Tuesday, March 30, 2021

A man in his 40s with a highly specific ECG

Case submitted by Charles Harris M.D. and Vitaliy Belyshev M.D., with edits by Pendell Meyers

A 43 year old man with no reported past medical history presented with acute onset chest pain and shortness of breath, as well as a syncopal episode. He stated he was walking into his house when he suddenly started coughing and had a syncopal episode. Over the past few days he had been noticing some intermittent central chest pain described as "burning" with associated shortness of breath. He had no cardiac family history, no drug use, no recent COVID infection. His vitals were normal except for mild tachycardia.

Here is his triage ECG (no prior available):

What do you think?

Meyers' comment: I was on a walk with my wife and new baby daughter in the park when I received a text message with this ECG (see below). In our department we have secure channels to ask each others' opinions on ECGs, echos, etc. You can see that I had no knowledge of the patient, not even age. 

After my interpretation, I was told "burning chest pain." There are certain rare ECGs like this one that are so pathognomonic that clinical context is almost irrelevant, or as in the case of the initial clinical context I got here ("burning chest pain"), can even be misleading in the context of a pathognomonic ECG. There is nothing smart or exceptional about this interpretation, it is simply pattern recognition of squiggly lines. I've seen this exact ECG many times (see below for our other posts on this), have followed up the outcome, and learned from the mimics, to the point that I recognize this ECG instantly and pathognomonically. Anyone can do it, and a computer AI / deep neural network could do it much better than I ever could. I later sent this ECG to Dr. Smith, who instantly said "PE."

ECG Interpretation:

Raw findings:
 - Sinus tachcyardia
 - QRS is narrow with RAD and very poor R wave progression
 - Very slight STE in V2, V3 with convex morphology
 - Terminal T wave inversion in V2 and V3
 - Inferior T wave inversion (III and aVF)
 - S1Q3T3

Subjective Interpretation (Meyers):
 - Pathognomonic for acute severe R heart strain (the most common etiology by far being acute PE)
 - V2-V3 have the most important pathognomonic morphology here, with the small R wave followed by large S wave, then slightly convex ST segment followed by terminal-to-whole T wave inversion
 - paired with the classic simultaneous "inferior and anterior" T wave inversion
 - by the way, sure, there is S1Q3T3, which is by far the least important supportive finding of all the above, because it is the least specific
 - Not consistent with anterior reperfusion (Wellens' morphology), it does not have the right morphology of either the QRS complex or the STT waves. This is hard to describe and can really only be learned by comparison: 

Examples of acute right heart strain from PEs vs. Anterior MI (with reperfusion pattern):

Note that, as Kosuge's study found, ALL cases of PE with precordial T-wave inversion have an inverted T wave in lead III and ALL cases of MI have an upright T wave in lead III:

Examples of anterior reperfusion (Wellens):

Notice that this last one (further along in the reperfusion sequence) has some characteristics in V2-V3 similar to the PE pattern I'm describing, but the differences are easy: PE affects the RV, which should have findings proportionally maximal in V2-V3 and usually not extending leftward beyond V4-5, but this example of Wellens shows the T wave inversions in V2-V6, as well as I, II, aVL. The T waves are upright in III and aVF, whereas they are usually inverted in active right heart strain. 

Back to the case:

A bedside echocardiogram was performed by one of our ultrasound fellowship-trained EM faculty, shown below.

The apical 4 chamber view above was interpreted as having RV dilation and McConnell's sign. Color doppler was applied and showed moderate tricuspid regurgitation.

This was followed by a bedside DVT ultrasound, which shows a non-compressible left popliteal vein as shown below.

Based on all the above information, the patient was given 1mg/kg enoxaparin. The CT pulmonary angiogram was performed approximately 20 minutes later, showing "severe pulmonary thromboembolic disease involving the main pulmonary arteries and lobar supply to all lobes. Imaging evidence of associated right heart strain."

