Anesthesiology
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Twenty patients requiring ventilation for acute respiratory failure were studied to determine whether intrapulmonary shunt fraction (Qs/Qt) measured at an inspired oxygen concentration (FIO2) of 1.0 differs from Qs/Qt measured at the clinically indicated FIO2 and, if so, the mechanism by which this occurs. Qs/Qt increased from 15.5 +/- 1.8 per cent (mean +/- SE) at the clinically indicated inspired oxygen fraction (FIO2 0.3-0.6) to 21.7 +/- 2.1 per cent after 20 minutes at FIO2 1.0. Functional residual capacity (FRC) decreased by 6 +/- 6 per cent and total compliance (CT) by 10 +/- 6 per cent. ⋯ Patients with increased PCWP showed smaller increases in Qs/Qt with 100 per cent oxygen. These findings suggest two mechanisms responsible for the increase in Qs/Qt: 1) redistribution of blood flow to nonventilated areas, resulting from the vasodilating effect of an increased oxygen tension in the vessels of hypoxic lung segments; 2) resorption atelectasis. Of the total change in Qs/Qt observed during ventilation with oxygen, 63 per cent was calculated to be due to factors other than a decrease in FRC. (Key words: Ventilation, positive end-expiratory pressure; Oxygen, pulmonary shunt and; Lung, compliance; Lung, shunts.)
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The transformation of lymphocytes in response to phytohemagglutinin stimulation was investigated in 77 patients undergoind anesthesia with and without coincident surgical operation. A depression of lymphocyte transformation apparent immediately following major operations was related primarily to the extent of tissue trauma and not to the anesthetic agent or technique. No depression of lymphocyte transformation followed anesthesia for treatment of pain or for minor operations. ⋯ The leukocyte count did not increase after comparable operations performed with regional anesthesia. Postoperative depression of lymphocyte transformation is primarily due to nonspecific stress, perhaps because of associated sympathetic and adrenocortical stimulation. The depressant effect of anesthesia alone is minimal.
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The authors previously showed that cyclopropane-epinephrine-induced bigeminal arrhythmias can best be explained by a re-entrant mechanism. They have now obtained evidence for reentry in bigeminal arrhythmias during infusions of epinephrine (.5-3 mug/kg/min) in dogs anesthetized with .8 per cent halothane. Both a critical level of blood pressure and a critical increase in heart rate were necessary for arrhythmias to be induced in any given animal. ⋯ Under these conditions further acceleration of the heart rate could reinstate a bigeminal arrhythmia that was again sensitive to further increases in the frequency of vagal stimulation, and it is concluded that the vagus acts on the spread of the re-entrant impulse. This is best shown with cyclopropane anesthesia, because AV-nodal block occurs more easily with halothane. In addition, very brief periods of increased heart rate caused prolonged periods of bigeminy, which indicates that changes in heart rate may alter the electrophysiology of the halothane-sensitized myocardium to promote bigeminal arrhythmias by a re-entry mechanism.