Syncope, chest pain, and inferior ST Elevation with Reciprocal ST depression in aVL

A 26 year old male presented with syncope and chest pain.  Syncope was sudden and without prodrome, and resulted in head trauma with a scalp laceration.

Here is his ECG:

There is significant ST Elevation in inferior leads, with reciprocal ST depression in aVL.

This appears to be an inferior OMI

What do you think?

Smith: I recognize this as a STEMI mimic.  I was not alarmed.  The providers showed me the ECG and I told them that I thought it was a fake.  It is a sad fact that although pericarditis with STE in inferior leads rarely has reciprocal ST depression in aVL, normal variant ST Elevation sometimes does manifest STD in aVL

He had a previous ECG on file from one year prior:

There is some abnormal atrial activation, but no ST Elevation

Does this mean that the new one is necessarily due to OMI/ischemia?

No.

What does the Queen of Hearts think?

"No signs of OMI"

The chest pain resolved after some time, and another ECG was recorded:

The ST Elevation is nearly gone.  

Doesn't this necessarily mean that he was having ischemia?

Unfortunately, life is not so simple.  I recognize this as a normal variant.  Amazingly, the Queen also recognizes it as "Not OMI".  She is very good.

The first troponin was < 3 ng/L.  The 2 hour troponin was < 3 ng/L.

He was admitted for monitoring and had no dysrhythmias.

He had a formal contrast echo that was completely normal:

Normal estimated left ventricular ejection fraction; 69%.

No left ventricular wall motion abnormality identified.

Normal LV cavity size and borderline wall thickness.

Normal right ventricular size and function.

No hemodynamically significant valvular abnormalities.

I want to emphasize that it is not the patient's age which made me think the ECG was a mimic.  It was the ECG morphology.  The queen does not know the patient's age.  And I have long warned doctors that young people have acute MI and OMI.

Especially, if a young woman has OMI, she is likely to be disregarded with a "Nah, couldn't be OMI!"

See here for young women with OMI

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MY Comment, by KEN GRAUER, MD (1/9/2025):

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I found today's case challenging — and an excellent example of how despite my not being certain of the diagnosis from the history and initial ECG — careful follow-up yielded the answer.

• To facilitate comparison in Figure-1 — I've put together the 3 ECGs from today's case.

Why I was Uncertain about ECG #1

I found today's initial ECG and the history to be study in contrasts.

• The history of syncope that was sudden and without prodrome, and severe enough to result in head trauma on falling — is concerning. The most common cause of syncope in a previously healthy young adult like today's patient — is vasovagal syncope. But vasovagal syncope typically has a prodrome — such that further evaluation of today's patient may be needed as an outpatient to better assess for the cause of his sudden syncope.
• Concern about this patient's initial ECG was enhanced by the history of "chest pain" — although: i) We are not told the specifics regarding this chest pain (ie, Whether or not this truly was cardiac-sounding CP?); — but, ii) In a previously healthy 26-year old man — syncope is not a common accompaniment of an acute MI.

Regarding the initial ECG:

• There is no denying the presence of nearly 2 mm of ST elevation in each of the inferior leads. In addition, there appears to be some ST segment straightening in these inferior leads — which adds to potential concern in a patient with CP.
• That said, there were features less commonly seen with acute OMI. These included subtle J-point notching in each of the inferior leads (typically a benign finding) — with a QTc that looked relatively short — and a "funny-looking" ST-T wave shape that did not necessarily look acute despite the ST elevation.
• I was not convinced that lead aVL was showing "reciprocal" ST depression — as the T wave vector often follows closely behind that of the QRS, such that the very shallow T wave inversion in aVL in which the QRS was essentially all negative might be a normal finding.
• Finally — I added question marks over the ST-T waves in leads V1,V2,V3 because the progression of the QRS and ST-T waves did not make sense. That is — the R wave decreases from V1-to-V2, but then increases from V2-to-V3 — and the ST segment suddenly becomes flat in lead V2, before abruptly becoming quite large in lead V3 (which interestingly manifests a similar amount of ST elevation and a similar ST-T wave shape as is seen in the inferior leads). At the least — I thought there may be some lead malposition. But the shape of the ST-T waves in these 3 anterior leads certainly did not suggest posterior OMI, which is such a common accompaniment IF there is ongoing inferior OMI.

BOTTOM Line about ECG #1: There is no denying that despite the young adult age of this patient — he presented to the ED with chest pain and syncope — and his initial ECG shows nearly 2 mm of ST elevation in each of the inferior leads.