CT images shown below:

The patient was activated as a "Code PE" by our hospital protocol, which facilitates rapid consultation with critical care, interventional radiology, CT surgery, as needed. He continue to have normal oxygen saturation on room air, with no respiratory distress, and BNP 477 and high sensitivity troponin T 55 ng/L (URL = 14 ng/L). He was deemed appropriate for non-ICU status in a medical telemetry bed.

He had an unremarkable 2-day hospital stay on the medical floor, without even requiring any oxygen. He had no obvious coagulopathy discovered, but with further outpatient workup planned. He was discharged on a novel anticoagulant.

Three hours later the ECG was unchanged:

Learning Points:

In a very small subset of PE with at least submassive right heart strain, the ECG can be highly specific or even pathognomonic as detailed by the findings above. The ECG is not at all sensitive for all PE.

Don't forget that severe PE can also present with much more difficult findings on ECG, including RBBB and inferior/RV/anterior STEMI mimics.

Use your bedside echo to correlate ECG findings. 

Wellens (anterior reperfusion) can be differentiated from acute right heart strain as detailed above. 

Consider having a (secure, de-identified, approved) channel for you and your colleagues to help one another recognize and interpret ED-based images for which there is no radiologist or other expert, such as the ECG and bedside ultrasound. It may improve patient care, resident education, and departmental camaraderie.

See some of our prior PE cases:

A crashing patient with an abnormal ECG that you must recognize

Chest pain, ST Elevation, and tachycardia in a 40-something woman

Primer on the ECG in Pulmonary Embolism:
These are findings of acute right heart strain, and could be seen in any condition which results in a rapid rise in pulmonary artery pressure. This includes hypoxia because of "pulmonary hypoxic vasoconstriction" 

The ECG is not sensitive for PE, but when there are findings such as S1Q3T3 or anterior T-wave inversions, or new RBBB, then they have a (+) likelihood ratio and the S1Q3T3, or even just the T3, may help to differentiate Wellens' from PE. 

Stein et al. found normal ECGs in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE.  Today, however, that number would be higher because we diagnose more of the submassive PEs that have minimal symptoms.

This is a paper worth readingMarchik et al. studied ECG findings of PE in 6049 patients, 354 of whom had PE.  They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. 

What is an S1Q3T3?  Very few studies define S1Q3T3.  It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV).  In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS.  In this study, (quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

Witting et al. looked at consecutive patients with PE, ACS, or neither. They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6% of controls.  This does not contradict the conclusions of Kosuge et al. that when T-wave inversions in the right precordial leads and in lead III are indeed present, then PE may indeed by more common.  In my experience, this is true, but needs validation in a study of similar methodology. Supporting Kosuge, Ferrari found that anterior T-wave inversions were the most common ECG finding in massive PE. 

Sunday, March 28, 2021

Nonspecific symptoms with RBBB and New ST Elevation. Anterior STEMI, right? What does the echo show?

A 50-something male with a history of COPD and substance use disorder who presented with generalized weakness and exacerbation of chronic back pain that is now radiating to his neck, and headache. He also developed nausea, alternating "hot and cold flashes", and generalized weakness the previous evening. He became anxious about his symptoms and then used crack cocaine as well as drank alcohol last night. His symptoms have persisted since then. He states he has felt short of breath since last night. He denies any chest pain, though notes he has a "odd" sensation in his chest. 

Vital signs were normal and physical exam was unremarkable

He had an ECG recorded:

This is RBBB, which normally does not have ST Elevation anywhere.  In fact, it normally has ST depression in V1-V3 that is discordant to the previous R'-wave.  

In this case, there is no R'-wave in V1, which is unusual in RBBB.  
V2 and V3 do have rSR', and both of those also have ST elevation that is concordant to the R'-wave.  This usually is an indicator of LAD occlusion.
This is all but diagnostic of lead V1 - lead V3 lead reversal
Nevertheless, the T-waves appear hyperacute.

