Mechanical determinants of myocardial oxygen consumption in conscious dogs

Abstract

A new practical descriptor of metabolic to mechanical myocardial energy transfer (MET), termed the virtual work model, was evaluated in 32 conscious dogs and in 8 isolated canine hearts. An index of total mechanical energy expenditure (TME) was calculated as the sum of external energy (stroke work) and an internal energy index of heat (left ventricular end-diastolic volume times left ventricular mean ejection pressure). Physiological comparison of TME (x-axis) and myocardial oxygen consumption (MVO2; y-axis) yielded highly linear MET relationships (mean r = 0.93 +/- 0.07), with an average slope of 0.86 +/- 0.39 (SD) and a y-intercept of 9.1 +/- 6.4 mW/ml myocardium. The linear MVO2-TME relationship did not vary under steady-state vs. dynamic vena caval occlusion, increased heart rate, increased afterload, or increased inotropic state with calcium infusion. Compared with five other indexes of myocardial energetics, the virtual work model of MET was the most linear, the most practical in not requiring determination of the end-systolic pressure-volume relationship, and the most accurate predictor of MVO2 under normal and altered hemodynamic conditions.

Cardiac Basal Metabolism.

“…Thus Vanoverschelde [138] has reported a mean VO 2 of 5 ml O 2 100 g Ϫ1 min Ϫ1 (ϳ17 mW g Ϫ1 ) compared with the expected textbook values for man of 26-33 mW g Ϫ1 . In conscious dogs in vivo, Elbeery et al [139] reported a low value (17 mW g Ϫ1 ), but found a mean value of 36 mW g Ϫ1 in isolated hearts studied in parallel. Part of the reason for the lower VO 2 values relates to the lower heart rates and lower end-diastolic volumes in the conscious animals.…”

Oxygen-Wasting Effect of Inotropy

“…First, whether an oxygen-wasting effect is truly an effect of inotropic drugs is uncertain because it can be partly explained by the particular mechanical index used for the assessment. An energetic cost can be calculated without excessive oxygen consumption by using, for instance, the pressure-work index proposed by Rooke and Feigl 14 or the total mechanical energy (TME) model developed by Elbeery et al 15 Second, most of these studies have been conducted in isolated hearts and not in vivo. Therefore, this phenomenon could, in large part, be restricted to the isolated-heart models.…”

“…Therefore, this phenomenon could, in large part, be restricted to the isolated-heart models. 15 Finally, the doses of inotropes needed to show such a wasting of oxygen in vivo have been excessive, inducing profound tachycardia and blood pressures exceeding clinical goals. 16,17 In this study, we investigated whether the inotropic drugs dobutamine and levosimendan have relatively increased oxygen consumption (oxygen wasting) in clinically relevant doses applied in a large-animal model of postischemically reduced left ventricular function.…”

“…Total left ventricular mechanical work was calculated as the pressure-volume area (PVA), 2 the tension-time index (TTI), 19 and the TME. 15 The TTI was calculated from the formula TTIϭ͐Pdt, 19 which is the area under the systolic ventricular pressure curve during 1 steady-state beat. TME was calculated from the formula TMEϭ[(MEP ⅐ EDV/ k)ϩSW]; where MEP is mean ejection pressure 21 and k equals 2.28, a factor correcting for the omission of V w (x intercept of the SW-EDV relation) and a constant parallel conductance volume Vp.…”

“…TME was calculated from the formula TMEϭ[(MEP ⅐ EDV/ k)ϩSW]; where MEP is mean ejection pressure 21 and k equals 2.28, a factor correcting for the omission of V w (x intercept of the SW-EDV relation) and a constant parallel conductance volume Vp. 15,22 Left coronary blood flow was estimated from the formula LVCBFϭCBF/W ⅐ LVW; where LVCBF and CBF are left ventricular and total coronary blood flow, respectively. W and LVW are total and left ventricular myocardial weight, respectively.…”