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.
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