There was a previous ECG from 3 months prior
This ECG does have an R'-wave in V1, and (appropriately) without STE.  V2 and V3 are lacking an R'-wave; in fact, they have a wide S wave which is usually only seen in lateral leads of RBBB.  There is STE which is discordant to that wide S-wave; usually the ST segment in RBBB is isoelectric even AFTER the wide S-wave.

So this is an abnormal baseline ECG, but the acute ECG looks far more worrisome.

Let's look at V1-V3 side by side, presentation ECG on the left and old one on the right:

V1 T-wave sure looks hyperacute compared to the old one.
I have not applied the term "Terminal QRS distortion" to RBBB, but if one did so, then the acute ECG would definitely qualify in lead V3 (R'-wave does not return to baseline).

A Bedside echo (POCUS) was recorded:

Notice only the apex contracts; the base does not.  

Is it just an apical wall motion abnormality due to LAD occlusion?  

One might think so.


--Large RCA without significant disease.  

--Left main is large with mild proximal plaque

--Circumflex is a small caliber vessel and supplies two small OM branches

--There is a medium caliber, multi-branching ramus intermediate without

significant disease.

--LAD is a large caliber vessel that extends to the apex.  No significant coronary artery disease is noted in the LAD, but the LAD is noted to dilate with IC nitroglycerin. LAD supplies four small caliber diagonal branches

--Left ventricular end diastolic pressure (LVEDP) 24-27 mm Hg (elevated) in the setting of SBP < 85


Impression and recommendation:

--No significant obstructive coronary artery disease to explain elevated troponin, dyspnea and ECG changes

--No evidence for plaque rupture or vessel occlusion

--Significant elevated left ventricular filling pressure in the setting of relative hypotension

--Consider non-ischemic cardiomyopathy; troponin elevation could be caused by decrease coronary perfusion pressure in the setting of elevated LVEDP.  Would not recommend further treatment of ACS

Contemporary troponin I peaked at 0.393 ng/mL, which is typical for a Non-OMI, but also for a variety of "acute myocardial injury" diagnoses.

An ECG was recorded the next AM:

Less hyperacute, but still has ST Elevation in V1-V3

Formal echo with contrast:

Possible atypical stress cardiomyopathy with sparing of the apex (It looked similar to the POCUS echo)


Intracoronary nitroglycerin suggests a component of coronary vasospasm, LVEDP was elevated to 24. Serial troponin testing was 0.227, 0.222, 0.343, 0.393 ng/mL. TTE revealed LVEF of 40-45% and possible atypical stress cardiomyopathy with sparing of the apex.  There may be some contribution of cocaine toxicity to epicardial and microvascular coronary spasm.

Apical takotsubo or "Reverse" Takotsubo.  (Of course it should not be called takotsubo because that name comes from the japanese octopus trap, which implies apical ballooning with good contraction of the base.)

Read about Reverse takotsubo here: 

Respiratory Failure and ST Depression: Is there Posterior STEMI?

Thursday, March 25, 2021

20-something with anxiety. Pulse is 169. Then 229. Then 169. Then 229. Latent conduction vs. Concealed Conduction. 3 Pathways.

A young woman in her third trimester of pregnancy had complained of panic attacks on multiple occasions.  

She presented to the ED this time, instead of to a clinic, for the same complaint and her pulse was palpated at "very fast".

Side note: Many panic attacks are diagnosed as SVT by 3 year followup. In other words, the patient was wrongly diagnosed and treated for psychiatric disease for up to 3 years.

Lessmeier TJ, Gamperling D, Johnson-Liddon V, et al. Unrecognized paroxysmal supraventricular tachycardia. Potential for misdiagnosis as panic disorder. Arch Intern Med. 1997;157(5):537-543. More Info

EMA July 1997: Unrecognized Paroxysmal Supraventricular Tachycardia: Potential For Misdiagnosis As Panic Disorder. EM:RAP. https://www.emrap.org/episode/ema-1997-7/abstract5. Updated September 20, 2017. Accessed September 24, 2020.

