Friday, October 22, 2021

An elderly man who dies 12 hours later - could he have been saved?

Sent by Anonymous, written by Pendell Meyers and Steve Smith

An elderly man with good neurologic baseline but history of CABG presented to the ED with acute lightheadedness, shortness of breath, and chest pressure radiating to both arms. He had just recently been admitted for similar symptoms which had been diagnosed as an NSTEMI, and he received a stent to the ostial LCX one week ago. At that time his EF was 30%. 

He returned to the same hospital where he had just received his LCX stent.

Here is his first ECG at triage, with chest pain temporarily resolved:

He then had spontaneous return of chest pain while in the ED, with this ECG:

What do you think?

The first ECG has an intra-ventricular conduction delay (IVCD) which is of the LBBB type (for textbook LBBB most would list a monophasic R wave in lateral leads V6 which is not present in this case).  For such a QRS complex, the modified Sgarbossa criteria should be used. With the exception of lead V2, there is appropriate ST segment discordance.  However, in V2 there is no discordance (i.e., it is isoelectric, which suggests that there is relative ST depression).  Moreover, the ST segment is downsloping, which should never happen in LBBB. This is nearly diagnostic of posterior OMI, to the point where serial ECGs and close investigation is mandated.  Additionally, there may be evidence of inferior involvement, with slightly too much STE and large volume T waves.

The 2nd ECG does indeed evolve to the point where the modified Sgarbossa rule is positive, with concordant STD in V2 and V3 (and also in V4,5)

Bottom line: the 2nd ECG clearly meets original and modified Sgarbossa criteria with concordant STD maximal in V1-V4. It is diagnostic of acute posterior OMI until proven otherwise, in the setting of this patient with clear ACS symptoms.

Here was his most recent ECG on file (not a baseline, recorded at the end of his stay for his NSTEMI)

Looks like posterior reperfusion T waves, which would make sense for a LCX STEMI(-) OMI. Notice the QRS is narrower at this time, without LBBB, but you could call it LAFB.

The EM provider diagnosed positive Sgarbossa criteria given the concordant STD in leads V2 and V3, and activated the cath lab.

The cardiologist cancelled the activation. 

The first troponin (high sensitivity trop T) returned at 1600 ng/L.   Again they tried to get the patient considered for emergent cath, with ongoing pain despite aspirin and heparin. But the cardiologist refused.

Side note: high sensitivity troponin T cannot directly be translated to compare to the older assays with which we have studied OMI, but we can make a rough guess: 2,000 ng/L roughly equals 2.00 ng/mL, well above our cutoffs used in our OMI studies (1.00 ng/mL for contemporary troponin T assays). This is a large MI.  (This level of troponin T is roughly equivalent to high sensitivity troponin I of over 20,000.)  

See this study of hs trop T in OMI: Baro R, Haseeb S, OrdoƱez S, Costabel JP. High-sensitivity cardiac troponin T as a predictor of acute Total occlusion in patients with non-ST-segment elevation acute coronary syndrome. Clin Cardiol [Internet] 2019;42(2):222–6. Available from:

Troponin peaked at 2000 ng/L in the middle of the night.

Early the next morning the patient developed progressively worsening hypoxemia and hypotension.

He coded and died about 12 hours after ED arrival.

No angiogram was ever done during that visit, and no autopsy was requested.

It is clear that this patient died of untreated posterior OMI, leading to cardiogenic shock, with the thrombosis at the new LCX stent being the obvious culprit. 

This patient had countless indications for emergent cath, and several advocates who tried to get this patient the correct care. But still was denied proper treatment and died.

I get these cases all the time. Sadly, it is a normal event in 2021 under the STEMI paradigm, despite the fact that it is so easily diagnosable, and even when it is not diagnosed on ECG, there are multiple guidelines that indicate that this patient deserves angiogram for ongoing ACS despite medical management and ACS with cardiogenic shock.