• I wondered if there might be more details in the history that could suggest acute myocarditis, which could be a better "fit" than an acute OMI for the findings in ECG #1.
• I felt more evaluation was needed before being able to completely rule out an acute event.

Figure-1: I've labeled the the 3 ECGs in today's case.

A Previous ECG is Found:

Optimal comparison of serial ECGs is best performed by placing both tracings side-by-side, as I have done in Figure-1.

• There is no denying the change in appearance between ECG #2 (done ~1 year earlier) — and today's initial tracing ( = ECG #1). There is virtually no ST elevation on the earlier tracing — and the T wave is clearly upright in lead aVL.
• Of interest, upward sloping ST elevation with J-point notching (BLUE arrows) is seen in ECG #2 (that was done a year earlier) — whereas these findings are not seen in leads V2,V4,V5,V6 of today's initial ECG. Considering the normal R wave progression — plentiful QRS amplitude — and the 6 BLUE arrows highlighting J-point notching in ECG #2 — this previous tracing is typical of a repolarization variant.

The ECG is Repeated:

The 3rd ECG in today's case appears at the bottom of Figure-1.

• With the exception of now manifesting a nice normal sinus P wave and a slightly faster heart rate — ST-T wave morphology in ECG #3 looks very similar to that in baseline ECG #2.
• Comparing ECG #3 to the initial ECG in today's case — the inferior lead ST elevation has resolved — the T wave in lead aVL is now clearly upright — and upward sloping ST elevation with J-point notching is more prominently seen in the chest leads.

Putting the Case Together:

In this young adult man who presented to the ED for chest pain and syncope — the ST elevation manifest on his initial ECG resolved while he was in the ED undergoing evaluation.

• That said, rather than reperfusion changes of an evolving OMI — the principal change between ECG #1 and the repeat ECG ( = ECG #3) is reestablishment of the repolarization variant pattern that was seen on this patient's baseline ECG.
• Troponins were negative.
• Overnight telemetry showed no arrhythmias (important to reduce the risk of worrisome arrhythmia given this patient's chief complaint of sudden syncope without prodrome).
• Formal contrast Echo showed normal LV function without wall motion abnormality.
• The patient was discharged home.

Learning Points:

• There are features in today's patient's initial ECG that are not typical for an acute OMI. Despite this — given the presentation to the ED of chest pain and ST elevation — "Prudence is the better part of valor" — so a period of monitoring during evaluation with Troponins, repeat ECG and Echo were indicated to attain 100% comfort before discharge the next day.
• The ST-T wave appearance in repolarization patterns is not always constant. Instead, the ST-T wave appearance may change in serial tracings recorded over the course of a single ED visit. Although this is not a common phenomenon — You will see it on occasion (See the June 30, 2023 post — the November 27, 2023 post — and the July 24, 2013 post in Dr. Smith's ECG Blog). As in today's case — the potential for the ST-T wave appearance of repolarization patterns to vary can be easily confused with "dynamic" ECG changes indicative of an acute evolving OMI.
• Greenfield and Rembert have noted that up to 1/3 of patients with ER (Early Repolarization) but no cardiac symptoms — may show marked variation in the amount of ST elevation from one tracing to the next. These ER patients do not have ischemia — and the variation in ST elevation has not been shown to be related to either heart rate or QRS amplitudes (Variation in ST-Segment Elevation in Early Repolarization: Electrocardiography 40:10,2007).

Online QT calculator for wide QRS (LBBB, RBBB, etc.)

This on-line QT calculator that we link to below was created by Arron Pearce. It is a work in progress — as Arron anticipates making this even more user friendly. But in the meantime — Try it out!

Click on the link:

•  On-line QT calculator for wide QRS (LBBB, RBBB, etc.).

NOTE: This calculator works on an Excel spreadsheet. So after you click on the above link — You may need to download this calculator in Excel format.

Figure-1: Depending on your browser and computer — after clicking on the above link — you should get a worksheet looking something like this.
— Click on File.

Figure-2: After clicking on File — Click on Download in the menu.

Figure-3: Download the Microsoft Excel ( .xlxs ) format. And now when you open the downloaded Excel file on your computer — it should be easy to enter the heart rate and QT interval that you measure to instantly see QTc calculations in each of the 5 methods shown.
= = = = = 
For the modified QTc (when the QRS is wide) — Remember that QRS duration is in milliseconds (ie, a wide QRS = 0.15 second = 150 ms).
— The Rautaharju QTc calculation comes up immediately.
— To get the Bogossian QTc value, you'll need to enter the modified QT value into the QTc calculator on the left side of the page.