Here is the 12-lead ECG:

Narrow complex tachycardia at a rate of 229

She was brought to the critical care area and put on monitors.  Her heart rate on the cardiac monitor constantly changed from narrow complex at 170 to narrow at 230 and back again.

She was hooked up to a continuous 12-lead ECG machine so that the different rates could be recorded.

Here is the slower rate:

Narrow complex tachycardia at a rate of 169

Here I point out the retrograde P-waves with arrows.

So this is clearly a re-entrant paroxysmal SVT (SVT, or PSVT).  But it is at 2 different rates.  Why?

Time zero Trop < 4 ng/L

2 hour = 12 ng/L

No 4 hour troponin was measured, but I suspect it would have been above the 16 ng/L cutoff for acute myocardial injury (for women; 34 ng/L for men), and then she would have been diagnosed with a type II MI.

Type II MI: acute myocardial injury (rise and/or fall of troponin with at least one value above the 99th %-ile upper reference limit AND the injury is due to ischemia AND there is some identifiable source of supply demand mismatch, such as hypotension, anemia, severe hypertension, sustained tachydysrhythmia, etc.)

So this elevated heart rate did cause enough ischemia to result in troponin release.

Here is the post conversion EKG:

Sinus rhythm.  There are no delta waves.  
Absence of delta waves does NOT rule out an accessory pathway.  Some accessory pathways have "concealed conduction," in which delta waves are not evident on the baseline 12-lead because the pathway only conducts in the retrograde direction.

Side note: I was educated today by our electrophysiologist that a syndrome that occurs due to an accessory pathway should only be called WPW if there is a delta wave on the baseline ECG.  So although this patient can have the same orthodromic tachycardias of a patient with WPW, strictly speaking, she does not have WPW.  

This would seem to imply that a patient without a delta wave could not have an antidromic tachycardia (antidromic AVRT) since the accessory pathway cannot conduct in the anterograde direction.  However, some patients can have intermittent WPW; if this were the case for this patient, then she COULD have an antidromic AVRT.  

There is also what is called "latent WPW."  In this case, the transit time from the sinus node through the AV node is faster than the time to get to the accessory pathway, get through it, and begin to Pre-excite the ventricles.

Here is nice explanation of accessory pathways (AP) from Medscape

"An AP that does not manifest on ECG is revealed when the rate exceeds the refractory period of the AV node. This has been described as a latent AP. A latent AP can conduct both antegrade and retrograde transmissions."

"An AP in which only retrograde transmission of impulses can occur is called a concealed AP and is used only during circus movement tachycardia (CMT or ORT). A concealed AP is not detectable on the regular surface ECG findings, because the ventricle is not preexcited. Tachycardia due to a concealed AP should be considered when the QRS complex is normal and the retrograde P wave occurs well after completion of the QRS complex, out in the ST segment or even in the T wave (long R-P tachycardia)." 

Here is an important example of Latent WPW that resulted in failure to diagnose for years.


Formal Echocardiogram:
Regional wall motion abnormality-inferior septum/inferior wall.  This strongly supports acute type II MI.

She will undergo EP study after delivery.  She was placed on metoprolol until then.

Why were there two different rates?

Usually this is due to simultaneous:

1. "dual AV nodal pathways", which is the source of most SVT (AV nodal reentry tachycardia, or AVNRT) 

2. WITH ADDITIONAL Accessory pathway.

See images far below for dual AV nodal pathways

Most likely Explanation: There are 2 pathways in the AV node, just as there are in all cases of AVNRT.  But in this case, there is a third pathway, probably an accessory pathway.  The reentrant rhythm goes down through the AV node taking one or the other of the 2 pathways, switching back and forth, and up the accessory pathway.  This is an orthodromic SVT, but because the 2 pathways have different conduction velocities, there are 2 different rates.

Provisional Diagnosis: probable Dual AV nodal pathways PLUS bypass tract, with orthodromic SVT that changes rates depending on the AV nodal pathway taken (see images below).  Needs verification by EP study.

