor tells you, with pride, that their accuracy in diagnosing STEMI is 100%, since they have never sent a “false-STEMI” to the cath lab, then they are either (best-case scenario) lying, or they are (worst-case scenario) very bad at their job.

If you never send a “false-STEMI” to the cath lab, it means that you are probably NOT picking up on a bunch of “true-STEMIs.” If you aren’t taking a chance on the small or subtle STEMIs, then you might be hurting patients.

The surgeons have understood this about appendicitis for generations. At least before CT scans started being used, a good surgeon was defined by the number of “negative” appendectomies you performed:

  • Too many meant you were too quick to cut, and had no sense of clinical judgment.
  • Too few meant you were missing “true cases,” letting them perforate & get septic.

We could view empiric treatment of hyperkalemia like that – if you aren’t overtreating at least sometimes, then you are probably missing critical chances to treat a potentially lethal condition. And unlike going to the OR or the cath lab, the EMS therapy (calcium chloride) is pretty benign.

So perhaps we should take pride in over-reacting (within your guidelines and protocols, of course). Maybe we could start to track our “negative-K” rates, and even start to brag about them!

Nitro paste is NOT an emergency medicine drug – The Evidence

I have no idea why, but many paramedics clamor for including nitroglycerin paste in their drug bag. Baffles me. True, you don’t need to break the seal of the CPAP to give it, and you don’t need to use an IV. But this medication hardly belongs in the emergency department, let alone a 21st-century EMS rig.

Before I get to the most recent evidence, I first want to highlight this perspective about why prehospital use of paste doesn’t make sense.


First off, let me ask: In what other medical emergency, where a patient is diaphoretic, ghost-white, and tachy-crazy, do we apply an ointment – stat!



And why not? Because we already know that pharmacokinetics proves that this is not a “stat!” kind of drug:

  1. Nitro paste takes a looong while to reach a peak level (about 60 minutes), and
  2. You end up with pretty weak blood levels with paste. Like, 18 times lower blood levels, compared with IV.

So maybe a poultice of nitroglycerin and tail-of-toad was all the rage back in 1780, but we’ve made a few other medical advances since then…

Well, this was genius. But the rest of the medicine was garbage back then.

Well, this was genius. But the rest of the medicine was garbage back then.

But even more importantly, dosage is measured in inches?!? No other medication is measured this way! Even in the 19th century, the commonly prescribed (and completely toxic) mercury pills were prescribed in precise weights (e.g. 1 grain). Even if we don’t dose nitro paste in milligrams, you would at least expect that a liquid drug would be dispensed in 3-dimensional units (i.e. volume), or maybe even  2-dimensional units(i.e. area).

Instead, we administer it in 1-dimensional quantities, squeezed out of a fancy ketchup packet. Depending on how you rip the packet, and how thick (and how wide) your “1-inch” glob is, the patient could receive widely different doses.

Unfair comparison. Ketchup now has better packaging than NTG paste

Unfair comparison. Ketchup now has better packaging than NTG paste

Utterly nonsensical – It’s like we don’t even care about getting the dose right.

Well there’s a reason we don’t care: It doesn’t work.

The study: “Hemodynamic effects of NTG ointment in ED patients.”

This wasn’t randomized or controlled (but then again, the early studies that are usually cited in support of NTG paste weren’t exactly high-quality either). However, the data was collected prospectively.


Physicians in an emergency department enrolled patients who appeared to be in acute CHF, and who had NTG paste ordered for treatment.

Before the paste was slathered on, impedance cardiography (a noninvasive hemodynamic test) was performed. This test is supposed to provide data similar to that which could only be obtained with the use of complicated heart catheters (“Swans”) in the past. They measured not only the mean arterial pressure (MAP), but also systemic vascular resistance (SVR), cardiac output (CO), and thoracic fluid content (TFC), a rough measure of edema in the chest. This testing was repeated at intervals after the paste was applied.

MAP and SVR were the primary outcomes.


Most patients got “1 inch” of paste. Interestingly, while 20% of the patients received morphine, none got CPAP. Old school, brah!

Treat CHF with morphine? Then you likely know what this is.  Just sayin'.

Treat CHF with morphine? Then you likely know what this is.
Just sayin’.

A modest decrease in the MAP was seen after 120 minutes (106 mm Hg –> 99 mm Hg), but it’s unclear if this was because of the NTG paste.  Since this study was uncontrolled, this mild improvement could have been the natural course of the episode; i.e. regression to the mean, or “tincture of time.”