If you are a cardiologist reading this case, I would really appreciate your insights for the following questions: given the fact that this case was most likely an occlusion at the site of his LCX stent that had just been placed 1 week ago, what are the "repercussions" of that event in terms of metrics and statistics? Is the cardiologist disincentivized to cath the patient for fear of diagnosing a "complication" of the stent 1 week ago? What actual, tangible repercussions happen to the cardiologist? to the cardiology department? Please help us understand why these seemingly easy decisions are more complicated than we can see.

Learning Points:

Use the modified Sgarbossa criteria for LBBB (studied and proven), ventricular paced rhythm (studied and proven), and also for other LBBB-like QRS complexes (not yet studied). The principles of appropriate discordance can be applied to all wide QRS complexes in general.

In the setting of ACS clinically, whether in LBBB or in normal conduction, STD max in V1-V4 is posterior OMI until proven otherwise.

Regardless of the ECG, patients with ACS with ongoing ischemia (as shown by ECG ischemia or ongoing symptoms) despite medical management, or with electrical instability or cardiogenic shock, should receive emergent angiogram as per all guidelines. 

"NSTEMI" OMIs have almost double the mortality of NSTEMIs without OMI. Patients like this one make it obvious why this is. 

Monday, October 18, 2021

I thought the ECG diagnosis was obvious. But many missed it. So I'm showing it.

I was reading ECGs in the system and came across this one:

What do you think?

Computer diagnosis: 



I thought the ECG diagnosis was obvious, but no comment was made by the providers who ordered it.  That could be because they never saw it, as the patient eloped before full evaluation.  

But then I showed it to multiple smart providers and not a single one saw it.  So I thought it would be good to show it to blog readers.

Everyone went straight to the ST-T abnormalities, and came up with diagnoses such as pulmonary embolism, or subendocardial ischemia.

However: whenever you see ST-T abnormalities (abnormal repolarization), first look to see if they are secondary to (as a result of) abnormal QRS (abnormal depolarization).

Read the ECG systematically: Rate, rhythm, intervals, axes, voltages (QRS, ST, T), ratio of ST-T to QRS, morphologies

Here, the QRS is definitely abnormal.  The most obvious abnormalities are a large R-wave in V1 (and also V2, V3...) and also high voltage.  And also wide QRS interval -- so the QRS (depolarization) is clearly abnormal. But look more closely still: there is a short PR interval.  This should make you look for a delta wave.  

And there it is, pretty clearly evident in nearly all leads!!

This is WPW with typical repolarization abnormalities.  All of these ST-T abnormalities are expected, as they are secondary to the abnormal depolarization of pre-excitation.

I went to the chart:

This 20-something woman presented after smoking marijuana. She believes that it may have had some other drug added to it because she has had no similar reactions from past marijuana smoking. She reports that everything feels slow and distant. Endorses chest pain and auditory hallucinations. Denies EtOH/other drugs.

She had an ECG recorded and was put in the waiting room.  The wait was too long and she eloped.

After seeing this ECG, I called her back and made an appointment in Cardiology clinic.

Here are a number of interesting WPW cases:

WPW mimicking and obscuring acute MI (5 Cases)

(Case 5 is an amazing case that Pendell sent me when he was still an undergraduate)

Saturday, October 16, 2021

A 50s year old man with lightheadedness and bradycardia

 Written by Pendell Meyers with edits by Smith and Grauer

A man in his 50s with history of end stage renal disease on dialysis, prior bradycardia episode requiring transvenous pacemaker, diabetes, and hypertension, presented to the ED for evaluation of acute onset dizziness and lightheadedness starting several hours prior to arrival. These symptoms prevented him from going to dialysis, and his last session was three days ago. EMS found him with a heart rate of 30 bpm but normal blood pressure. He received 0.5 mg atropine with increased in heart rate to the 60s with improvement in symptoms. He denied chest pain or shortness of breath. 

