Search

We previously found the frequency distribution of the left ventricular (LV) effective afterload elastance ([E.sub.a]) of arrhythmic beats to be nonnormal or non-Gaussian in contrast to the normal distribution of the LV end-systolic elastance ([E.sub.max]) in canine in situ LVs during electrically induced atrial fibrillation (AF). These two mechanical variables determine the total mechanical energy [systolic pressure-volume area (PVA)] generated by LV contraction when the LV end-diastolic volume is given on a per-beat basis. PVA and [E.sub.max] are the two key determinants of the LV [O.sub.2] consumption per beat. In the present study, we analyzed the frequency distribution of PVA during AF by its [chi square], significance level, skewness, and kurtosis and compared them with those of other major cardiodynamic variables including [E.sub.a] and [E.sub.max]. We assumed the volume intercept ([V.sub.o]) of the end-systolic pressure-volume relation needed for [E.sub.max] determination to be stable during arrhythmia. We found that PVA distributed much more normally than [E.sub.a] and slightly more so than [E.sub.max] during AF. We compared the [chi square], significance level, skewness, and kurtosis of all the complex terms of the PVA formula. We found that the complexity of the PVA formula attenuated the effect of the considerably nonnormal distribution of [E.sub.a] on the distribution of PVA along the central limit theorem. We conclude that mean (SD) of PVA can reliably characterize the distribution of PVA of arrhythmic beats during AF, at least in canine hearts. end-systolic elastance; effective afterload elastance; frequency distribution; normality

A comprehensive equation defining the force of restitution and potentiation in terms of two preceding beat intervals was used in a computer simulation approximating the contractilities of irregular arrhythmic beats. The relationship among the different parameters under investigation was similar to the results of an experimental procedure previously undertaken. This suggests that mechanical restitution and potentiation are responsible for the variable contractilities observed in arrhythmia.