This case was kindly reviewed by Dr. Rehan Karim, one of our fine electrophysiologists.  He made the following comment (in addition to informing me that the term WPW is reserved only for those with delta waves):

"There are some other nuances, which might be out of scope of the blog:"

-         "Patients can have “more than one” slow pathways – that could result in multiple cycle lengths of AVNRT’s."

-         "I have had two patients with alternating cycle lengths during same tachycardia (every other beat alternating cycle length, rather than two different tachycardias) – one was accessory pathway mediated (AVRT) retrograde, and antegrade using fast and slow pathways as you have described; another one where patient had AVNRT with two different cycle lengths."

"Therefore, it’s difficult to be certain about it just looking at 12-lead ECG’s – but if I were to guess, the explanation that you give in your description is most likely correct!"

See these two cases: 

Case 1: Wide Complex Tachycardia in a 20 something.

This patient developed ventricular fibrillation from Cardioversion.

Case 2: A Very Fast Regular Narrow Complex, Followed by an Equally Fast Regular Wide Complex

1. Accelerated AV conduction
2. Left lateral accessary pathway

Above: Duel AV nodal pathways.  They have different conduction velocities.  They also have different refractory periods.  This is the substrate of AVNRT.

Dual AV nodal pathways with ADDITIONAL accessory pathway. 
But this circuit is the opposite direction of our patient today!
In this schematic, the conduction is ANTIDROMIC (down the bypass tract and up the AV node).  This would create a wide complex tachycardia that may mimic a very fast VT but at 2 different rates, depending on which pathway within the AV node is taken.  See this case.  This would be AV Reciprocating Tachycardia (AVRT).

In our patient, it is ORTHODROMIC: the impulse goes from the atrium to the AV node, then through either the fast or slow pathway (which determines the rate), then back up through the accessory pathway.

Tuesday, March 23, 2021

Does this ECG represent acute ischemia?

 I was shown this ECG, without any clinical data:

What do you think?

My answer: "I think it is a baseline ECG, not ischemic."

Why did I say that?  Because of the very high voltage.  Whenever you see voltage like that, ST-T abnormalities which at first appear to be ischemic are probably simply secondary to the abnormal depolarization and due to LVH or some other baseline disease.

And so it was indeed the patient's baseline ECG:  The patient had presented for nonspecific symptoms and had the ECG recorded.  So they searched for a previous ECG.  

Here it is from 20 months prior.  

Quite similar

It turns out the patient had had an echocardiogram 22 months prior:

Prominent trabeculation is noted in the distal LV segments but not definitive for Left Ventricular Noncompaction Cardiomyopathy (LVNC).

Serial troponins and Serial ECGs were negative.

Another ECG was recorded that day:

Slightly different, but not significantly so.  No evidence of developing ischemia.

The patient was discharged with followup.

Noncompaction Cardiomyopathy

A few pearls on LVNC copied from UpToDate (quotes):

Left ventricular noncompaction (LVNC) is a distinct phenotype characterized by prominent LV trabeculae and deep intertrabecular recesses. LVNC was previously also called spongy myocardium or hypertrabeculation syndrome but these terms should not be used interchangeably with LVNC.

LVNC is characterized by the following features:

An altered myocardial wall with prominent trabeculae and deep intertrabecular recesses, resulting in thickened myocardium with two layers consisting of noncompacted myocardium and a thin compacted layer of myocardium () [5-7].

Continuity between the LV cavity and the deep intertrabecular recesses, which are filled with blood from the ventricular cavity without evidence of communication to the epicardial coronary artery system.

As discussed below, criteria for the extent of noncompaction have been developed to help distinguish the trabeculation seen in LVNC from that seen in other forms of heart disease and in healthy individuals. However, criteria are evolving and there may be morphologic overlap between LVNC and other types of cardiomyopathy and other pathologic and nonpathologic phenotypes. (See 'Diagnosis' below and 'Differential diagnosis' below.)