Here is his triage ECG at 1533:

There is a regularly irregular rhythm with RBBB and possibly also LAFB morphology. The T waves are definitively peaked in many leads. The rhythm is possibly junctional with pauses or block, I'm not exactly sure. I asked Ken Grauer for help with this rhythm and he agrees it cannot be atrial fibrillation due to the irregular regularity, but with the artifact present also cannot definitively find atrial activity. His bottom line: "This rhythm is not 'following the rules' - so either hyperkalemia - or some other toxicity - or very severe and diffuse conduction system disease producing junctional escape with bifascicular block with some complex form of exit block." See his full comments reproduced at the end of the post. 

This ECG is diagnostic of significant hyperkalemia.

He was immediately given 2gm calcium gluconate, insulin and dextrose. Shortly after those therapies his heart rate is documented as improved to the 70s.

Initial labs showed a potassium level of 7.7 mEq/L.

Repeat ECG at 1801:

Improved heart rate and narrower QRS.

He later received a second dose of 2 gm calcium gluconate for down-trending heart rate.

He was emergently dialyzed and did well.

No more ECGs were recorded from this visit, unfortunately.

Approximately 1 year prior to this event, he had a similar event and presented with this ECG:

Junctional escape with similar RBBB and LAFB morphology, and peaked T waves. Notice the flat ST segments and narrow base of the T waves. This ECG was apparently not recognized as hyperkalemia (!). In my experience, these are some of the most commonly missed and dangerous hyperkalemia ECGs because many practitioners rely heavily on strikingly peaked T waves to start considering hyperkalemia on ECG. These T waves are in fact peaked, but they are more subtle than the textbook hyperkalemia ECG.

During this visit, the patient received transcutaneous pacing and an emergent transvenous pacemaker before the labs showed a potassium level of 7.3 mEq/L!

After treating his hyperkalemia, the pacemaker was successfully discontinued. He never received a permanent pacemaker.

After dialysis during that visit, a repeat ECG was recorded showing resolution of the RBBB/LAFB:

Notice the marked difference in the T-waves

Learning Points:

In medical school, I worry that the only consistent teaching you get about hyperkalemic ECG findings is peaked T waves and QRS widening. What should be taught includes the "Killer B's of Hyperkalemia": Broad (QRS widening), Brady (bradycardias), Blocks (AV blocks, bundle branch blocks), and Bizarre (bizarre morphology, OMI mimics, etc.). Some of the most important hyperkalemia ECGs are like the above: QRS widening that can be subtle or falsely blamed on RBBB alone, and T waves that are not perceived as classically peaked. Yet this ECG above is far more dangerous and far more hyperkalemic than the classic hyperkalemia ECG with only peaked T waves in the textbook.

Before you consider pacing a patient, consider hyperkalemia. I would go so far as to say that every patient about to be paced should receive calcium, unless there is certainty of a non-hyperkalemia diagnosis as the cause.


Ken Grauer's comments on the rhythm in the first ECG of this case (he was completely blinded to all case details, just the ECG):

This is tough — and I do NOT have a definite answer. I labeled the tracing (Figure-1):

Figure-1: The 1st tracing in today's case.

Artifact makes it difficult to assess for the presence of atrial activity. I thought BLUE arrows might represent retrograde P waves (as their placement seems pretty consistent) — but there is a lot of “noise” in the baseline — so I’m not sure if this really represents retrograde atrial activity or not …

What we DO know — is that the QRS is wide, and NO P wave precedes any QRS. We also know (as per Pendell) — that this isn’t AFib, because there is a definite pattern ( = a “regular regularity” to the rhythm) — with both the short intervals (between #1-2; 4-5; 6-7) all equal — and the long intervals (between #2-3; 5-6; 7-8) also all equal.

My #1,2,3 questions are what is the serum K+ level? We have a wide QRS and T waves really are peaked in multiple leads (even though the base of these T waves isn’t as narrow as is usually seen with hyper-K+) — but Hyperkalemia is notorious for QRS widening, brady rhythms and ALL SORTS of conduction disorders that do not “obey the rules” …

So if K+ is normal — then we really have an RBBB/LAHB configuration without sinus P waves — so suggesting perhaps origin of a ventricular rhythm near the left anterior hemifascicle — vs junctional escape with bifascicular block … (the surprisingly narrow initial part of the QRS suggests origin not directly from ventricular myocardium).

