Extremity tourniquet deflation increases end-tidal PCO2.
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Biomedical subjects
Publications and source records attributed to J G Giuffrida.
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We studied nine healthy adult patients having orthopedic surgical procedures requiring the use of a tourniquet under general anesthesia with controlled mechanical ventilation to determine changes in end tidal CO2 (EtCO2) and arterial blood gas values after tourniquet deflation. After deflation of the tourniquet, EtCO2 and PaCO2 increased maximally within one minute; EtCO2 returned to baseline at a mean time of 13 minutes 7 seconds +/- 5 minutes 17 seconds, while PaCO2 was still above baseline when the study was terminated. The pH level decreased significantly, with the maximal fall occurring within four minutes; it remained below baseline when the study was terminated. The PaO2 level decreased and the bicarbonate level increased, though neither change was statistically significant. After tourniquet release, hyperventilation may be indicated to facilitate the return of PaCO2 and pH levels to baseline; in patients whose acid-base status is compromised by preexisting disease, PaCO2 and pH should be monitored closely. The PaCO2 level could be predicted by monitoring the EtCO2 level.
While halothane was without mutagenic activity in the Salmonella mutagenicity assay, even in the presence of microsomal fractions, the urines of anesthesiologists induced mutations of the base-substitution type.
During surgical procedures in which nitrous oxide (N2O) anaesthesia was administered there was an increased concentration of both nitric oxide (NO) and nitrogen dioxide (NO2) in operating-room air. Preliminary studies suggest that the use of certain devices (e.g., electric cauteries, X-ray machines) capable of releasing energy in the operating-room produce the oxidation of nitrous oxide. Further evaluation of gas phase reactions of anaesthetic agents within the operating-room appear warranted, particularly in relation to the occupational risks of operating-room personnel.
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Hemodynamic changes resulting from anesthesia and endotracheal intubation were studied in 32 critically ill patients. Cardiac preload, afterload, and output were measured utilizing Swan-Ganz catheter, arterial catheter, and thermodilution technique. Group I: 15 patients with known cardiac disease. Group II: 10 patients with no known cardiac disease, but with non-specific ECG findings and/or mild cardiomegaly shown by x-ray. Group III: seven patients with no known cardiac disease and without the ECG and x-ray findings of group II. Anesthesia and endotracheal intubation caused an increase in heart rate, systemic arterial pressure, central venous pressure, and pulmonary artery wedge pressure, and a decrease in cardiac output and left ventricular function. Left ventricular function curves showed: group I - severe depression with no recovery; group II - moderate depression with only partial recovery; group III - moderate depression with full recovery. The severity of cardiovascular changes seen varied with the degree of pre-existing cardiac disease. It is concluded that patients with non-specific ECG findings and/or cardiomegaly indicated by x-ray have an increased risk of cardiac dysfunction during anesthesia and require similar preoperative and intraoperative management as do patients with cardiac disease.