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Grauer: The fact that you will see slightly different values in the above QTc calculator conveys the lack of universal agreement on QTc calculation at different heart rates. That said — 4 of the 5 methods are generally quite close to each other (You might mentally take an average of those readings for the value you select — or pick your "favorite" among the methods).

• In our experience — We find the Bazett method potentially problematic, in that it tends to overestimate the QTc for faster heart rates — and underestimate the QTc for slower heart rates.
• 
  
• For QTc estimation when the QRS is wide — I find the Bogossian method to be problematic because the simplified formula that is used by the Bogossian method to calculate the modified QT = QT minus ~50% of QRS duration. But since all this entails is to subtract ~50% of QRS width (ie, for a widened QRS = 0.16 msec — 0.08 msec would be subtracted from the QT you measured) — there is no compensation for any change in heart rate (and since we know the QTc is altered by faster or slower heart rates — I believe the Bogossian method is fatally flawed).

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Note: Below — Brief video demo showing how to use the Excel file:

 

 

Is it important to try to determine the culprit vessel based on ECG?

Written by Willy Frick

A man in his 60s with hypertension and prior stroke presented with three days of crushing chest pain. He reported intermittent chest pain for the last few months, but never lasting this long. He described it as substernal with radiation into the right arm.

With all of this information, we can feel reasonably confident even before looking at the ECG that we are dealing with OMI.

What do you think?

Right away, we notice different populations of R waves. On the V1 rhythm strip, R4 and R5 look like natively conducted beats. (Note, they are not sinus since the P waves are upside down in aVF. It looks like a low atrial rhythm.) The other beats are wider and have a different origin -- more on this later. Unfortunately, although natively conducted beats are the best ones for evaluating ischemia, we only have a few! Or do we?

Although printed ECGs in North America typically display 2.5 seconds of each lead plus one or more 10 second rhythm strips, most machines actually gather data for 10 seconds of all 12 leads! (I recently learned from Dave Richley that modern machines collect 10 seconds of data from leads I and II plus V1-V6. They do not actually measure III, aVL, aVR, aVF but rather calculate them.)

Smith comment: this is one of the major obstacles that Powerful Medical needed to overcome in digitizing 12-lead ECG images: all digital ECG recordings are 10 seconds of each lead, but the images only display 2.5 seconds.  So 75% of the image is missing!  Most computer scientists in the 12-lead ECG world said it was impossible.  But they did it.  They were also able to produce an XML file with 10 seconds of each lead out of these JPG, PNG, or PDF files.  This is critical because AI needs an XML file for analysis.

Case Continued

I like to take advantage of this fact by opening up the ECG in the reading software and reformatting it into 12 channels of rhythm.

Before reading further, see if you can figure out the rhythm. My interpretation is described in reference to the lead II rhythm strip below with annotations for clarity.

• Beats 4 and 5 have the narrowest QRS of all. These must be natively conducted beats. Note that the P waves indicated by the blue arrows have a superior axis (i.e. they are inverted in the inferior leads). Sinus rhythm has an inferior axis, so this must be a low atrial rhythm.

• Beats 1-2 and 7-10 are wider, uniform, and regular. In context of reperfused OMI (I will come back to this), we commonly see AIVR. This QRS complex is almost exactly 120 ms, which is on the narrow end for ventricular origin. And AIVR is commonly closer to 80-110 bpm. Still, this would be very fast for a junctional or ventricular escape rhythm under normal circumstances, so I favor AIVR.

• The red arrows associated with R waves 3 and 6 indicate P waves with sinus morphology -- upright in  I, II, aVF. (They are upside down in V1 and V2, but this is probably because the electrodes are too high.) Additionally, the PR intervals are very short and the QRS complexes are intermediate in morphology between the AIVR beats. Hence they are fusion beats [fusion between ventricular (wide) and conducted (narrow)].  R3 is mostly AIVR morphology, and R6 is mostly sinus conducted morphology.

• The green arrows indicate atrial activity that appears to have been beaten out by the AIVR (i.e., did not conduct because the AIVR beat came first). I doubt retrograde conduction because the RP interval is variable between 8 and 9. If the atrial activity were due to retrograde conduction, the interval from the R wave to the retrograde P wave would likely be the same between the two beats.

Moving on to ischemia, the ECG shows reperfused inferoposterior infarct. Specifically focusing on beats 4 and 5, we see:

• TWI in II, III, aVF

• Overly upright posterior reperfusion T waves most pronounced in V2-3*

• Reciprocally upright T waves in I/aVL (we would expect them to be inverted with the LVH strain pattern)

*Some of this may be the expected T wave in a patient with LVH strain pattern. It is hard to be sure, but this nuance does not impact the overall diagnosis.