The SVR did not show any improvement; also known as afterload, SVR is the main target when treating acute hypertensive CHF, so this is pretty disappointing.


One of the secondary outcomes, TFC, showed a statistically significant decrease, but the clinical significance of a drop of 0.5 kOhm(-1) is dubious (see here and here).

So, basically a negative study. The nitro paste didn’t change the hemodynamics.

So what do you expect us to do now?
Either maximize your use of sublingual tabs or oral spray, or work to get IV NTG included in your protocols.  If you are going to break the seal on the CPAP to give NTG tabs or spray, give a good amount, and maximize absorption.

  • Hypertensive acute CHF patients require a stout dose of NTG to address the afterload – 2, 3, or even 4 tabs of SL NTG may be needed, and are quite safe.
  • These same patients may have (paradoxically) dry mouths, and squirting a bit of saline can enhance absorption of the tabs.
  • If you are using the spray, be aware that you don’t have to get under the tongue, you can also paint the top of the tongue as well.

And if you really want to avoid messing with your nice mask seal, and your service can’t afford fancy IV pumps, advocate for “push-dose vasodepressors.” Bolus doses of IV NTG as high as 2 mg, or even 3 mg, have been shown to be both effective and safe.

30 Day Challenge


Today is July 11 and I have not had a drink in 30 days.

Some of you may know that my mother suffers from advanced dementia and requires round-the-clock care. She is on hospice and I have been out on FMLA leave helping with her care (which is why I missed SMACC in Chicago).

This time away from work has allowed me to do some soul searching about life. Life is hard. Working in the emergency services is hard. Being a caregiver is hard. Being a good husband and father is hard.

I was drinking a lot. My mother goes to bed between 3:30 and 4:00 p.m. and my Dad and I would sit down at the kitchen table and enjoy a honey whiskey and ginger ale. Mostly it was honey whiskey with a splash of ginger ale. Then we’d split a bottle of wine. My Mom’s illness has been hard on my Dad.

My GERD was getting worse. I was taking Prilosec and Zantac every day. The results of my annual physical came back. My liver enzymes were abnormal. I told myself it was probably from lifting weights.

It was subtle at first. Like tiny little stress fractures you’d need a magnifying glass to see. I think we in the emergency services have very strong coping mechanisms. Maybe we don’t have any choice.

We see abnormal things every day. We deal with people more screwed up than we are. We endure stress. Lots and lots of stress.

I thought to myself, “I should probably cut down on the drinking.” I was forgetting to take care of certain things. I was waking up almost every morning with a hangover. The gutters at my house were overflowing with pine straw. My wife and I were getting on each others’ nerves. She’s in a doctoral program and she’s under a lot of stress, too.

I quit drinking for a few days. I didn’t have any withdrawal symptoms. But then maybe I wouldn’t. After all, for the last 18 years I have had to be sober for 24 hours every third day. I went to a firefighter wedding and didn’t drink at all. For the first time I noticed how much people drink at a wedding. My wife and I left early.

Two days later I fell off the wagon and got really drunk at my Dad’s house. I felt bad about it. Not because I think I’m an alcoholic (that’s a whole other topic). Because I failed to do something that I said I was going to do. That bothered me.

The next day I enjoyed a glass of wine with my Dad and announced that I was going to take a 30 day break from drinking. That was June 10. Today marks 30 days. That’s probably the longest I’ve gone without drinking alcohol in 30 years.

I’ve learned a lot about myself in the last 30 days. I’ve learned that I don’t need alcohol. I like waking up without a hangover. I enjoy having my evenings back. My GERD has mostly resolved and I’m off my medication. I suddenly have a lot more money in my pocket.

I used to think I loved eating out. Now I realize that I went out to have sushi so I could drink saki. I went to an Italian restaurant so I could drink red wine. I went out to my favorite Mexican restaurant so I could enjoy a margarita or two. I’m an expensive drunk!

I don’t know if I’m going to start drinking again or not and it’s not my intention to tell you how to live your life. But I do know a thing or two about the emergency services, stress, and drinking alcohol. Chances are that you know a thing or two about it, too.

Do you recognize yourself in anything I’ve just written? If so, I challenge you to take a 30 day break from drinking alcohol.

It won’t hurt you. I promise. It might even help.

Computer misses it, but the medic catches it.