What is unusual for a simple block (or “exit block”) — is that the duration of the pauses. You can have an ectopic ventricular focus (even VTach) with various degrees of “exit block” out of the ventricular focus — but against the usual form of exit block is the fact that the long intervals (between #2-3; 5-6; 7-8) is clearly MORE than twice the shortest interval …

Of note — the R-R interval between beats #3-4 is LONGER than that between #4-5. I do not think this is for chance — and this is what you tend to see with Wenckebach phenomenon — but unlike typical Wenckebach phenomena is the overly long pauses (more than twice the shortest R-R interval). NOTE — You CAN have a ventricular rhythm (including VTach) with a Wenckebach-type of exit block … 

BOTTOM LINE: This rhythm is not “following the rules” — so either hyperkalemia — or some other toxicity — or very severe and diffuse conduction system disease producing junctional escape with bifascicular block (vs ventricular escape near the anterior hemifascicle) with some complex form of exit block …

Hope the above is helpful. Let me know if you find out more clinically about the patient — :) Ken


Here are a couple other cases of hyperkalemia with small, but peaked, T-waves:

Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer. (Physician also reads it as normal)

This is on a previous visit with K = 6.6:

After treatment: 

ST Elevation in I and aVL, with reciprocal ST depression in lead III

Thursday, October 14, 2021

A New Seizure in a Healthy 20-something

A 20-something year old who is the picture of good health presented with a new onset seizure.  A witness described what sounded like a 3 minute tonic-clonic seizure.  

Her seizure workup was negative and she was scheduled for an outpatient MRI and EEG.

Because she was persistently tachycardic, an ECG was recorded.  At the time her K was 3.2 mEq/L:

Here is the interpretation by the computer, confirmed by the over-reading physician:

P-R Interval 116 ms
QRS Interval 158 ms
QT Interval 422 ms
QTC Interval 485 ms
P Axis 259
QRS Axis 88
T Wave Axis 36

What do you think?

When I saw it, I was immediately alarmed:

First, I think there are P-waves underneath all that artifact, so it is not a junctional rhythm.  

The abnormality is in the QRS and QT intervals.  I measure QT at 500 ms, with Hodges correction (what our computer uses) = 582 ms, Bazett = 668 ms. Part of this long QT is the wide QRS, which the computer measured at 158 ms. If you deduct that extra QRS duration, you get a QT of 440 ms.  I think the QRS duration was also erroneously measured and it is really 130 ms.  Thus, the QT would be about 470 ms without this extra QRS duration, with the corrections at 552 ms (Hodges) and 628 (Bazett).  

What constitutes a long QT in the setting of prolonged QRS such as LBBB, RBBB, and Paced rhythm is complicated and beyond the scope of this post, but suffice it to say that the JT and JTc intervals are very useful, as is the T-peak to T-end interval, which measures the part of the QT which is most prolonged in patients at risk for Torsades: the last part of the T-wave.

The findings are NOT due to a K of 3.2.

A QRS of this duration in an otherwise healthy patient is also a red flag — extremely abnormal — always requiring further investigation.   

NEVER trust the computer QT measurement.  NEVER.  

Below I put in links to 7 of the many cases I have in which the computer missed a dangerously long QT.

Here we write about this (full text): 

Screening for QT Prolongation in the Emergency Department: Is There a Better “Rule of Thumb?”

Summary: if the heart rate is over 60, then use the rule of thumb that if the QT is more than half the RR interval, it is probably long and must be measured by hand.  If the heart rate is under 60, measure the QT and if the raw QT is over 485 ms, then it is too long.

Case Continued

I saw the patient in the ED and syncope never occurred to me.  It seemed so much like seizure by history that I did not even order an ECG.  Fortunately, after I left and before the patient was discharged, she did get an ECG recorded.

Unfortunately, the findings were not appreciated.

So when I was signing my charts the next day, and found that an ECG was recorded, I naturally looked at it (it is the ECG at the top of the post).