Back to the case:

Unfortunately for the patient, he presented on Friday morning to a facility that did not have cath lab coverage until the following Monday. The cardiology consultant notes that pain is "almost resolved."

Remember that in OMI, chest pain is a sign of ongoing infarction. "Almost resolved" means it is NOT resolved. There is active infarction. There either is ischemic chest pain or there is not.

The patient was loaded with aspirin and clopidogrel and started on continuous heparin infusion with plan for cath Monday. The note says that "if symptoms become refractory," the patient will need to be transferred for urgent cath over the weekend. (What does refractory mean if not days of unresolved chest pain which persists after starting medical therapy?) Initial hsTnI was 14,114 ng/L, repeat 12,651 ng/L, none further checked. Echocardiogram showed inferior wall hypokinesis. The patient was evaluated Saturday with no changes to plan.

On Sunday, the patient complained of dyspnea and angina while ambulating. Repeat ECG is shown.

Again, we see reperfusion in the inferior and posterior territories. There is just a hint of coving in leads III and aVF suggesting a component of active ischemia which fits with persistent pain.

The Queen of Hearts recognizes this as reperfused OMI:

This was interpreted by cardiology as "suggestive of anterior wall ST elevation MI." Yes, you read that right. It was hand written in two places in the note, so definitely not an accident.

Smith: yes, it is suggestive of anterior MI -- of OLD anterior MI.  But also of subacute inferior OMI.

Perhaps the cardiologist was attempting serial comparison and thought there was new STE in V3 without realizing that the prior ECG shows AIVR and fusion beats in V3. Fortunately for the patient, this mistaken interpretation at least got him urgently transferred to a cath capable facility where he underwent urgent angiography.

If interested, you can review the angiography in detail on my coronary angiography guide where you will find a lot more information about coronary angiography generally.

Here is an LAO cranial view showing TIMI 0 in the mid to distal RCA

Angiography was interpreted as showing chronic total occlusion of the RCA. (We know from the ECG that the RCA is actually the acute culprit!) The patient received DES to mid LAD and DES to diagonal, with no intervention to the culprit RCA.

Unfortunately, wrong vessel PCI is very common. In a prospective cohort of patients presenting with NSTEMI, 27% of patient receiving PCI had intervention solely to uninvolved arteries. In the same cohort, almost HALF (46%) have either the wrong infarct related artery selected, or the ultimate diagnosis is not ischemic in the first place!

Not surprisingly, the patient had persistent pain after PCI, continuing through the night. The following day, he returned to lab where a different operator performed repeat angiography. The second operator described the RCA as an acute thrombotic occlusion and placed three overlapping stents. The final shot is shown.

Learning points:

• Just because the cath report describes a lesion as "CTO" does not mean it is. It may still be an acute culprit.

• Wrong vessel PCI is very common, it happens in about 1 in 4 NSTEMIs.

• Angiography has inherent limitations. About half of NSTEMI diagnoses are incorrect.

• As always, effective OMI care requires putting the ECG in context of the patient's symptoms.

Here is another video explanation of a case in which the ECG was critical in finding the culprit:

Right Ventricular MI seen on ECG helps Angiographer to find Culprit Lesion

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MY Comment, by KEN GRAUER, MD (1/5/2025):

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Awareness that many modern ECG machines do not display all of the data they gather when writing out an ECG is a greatly underused concept. That said, uncovering much of this unused extra data by routinely displaying each beat in each of the 12 leads would not only prove cumbersome — but it would be unnecessary in the great majority of tracings that lack the great degree of morphology variation seen in today's case.

• Today's case by Dr. Frick illustrates an exception to the above generality. By reformatting the data collected into 12 channels of the rhythm — Dr. Frick facilitated interpretation not only of today's initial 12-lead ECG — but he also provides insight into the mechanism of today's fascinating initial rhythm.
• I focus my comment on exploring this mechanism.

Thanks to Dr. Frick — I was able to obtain a long lead II rhythm strip. In Figure-1 — I combine this derived lead II with the already displayed lead V1 rhythm strip to facilitate clarifying atrial activity in today's initial tracing.

