Severe diastolic dysfunction with preserved energy conversion efficiency after countershock.
The left ventricular (LV) mechanical performance and the LV myocardial oxygen consumption (VO2)-to-pressure-volume area (PVA; LV total mechanical energy index) relationship were measured in isovolumic contraction of isolated blood-perfused dog hearts before and after direct current (DC) countershocks. At a constant LV volume, DC shocks increased LV end-diastolic pressure progressively and strikingly with the progression of myocardial edema and a marked prolongation of the time constant of LV pressure decay. In contrast, DC shocks changed neither the slope of the LV end-systolic pressure-volume relationship nor the contractile efficiency (the slope of the Vo2-PVA relationship). The oxygen cost of contractility (the slope of the relationship between PVA-independent VO2 and LV contractility) increased 27% after DC shocks. However, the magnitude of this change was considerably smaller than that previously reported in postischemic stunned myocardium (123%), suggesting that the adverse effect of DC shocks on the energy cost of excitation-contraction coupling is relatively minor. Thus, despite the severe diastolic dysfunction, DC shocks do not substantially impair either the efficiency of cross-bridge cycling or calcium cycling. Myocardial interstitial edema is more likely a potential mechanism of diastolic dysfunction after DC shocks.
Yasuda
S
S
Department of Internal Medicine, National Cardiovascular Center, Osaka, Japan.
Shishido
T
T
Goto
Y
Y
D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D001834:Body Water / Q000378:metabolism; D003971:Diastole; D004285:Dogs; D004554:Electric Countershock; D004734:Energy Metabolism; D006352:Heart Ventricles; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D018487:Ventricular Dysfunction, Left