We studied the effects of ventricular end-systolic elastance (Ees) and effective arterial elastance (Ea) on the efficiency of energy transfer from pressure-volume area (PVA) to external mechanical work (EW) in the left ventricle of anesthetized closed-chest dogs. PVA represents the total mechanical energy generated by ventricular contraction, which is an intermediate form of energy between oxygen consumption, the total energy input, and EW, the effective energy output. PVA and EW were determined from ventricular pressure and volume, which were continuously measured with a volumetric conductance catheter. Measurements of Ees were obtained by transiently increasing afterload by an inflation of a Fogarty catheter in the thoracic descending aorta. Ea was determined as the ratio of end-systolic pressure to stroke volume. The EW/PVA efficiency of a steady-state contraction increased from 55% to 64%, with a 58% increase in Ees after dobutamine. Ees, which was smaller than Ea before dobutamine, became nearly equal to Ea after dobutamine, maximizing EW for a given end-diastolic volume. EW/PVA efficiency decreased with an abrupt increase in afterload before and after dobutamine. The sensitivity of the decrease in the EW/PVA efficiency to an increase in end-systolic pressure was significantly less after than before dobutamine. We could account for all these changes in EW/PVA efficiency by the relative changes in Ees and Ea in the pressure-volume diagram.
The present study attempted long term hemodynamic maintenance in 16 adult brain-dead patients, 14 with head injury and 2 with cerebrovascular accidents. In addition to respiratory and fluid management, 10 were treated with continuous infusion of epinephrine to maintain systolic blood pressure above 90 mm Hg. The remaining 6 patients each received a continuous infusion of synthetic arginine vasopressin (ADH) at a rate of 1 or 2 units/hour (285 +/- 45 microunits/kg/minute) simultaneously with epinephrine. The 10 patients treated with epinephrine alone all succumbed to cardiac arrest within 48 hours of brain death, with a mean survival time of 24.1 +/- 17.2 hours. In the patients who received simultaneous ADH infusion, a minimal dose of epinephrine of no more than 0.5 mg/hr in most instances sufficed to maintain blood pressure. Their mean survival time after brain death was remarkably prolonged to 23.1 +/- 19.1 days. In brain death, ADH plays a critical role in hemodynamic maintenance, and ADH administration permits long term hemodynamic stabilization of brain-death patients, offering increasing opportunities for organ transplantation.
We theoretically considered the relation between left ventricular O2 consumption (MVO2) and a contractility index (Emax), searching for an optimal Emax that minimizes MVO2 for a given external mechanical work. We used one equation relating Emax with ventricular pressure and volume and another equation relating MVO2 with pressure-volume area (PVA). PVA is theoretically and experimentally a good predictor of MVO2 with Emax as a parameter. Then we could theoretically show the existence of the optimal Emax. For example, MVO2 was minimized to 8.9 ml O2.min-1.100 g-1 at an Emax of 6.3 mmHg.ml-1.100 g when cardiac output was 1.2 l/min, afterload pressure was 100 mmHg, and heart rate was 150 beats/min. These values can be observed experimentally in a 10- to 15-kg dog. Optimal Emax values for a wide range of external work fall in the middle of the normal working range of Emax. Thus our MVO2-PVA-Emax relationship supports the contemporary concept of the optimal contractility that MVO2 for a given cardiac external work is minimum at a middle level of ventricular contractility.
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