“…Clinical hypercalcemia, whether secondary to hyperparathyroidism, neoplastic disease, or other causes, is usually characterized by a prolongation of A-V conduction time, widening of the QRS interval, the appearance of a J wave or Osborne wave, abbreviation of the ST segment, and, particularly in patients with extreme hypercalcemia (> 16 mg/dL; normal value, 8.2 to 10.4 mg/dL), changes in the morphology (biphasic, notched), polarity (inverted), and amplitude (flat) of the T wave of the surface ECG. 56 Most if not all of these changes can be explained based on the differential effects of high calcium in canine ventricular epicardium and endocardium. The calcium-induced accentuation of the action potential notch in epicardium can account for the appearance of a J wave, the slight slowing of conduction for the widening of the QRS, and the disparate effects on APD90 in epicardium and endocardium for the inversion or flattening of the T wave.14 Possible Limitations of the Study Although some of the results of the study are discussed in terms of changes in intracellular calcium levels, we clearly have not demonstrated an increase in Ca, in either epicardium or endocardium after exposure to high [Ca'2+] and rapid pacing.…”