Orris

In Torsades de Pointes : qt prolongation reflects prolonged repolarisation period due to ion channel dysfunction. This can give rise to early after depolarisation which manifest as tall U waves on ecg and if those u waves reach threshold they may manifest as PVCs and cause Polymorphic Ventricular Tachycardia. Does this happen?

Reading File
Reading File
Searching PubMed

"Torsades de Pointes"[MeSH Terms] AND "early afterdepolarization"

Finding Sources
Finding Sources
Reading File
Reading File
Yes, your chain is essentially right. Two details need correcting: the link to U waves, and what actually sustains the arrhythmia.
What the textbooks support
  • Prolonged repolarisation lets inward currents recover (L-type calcium, and late sodium). This produces early afterdepolarisations (EADs) that cause PVCs. Prolonged repolarisation also makes repolarisation uneven across the ventricle, which favours reentry. - Braunwald's Heart Disease, "Acquired Long QT Syndrome and Torsade de Pointes"
  • EADs occur during phases 2-3 of the action potential. They are favoured by intracellular calcium loading. When the QT is prolonged unevenly across the ventricles, EADs can trigger abnormal depolarisation wavefronts, which gives TdP. - Harrison's Principles of Internal Medicine 22E, "Afterdepolarizations and Triggered Arrhythmias"
  • Hypokalaemia, hypomagnesaemia and bradycardia all predispose to EADs. - Harrison's 22E
  • Rosen's Emergency Medicine also names acquired TdP as the classic arrhythmia of EADs.
Corrections
  1. An EAD is not the same thing as a U wave. An EAD is a cellular event: a membrane potential oscillation during phase 2 or 3, before repolarisation is complete. Prominent U waves or notched T-U complexes often accompany long QT, especially with hypokalaemia. They may partly reflect EAD activity or M-cell repolarisation, but the mechanism of the U wave is debated, and "EADs appear as tall U waves" is a simplification. Clinically, the diagnostic signs are a prolonged QTc (usually above about 0.48 s before the event), T-U abnormalities, and PVCs.
  2. The EAD itself must reach threshold, not the U wave. When an EAD reaches threshold, it fires a premature beat, which is the PVC. That PVC often lands on a vulnerable, prolonged T wave.
  3. The trigger is usually pause-dependent. Braunwald notes that episodes are usually initiated by heart rate slowing or a PVC-induced pause. The classic sequence is short-long-short: a PVC, then a compensatory pause, then a sinus beat with an even longer QT, then a PVC that starts TdP. Slow rates favour EADs, and rapid pacing or drugs that shorten the action potential suppress them (Goldman-Cecil Medicine). Bradycardia can also deepen the pause-dependent effect.
  4. EADs are probably the trigger, and reentry the sustaining mechanism. The EAD-driven PVC starts the arrhythmia. Heterogeneous repolarisation across the ventricular wall (transmural dispersion) then allows reentry to maintain the polymorphic VT. The twisting QRS axis is the ECG result of this. Episodes are often self-terminating, but they can degenerate to VF.
  5. Ion channel dysfunction is not the only cause of QT prolongation. In congenital long QT it is channel mutations (for example loss of function in IKr/IKs, or gain of function in late INa). In acquired long QT it is mostly IKr-blocking drugs, plus electrolyte problems, bradycardia and female sex.
Why magnesium and pacing work Magnesium inhibits the calcium currents that cause EADs (Tintinalli's Emergency Medicine). Braunwald recommends 1-2 g IV magnesium, correcting bradycardia with isoproterenol or pacing, stopping the offending drugs, and correcting electrolytes. Sustained TdP needs immediate defibrillation.
I ran a short PubMed search for recent systematic reviews and meta-analyses on this mechanism. It found nothing that changes or contradicts the textbook account.
This is a shared conversation. Sign in to Orris to start your own chat.