Nitrous oxide and vaporizer outputs; transient or continuous effect?
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Anesthesia, Inhalation↗
Biomedical subjects
R Knill
Publications and source records attributed to R Knill.
Components of respiratory depression after narcotic premedication in adolescents.
The effects of narcotics on ventilatory control were assessed in 13 adolescents and young adults. Both a narcotic and narcotic-phenothiazine significantly depressed the CO2 response curve. Using an occlusion pressure technique (Pm100) to evaluate those neuromuscular processes that generate forces acting on the ventilatory pump, it was found that narcotic agents reduced neuromuscular drive. In most subjects, narcotics had an additional action that contributed to the overall ventilatory depression. Using carbon dioxide to vary neuromuscular drive before and after drug administration at constant levels of neuromuscular drive the drugs reduced tidal-volume responsiveness of the pump. We conclude that narcotics impair ventilation through a combination of two effects; first, reduced neuromuscular drive, most probably due to central depression, and second, increased impedance of the ventilatory pump, most probably due to a decrease in chest-wall compliance.
Adolescent↗
An intercostal-phrenic inhibitory reflex in human newborn infants.
An effect of phasic distortion of the rib cage on inspiratory time was studied in thirty sleeping newborn infants. Distortion was produced by both manual compression of various rib cage diameters, and by occluding the airway at functional residual capacity, allowing diaphragmatic contraction to alter rib cage shape. With rapid distortion produced by these maneuvers, inspiration was often terminated prematurely. The effect was dependent upon there being a rapid rate of distortion, and was most readily elicited when inward motion involved the lower lateral rib cage. The results indicate a potent inspiratory inhibitory reflex, originating most probably from the spindles of intercostal muscles. This reflex acts to decrease tidal volume and ventilation when rates of rib cage retraction are high during spontaneous breathing.
Airway Obstruction↗
Respiratory load compensation in infants.
We have studied the respiratory compensation for elastic loads in 15 term and preterm infants. Elastic loads, approximately equal to the infant's effective elastance, were applied to the airway for five breaths while tidal volume and mask pressure were monitored. Motion of the rib cage and abdomen were monitored simultaneously with magnetometers. The studies were done both in active or REM sleep and in quiet or non-REM sleep. During quiet sleep the load immediately reduced the tidal volume by about 50% but a progressive increase in tidal volume occurred over the next four loaded breaths. During active sleep load compensation was disorganized with respect to both tidal volume and frequency, and compensation was significantly less. Active sleep was also characterized by marked rib cage distortion. We suggest that during active sleep there is tonic inhibition of the intercostal muscles, allowing the diaphragm to distort the rib cage. This distortion impairs load compensation by a direct mechanical effect and indirectly by initiating an intercostal-phrenic reflex.
Abdomen↗