I texted the ECG and the story to our electrophysiologist, and he texted back "WOW!"


Next day she returned after I called her back.  This was her ECG with a K of 4.0:

Now there are prominent U waves in almost all leads, creating a long QU interval.  The QRS is again long at 140 ms.

Here is another:

And this one is STANDING (which is useful in congenital long QT syndrome)!!

There is more to the story which makes it even more fascinating, but that will have to wait for a formal published case report.

More cases of long QT not measured correctly by computer (these are all fascinating ECGs/cases):

Bupropion Overdose Followed by Cardiac Arrest and, Later, ST Elevation. Is it STEMI?

Friday, October 8, 2021

Hyperkalemia: is it the cause of this AV Block, ST Elevation, and T-wave inversion?

I was texted this ECG:

What do you think?

This was my response: "Yikes. Pacer and Cath Lab!!"

He asked: "Could this all be due to hyperK?"

I said: "Always possible. But it does not look like it.  Among the reasons I do not think it is all due to potassium is that the QRS is not wide."  Also, there are obvious signs of OMI, and though these can sometimes be mimicked by hyperkalemia, the K must be very high.

ECG analysis: Sinus tachycardia with third degree AV block and a junctional escape.  QRS is 100 ms.  There are inferior Q-waves with inferior ST Elevation of OMI, and T-wave inversion, suggesting reperfusion or subacute OMI.   The inverted T-waves are large, which is evidence of significant viable myocardium.  The lead reciprocal to lead III is aVL, and there is the obligatory reciprocal ST depression, but also a reciprocally large upright T-wave (a mirror image to the inferior inverted (reperfusion) T-wave.   There is also STD in V2 and V3, with large upright T-waves indicating reperfusion of the posterior wall.  There is STE of OMI in V5 and V6, with terminal T-wave inversion, also suggestive of subacute or reperfusing lateral OMI.

The tall upright T-waves in aVL and V3 might conjure up hyperK in your mind, but these T-waves are reciprocal to large inverted reperfusion T-waves: aVL reciprocal to III, and V3 is a posterior reperfusion T-wave, reciprocal to an imaginary inverted T-wave of the posterior wall.  

See my article on posterior reperfusion T-waves.  Posterior reperfusion T-waves: Wellens' syndrome of the posterior wall

Comment: Heart block with junctional escape is typical of inferior infarctions.  The RCA supplies the AV node.  The escape in LAD occlusion is below the AV node because if results in ischemia of the bundle of His and Purkinje fibers.  

Summary: subacute, reperfusing inferior, posterior, and lateral OMI with complete AV block

The clinical story came later:

It turns out that this patient presented with several days of vomiting, diarrhea, and syncope.  He denied any chest pain or SOB.  His vital signs were normal except for some bradycardia.  

He had had a prehospital ECG:

Pretty much the same, except P waves are more difficult to discern.

On further evaluation, he was in DKA, with glucose of 904 and K of 5.8.  They got the K down to 4.8 and repeated the ECG:

T-waves are larger still, which is a normal progression of reperfusion T-waves

Before the patient left for the cath lab, the initial troponin I returned at 31,000 ng/L (very high, a level only seen in OMI, and an initial one this high is only seen in subacute OMI).  So this is a subacute OMI.

Angiographic findings:

1. Left main: no stenosis.

2. LAD: type II, luminal irregularities, no stenosis. It supplies a D1 without stenosis.

3. Ramus intermedius: luminal irregularities, no stenosis.

4. LCX: non-dominant, supplies a small caliber OM that has an 80% stenosis (TIMI III flow).

5. RCA: dominant. Supplies an RPDA and at least 2 RPDAs. It is thrombotically occluded in the proximal segment.

Comment: The ECG shows evidence of reperfusion.   

I do wonder if:

1) the artery re-occluded between the last ECG and the angiogram, or if 

2) collateral circulation developed before the ECGs were recorded.

Formal Echo:

Normal left ventricular size.

The estimated left ventricular ejection fraction is 55%.

Regional wall motion abnormality:

-mid and basal inferior, akinetic. (this is the posterior wall)

-basal inferoposeptum, akinetic.

