POTD: QT Prolongation
Today’s POTD is thanks to Dr. Haines, who pointed out to me the weird values on the top left of our EKG’s. Namely, the QTcF vs. QTcB. Simply put, they’re just different ways of calculating the QTc.
Briefly about the QT interval.
What is it?
Time from the start of the Q wave to the end of the T wave. Represents time taken for ventricular depolarization and repolarization.
- QT interval shortens at faster heart rates
- QT interval lengthens at slower heart rates
- A quick way to estimate prolonged QT the QT should be less than half the preceding RR interval
Prolonged values are…
· > 440ms in men
· > 460ms in women
· QTc > 500 is associated with an increased risk of torsades de pointes
· QTc < 350 is short
Causes of QTc prolongation
- Medications – the list is EXHAUSTIVE. Common one’s we see.
o Antipsychotics – Haloperidol, droperidol, chlorpromazine, quetiapine, olanzapine
o Benadryl
o Zofran (ondansetron)
o Amiodarone
o Antidepressants
o Antbiotics – the -ofloxacin’s, Bactrim, macrolides (azithromycin)
o Antifungals
o Methadone
- Electrolytes – HypoK, HypoMg, Hypocalcemia
- Hypothermia
- Myocardial Ischemia
- Congenital Prolonged QT Syndrome
Torsades de Pointes (TdP) and QT prolongation
Torsades, a form of polymorphic ventricular tachycardia, is the complication that occurs with QT prolongation. The pathophysiology revolves around the delayed repolarization reflected in the QT prolongation, which can cause early after-depolarizations (can manifest as PVCs). If the PVC occurs concurrently with the T wave, known as “R on T” phenomenon, it can cause degeneration of the rhythm into TdP. Incidentally, this is also why we always use synchronized cardioversion on patients with a pulse rather than defibrillation, as shocking a patient on their T wave can also cause “R on T” phenomenon.
TdP is usually short and self-resolving, so mainstays of treatment involve prevention of recurrent TdP. With active TdP, shock. Otherwise, there are a few therapies for potentially preventing future TdP episodes.
Treatment:
- As for other ventricular tachyarrhythmias, synchronized cardioversion if unstable and defibrillation if pulseless (many times the defibrillator may not be able to sync anyways, so just shock)
- Magnesium 1-2g IV over 10-15 min, can be repeated, followed by an infusion
- Treat underlying cause – correct electrolytes, stop offending drugs, cardiac reperfusion therapy, etc.
- Lidocaine – for refractory TdP. Only non-QT prolonging agent compared with amiodarone and procainamide.
Prevention of TdP:
- Overdrive pacing – no great evidence. The idea is to increase the HR of the patient to shorten the QT interval. Transvenous is preferred. Target is typically ~100-110BPM
- Isoproterenol – also no great evidence, can use prior to pacing to medically increase the HR.
o 5mcg/min (0.1mcg/kg/min in children) target HR 100 or 30 above natural HR
o For both overdrive pacing and isoproterenol, may need to titrate HR to whatever will prevent the patient from going into TdP
Now, back to the original clinical question…
The QTc estimates the QT interval at a standard heart rate of 60 BPM. If the HR is 60 on your EKG, you can just use the QT =).
· Bazett formula: QTC = QT / √ RR
· Fridericia formula: QTC = QT / RR 1/3
· Note: The RR interval is given in seconds (RR interval = 60 / heart rate).
The Bazett formula is the most commonly used because of its simplicity. The Bazett formula overcorrects at HR > 100 and under corrects at HR < 60. If the HR is >100 or <60, the Fridericia formula should be used instead. No, I’m not savvy enough with math to explain why.
Some tips when calculating your own QTc
- Use the lead with the longest, easily measurable QT interval
- Where the maximum slope of the T wave intersects the isoelectric line determines the end of the QT interval
MDCalc has great calculators for calculating your own QTcs.
Random Questions
1) Does magnesium decrease the QTc?
A: No. Thought to stabilize the myocardium through an unknown mechanism.
2) What do I do with my asymptomatic patient’s with QTc > 500?
A: Admit them? Honestly, I have (although they were sent in by their cardiologist for elevated QT). Doesn’t appear to be a clear cut answer… likely hinges on multiple factors like ability to follow-up, comorbidities, number of QT prolonging medications, discussion with PCP, etc.
https://litfl.com/qt-interval-ecg-library/
https://litfl.com/polymorphic-vt-and-torsades-de-pointes-tdp/
https://first10em.com/torsades-de-pointes/