• Without Dr. Frick's reformatting the 10 beats in today's initial tracing into 12 channels of rhythm — I would never have realized that there are 2 atrial foci in the initial rhythm. (Although P wave morphology of sinus P waves may vary some from one beat to the next — I would not expect as much variation as we abruptly see for just 2 beats in today's initial rhythm).
• As per Dr. Frick — the P waves that precede beats #4 and #5 are predominantly negative in lead II, therefore presumably of low atrial origin (BLUE arrow P waves in Figure-1).
• RED arrows in Figure-1 highlight sinus P waves that are upright in lead II. Of these, P waves c and f are the only P waves clearly seen. Dr. Frick pointed out P waves h and i that appear shortly after beats #8 and 9 in lead II (albeit they are not seen in lead V1).
• Given sinus P waves f, h and i — it seems logical that another on-time sinus P wave will almost certainly be hiding within the QRS complex of beat #7 (WHITE arrow).
• Motivated to look even closer for "hidden" P waves — the slight angulation just before the QRS of beat #2 is not present in other beats (strongly suggesting that b represents another on-time sinus P wave).
• Finally — the subtle notch that simulates an r' deflection at the end of the QRS of beat #1 falls in a perfect place to be hiding a final on-time sinus P wave. (This rhythm simply makes more sense if we postulate more regular atrial activity — and the highlighted atrial deflections support this premise).

Whereas atrial activity is best displayed in the long lead II rhythm strip of today's initial ECG — I thought the variation in QRST morphology to be best displayed in the long lead V1.

• As per Dr. Frick — the pathology underlying today's case is an acute inferior OMI — now with reperfusion T waves (best seen in the inferior leads of this initial tracing) and with AIVR (Accelerated IdioVentricular Rhythm) that is so commonly seen as a reperfusion arrhythmia.
• Focusing on QRST morphology in lead V1 of Figure-1 — beats #1,2; and 7,8,9,10 are all wide and not preceded by any P wave. These are all ventricular beats at a regular and slightly accelerated rate of ~60/minute (which is perfectly consistent with AIVR).
• The 2 low atrial P waves ( = d and e) are conducted normally to the ventricles (ie, beats #4 and 5 are narrow QRS complexes).
• Beats #3 and #6 are Fusion beats (F). We know this — because both of these beats: i) Manifest a QRS and T wave morphology that is intermediate to the beat before and the beat after it (ie, QRST morphology of beat #3 is intermediate to that of beats #2 and #4 — and QRST morphology of beat #6 is intermediate to that of beats #5 and #7); — and, ii) Both beats #3 and 6 are preceded by P waves that have a chance to partially conduct (and as would be expected with fusion beats — beat #6 with a slightly longer PR interval provides slightly more time for the sinus P wave preceding it to conduct in the ventricles, which is why fusion beat #6 looks more like normally conducted beats #4 and 5 than does beat #3 which is preceded by a shorter PR interval).

Why was AIVR able to appear in this initial tracing?

• Whereas the R-R interval of ventricular beats in Figure-1 remains quite constant — the atrial rate of sinus P waves varies somewhat. As a result — slowing of the sinus P wave rate facilitates intermittent appearance of either a low atrial escape rhythm or of AIVR.
• P.S.: As often occurs — there may be slight lag in the intermittent appearance of AIVR. But the "theme" of this initial rhythm, is that OMI reperfusion results in a slightly accelerated AIVR that in general makes its presence around the time that the sinus rate slows. A longer period of monitoring would be needed to know for certain — but the back-and-forth between wide and narrow QRS complexes is almost like that seen with isorhythmic AV dissociation, albeit complicated by low atrial escape.

Figure-1: Combined lead II and lead V1 rhythm strip.

My Proposed Laddergram:

• Sinus P waves a,b and g are not conducted to the ventricles — because ventricular beats #1,2 and 7 have rendered the AV nodal area refractory to supraventricular impulses.
• Sinus P waves h and i are not conducted to the ventricles — because these P waves occur after the QRS of beats #8 and 9 during the ARP (Absolute Refractory Period).
• Escape low atrial impulses d and e occur at just the right time to be able to conduct normally to the ventricles to produce beats #4 and 5.
• Sinus P wave c occurs just before the QRS of beat #3. As a result — this P wave is only able to conduct a short distance in the ventricles before being stopped by the AIVR impulse. This fusion beat therefore looks very much like other AIVR impulses.
• Sinus P wave f manifests a slightly longer PR interval than did c. As a result — this P wave penetrates further in the ventricles — which leads to a fusion beat that looks much more like normally conducted beats #4 and #5.

Figure-2: Proposed laddergram for today's initial rhythm. 

 

Torsade in a patient with left bundle branch block: is there a long QT? (And: Left Bundle Pacing).

By Smith with comments from our electrophysiologist, Rehan Karim.  (And of course Ken's comments at the bottom)

An elderly obese woman with cardiomyopathy, Left bundle branch block, and chronic hypercapnea presented hypoxic with altered mental status.

