Prolonged QT/Torsades

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MedicineZ0Z

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Hello,

A concept I've had trouble with is identifying a true case of QT prolongation and what the real risk of torsades is.

One patient I've seen had a QTc (HR 120) of 440 and 460 taken an hour or two after an episode of rapid heart rate and lightheadedness. Patient takes a QT prolonging drug but is healthy otherwise.

So how do we suspect torsades in a case like this where a tachycardia episode occurred? My understanding is that a <QTc of 500 is not that significant and that torsades is quite rare. But when do we truly suspect it?

Thanks!
 
What do you mean an hour or two after an episode of rapid heart rate and lightheadedness?

People with torsade don't usually feel a touch of the lightheadedness. If they survive, they usually come in with a mandle or a zygomatic arch fracture or a broken arm and bruises everywhere. You don't get a little lightheaded and ease yourself to the ground with TdP or polymorphic VT. Cardiac output literally goes to zero and you lose consciousness and all muscle tone. You don't stop yourself from going down. Think tree falling in the woods.

TdP is rare with QTc <550.

The TdP I have seen had QTs of 550- 700
 
What do you mean an hour or two after an episode of rapid heart rate and lightheadedness?

People with torsade don't usually feel a touch of the lightheadedness. If they survive, they usually come in with a mandle or a zygomatic arch fracture or a broken arm and bruises everywhere. You don't get a little lightheaded and ease yourself to the ground with TdP or polymorphic VT. Cardiac output literally goes to zero and you lose consciousness and all muscle tone. You don't stop yourself from going down. Think tree falling in the woods.

TdP is rare with QTc <550.

The TdP I have seen had QTs of 550- 700
Hmm I see.. Doesn't it normally cease on its own after a brief episode and uncommonly goes into vfib?
How rare is it generally (hard to verbalize I'm sure) among those using QT prolonging drugs?
 
Hmm I see.. Doesn't it normally cease on its own after a brief episode and uncommonly goes into vfib?
How rare is it generally (hard to verbalize I'm sure) among those using QT prolonging drugs?

It often ceases but is life threatening. It is polymorphic VT

It is rare. Zofran, fluoroquinolones Macrolides, haldol and many other commonly prescribed meds significantly prolong the QT interval but we don't see TdP all that often.
 
It often ceases but is life threatening. It is polymorphic VT

It is rare. Zofran, fluoroquinolones Macrolides, haldol and many other commonly prescribed meds significantly prolong the QT interval but we don't see TdP all that often.

Interesting, I never knew cardiac output basically drops entirely in polymorphic VT (I'm an MS-III).
Are PVCs in the presence of QTc in the mid to high 400s a true risk in any way for anything in the absence of structural heart disease or any congenital factors?

Like an otherwise healthy athlete comes in with some PVCs and mildly prolonged QTc. Do we really do anything? Keep K above 4 and Mg above 2.5 and let them be?
 
Most of the TdP I have seen is related to heavy methadone use due to high drug related probs in the city where I’m training. Rarely seen it degenerate into VF.
 
Interesting, I never knew cardiac output basically drops entirely in polymorphic VT (I'm an MS-III).
Are PVCs in the presence of QTc in the mid to high 400s a true risk in any way for anything in the absence of structural heart disease or any congenital factors?

Like an otherwise healthy athlete comes in with some PVCs and mildly prolonged QTc. Do we really do anything? Keep K above 4 and Mg above 2.5 and let them be?

That is why people die with PMVT... it is an unstable rhythm. Your CO goes to zero. When you have an a-line, it goes flat.

Actually a young person with long QT gets people a lot more anxious even if mildly prolonged. These people often undergo testing to look for the various channelopathies that cause long QT syndromes. Other than HoCM, these channelopathies are one of the more common causes of sudden death in an otherwise young healthy person.
 
Most of the TdP I have seen is related to heavy methadone use due to high drug related probs in the city where I’m training. Rarely seen it degenerate into VF.
Makes sense. How do you know if they had TdP when they present after the episode (aside from the physical signs described above)?
 
That is why people die with PMVT... it is an unstable rhythm. Your CO goes to zero. When you have an a-line, it goes flat.

Actually a young person with long QT gets people a lot more anxious even if mildly prolonged. These people often undergo testing to look for the various channelopathies that cause long QT syndromes. Other than HoCM, these channelopathies are one of the more common causes of sudden death in an otherwise young healthy person.
Interesting. On this note, is the usual QTc formula reliable outside of the pulse ranges of 60-100? Just mathematically, doesn't sinus tachy artificially increase the QTc?
 
Makes sense. How do you know if they had TdP when they present after the episode (aside from the physical signs described above)?
Clinical history, QT prolongation, and the couple obvious times they had a recurrence.
 
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