True fact: I failed out/dropped out of grad school in mathematics. But despite having little enthusiasm for topology or complex analysis, nothing drives me more nuts than people who say stuff like “I’m not good at math – just not a math person, I guess.” This attitude is not just incorrect, it’s harmful. Most mathematics is quite straight-forward, if you practice and study conscientiously. Same with ECGs.

Stratford EMS was called for a (quite) elderly woman who wasn’t feeling well. And of course, she lived on the 5th floor of a building with narrow, twisting stairs. Nonetheless, the paramedic Jay and his crew humped all their gear, including the Like-Pak, up those stairs. Good thing too.

There was a small language barrier, but Jay ascertained that the woman was complaining of a “burning” in her epigastrium that she also felt in her back. This had started within the last hour. VS were normal, as was the exam, except that she “didn’t look right.” Time for the 12-lead!


Does it meet STEMI criteria? There’s a bunch of ST segment depression in the inferior and lateral leads, but (as you all know) that doesn’t usually count for field activation. There is ST segment in aVL, but it is < 1mm, and aVR shows only minor STE, while lead I shows none.

V2 and V3 show some STE, but it isn’t much, and it would have been easy for Jay to tell himself that, since the computer didn’t “see” it, it wasn’t really there. Instead, he turned his attention to V4….


… and noted that the T wave seemed pretty darn tall, relative to the R wave. Along with a hint of STD in V3, it triggered Jay to consider a de Winter-ish pattern.



The strict de Winter criteria require more ST depression, however, at least 1 mm, and we already have minor (but significant) anterior STE, so this ECG isn’t a “pure” example. However the morphology of V4 is pretty similar to that seem in a number of cases that Dr. de Winter evaluated, and who all turned out to have proximal LAD occlusions:

From http://dare.uva.nl/document/2/90500

From http://dare.uva.nl/document/2/90500

This pattern convinced Jay to call this in as a STEMI, activating the cath lab from the field. To be specific, activating it from the 5th-floor back bedroom.

Good thing too – it was “after-hours,” and the cardiology team needed time to get in to the lab form home. Also, extrication turned out to be a flail, squeezing the patient down narrow, winding stairs.

A second ECG obtained 10 minutes later, during the perilous descent to the rig:


The computer still doesn’t get it, but the ST segments in both lead I and V3 have started to straighten and move up, suggesting that the first diagonal is occluded, likely because the proximal LAD is blocked.


The Life-Pak finally made the call 15 minutes after the initial ECG. By this time, however, the patient was starting to look a lot worse, and the pressure was dropping. A fluid bolus was given, keeping the SBP barely above 90.


By the time the rig was pulling into the ED, 30 minutes after the initial ECG, the 12-lead wouldn’t have been missed by an EMT-B student during their ED observation time. At this point, however, the patient was in frank cardiogenic shock, and the Stratford EMS team was directed to bypass the ED, since they had given the cath team sufficient heads-up to prep the lab. Without the “bedroom-activation” that Jay made, this patient could have arrested while waiting in the ED.

Bring your gear in on every call. Every call.
Navy SEALS don’t leave their gear behind while they “just go check it out first,” and neither should EMS. A paramedic without their gear, and especially without their monitor/defib, is not that helpful.

Get serial ECGs when you suspect something.

Don’t be satisfied if the computer “didn’t say there was a STEMI.”

Practice, practice, practice your ECG skills! Jay felt comfortable committing to the early activation because he has worked hard at reading 12-leads, seeking feedback, and pushing his skills. He has developed a “gut sense” after hours of study, and hundreds of ECGs. He hasn’t been afraid to ask questions, accept criticism, and learn.

Conclusion to 59 Year Old Male: Unwell

This is the conclusion to our latest case, 59 Year Old Male: Unwell. I suggest starting there and reviewing the scenario before diving into this discussion.

I was glad to see our latest case generated quite a bit of debate. This is a difficult tracing coupled with an equally difficult clinical scenario, so it wasn’t surprising there were a variety of treatment plans. What’s less debatable, however, is the interpretation of the first two ECG’s:

Initial ECG

Fig. 1. Initial ECG showing STEMI with rapid AF and a bifascicular block. Click to enlarge.

  • Atrial fibrillation with rapid ventricular response
  • Right bundle branch block (RBBB) + left anterior fascicular block (LAFB) [Bifascicular block]
  • Acute STEMI due to a LMCA or proximal LAD culprit

I’m going to have to put together a second post where we actually discuss the management of this patient, but this article is going to focus purely on the electrocardiograms. There’s a lot of fine details we can (and will) pick apart, but the three points above should be spot-diagnoses in a case like this.