She was intubated.

Bedside cardiac ultrasound showed moderately decreased LV function.

CT of the chest showed no pulmonary embolism but bibasilar infiltrates.

She was managed for sepsis with antibiotics including azithromycin, had hypotension with arterial and central lines placed and pressors.

She had an ECG recorded:

This is left bundle branch block (LBBB), with appropriate proportional discordance.  T-waves are quite tall and possibly peaked (HyperK?), but potassium returned normal.  I do not see OMI here and all trops were only minimally elevated, consistent with either chronic injury from cardiomyopathy or with acute injury from sepsis.  

What is the QT interval?

In LBBB, the QT interval is partly prolonged by the wide QRS.  A normal QRS is about 100 ms, and a typical LBBB is 150 ms.  Thus, 50 ms is added to the QT interval even if repolarization is not prolonged.   So the best way to measure whether there is prolongation within an individual is to measure changes in either the JT interval or the T-peak to T-end interval (1, 2).  

However, in order to correct for rate, one needs a full QT interval.  Bogossian et al. (1) showed that one can create a modified QT with this formula:

Modified QT = measured QT - 0.485 x measured QRS duration.  

Then we can correct that modified QT for heart rate.

Here the QT = 440 ms.  The QRS = 160 ms.  So the modified QT = 365 ms.  The modified QTc then at a heart rate of 98, using the Hodges formula, is 432 ms (by Bazett it is 466 ms)

In any case, the QT does not appear to be prolonged, or at least not much.

1. Bogossian H, Frommeyer G, Ninios I, Hasan F, Nguyen QS, Karosiene Z, Mijic D, Kloppe A, Suleiman H, Bandorski D, et al. New formula for evaluation of the QT interval in patients with left bundle branch block. Heart Rhythm [Internet]. 2014;11:2273–2277. Available from: https://www.sciencedirect.com/science/article/pii/S1547527114009151   

2. Dodd KW, Elm KD, Dodd EM, Smith SW. Among patients with left bundle branch block, T-wave peak to T-wave end time is prolonged in the presence of acute coronary occlusion. Int. J. Cardiol. [Internet]. 2017;236:1–4. Available from: http://dx.doi.org/10.1016/j.ijcard.2017.01.064

Online QT calculator for wide QRS (LBBB, RBBB, etc.)

(This was created by Arron Pearce (https://x.com/arron_pearce_)

Comment by our electrophysiologist, Dr. Karim: 

"The importance of accurately measuring QT interval cannot be overemphasized. Dr. Smith has provided excellent overview of measuring and correcting QT interval in scenarios where QRS duration is prolonged (e.g., LBBB, ventricular pacing, etc.)."

CASE CONTINUED

She was admitted to the ICU.

In the middle of the night, a "code" was called, and multiple rhythms like this were recorded.  There were short bursts of chest compressions, but the non-perfusing rhythm was intermittent.  During the arrest, amiodarone was given.

Here is one of the strips

This is clearly polymorphic VT and probably torsade de pointes

Subsequent ECGs.

LBBB; QT = 440, QRS = 135 ms

Modified QT = measured QT - 0.485 x measured QRS duration.  

Then we can correct that modified QT for heart rate.

Modified QT = 440 - 65 = 375 ms.  

Correct for rate of 100:

Bazett = 484 ms

Hodges = 445 ms

Fridericia = 445 ms

So this ECG has a borderline long QT

Another ECG was recorded:

This ECG is classic one for patients at risk of torsades.  

There is ventricular bigeminy with bizarre appearing wide T-waves

See even more striking cases of this at the bottom of the post.

The plan:

1. Discontinue all negative chronotropic agents, since the risk of torsade is much higher with bradycardia or pauses.

See this post: How a pause can cause cardiac arrest

2. Place temporary pacemaker

3. Discontinue amiodarone, since it prolongs the QT

4. Use Lidocaine instead (lidocaine prevents the PVCs which cause R on T, and does not prolong the QT.)

5. Discontinue all QT proloning medications, including azithromycin

6. Finally, do a coronary angiogram

Possible alternative to pacing is to give a beta-1 agonist to increase heart rate.  The classic one is isoproterenol, but that is difficult to obtain now.  Dobutamine is an acceptable alternative.