-basal inferolateral, akinetic.

Translation: inferior, lateral, and posterior OMI

Learning Point:

1. If hyperK is causing a PseudoSTEMI or PseudoOMI pattern, it will ALWAYS also cause a wide QRS.

2. If hyperK is causing a PseudoSTEMI or PseudoOMI pattern, the K will virtually always be above 7.0

Below are a number of cases of OMI mimics (PseudoSTEMI) due to severe hyperkalemia.  All had K of at least 7.0 mEq/L.

"Steve, what do you think of this ECG in this Cardiac Arrest Patient?"

Hyperkalemia and ST Segment Elevation, Post 1

35 minutes later:

A patient with chest pain and ST Elevation in V1 and V2

Massive STE in DKA (no OMI)

Tuesday, October 5, 2021

A man in his 60s woken from sleep by epigastric pain. Would you have been able to correctly diagnose him?

Written by Pendell Meyers

A man in his mid 60s with history of CAD and stents experienced sudden onset epigastric abdominal pain radiating up into his chest at home, waking him from sleep. He called EMS who brought him to the ED. He had active chest pain at the time of triage at 0137 at night, with this triage ECG:

I sent this ECG, without any text at all, to Dr. Smith, and he replied: "LAD OMI with low certainty. V3 is the one that is convincing." 

After his response I sent him the baseline ECG (below), still with no context at all except that this was his prior ECG:

Dr. Smith replied: "Now high certainty. By the way, the formula using QTc of 410 and STE60V3 of 3.5 was 19.4. I bet this LAD occlusion was missed."  (Also, R-wave amplitude in V4 of 12, and QRS in V2 of 16)

I replied: "You're right about both. It was LAD occlusion, and of course it was not seen until about 6 hours later." 

Here is the ECG again: 
The computer QT / QTc is 428 and 461 msec.

Using the computer's QTc of 461 ms instead of Smith's, which was measured by him (at 410 ms) while looking on an iPhone screen, you can see the formula value below.  

There is sinus rhythm with overall normal QRS complexes, normal R wave progression. There is STE in V2-V4, maximal in V3. The T wave in V3 and V4 is likely hyperacute, as it is fat, broad, full, and nearly symmetric in V4. A prior ECG, if available as in this case, would help to confirm or deny whether these are truly hyperacute, and the baseline ECG above shows that they are indeed all new and diagnostic. 

A couple other supportive findings that are not necessary for the diagnosis: 1) there are inferior Q-waves of old MI; this helps to establish the presence of coronary disease. 2) PVC, which also is more likely in patients with old and/or new MI.

See side by side below:

Comparison makes it obvious: huge fat hyperacute T waves in V3-V4.

The computer measurement of the QT might be slightly longer than actuality. But no matter, the formula is grossly positive.

Unfortunately, the ECG was not understood by the provider. Here is the EM decision making:

"The patient's EKG revealed some repolarization abnormalities but no clear signs of a STEMI. The patient's laboratory studies revealed troponin mildly elevated at 25 ng/L but liver enzymes, lipase were normal. Gallbladder ultrasound was negative for stones. Chest x-ray was normal. I ordered  morphine but he refused. I tried a GI cocktail but this did not significantly help. I felt the patient warranted admission for following his cardiac enzymes and EKG."

"ED Diagnoses:
1. Epigastric pain
2. Elevated troponin"

Cardiology was not notified of the patient at all. He was admitted to general medicine floor. No more troponins were ordered by the EM physician.

The hospitalist then came down to the ED to evaluate the patient. Their documented assessment included:
"Epigastric pain with odynophagia. ? gastritis vs. ulcer with recent Goody powder use. Atypical chest pain with elevated troponin. Patient will be started in IV PPI. Consult GI services in a.m. May need endoscopy. Currently denies dark stools. Lipase normal. Stool occult will be obtained. Patient claims 10 years ago when he had stents placed he had witnessed similar symptoms, due to mildly elevated troponin repeat troponin will be obtained. CT angio chest due to concerns of epigastric pain radiating to back, but suspicion for dissection less. No aspirin or lovenox until CT is obtained."

