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Gamsu and coworkers[109] compared the rate of tantalum clearance from the lungs of postoperative patients who had received general anesthesia for intra-abdominal or lower extremity operations. Patients who underwent lower extremity surgery demonstrated no significant difference in tantalum clearance when compared with a control group measured using tracheography. These patients also did not develop atelectasis. In contrast, retention of tantalum was demonstrated for as long as 6 days after intra-abdominal surgery, with an average retention time three times greater than that observed in the control group. Retention of tantalum was gravity dependent and correlated with the retention of mucus demonstrated in areas of atelectasis. Disappearance of tantalum from these atelectatic areas occurred only after reexpansion of collapsed lung segments. Teflon disks placed on the tracheal mucosa and observed with fiberoptic bronchoscopy were used to study tracheal mucus velocity in young women undergoing gynecologic surgery.[110] The average velocity of mucus in the awake volunteers was 20 mm/min. Administration of halothane (1% to 2%) and nitrous oxide (60%) rapidly decreased the rate of mucus movement to 7.7 mm/min. Little or no mucus motion was observed after 90 minutes of halothane-nitrous oxide exposure. Inspired gases were humidified, but the use of high inspired concentrations of oxygen, a cuffed endotracheal tube, and positive-pressure ventilation were confounding factors in this study. Bronchial mucosal transport velocity was also determined using radiolabeled albumin microspheres deposited distally in the mainstem bronchi using a
Figure 6-7
Effect of halothane on phosphatidylcholine (PC) synthesis
by alveolar type II cells. PC synthesis measured as the incorporation of [3
H-methyl]-choline
into PC and expressed as disintegrations per minute per microgram of intracellular
protein (*P < .05, **P
< .01 versus respective control.) A, Effect of
increasing halothane concentration with 4-hour exposure. B,
Effect of increasing exposure time to 2% halothane. (Adapted from Molliex
S, Crestani B, Dureuil B, et al: Effects of halothane on surfactant biosynthesis
by rat alveolar type II cells in primary culture. Anesthesiology 81:668, 1994.)
Konrad and coworkers[112] have shown that smokers have significantly slower bronchial mucus transport velocities than nonsmokers in patients undergoing abdominal or thoracic surgery. The investigators postulated that this observation may be related to an increased incidence of postoperative pulmonary complications in smokers.[112] Some evidence exists to support the contention that patients with chronic obstructive pulmonary disease (COPD) receiving regional anesthesia demonstrate a lower incidence of respiratory failure than those having general anesthesia,[113] but other studies have failed to confirm this hypothesis. The consequences of the specific procedure with intrathoracic and intra-abdominal surgery appear to be of greater importance in determining morbidity related to compromised respiratory function compared with peripheral procedures performed under regional anesthesia.
Mucociliary function impairment also occurs after lung transplantation. The mechanism for this dysfunction
Many factors contribute to postoperative pulmonary complications. The specific roles of depressed mucociliary function and alterations in type II alveolar cells in such complications are unclear. Prolonged administration of inhaled anesthetics may produce mucus pooling and adversely alter alveolar cell surfactant metabolism. These actions may result in deleterious effects on pulmonary function including atelectasis and infection. Those at greatest risk appear to include patients with excessive or abnormal mucus or surfactant production (e.g., chronic bronchitis, asthma, cystic fibrosis, chronic mechanical ventilation).
Controlled studies of the effects of inhaled anesthetics on mucociliary function and surfactant metabolism in patients with compromised pulmonary performance have yet to be undertaken, nor has the precise action of inhaled anesthetics on the incidence of pulmonary complications been clearly defined. The specific actions of the newer volatile anesthetics desflurane and sevoflurane on mucociliary function have not been adequately studied, although there are no compelling reasons to suspect a clinically significant difference should exist between these agents and other inhaled anesthetics.
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