Comment on beta agonists, from Dr. Karim, our electrophysiologist: 

"With prolonged QT interval causing torsades de points, in addition to correcting electrolytes abnormalities like hypokalemia and hypomagnesemia, increasing the heart rate can suppress (or overdrive) ventricular ectopy. As noted by Dr. Smith, this can be accomplished by either using beta-one agonists or temporary transvenous pacing. It should be kept in mind that on occasions, beta-one agonist can result in increased ventricular ectopy – e.g., in severe myocardial ischemia (by increasing myocardial demand), or sometimes with congenital long-QT syndrome. Therefore, I usually prefer temporary pacing which might be more controlled and is more predictable."

In order to stabilize the patient, a temporary pacer was placed and she was given overdrive pacing (overdrive pacing prevents any pauses, which are the substrate for torsades):

Ventricular Paced Rhythm: Is there a long QT here?

It is a paced rhythm, for which a modified QT formula is the same as for LBBB.

The measure QT = 500 ms

The QRS duration is 160 ms

modified QT = 500 - (0.485 x 160) = 422 ms

Heart rate = 100

Correcting for heart rate: 

QTc = 545 ms by Bazett correction

QTc = 492 ms by Hodges correction

QTc = 500 ms by Fridericia correction

QTc is indeed quite long!!

Coronary Angiography 

 

No angiographic significant obstructive disease.

Echo:

Decreased left ventricular systolic performance-severe.

The estimated left ventricular ejection fraction is 25%.

Regional wall motion abnormality-anterior septum and apex, akinetic.

Asynchronous interventricular septal motion, LBBB/paced rhythm.

Permanent pacer placement

Later, a biventricular pacer was placed for "Cardiac Resynchronization Therapy (CRT)"  (This is indicated for patients with LBBB and QRS duration > 130 ms and heart failure and vastly improves heart failure).  This usually done by a pacer lead placed through the coronary sinus (LV venous system).  See Dr. Karim's further thoughts on this below.

In this case, it was Left Bundle Branch (LBB) area pacing.  Dr. Karim explains how it is done: "We capture the left bundle (or portion of it) by placing the lead deep into the interventricular septum where a bundle or a fascicle (especially the posterior fascicle) is located. "

I asked if it requires penetration of the septum with a needle, and he responded: 

"No, it's primarily a combination of anatomical location along with 12-lead EKG morphology of septal pacing, and then analyzing the intracardiac local electrograms for left bundle / fascicular signal and lead impedance. The septum is “punctured” with the active fixation screw of the lead - so essentially you bore the septum with the screw helix."

Because she has cardiomyopathy and ventricular dysrhythmias, the pacer included an Implanted Cardioverter-Defibrillator (ICD)

Echo 6 days later after CRT:

Normal estimated left ventricular ejection fraction .

No wall motion abnormality .

The estimated left ventricular ejection fraction is 55-60%

This is somewhat miraculous to me; I don't think such an improvement is common.

ECG with biventricular left bundle CRT pacing:

The QRS is now much narrower, and the QT interval is now much narrower than it was.

Final thoughts from Dr. Karim:

Since this patient had previously known LV dysfunction / cardiomyopathy, along with LBBB, and it was strongly felt that she might have underlying ion-channelopathy (given that single dose of QT prolonging medication resulted in such a profound clinical presentation with hemodynamically unstable ventricular arrhythmia; will be planning to discuss genetic testing as outpatient), decision was made to proceed with cardiac resynchronization. In this specific case, Left Bundle Branch (LBB) area pacing was pursued to achieve cardiac resynchronization. EKG with paced complexes shown below shows much narrower QRS complex and echocardiogram showed improved LV systolic function primarily due to improvement in LV dyssynchrony. (J Am Coll Cardiol. 2019 Dec, 74 (24) 3039–3049) https://doi.org/10.1016/j.jacc.2019.10.039

Examples of bizarre ECGs that lead to torsades de pointes

 

Long QT Syndrome with Continuously Recurrent Polymorphic VT: Management

Polymorphic Ventricular Tachycardia

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MY Comment, by KEN GRAUER, MD (1/2/2025):

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Today's case highlights a number of important concepts to apply in the assessment of the QTc (corrected QT interval) in patients with a prolonged QRS in their baseline ECG. I'll add the following thoughts to the above insightful discussion by Dr. Smith.

