Anesthesia and analgesia
-
Anesthesia and analgesia · Jan 1999
The influence of surgical sites on early postoperative hypoxemia in adults undergoing elective surgery.
To determine the influence of the surgical sites on early postoperative hypoxemia, we studied postoperative hypoxemia in 994 patients, ASA physical status I or II, aged 18-68 yr, scheduled for various types of elective surgery. Patients were divided into three groups on the basis of the surgical sites: Group 1 = elective superficial plastic surgery (n = 288); Group 2 = upper abdominal surgery (n = 452); and Group 3 = thoracoabdominal surgery (n = 254). Anesthesia was maintained with 1%-2% enflurane and 67% nitrous oxide in oxygen; thiopental or fentanyl was given IV as required. SpO2 levels were recorded while patients breathed room air shortly after arrival in the recovery room (0 min) and 5, 10, 15, 20, 30, 40, 50, 60, 120, and 180 min thereafter. The results showed that during the early postoperative period, the degree of arterial desaturation and the incidences of hypoxemia (SpO2 86%-90%) and severe hypoxemia (SpO2 85%) were closely related to the operative sites and were greatest for thoracoabdominal operations, less for the upper abdominal operation, and least for the peripheral surgery. The incidence of hypoxemia and severe hypoxemia in the recovery room was 7% and 0.7%, respectively, in Group 1, 38% and 3% in Group 2, and 52% and 20% in Group 3. Mild airway obstruction and hypothermia in the postanesthesia recovery unit (PAR) were the predictive factors of early postoperative hypoxemia. We conclude that during the early postoperative period, there were significant differences in SpO2 levels and incidences of hypoxemia and severe hypoxemia among the three groups. ⋯ We found that the severity of arterial desaturation and the incidence of hypoxemia during the early postoperative period are closely related to the surgical sites and are strongest for thoracoabdominal surgery, less for upper abdominal surgery, and least for peripheral surgery.
-
Anesthesia and analgesia · Jan 1999
The effects of ketamine and propofol on neuronal nicotinic acetylcholine receptors and P2x purinoceptors in PC12 cells.
We studied the effects of ketamine and propofol on two ligand-gated ion channels mediating fast synaptic transmission through sympathetic ganglia, neuronal nicotinic acetylcholine receptors (nAchRs), and P2X purinoceptors in a rat pheochromocytoma cell line PC12 using whole cell voltage clamp recording. Ketamine and propofol similarly inhibited the nicotine-induced inward current reversibly and dose-dependently at the membrane potential of -60 mV but had no effects on the adenosine triphosphate-induced current. Both anesthetics accelerated the current decay during agonist application, resulting in greater inhibition on the steady current than the peak current. The 50% inhibition concentration values for the steady current were lower than the clinically relevant concentrations for ketamine (2.8+/-0.6 microM) and higher than those for propofol (5.4+/-0.6 microM). Both anesthetics induced an addition of the fast component to the decay phase and an acceleration of the slow component, which suggests an open channel blockade or an enhancement of desensitization as a mechanism. The effects on closed channels seemed to be small because preincubation with the anesthetics did not significantly augment the block. Inhibition was voltage-independent at membrane potentials between -20 and -70 mV and was consistent with a noncompetitive block. Inhibition of the neuronal nAchR-mediated current may lead to the suppression of synaptic transmission in sympathetic ganglia by ketamine, but not by propofol, at the clinically relevant concentrations. However, these results are not consistent with changes in sympathetic nerve activities reported for animals or humans anesthetized with ketamine or propofol, which suggests effects from other systems, such as the central nervous system in vivo. ⋯ Ketamine (at smaller than clinically relevant concentrations) and propofol (at larger than clinically relevant concentrations) inhibited neuronal nicotinic acetylcholine receptor-mediated current in PC12 cells, which possess the receptors that resemble those in postganglionic sympathetic neurons. These findings are not consistent with in vivo experiments, which suggests that effects from other systems, such as the central nervous system, are of importance.