Pathophysiological basis for monitoring of whole heart conductance by 2-lead system

The defibrillation threshold (DFT) is elevated during myocardial ischemia, but the underlying mechanism remains to be elucidated. The hypothesis tested by the present study was that whole heart conductance (WHC) is a determinant of DFT.

WHC was monitored across the longest diameter of the isolated perfused rat heart, using a 2-electrode instrument under various conditions including ischemia-reperfusion (IR). In the control study, WHC was influenced by the conductivity and flow rate of the solution. In IR, WHC decreased immediately after the onset of perfusion arrest in a single exponential manner, then declined again gradually. The second decrease was augmented and accelerated by pretreatment with 1.0 mmol/L heptanol (p<0.005) or high-[Ca2+]e (p<0.001), and was attenuated and delayed by pretreatment with 1.0 micromol/L verapamil (p<0.01). WHC after reperfusion was greater than the pre ischemic level. The postischemic increase in WHC was proportional to the ischemic interval and tissue water content as assessed by desiccation method.

Although time-dependent alterations in DFT in ischemic hearts may be attributable at least in part to dynamic changes in WHC, WHC should be interpreted carefully because it reflects many physiological factors such as coronary perfusion, electrical coupling of cardiac myocytes and tissue edema.