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

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).