Effect of airway anaesthesia on the ventilatory and heart rate responses to isocapnic progressive hypoxia.

Abstract

The effect of airway anaesthesia by lidocaine inhalation on the hypoxic ventilatory response was examined together with the heart rate response by the isocapnic progressive hypoxia test in human subjects. During the test, end-tidal P~o2 (PETCo2) was maintained at the resting level. However, because resting PETCoz tends to decrease by airway anaesthesia, we conducted the test at the resting PETCo2 determined both before (normocapnic) and after lidocaine (hypocapnic). Ventilatory and heart rate response were evaluated as a linear function of oxygen saturation of the arterial blood (Sao2). In the "hypocapnic" runs, ventilatory responses tended to be depressed, while the slope of heart rate response-PET~o2 relationship increased after lidocaine. However, when PETC02 was restored to the normocapnic level, ventilation apparently increased from the control, and the augmented slope in the heart rate response disappeared. Although the elevated ventilation in normocapnic hypoxia might be due simply to the increased ventilatory response to C02, we suggested that the augmented slope in the heart rate response in hypocapnic hypoxia might be related not only to PET~o2 level itself but also to the direct effect of airway anaesthesia.Key words : airway anaesthesia, hypoxia, control of breathing, control of heart rate.It has been repeatedly confirmed by many investigators that airway anaesthesia induces enhanced ventilatory response to hypercapnia (CROSS et al., 1976; SULLIVAN and YU,1983;WINNING et al., 1985). However, it seems uncertain at present if this is also the case with response to other ventilatory stimuli. Recently, SULLIVAN and DEWEESE (1985) reported the lack of effect of lidocaine inhalation on hypoxic ventilation, and stated that only hypercapnic ventilation is increased after airway

Effect of Unilateral Pulmonary Vagotomy on Respiratory Control in Man

“…They suggested that afferent vagal informa tion is required to elicit an increased rate of breathing in response to hypercapnia and hypoxemia. Little or no effect of airway anesthesia on the hypoxic venti latory and occlusion pressure responses in healthy subjects was reported by Tanaka et al [17] at our insti tute. Three possibilities may account for the discre pancy between those data and the results in this study.…”