Clinical manifestations of LVNC are variable and may include dyspnea, chest pain, palpitations, syncope, or an abnormal electrocardiogram (ECG) or echocardiogram [8,11,43]. Cardiac symptoms and signs may not be present. The major complications of LVNC are HF, atrial and ventricular arrhythmias, sudden cardiac arrest, and thromboembolic events, including stroke [5,11,18,44].

Echocardiography criteria

The presence of all four of the following echocardiographic criteria are required for diagnosis:

A thickened LV wall consisting of two layers: a thin compacted epicardial layer and a markedly thickened endocardial layer with numerous prominent trabeculations and deep recesses with a maximum ratio of noncompacted to compacted myocardium >2:1 at end-systole in the parasternal short-axis view ().

Color Doppler evidence of flow within the deep intertrabecular recesses.

Prominent trabecular meshwork in the LV apex or midventricular segments of the inferior and lateral wall.

Compacted wall thickness ≤8.1 mm. The criterion of maximal systolic compacta thickness of ≤8.1 mm was found to be very specific for myocardial thickening in LVNC compared to normal controls or patients with aortic stenosis [54].

Great Full Text Review Article on Noncompaction Cardiomyopathy from the Journal of the American College of Cardiology.  Hussein A et al.  JACC 2015;66(5):578-586. 

Some Pearls on the ECG from this article: 

"94% of patients had an abnormal electrocardiogram (the most common abnormality was left bundle branch block, observed in 44%)."

"Resting electrocardiogram abnormalities are found in most patients, but findings are nonspecific and include left ventricular hypertrophy, repolarization changes, inverted T waves, ST-segment changes, axis shifts, intraventricular conduction abnormalities, and atrioventricular blocks. Arrhythmias are common, including ventricular tachyarrhythmias, atrial fibrillation, and paroxysmal supraventricular tachycardia, all of which can precipitate sudden death."

This table is from this paper

Friday, March 19, 2021

A man in his 50s with acute chest pain and diffuse ST depression

Submitted by Alex Bracey, with edits by Meyers and Smith

A man in his 50s with history of type B aortic dissection with prior TEVAR experienced acute onset chest pain at rest and presented to the Emergency Department. 

Here is his ECG on arrival:

What do you think?

Here is a prior ECG on file (presumed baseline):

There is sinus rhythm with minimal STD in V5, V6, II, III, aVF. There is the tiniest amount of STE in aVL, but the T wave is not hyperacute (instead there is a terminal inversion). I would call this ECG consistent with subendocardial ischemia, but also the question of possible high lateral OMI (for which I am not yet convinced and would need serial ECGs, echo, etc.). 

The team was worried foremost for possible aortic dissection given his history and presentation. He was neurologically intact with ongoing pain, without obvious vascular signs.

A CT aortogram was performed and is shown below:

This was read as an acute type A aortic dissection.

He was transferred to a surgical center for management.

On arrival he complained of increasing chest pain, and a repeat ECG was ordered:

This ECG shows interval increased severity of diffuse subendocardial ischemia (non-occlusion ischemia). There is now STD from V3-V5 (maximal in V5 slightly greater than V4), as well as leads I, III, aVF, I (maximal in II), with obligatory reciprocal STE in aVR. I see no signs of superimposed high lateral OMI which we were considering from the first ECG.

Knowing that the patient has aortic dissection, the most likely explanation is that the dissection is involving, but not fully occluding, the left main (or potentially both left main and RCA). Potentially this supply/demand mismatch could be due to increased demand from hypertension, pain, etc., but typically these etiologies alone would not produce the severity of ECG findings seen above.

Additionally, the patient complained of new pain in the right arm, and it was found to be newly pulseless. Review of the CT scan revealed that the dissection extended circumferentially around the annulus involving both left and right coronary arteries. It also extended to the right subclavian artery. 

He underwent surgery and survived.

See many more cases of diffuse STD with reciprocal STE in aVR:

A man in his 50s with witnessed arrest and ST elevation in aVR

Recommended Resources