Cell calcium in the pathophysiology of ventricular fibrillation and in the pathogenesis of postarrhythmic contractile dysfunction.

The mechanism of ventricular fibrillation is poorly understood at the cellular level. We explored the role of intracellular free calcium in the pathophysiology and pathogenesis of ventricular fibrillation in perfused ferret hearts loaded with the Ca2+ indicator 5F-BAPTA. Nuclear magnetic resonance spectroscopy was used to measure [Ca2+]i, pH, and high-energy phosphates. During ventricular fibrillation induced by burst pacing, [Ca2+]i rose rapidly and dramatically, exceeding by four times the control within 5 minutes. [Ca2+]i remained markedly elevated throughout 20 minutes of fibrillation, but it returned to control values shortly after defibrillation. In a group of hearts kept isovolumic by a balloon in the left ventricle, acidosis and high-energy phosphate depletion developed despite the maintenance of normal coronary pressure. To distinguish the effects of superimposed ischemia from those of the arrhythmia itself, we lowered left ventricular volume during fibrillation in a second group of hearts. This ...