The effects of constant positive airway pressure applied via a nose mask through the nares (nasal CPAP) on the swallowing reflex were studied in eight adult humans. The swallowing reflex was induced by bolus injections of a small amount of distilled water (0.5 ml) into the pharynx at four different values of endexpiratory airway pressure (0,5,10, and 15 cm H2O CPAP) or by continuous infusion of water (3 ml/min) at two different values of endexpiratory airway pressure (0 and 15 cm H2O CPAP). The latency of response from the time of bolus injection of water to the occurrence of the first swallow as well as the number of swallows elicited during the period of 10 s immediately following the water injection were measured. Our results showed that increases in endexpiratory airway pressure progressively prolonged the latency of response and decreased the number of swallows. Also, the frequency of swallows decreased greatly at nasal CPAP of 15 cm H2O during continuous infusion of water. These results indicate that nasal CPAP exerts an inhibitory influence on the swallowing reflex.
"Pendelluft", or out-of-phase movement of the airway gas between the intact and flait-chest-side lungs has long been believed to be the major contributor to respiratory dysfunction in patients with flail chest. However, conflicting findings have also been reported mainly from animal studies. The aim of this study was to provide a mathematical projection on this classical problem. We measured respiratory impedance (ZRS) of dogs with flail chest using a pseudorandom forced oscillation method. A mathematical model implementing flail chest was fitted toZRS. The fitted results were used in simulating the mechanical behavior of a respiratory system with flail chest during spontaneous breathing. Our results suggest that the paradoxical movement of breathing between the flail segment and the intact chest wall does not create substantial pendelluft and that alveolar hypoventilation is created by the wasting movement of the flail segment which interferes with effective thoracic expansion.
To clarify the difference of negative inotropic effects, we evaluated the effects of 0, 0.5, and 1 MAC halothane and enflurane on systolic performance in anesthetized, mechanically ventilated, vagotomized dogs. Left ventricular myocardial contractility was assessed by the slope of the end-systolic pressure-diameter relationship (EES), which have been reported to be independent of alterations in preload and afterload but sensitive to changes in myocardial contractility. Both anesthetics decreased heart rate and dose-dependently decreased left ventricular systolic pressure. Enflurane decreased heart rate and left ventricular systolic pressure more than an equivalent MAC of halothane. Both anesthetics increased left ventricular end-diastolic diameter without any change in % shortening of the left ventricular internal diameter. TheEES was decreased to a similar extent at both 0.5 and 1 MAC halothane. TheEES was decreased with increasing concentrations of enflurane. TheEES was significantly larger (P<0.05) with 1 MAC of halothane than with 1 MAC enflurane. These results suggest that halothane preserves myocardial contractility better than enflurane in the presence of fentanyl.
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