RESUMEN
UNLABELLED: We compared outpatients transported to the postanesthesia care unit (PACU) while breathing room air to 2-4 L/min nasal cannula oxygen (O2) to test the hypothesis that routine supplemental O2 during transport is not required after general anesthesia in an ambulatory surgery center. We also examined whether the arbitrary arrival PACU O2 saturations of > 92% may be used to predict an infrequent incidence of subsequent significant desaturations (< 90%) in the PACU. One-hundred-ninety patients were randomized to receive either room air or 2-4 L/min nasal cannula for transport to PACU after receiving general anesthesia. O2 saturations were recorded before surgery, just before leaving the operating room, and upon arrival in the PACU. The lowest O2 saturation occurring in the PACU was also recorded. The mean arrival PACU O2 saturation was 95.0 in the Room Air group, compared with 97.2 for the Nasal Cannula (NC) group, a statistically significant difference (P < 0.001). In the Room Air group, 20% had arrival O2 saturations < or = 92%, and half of these (10%) had O2 saturations < 90%. In the NC group, 6% had O2 saturations < or = 92%, of which one third (2%) were < 90% on arrival in the PACU. All of these initial desaturations were easily corrected with face-tent O2 administration, deep breathing, or both. Subgroup analysis revealed that patients whose ages were 60 yr or older or those weighing 100 kg or more had lower arrival room air saturations than their younger or slimmer counterparts. In the Room Air group, only three (3.9%) of the patients that arrived in PACU with O2 saturations > 92% had subsequent desaturations < 90%, compared with seven (7.9%) in the NC group. We conclude that most adult patients undergoing ambulatory surgery can be transported safely to the PACU breathing room air after general anesthesia. However, patients whose age was > or = 60 yr or weight was > or = 100 kg, or for whom transient O2 desaturation on transport may be harmful, should be transported while breathing nasal O2 via nasal cannula. IMPLICATIONS: Most adult patients undergoing ambulatory surgery can be transported safely to the PACU breathing room air after general anesthesia. However, patients whose age was > or = 60 yr or weight > or = 100 kg, or for whom transient O2 desaturation on transport may be harmful, should be transported while breathing oxygen via nasal cannula.
Asunto(s)
Procedimientos Quirúrgicos Ambulatorios , Anestesia General , Terapia por Inhalación de Oxígeno , Transporte de Pacientes , Adulto , Asma/complicaciones , Método Doble Ciego , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Respiración Artificial , FumarRESUMEN
Centrilobular liver necrosis results when halothane is administered to rats pretreated with phenobarbital. Using radioactive microspheres in Wistar rats weighing 300 to 360 g each, the authors determined cardiac output and hepatic arterial and portal blood flows in normoxic (FlO2 = 0.20) unanesthetized animals pretreated with phenobarbital and in similarly pretreated animals that received halothane with adequate oxygen (FlO2 = 0.50) and while hypoxic (FlO2 = 0.08 to 0.10). Cardiac output averaged 122 +/- 8 ml/min (mean +/- SEM) in unanesthetized normoxic rats and 119 +/- 23 ml/min in unanesthetized hypoxic rats. When halothane, 0.6% in 50% oxygen, was administered cardiac output decreased significantly to 89 +/- 8 ml/min and when halothane was administered during hypoxia cardiac output was decreased further to 80 +/- 11 ml/min. During hypoxia without halothane portal venous blood flow decreased significantly but the percentages of cardiac output delivered to the hepatic artery and portal vein were not significantly different from the normoxic awake animals. When halothane was administered with adequate oxygen the percentage of the cardiac output delivered to the hepatic artery significantly increased but there was no change in absolute blood flow to either the hepatic artery or portal vein. When hypoxic animals received halothane the percentage of the cardiac output delivered to the hepatic artery and portal vein was unchanged but the absolute blood flows to the hepatic artery and portal vein decreased significantly. It is concluded that halothane combined with hypoxia is associated with changes in hepatic blood flow but that these changes are similar to changes caused by hypoxia alone. It is unlikely that hemodynamic factors account for the liver injury seen after halothane and hypoxia in phenobarbital-treated rats.
Asunto(s)
Anestesia por Inhalación , Anestesia Intravenosa , Halotano/farmacología , Hipoxia/fisiopatología , Circulación Hepática/efectos de los fármacos , Fenobarbital/farmacología , Animales , Gasto Cardíaco/efectos de los fármacos , Masculino , RatasAsunto(s)
Anestesia por Inhalación , Enfermedad Hepática Inducida por Sustancias y Drogas , Halotano/toxicidad , Hipoxia/complicaciones , Hígado/efectos de los fármacos , Fenobarbital/farmacología , Animales , Enfermedad Hepática Inducida por Sustancias y Drogas/enzimología , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Sistema Enzimático del Citocromo P-450/metabolismo , Inducción Enzimática , Fluoruros/sangre , Glutatión/metabolismo , Halotano/administración & dosificación , Hipoxia/enzimología , Hipoxia/metabolismo , Hígado/enzimología , Hígado/patología , Masculino , Microsomas Hepáticos/enzimología , Necrosis , Fenobarbital/administración & dosificación , RatasRESUMEN
A prospective study in 12 adult male patients undergoing coronary-artery revascularization was conducted to compare the effects of a morphine versus a halothane anesthetic technique on several indices of myocardial oxygen supply and demand. Indices reflecting myocardial contractility, preload, afterload, and heart rate were measured. Undesirable increases in systemic and pulmonary capillary wedge pressure were minimized using sodium nitroprusside as needed. In the period after sternotomy but before revascularization, patients anesthetized with morphine (mean 2.1 mg/kg) had significant (P less than .05) increases in rate-pressure product, tension-time index, blood pressure, and heart rate, as well as relative myocardial ischemia, evidenced by significant ST-segment depression in the V5 lead of the EKG and a decreased diastolic pressure-time index/tension-time index compared with patients anesthetized with halothane (mean .75 per cent inspired). Few difficulties associated with myocardial depression were seen in patients anesthetized with halothane. Halothane, at least in a well-monitored environment, is safe for use in patients without severe ventricular dysfunction undergoing coronary-artery revascularization.
Asunto(s)
Anestesia General , Halotano , Corazón/fisiología , Morfina , Revascularización Miocárdica , Consumo de Oxígeno , Presión Sanguínea/efectos de los fármacos , Vasos Coronarios/fisiología , Frecuencia Cardíaca/efectos de los fármacos , Humanos , Masculino , Contracción Miocárdica/efectos de los fármacos , Resistencia Vascular/efectos de los fármacosRESUMEN
Hepatic drug-metabolizing enzymes and hepatic ultrastructure were studied in rats after two hours of anesthesia with 1 MAC halothane or diethyl ether. Twelve hours after cessation of either anesthetic smooth endoplasmic reticulum was increased in centrilobular but not in periportal hepatocytes. This change persisted at 24- and 36-hour sampling times. Microsomal cytochrome P450 and cytochrome b5 decreased after halothane anesthesia (by 7 to 20 per cent of control). Diethyl ether caused increased cytochrome P450 and cytochrome b5 (27 and 18 per cent, respectively) at the 36-hour sampling time. NADPH cytochrome c reductase did not change significantly after either agent. The authors interpret these results to mean that both agents promote conversion of rough endoplasmic reticulum to smooth endoplasmic reticulum or, alternatively, that the anesthetics decrease degradation of smooth endoplasmic membranes. Since only ether caused an increase in the microsomal content of enzymes of the drug-metabolizing enzyme system, it is concluded that these two anesthetics act on hepatic cells by dissimilar mechanisms.