Interpretation of pulmonary artery wedge pressure and pullback blood gas determinations during positive end-expiratory pressure ventilation and after exclusion of the bronchial circulation in the dog

Left atrial pressure (LAP) and pulmonary artery wedge pressure (PWP) were measured at different heights during graded increases in positive end-expiratory pressure (PEEP). Six healthy anesthetized dogs were placed in lateral decubitus positions with a balloon-tipped pulmonary artery catheter inserted in each lung. PWP in the gravitationally superior lung overestimated LAP at 15 and at 20 cm H2O PEEP (p less than 0.05). PWP in the dependent lung was virtually identical to LAP at all degrees of PEEP. Wedge blood could be aspirated through the distal lumen of the pulmonary artery catheters during balloon inflation at all degrees of PEEP except for 3 attempts. PCO2 in wedge blood in both the nondependent and dependent lungs at all degrees of PEEP was consistently lower than PCO2 in arterial blood (p less than 0.05). Wedge blood was arterialized, i.e., oxygen saturation greater than 95%, in all but 4 specimens. Surgical elimination of the bronchial artery supply to the lung in 3 dogs did not affect PWP or blood gas measurements. We conclude that in this animal model: (1) the tip of a pulmonary artery catheter must be below the level of the left atrium, Zone III location, to accurately reflect LAP at high degrees of PEEP; (2) arterialization of wedge blood samples does not guarantee that PWP reflects LAP; (3) bronchial artery blood supply does not affect PWP or wedge blood gas measurements, even at high degrees of PEEP.     

Continuous monitoring of oxygen tension with a transcutaneous sensor during hypotensive anesthesia

Transcutaneous oxygen tension (TCPO2) is a useful noninvasive technique for monitoring arterial oxygen tension under stable circulatory conditions. This study was undertaken to determine if TCPO2 is also reliable during sodium nitroprusside-induced hypotension under general anesthesia. Arterial blood gases and TCPO2 were measured prior to inducing hypotension (baseline), at 20-min intervals during hypotension, and when systemic arterial pressure had returned to within 10% of the control (pre-hypotension) value. With induced hypotension, PaO2 and TCPO2 decreased significantly (P less than 0.05), and were well correlated by linear regression (r greater than 0.85); however, regressions were strongly dependent on the individual patient. The mean regression line for all patients as a group was given by TCPO2 = 0.69 PaO2 + 20.7 mmHg (r = 0.93, P less than 0.01); significantly different regressions were obtained for each patient (P less than 0.0001). Comparing changes in TCPO2 versus those in PaO2 (relative change from baseline values) did not substantially reduce the variability among patients. It is concluded that TCPO2 reliably reflects changes in arterial oxygen tension during controlled hypotension under general anesthesia, but that a separate calibration of TCPO2 vs. PaO2, obtained prior to inducing hypotension, may be required for each individual patient.     

Propranolol prevents hemodynamic and humoral events after abrupt withdrawal of nitroprusside

Hemodynamic and humoral events after intraoperative discontinuation of nitroprusside were studied in subjects without and with pretreatment with intravenous propranolol, 0.1 mg X kg-1. Nitroprusside-induced hypotension was associated with increases in heart rate, cardiac output, plasma renin activity (PRA), and catecholamine levels; these changes were prevented by propranolol. In subjects pretreated with propranolol, dose requirements of nitroprusside for hypotension of comparable degree and duration decreased 40%. On discontinuation of nitroprusside, mean systemic pressure rose to 100.2 mm Hg--a level higher than prehypotension and awake values--because of increased systemic vascular resistance. Hemodynamic events were associated with persistent elevations of PRA and catecholamine levels. These rebound changes were maximal 15 min after nitroprusside withdrawal and returned to control levels 30 to 60 min later. Pretreatment with propranolol completely prevented rebound hemodynamic events after nitroprusside. Persistent elevations of PRA and catecholamine levels after nitroprusside action subsided were responsible for the effects of withdrawal.