For most providers they aren’t.

And it actually has very little to do with individual skill or experience. Looking at the comments when we first posted the case, a lot of folks—including those who usually nail even our toughest cases—got distracted by the “wide and fast” rhythm. Unlike most of our other cases where we encourage a step-by-step analysis, this particular situation is one where strict pattern recognition may initially serve you better since over-thinking it can get you in trouble.

Once you train yourself to recognize the underlying pattern, however, the above diagnoses should come to you like instinct. After initially stabilizing the patient you can take a second look at the ECG’s to tease out more details and consider whether you might be might be dealing with a STEMI mimic (hyperkalemia comes to mind)—some would term that “System II” thinking—but your goal at the end of this article should be to recognize the three major findings listed above within seconds.

Rather than going step-by-step starting with the rate, rhythm, axis, etc… as we are all trained, I’m going to discuss it in the order my brain actually processed the images the first time I saw them.


The Pattern

Let’s start by running through the pattern that initial ECG brought to mind the moment I saw it: RBBB, LAFB, and massive antero-lateral STEMI.

ECG reproduced from this case at Dr. Smith's ECG Blog.

Fig. 2. Sinus tach, RBBB, LAFB, and massive STEMI. ECG reproduced from this case at Dr. Smith’s ECG Blog.

01 - 85yo M

Fig. 3. Uncertain irregular rhythm with RBBB, LAFB, and massive STEMI. ECG reproduced from this case on our blog.

Sinus tach (with extopy), RBBB, LAFB, and massive STEMI. Image reproduced from Figure 1 of the Invasive Cardiology article linked here.

Fig. 4. Sinus tach (with extopy), RBBB, LAFB, and massive STEMI. Image reproduced from Figure 1 of the Invasive Cardiology article linked here.

Image reproduced from the NEJM article linked here.

Fig. 5. Uncertain regular rhythm with RBBB, LAFB, and massive STEMI. Image reproduced from the NEJM article linked here.

Image reproduced from Figure 2 of the Journal of Electrocardiology article linked here.5

Fig. 6. Sinus tach with RBBB, LAFB, and massive STEMI. Image reproduced from Figure 2 of the Journal of Electrocardiology article linked here.

In all of these cases the patients experienced large STEMI’s due to a culprit in the LMCA or proximal LAD. Commit these tracings to memory.


Is There Really A STEMI?

While the pattern seems to fit, it’s still hard to pick out whether we’re actually looking at true ST-elevation on the initial ECG.

To be honest, the first thing I look at on almost any EKG is the ST-segments. As Willie Sutton [allegedly] said, “…that’s where the money is.” It’s electrocardiographic heresy to admit you don’t perform a step-wise analysis starting with the rate, rhythm, axis, etc… (though anyone in-training should and I still do when practicing), but my gut doesn’t care that the complexes are wide, fast, and irregular—if I’m not immediately cardioverting the patient or pushing calcium (another discussion), my next priority is identifying STEMI.

I chose to share the messy ECG at the top of the page several hours before updating the case with a cleaner tracing for a very specific reason: though you cannot accurately assess the precordial leads on that first ECG, it’s still diagnostic for STEMI.

Keeping with our policy of going right for the money, rather than trying to dissect out the J-points in all the leads or wading through the precordial artifact, let’s just focus on the two leads with the most prominent ST-deviations: III and aVL.

ST-elevation in aVL with marked ST-depression in III.

Fig. 7. ST-elevation in aVL with marked ST-depression in III.

Now those two leads slightly deceiving. Given only Figure 7 you might think the QRS duration is only 90 ms instead of its actual measurement of something like 160 ms (more on that later), but that’s okay. I usually don’t condone self-deception or sloppy interpretations but in this case it doesn’t really matter whether the QRS is 90 or 160 ms wide; there is significant ST-elevation in aVL with a large amount of ST-depression in lead III.

That alone is diagnostic of a STEMI.

Nothing else will give you that pattern of ST-elevation in aVL with marked ST-depression in lead III. For an example with much more subtle ST-deviations check out this case: The 360 Degree Heart – Part II. Since the “high-lateral” territory is poorly covered by the 12-lead ECG, III and aVL are all is necessary to seal the diagnosis of “high-lateral” STEMI—even without “two contiguous leads” showing ST-elevation.

