Journal of cardiothoracic anesthesia
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J Cardiothorac Anesth · Oct 1989
Continuous oxygen insufflation in addition to IPPV causes air trapping in a mechanical lung model.
It has previously been reported that continuous insufflation of either supracarinal or subcarinal oxygen in addition to intermittent positive-pressure ventilation (IPPV) in patients under general anesthesia, and in critically ill patients in the intensive care unit, causes increased proximal airway pressure, decreased systemic blood pressure, and decreased cardiac output. The investigators hypothesized that these deleterious hemodynamic effects were due to intrapulmonary air trapping, resulting in an increased distal intrapulmonary pressure and volume. The purpose of this study was to test this hypothesis in an appropriate mechanical lung model. ⋯ With each insufflation catheter system (sequences 3, 4, and 5), each incremental increase in insufflation flow rate resulted in significant increases in lung pressure and volume. Increasing expiratory times (sequences 6 and 7 compared with 3, 4, and 5) decreased lung pressure and volume. Increasing the airway diameter (sequence 8) had only slight effect on lung pressure and volume.(ABSTRACT TRUNCATED AT 250 WORDS)
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J Cardiothorac Anesth · Oct 1989
Anesthetic management of abdominal aortic surgery: a retrospective review of perioperative complications.
The incidence of perioperative complications was retrospectively reviewed in 103 patients who underwent replacement of the abdominal aorta from 1981 to 1987. Eighty-nine of the patients had associated systemic diseases, with hypertension being the most frequent (63%). Ischemic heart disease and cerebrovascular disease had an incidence of 12% and 13%, respectively. ⋯ Deterioration in renal function occurred in 6 patients, but with no difference between groups. There were three perioperative deaths (2.9%), with two of them resulting from cerebrovascular accidents in patients with a history of cerebrovascular disease. The overall morbidity and mortality were independent of the anesthetic technique.
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J Cardiothorac Anesth · Oct 1989
The mechanism of nitrous oxide-induced changes in pulmonary vascular resistance in a dog model of left atrial outflow obstruction.
Nitrous oxide has been reported to increase pulmonary vascular resistance (PVR) in patients with pulmonary hypertension secondary to mitral stenosis. Additional data suggest this response involves sympathetic stimulation because the increase in PVR can be prevented by alpha-adrenergic and ganglionic blockade. Whether or not active pulmonary vasoconstriction occurs remains unclear. ⋯ The inspired gas was then changed to 67% N2O and 33% O2 for 10 minutes, and then returned to the N2/O2 mixture. Once baselines had been reestablished (about 10 minutes), phentolamine, 0.75 mg/kg, was administered, and the response to 10 minutes of N2O again observed. N2O did not change vascular resistance in the isolated lobe, but increased intact-lung PVR.(ABSTRACT TRUNCATED AT 250 WORDS)