The CT showed no dissection or PE, nor any other acute pathology.

The second troponin returned around 0345, at 1,345 ng/L.

So aspirin and heparin are given, and a repeat ECG was finally ordered and obtained at about 0400:

This was interpreted as "no significant change from initial EKG at 0137."

Obviously it is importantly different, and remains diagnostic of ongoing, progressing LAD OMI. There is new R wave diminution in V3, new pathologic Q waves in V3-V4, new STE in V4. This ECG almost meets STEMI criteria, except that lead V3 in a man older than 40 would require 2.0 mm, whereas he has only 1.5 mm by my zoomed in measurement. V4 certainly has the necessary 1.0 mm.

This ECG was somehow interpreted as no change from the first ED ECG. But due to increased troponin, cardiology was called to see him for "NSTEMI management."

He continued to refuse morphine multiple times during this time period.

Notice how everyone involved (EM, IM, and cardiology) openly and blatantly violate all NSTEMI guidelines that state that NSTEMI with ongoing ischemic symptoms despite medical management requires less than 2 hour angiogram! All of them believe that this is just normal "NSTEMI management." That's because this is how patients are managed in the majority of settings, still, in 2021. The guidelines are simply ignored.

Another troponin was sent, which returned at 5,178 ng/L.

So more ECGs were ordered at 0532 and 0539:

Ongoing progression of OMI is seen, however at this moment there is small terminal T wave inversion suggesting momentary slight reperfusion. 

Only 20 minutes later, the T waves have pseudo-normalized, meaning the terminal inversion has been replaced again by hyperacute T waves in V2-V4. The artery is occluded again.

The ECGs before the angiogram are never recognized as a "STEMI" or "OMI".  They never actually meet STEMI criteria. 

The patient finally gets to go to the cath lab at 0744 (more than 6 hours after arrival and immediate what could have been an immediate ECG diagnosis of LAD OMI), where they of course find a complete 100% thrombotic occlusion of the mid LAD, at the site of his prior LAD stent. It is stented with good angiographic result. EF at cath is estimated at 35% with hypokinesis of "inferoapical" myocardium.

All subsequent troponins returned at greater than 25,000 ng/L (our lab's upper reporting limit).

Formal echo confirmed EF of 35-40%, with moderate hypokinesis of the mid-apical inferoseptal, mid-apical inferior, and mid-apical anteroseptal myocardium.

Here are some ECGs over the next few days after cath, showing a huge amount of anterior wall loss, QS waves, LVA morphology, and some amount of tissue saved as evidenced by evolving reperfusion T waves:

This OMI is one of the highest risk for long term morbidity and mortality. 

He survived the hospitalization, with a final diagnosis of "NSTEMI."

Learning Points:

Use the formula.

Learn hyperacute T waves. See thousands of them on this blog.

This case makes it painfully obvious why Khan et al have shown in their meta analysis of more than 40,000 NSTEMI patients, why NSTEMI patients with OMI have double the mortality and worse morbidity, at every time point, than NSTEMI patients without OMI. 

Anyone with high quality ECG training could have shortened his door to balloon time by 6 hours. Anyone who had simply followed the ACC/AHA NSTEMI guidelines could have improved his care by at least 3 hours. But neither of these things is normal in 2021 - not because providers are dumb and evil - because they have been trained that STEMI is what matters. Even when the patient almost/barely meets STEMI criteria as in the repeat ECG before cath above, the STEMI paradigm cripples their minds and prevents them from recognizing evolving changes other than ST elevation. And this patient's long term outcome is the result. This patient happens all over the world, every day. I find and present only a tiny fraction of them.

I can't speak for interventional cardiologists, but EM doctors should not be expected to attain this level of ECG expertise. We have to be good enough at everything, we cannot be expected to be expert at every difficult task. In other areas of imaging that requires intense training and expertise, we have radiologists to help us. We have no such resource for ECGs. Hopefully soon we can make AI that reads ECGs this well or better. Until then, maybe we need an ECG radiologist. Or cardiologists if they would be willing to learn this. Many on Twitter see this case and tell me that they would never let this happen. But in the real world, I have a new case of this to post every day.