To make life easier we do have a lead contiguous to aVL showing ST-elevation though: lead I.

Fig. 8. ST-elevation in lead I.

Fig. 8. ST-elevation in lead I.

There’s too much movement to properly assess the precordials on the initial ECG but at this point in our interpretation it doesn’t matter—our patient is experiencing a STEMI. I keep saying it because it’s equal part simple and important. Once we’ve reached that conclusion, we don’t need to waste time trying to dissect the other leads. Whether the STEMI is lateral, antero-lateral, or antero-septal-postero-lateral (I’m not making up that distribution), our initial management is going to be the same, so time spent searching for further ST-elevation on the ECG is time wasted during the initial phase of our management.

Thankfully, for the curious, we do have a cleaner tracing to work with. It was obtained approximately 20 minutes after the first (and of course there were others performed in-between as well).

Fig. 9. Second ECG.

Fig. 9. Second ECG.

Fig. 10. Precordial ST-elevation on the second ECG.

Fig. 10. Precordial ST-elevation on the second ECG.

On rare occasions you can actually encounter a rate-related STEMI due only to the demand ischemia of an increased heart rate in patients with stable coronary artery disease. For that reason it is important to repeat the ECG after the heart slows down in a case like this to evaluate for resolution of the ischemic changes. In our scenario the ST-deviations are less impressive after slowing but still very evident.

Fig. 11. ECG after rate control.

Fig. 11. ECG after rate control.

So it looks like our patient definitely needs the cath lab…


Bifascicular Block

In addition to his STEMI this patient also has a bifascicular block.

Most of the time bifascicular blocks aren’t that concerning from a prehospital and emergency medicine perspective. Folks walk around with them all the time and until they start experiencing syncope or high-degree AV-blocks the finding is of minimal importance. That stops being true in the patient who is acutely unwell and experiencing a STEMI.

Digressing for a moment, as a specialty we’ve spent years obsessing over “new LBBB” as a criteria for STEMI activation, but it’s actually pretty rare to encounter a truly new LBBB during acute STEMI. Most of what we presume to be “new LBBB’s” are probably chronic findings that just haven’t been documented yet (+/- acute STEMI). That’s because the left bundle branch is a pretty robust system, with the anterior (superior) fascicle supplied by the LAD and the posterior (inferior) fascicle supplied by the posterior descending artery (PDA). Since it receives a dual blood supply, it’s pretty difficult to knock-out both the anterior and posterior fascicles at the same time and create an acutely new LBBB (though it does happen occasionally). Instead, it usually takes long-term processes like aging, fibrosis of the conduction system, or cardiac remodelling to elicit a LBBB.

It’s not often taught or emphasized, but what’s more common (and actually more deadly) during an acute anterior STEMI is a new RBBB. Obviously we still run into the issue of debating whether the RBBB we see is truly “new” or just “new to us,” but because the right bundle branch receives its blood supply solely from the LAD, proximal occlusions of the LAD (or the LMCA supplying it) are more likely to produce a truly new RBBB rather than LBBB.

When that happens it signifies a very high-risk lesion in the proximal coronary arterial tree with a large area of injured and ischemic myocardium. These patients are salvageable but will do poorly without immediate revascularization (and often experience significant morbidity or mortality in spite of our efforts).

So not only does our patient need the cath lab, he needs it as soon as is humanly possible, with the understanding that there is a high likelihood he will deteriorate on the way…


Wide Complex Tachycardia


Fig. 12. Our second ECG in a more rhythm-friendly format.

Fig. 12. This is the ECG from Figure 9 in a more rhythm-friendly format.

The first two tracings demonstrate a fast, mildly irregular, wide-complex tachycardia (WCT). Here’s our differential.

  • Rapid atrial fibrillation or flutter
  • Ventricular tachycardia
  • Sinus tachycardia with frequent PAC’s
  • Atrial fibrillation or flutter with an accessory pathway

Picking the low-hanging fruit, there’s no changing QRS morphology so that makes AF with an accessory pathway highly unlikely. Also, while sinus tach can hide P-waves, the irregularity of sinus tach w/ frequent PAC’s makes it much harder to hide atrial activity during compensatory pauses. I see no convincing atrial activity here so that’s off the table as well. Finally, while the irregularity is somewhat subtle, there’s no pattern to it and again no visible atrial activity, so it’s not a-flutter.

