Human chest wall function while awake and during halothane anesthesia. II. Carbon dioxide rebreathing.

BACKGROUND

Changes in the distribution of respiratory drive to different respiratory muscles may contribute to respiratory depression produced by halothane. The aim of this study was to examine factors that are responsible for halothane-induced depression of the ventilatory response to carbon dioxide rebreathing.

METHODS

In six human subjects, respiratory muscle activity in the parasternal intercostal, abdominal, and diaphragm muscles was measured using fine-wire electromyography electrodes. Chest wall motion was determined by respiratory impedance plethysmography. Electromyography activities and chest wall motion were measured during hyperpnea produced by carbon dioxide rebreathing while the subjects were awake and during 1 MAC halothane anesthesia.

RESULTS

Halothane anesthesia significantly reduced the slope of the response of expiratory minute ventilation to carbon dioxide (from 2.88 +/- 0.73 (mean +/- SE) to 2.01 +/- 0.45 l.min-1.mmHg-1). During the rebreathing period, breathing frequency significantly increased while awake (from 10.3 +/- 1.4 to 19.7 +/- 2.6 min-1, P < 0.05) and significantly decreased while anesthetized (from 28.8 +/- 3.9 to 21.7 +/- 1.9 min-1, P < 0.05). Increases in respiratory drive to the phrenic motoneurons produced by rebreathing, as estimated by the diaphragm electromyogram, were enhanced by anesthesia. Anesthesia attenuated the response of parasternal electromyography and accentuated the response of the transversus abdominis electromyography to rebreathing. The compartmental response of the ribcage to rebreathing was significantly decreased by anesthesia (from 1.83 +/- 0.58 to 0.48 +/- 0.13 l.min-1.mmHg-1), and marked phase shifts between ribcage and abdominal motion developed in some subjects. However, at comparable tidal volumes, the ribcage contribution to ventilation was similar while awake and anesthetized in four of the six subjects.

CONCLUSIONS

Halothane anesthesia enhances the rebreathing response of neural drive to the primary respiratory muscle, the diaphragm. These findings provide direct evidence that, at the dose examined in this study, halothane-induced respiratory depression is caused by alterations in the distribution and timing of neural drive to the respiratory muscles, rather than a global depression of respiratory motoneuron drive.