Ventricular fibrillation in ischaemia and its defibrillation
ECG signals were recorded from isolated, Langendorff-perfused rabbit hearts to establish the relationship between dominant frequency and myocardial perfusion during ventricular fibrillation. Lower perfusion rates produced faster rates of dominant frequency decline, to lower steady state values. Optically mapping the anterior epicardial surface demonstrated heterogeneity of dominant frequency in ventricular fibrillation. During low-flow ischaemia, the dominant frequency reduction was restricted to the left ventricle. Application of individual ischaemic components during ventricular fibrillation demonstrated that raised [K+]EC, but not hypoxia or acidic pHEC, reproduced the ischaemic reduction of dominant frequency in the ECG, pseudoECG and over the left ventricular epicardial surface. In contrast, minimum defibrillation energies were increased by hypoxia and acidic pHEC, and not by raised [K+]EC. The dominant frequency heterogeneity during ventricular fibrillation in low-flow ischaemia and raised [K+]EC was not due to differential prolongation of repolarisation or post-repolarisation refractoriness in the left ventricle. Monophasic action potential studies showed that APD90 was reduced to similar degrees in each ventricle by low-flow ischaemia and raised [K+]EC. Effective refractory period was not altered in either ventricle by either condition. Low-flow ischaemia decreased conduction velocity in the left, but not the right ventricle. Conduction velocities were unaltered by raised [K+]EC in either ventricle. The activation threshold of the left ventricle was increased in low-flow ischaemia and raised [K+]EC, whilst the threshold of the right ventricle was unchanged. The increased activation threshold was associated with decreased upstroke velocity and diastolic depolarisation.