Shock-induced epicardial and endocardial virtual electrodes leading to ventricular fibrillation via reentry, graded responses, and transmural activation.

INTRODUCTION

The mechanism of ventricular fibrillation (VF) induction by T wave shocks has been attributed to reentry, propagated graded responses (PGR), and triggered activity. The limitation of recording transmembrane potential (V(m)) from only a single surface has hampered efforts to elucidate the relative role of these phenomena and their relationship to shock-induced virtual electrodes.

METHODS AND RESULTS

V(m) patterns from epicardial and endocardial surfaces of isolated sheep right ventricles were recorded with two CCD cameras for monophasic (M) and biphasic (B) shocks delivered at various coupling intervals (CI) from a unipolar mesh electrode on the epicardium. VF was induced via (1) the formation of reentry following make or break excitation; (2) propagated graded responses during apparent isoelectric window; and (3) breakthrough activation patterns coincident with endocardial-to-epicardial gradients in V(m). M shocks depolarized both surfaces at long CIs and polarized epicardial and endocardial surfaces oppositely at short CIs. At intermediate CIs, postshock V(m) patterns could lead to reentry on one surface or endocardial-to-epicardial gradients resulting in breakthrough. B induced VF less than M for short and intermediate CIs due to more homogeneous end-shock V(m) patterns. However, at long CIs these homogeneous patterns resulted in more VF induction because B left the tissue closer to the V(m) threshold for propagation.

CONCLUSION

Postshock activity occurred either immediately via epicardial or endocardial reentry, or after a delay caused by transmural propagation or propagated graded responses. These findings could explain the isoelectric window and focal activation patterns observed on the epicardium following VF induction shocks.