That leaves rapid AF and ventricular tachycardia as possibilities. I know, most folks would have eliminated VT the moment they noted the WCT to be irregular, but I kept it in because it’s both an important diagnosis that affects management and the next-most-likely option after rapid a-fib. I also kept it in because VT can exhibit irregularity in certain situations, including (but not limited to):

  • In the presence of frequent capture and fusion beats.
  • Minor variations soon after onset, while the arrhythmia “settles in.”
  • If there’s a complex scar allowing multiple exit points for the VT.

There is also a slight irregularity to even “regular” VT at times, but it’s usually less than 40 ms of variation and barely perceptible on the surface ECG. What simplifies things for us here is that there are cycle-length variations exceeding 160 ms, ruling out physiologic variation. Also, the QRS morphology is pretty static, ruling-out capture or fusion beats or multiple exit sites.

Really, the only diagnosis we’re left with is rapid atrial fibrillation.


The Shortcut

Of course we don’t have time run through a step-by-step differential like that with a critical patient in front of us, so here’s how I actually diagnosed the rhythm:

  1. I recognized the pattern of massive STEMI with a bifascicular block.
  2. Based on the extensive infarction and “shocked” presentation, I was expecting a compensatory tachycardia like sinus tach or rapid AF.
  3. Knowing the QRS morphology was “typical” for that kind of STEMI, I ignored it as a factor in the rhythm and mostly focused on regularity. It was irregular, ruling-out sinus tach and ruling-in AF.

That took all of 10 seconds. Then, when I had a chance a few minutes later, I spent more time dissecting the rhythm to make sure I wasn’t missing anything like irregular VT.



As typically occurs with these cases of STEMI + bifascicular block, there was a lot of confusion over the actual width of the QRS and where to measure the J-point. After spending too much time drawing plumb-lines and playing with a set of screen calipers, I’m calling the true QRS duration 174 ms.

Fig. 13. QRS duration.

Fig. 13. QRS duration.

Turns out I could have saved myself a lot of time because that is the same exact measurement the computer calculated (see Fig. 12). Still, I always say that the sicker the patient is the less you can trust your computerized measurements, so now I can sleep soundly knowing that is probably the right value.



So what happened? The patient obviously got his rate controlled as stabilization (see Fig. 11) and then went for emergent cardiac catheterization where an ostial LAD lesion was identified and removed with suction thrombectomy. Although he now has a residual decreased EF (approx. 35%) and congestive heart failure, he has survived several years since his near-fatal MI and maintains a decent prognosis for the time-being.

For more discussion on the actual management of this case look forward to Part 2 of our conclusion next week.

59 Year Old Male: Unwell

It’s the middle of the afternoon when you are dispatched to the residence of a 59 year old male with a chief complaint of general illness.

When you arrive on scene you encounter a middle-aged man in obvious distressed lying on a couch. He is pale, gray, diaphoretic, and drowsy. He states that he has felt drained for the past 8 hrs; unable to catch his breath or get up off the couch with a heavy sensation in his chest. 30 minutes prior to your arrival he vomited and felt like he was going to pass-out so he decided to call 911.

His radial pulse is faint, rapid, and irregular while his skin cold and moist.

  • HR – 150 bpm, irregular
  • SpO2 – Unable to get a clear waveform
  • BP – 72/42 mmHg
  • RR – 26. labored
  • Temp – 36.6 C (97.9 F)

Breath sounds reveal crackles bilaterally.

Multiple 12-lead ECG’s are performed but suboptimal due to the patient’s increased work of breathing and inability to stay still. This is the best of the bunch:

Initial 12-Lead

BGL is 156 mg/dL.

He is a bit lethargic but properly oriented and answers questions appropriately, albeit slowly.

  • S – As above
  • A – No known drug allergies
  • M – None
  • P – Appendectomy @ 24yo
  • L – Soup 45 min prior, which he vomited soon after
  • E – Can’t recall—states he has felt terrible “all day.”

Regarding the chest heaviness…

  • O – Gradually through the morning
  • P – Nothing makes it better or worse
  • Q – Heaviness
  • R – None
  • S – Unable to quantify
  • T – Worsening x 8 hrs

What are your management priorities for this patient?

What is your interpretation of the ECG?


 ***UPDATE (2015/6/29/ 14:00 EDT)***

After carefully transferring the patient to the ambulance and finding him a position of comfort (head-of-bed at 60 degrees—he doesn’t like to lie flat), you succeed in obtaining a cleaner EKG. Does this change your approach to the case?

02 - 12-Lead 02