Page 120 - YORAM RUDY BOOK FINAL

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Figure 4.5. Effects of extracellular potassium concentration on action potential and ECG wave-
form. I is proportional to ([K ] )½ and is shown together with the action potential (dashed lines).
+
o
Kr
Hypokalemia ([K ] =2mmol/L, center) prolongs the QT interval and flattens the T-wave relative to
+
o
control (center). Hyperkalemia ([K ] =6mmol/L, right) shortens the QT interval and augments
+
o
the T-wave amplitude. These changes are consistent with experimental results obtained in an
arterially perfused ventricular wedge preparation. Reproduced from Gima and Rudy [247]. The
bottom panel is excerpted from Yan and Antzelevitch [250]. All panels are reproduced with
permission from Wolters Kluwers Health, Inc.

Because of the smaller I of M cells (smaller total repolarizing current), I reduction (LQT2)
Ks
Kr
prolongs their action potential to a greater extent than that of epicardial or endocardial cells.
Because repolarization of the M cells determines the end of the ECG T-wave, QT prolongation is
accompanied by widening of the T-wave and increased TDR. Also, the greater difference between
the M cells action potential and the action potentials of the other cell types augments the V m

gradient during repolarization, and consequently, the T-wave amplitude.
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In LQT3, prolongation of the action potential is caused by a late mutant I that shifts the
Na
delicate balance of transmembrane currents during the action potential plateau in the inward
(depolarizing) direction. Similar to LQT2, the effect is greater in M cells than other cell types