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The role of hemodynamic and regulatory factors in the arterial pressure response to hemodialysis induced hypovolemia was investigated by means of a computer model of the cardiovascular system, including the main short-term pressure regulatory mechanisms. The model mimics the arterial and venous systemic circulation, Starling's law and inotropic heart regulation, arterial and cardiopulmonary baroreflex controls of resistance, and capacitance vessels. All of the model parameters have a clear physiologic meaning: 10 represent the systemic circulation, 4 describe cardiac pump performance, and 3 characterize baroreflex regulation. Sensitivity analysis is performed to determine the effect of each parameter on the pressure response to mild hypovolemia (a 10% blood volume reduction after 4 hours). The results demonstrate that circulatory parameters, such as resistances and compliances, have no relevant effect upon the pressure response. Conversely, regulation of venous capacity seems to play a pivotal role in sustaining arterial pressure during hemodialysis induced hypovolemia. Regulation of systemic peripheral resistance exerts a compensatory action only as long as the blood volume reduction is < 5%, but it is inadequate to compensate for a larger blood volume reduction when venous capacity regulation is absent. A paradoxical arterial pressure increase during hypovolemia can be referred to a prevalence of cardiopulmonary afferences in the regulatory process.

Objective: To evaluate the effect of acute changes in minute ventilation (VE) on oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory quotient, and energy expenditure during volume-controlled mechanical ventilation in the critically ill surgical patient. The effects on some oxygen transport variables were assessed as well., Design: Prospective, randomized clinical study, Setting: Adult surgical intensive care unit of a university teaching hospital., Patients: Twenty adult critically ill surgical patients were studied during volume-controlled mechanical ventilation., Interventions: After a basal period of stability (no changes over time in body temperature, energy expenditure, blood gases, acid-base status, cardiac output, and ventilatory parameters), VE was then randomly either increased or reduced (+/-35%) by a change in tidal volume (VT), while respiratory rate and inspiratory/expiratory ratio were kept constant. Settings were then maintained for 120 mins. During the study, patients were sedated and paralyzed., Measurements and Main Results: VO2, VCO2, and respiratory quotient were measured continuously by a Nellcor Puritan Bennett 7250 metabolic monitor (Nellcor Puritan Bennett, Carlsbad, CA). Hemodynamic and oxygen transport parameters were obtained every 15 mins during the study. Despite large changes in VE, VO2 and energy expenditure did not change significantly either in the increased or in the reduced VE groups. After 15 mins, VCO2 and respiratory quotient changed significantly after ventilator resetting. VCO2 increased by 10.5 +/- 1.1% (from 2.5 +/- 0.10 to 2.8 +/- 0.12 mL/min/kg, p< .01) in the increased VE group and decreased by 12.4 +/- 2.1% (from 2.7 +/- 0.17 to 2.4 +/- 0.16 mL/min/kg, p< .01) in the reduced VE group. Similarly, respiratory quotient increased by 16.2% +/- 2.2% (from 0.87 +/- 0.02 to 1.02 +/- 0.02, p< .01) and decreased by 17.2% +/- 1.8% (from 0.88 +/- 0.02 to 0.73 +/- 0.02, p< .01). VCO2 normalized in the reduced VE group, but remained higher than baseline in the increased VE group. Respiratory quotient did not normalize in both groups and remained significantly different from baseline at the end of the study. Cardiac index, oxygen delivery, and mixed venous oxygen saturation increased, while oxygen extraction index decreased significantly in the reduced VE group. Neither of the mentioned parameters changed significantly in the increased VE group., Conclusions: We conclude that, during controlled mechanical ventilation, the time course and the magnitude of the effect on gas exchange and energy expenditure measurements caused by acute changes in VE suggest that VO2 and energy expenditure measurements can be used reliably to evaluate and quantify metabolic events and that VCO2 and respiratory quotient measurements are useless for metabolic purposes at least for 120 mins after ventilator resetting.