• Assessment of the QTc is different when the QRS complex is wide — be this because of preexisting BBB (Bundle Branch Block) or cardiac pacing.
• Dr. Smith offers a quantitative correction factor that accounts for the anticipated amount that QRS widening from a conduction defect is likely to add to calculation of the QTc.
• In the interest of simplicity — I'll suggest that in the emergency setting, the most important thing I want to know is a qualitative determination of the QTc for the patient in front of me (ie, whether the QTc is normal — borderline — or increased — and if the QTc is increased, whether it is likely to be minimally or much more than that increased). Practically speaking — precise numerical (quantitative) determination of the QTc is less important for initial management in the emergency setting.
• More precise measurement of the QTc becomes important for cases in which we need to serially follow a given patient, as may be the case if our intervention includes some parameter that may further increase our patient's baseline QTc (ie, Use of a medication that may prolong the QTc — or worsening hypo-K+ or hypo-Mg++).
• As long as we are consistent with the method we employ to measure the QTc — we will know whether or not the QTc is further increasing (ie, regardless of whether the initial QTc in our patient was 480 or 520 msec — we'll be able to tell if the QTc is getting longer).
• To keep in mind that the 3 different methods cited by Dr. Smith in his discussion (ie,  Bazett, Hodges and Fridericia correction formulas) — produce a ~10% variation in the predicted QTc. This tells us that universal agreement for QTc estimation is not perfect. Clinically, it is well to remember that this variation in QTc estimation is greater at faster heart rates (with faster heart rates being common in "sicker" patients, for whom we are most likely to need to assess the QTc).
• BOTTOM Line: As per Dr. Smith — the KEY point in today's case, is that whereas the QTc was no more than minimally (if at all) prolonged for the initial ECG (which showed sinus tachycardia with LBBB and those tall peaked T waves) — the QTc for the ECG done later with overdrive ventricular pacing from a temporary pacemaker had clearly become, "quite long!" (ie, between 492-to-545 msec, depending on which correction formula is chosen).
• As described above by Drs. Smith and Karim — Pacing in today's case is an effective intervention — as doing so prevents the bradycardia and pauses that are likely to precipitate additional episodes of Torsades de Pointes. (For more on Torsades de Pointes vs PMVT — See My Comment in the October 18, 2023 post and the September 2, 2024 post in Dr. Smith's ECG Blog).
• 
  
• NOTE: A handy link that I favor to provide near instant correction of the measured QT according to heart rate (at least in cases with normal QRS duration) = MD CALC — which allows calculation of the QTc by any of the 5 most commonly used corrective formulas ( = Bazett — Fridericia — Framingham — Hodges — Rautaharju).

My Approach: Rapid Qualitative Assessment ...

Although I did not precisely calculate the QTc for the ventricular paced ECG in today's case — I instantly recognized that despite the tachycardia at ~100/minute — the QTc for this markedly widened paced QRS complex was significanatly prolonged because:

• The measured QT interval for this tracing qualitatively looks to be well over 2/3 the R-R interval in this tracing. 
• Even with tachycardia and a paced QRS duration of ~0.16 second — I immediately knew there is no way this relative increase in QT duration (compared to the R-R interval) is going to be "normal".

2 Quick Approximations that I Use:

As I discuss in My Comment in the March 19, 2019 post in Dr. Smith's ECG Blog — 2 quick methods for rapid assessment of the QTc have worked well for me over the past 3+ decades:

• When the heart rate is not too rapid (this method works less well with heart rates >90-100/minute) — I favor the “Eyeball” Method to tell at a glance if the QTc is likely to be prolonged. Using this method — one may suspect that the QTc will be long IF the longest QT interval that you can clearly see on the tracing is more than half the R-R interval.
• 
  
• To quickly estimate a numerical value for the QTc — I developed a Correction Factor that has been surprisingly accurate for me in assessing too-numerous-to-count QTc values that I’ve estimated during the course of my career. As per the text under the ECG in Figure-1 — you only need to remember 3 values (ie, 1.1 for a rate ~75/min — 1.2 for ~85/min — and 1.3 for ~100/minute). With a little practice using this method — you can estimate the QTc within seconds.
• Applying my method to the March 19, 2019 case that I show in Figure-1 — the rhythm in this Figure-1 ECG is regular, with an R-R interval just under 4 large boxes. Thus, the heart rate is just a bit over 75/minute (ie, 300÷4). 
• I selected lead V3 in Figure-1, as one of the leads where we can clearly define the onset and offset of the QT interval. I measure the QT in this lead to be ~2.4 large boxes = 480 msec. 
• Using a correction factor of 1.1 (since the heart rate ~75/minute) — I estimate the QTc = 480 + [480 X .1 = 48) = 480 + 48 ~528 msec. For speed and ease of calculation — I usually round off values (it’s all an estimate anyway! ) — but I’ve enjoyed being able to get very close to computer-calculated QTc values by this simple correction factor method.

Figure-1: My "correction factor" for QTc estimation when the QRS is not wide (from My Comment in the March 19, 2019 post in Dr. Smith's ECG Blog).