Does nifedipine enhance the cardiovascular depressive effects of bupivacaine?

Inadvertent intravenous administration of bupivacaine has been shown to cause cardiovascular collapse in patients. Patients undergoing peripheral vascular surgery have a high incidence of coronary artery disease and frequently receive calcium channel antagonists such as nifedipine for treatment of angina. In this study, the effects of an accidental intravenous injection of bupivacaine during regional anesthesia in patients taking nifedipine was simulated using dogs. The sling-trained dogs had baseline hemodynamic values recorded. Each dog was given a 10-mg sublingual loading dose of nifedipine in alcohol solvent followed by intravenous infusion of nifedipine at a rate of 5/micrograms/kg/min. After hemodynamic measurements were taken, increasing boluses of intravenous bupivacaine were administered until a 50% decrease in maximum left ventricle change in pressure with respect to time (LV dP/dt max) was observed. On the next day of the experiment, baseline hemodynamic measurements were recorded. The dog was given only the alcohol solvent portion of the nifedipine solution at a dosage and rate equivalent to that of the first day of the experiment. Next, increasing boluses of intravenous bupivacaine were administered exactly as on the first day until a 50% decrease in LV dP/dt max was observed. The results demonstrated that the total dose of bupivacaine given with nifedipine (8.7 +/- 3.7 mg/kg) to reach a 50% drop in LV dP/dt max was significantly less than the total dose of bupivacaine given without nifedipine (14.5 +/- 4.9 mg/kg); and the main effect of the combination of nifedipine and bupivacaine was to accentuate the decrease in LV dp/dt max caused by bupivacaine with the elimination of the compensatory increase in systemic vascular resistance to maintain blood pressure.

Oxygen consumption during spontaneous ventilation with acute lung injury in anesthetized pigs.

Acute lung injury causes a restrictive pulmonary defect, decreases lung compliance, and increases the work of breathing. We wished to determine the oxygen cost of the increased elastic work of breathing associated with acute lung injury. Extracorporeal venous circulation with a membrane lung was used to extract CO2 and to induce apnea in 14 anesthetized pigs. Data were collected during 4 experimental states: during spontaneous ventilation and apnea when the animals' lungs were normal, and after acute lung injury developed because of oleic acid administration. Acute lung injury decreased lung compliance from 101 +/- 79 (mean +/- SD) to 52 +/- 25 ml/cm H2O (p less than 0.04), and increased the elastic work of breathing from 700 +/- 590 to 1,060 +/- 630 ml.cm H2O (p = 0.01). During spontaneous ventilation, the increases in total O2 consumption and the O2 cost of breathing caused by acute lung injury were sufficiently small as to be undetectable, and, therefore, less than 3 to 4% of basal O2 consumption despite markedly increased elastic work and ventilatory power requirements. The increase in O2 consumption imposed by acute lung injury was small enough (less than 3 to 4% of total O2 consumption) that it appears to be clinically insignificant.

Airway pressure release ventilation.

Airway pressure release ventilation (APRV) delivers continuous positive airway pressure (CPAP) and may support ventilation simultaneously. This investigation tested whether, after acute lung injury (ALI), APRV promotes alveolar ventilation and arterial oxygenation without increasing airway pressure (Paw) above the CPAP level and without depressing cardiac function. Ten anesthetized dogs randomly received either intermittent positive-pressure ventilation (IPPV) or APRV. APRV was delivered with a continuous-flow CPAP system. Expiration occurred when a switch in the expiratory limb opened and Paw decreased to near-ambient, which decreased lung volume. After baseline data collection, ALI was induced by infusing oleic acid iv. Two hours later, IPPV and APRV were administered randomly, and data were collected. With normal lungs, APRV and IPPV achieved similar gas exchange and hemodynamic function. During ALI, arterial oxygenation was improved, and peak Paw which did not exceed the CPAP level, was lower during APRV. Similar minute ventilations were delivered by both modes but resulted in lower PaCO2 with APRV. Thus, APRV decreased physiologic deadspace ventilation. Hemodynamic status was similar during both modes. Therefore, APRV is an improved method of oxygenation and ventilatory support for patients with ALI that will allow unrestricted spontaneous ventilation and may decrease the incidence of barotrauma.