Notice how this LAD OMI has no reciprocal STD on the standard 12 lead. Only approximately 50-60% of big obvious anterior STEMIs have reciprocal STD in the inferior leads. When the OMI is harder to see than an obvious STEMI, that number is even less.

Monday, October 4, 2021

A woman in her 60s with misdiagnosed palpitations, part 2: Case follow up!

 Written by Pendell Meyers

This post will be follow up information on the patient from this recent case linked below. Make sure to read that one first, then see what happened to this patient in this post below!

A woman in her 60s with palpitations, chest discomfort, and multiple misdiagnoses by both EM and Cardiology!!

Here is the ECG:

Here is the explanation:

We see a regular, narrow, monomorphic tachycardia, for which the full differential would include sinus tachycardia, SVT (an umbrella term including many different rhythms), and atrial flutter. 

This ECG has a large negative atrial wave just before the QRS complexes in the inferior leads, with only one of these waves visible for each QRS complex. These waves are of course fully upright in V1. The differential includes a low ectopic atrial tachycardia near the AV node, or a relatively high AVNRT such that the circuit activates the atrial retrogradely before the circuit can activate the ventricles anterogradely during each lap of the circuit.

It is not atrial flutter, because with such a prominent atrial wave seen in the inferior leads we should be able to see a second set of these waves midway between the visible ones.

Whatever the atrial waves are, their QRS complexes in the inferior leads are followed by ST segments which seem to be slightly above the baseline in III and aVF. Because I have been fooled by this phenomenon before, and because it does not match OMI patterns I've seen before, I can see that this morphology is likely due to the upright atrial repolarization wave from the dysrhythmia. If there were any question whether it were due to OMI, I would first convert the patient out of this dysrhythmia then reevaluate the ECG for OMI.

In this case, however, the EM provider was worried for possible STEMI in the inferior leads, and the cardiology provider misdiagnosed the rhythm as atrial flutter, starting the patient on eliquis. Based on our ECG interpretation, neither of those is correct!

Case continued:

The patient was scheduled for electrophysiology follow up for her "new onset atrial flutter." So I looked up which provider she was scheduled to see, and I wrote that physician a message explaining my thoughts from the post above, explaining that I thought it wasn't atrial flutter, she likely doesn't need eliquis, and her actual dysrhythmia could likely be diagnosed and solved with an EP study. 

The electrophysiologist wrote me back and agreed.

The patient was then seen in follow up clinic by the electrophysiologist, and soon scheduled for an EP study.

Several days later she underwent the EP study. Ultimately, she had focal ectopic atrial tachycardia confirmed and successfully ablated, after which it was no longer inducible. Here are some relevant excerpts with much more detail for those interested:

"Patient had easily inducible and incessant atrial tachycardia that initially appeared to be the earliest in the proximal coronary sinus atrial electrograms in the proximal and distal representing the left atrium revealed late signals." 

"Atrial signals were obtained during atrial tachycardia throughout the right atrium. Earliest signals were noted both intracardiac and with 3-dimensional mapping with CARTO activation mapping to be at least 65 ms pre-earliest atrial activation which was the proximal coronary sinus. This was at the 6 o'clock tricuspid annulus."

"Following ablation, initial ablation within a few seconds the tachycardia terminated with no further atrial tachycardia....With infusion of dobutamine and waking patient up from sedation, no further atrial tachycardia was induced with singles and double extra stimuli as well as burst atrial pacing. Prior to ablation patient had easily inducible atrial tachycardia. After waiting approximately 30 minutes from the time of the successful ablation, no further PAC's or atrial tachycardia was noted."

"Impressions: Incessant focal atrial tachycardia arising from the posterior inferior tricuspid annulus (6 o'clock) status post successful ablation."

Eliquis was discontinued. Metoprolol was continued for now. 

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