Human chest wall function while awake and during halothane anesthesia. II. Carbon dioxide rebreathing
Related Experiment Video
Updated: Aug 19, 2026

Expired CO2 Measurement in Intubated or Spontaneously Breathing Patients from the Emergency Department
Published on: January 29, 2011
1Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota 55905.
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.
More Related Videos
08:34Investigation into Deep Breathing through Measurement of Ventilatory Parameters and Observation of Breathing Patterns
Published on: September 16, 2019
05:45Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
Published on: October 25, 2019
Related Concept Videos
Breathing
Assessment of Diffusion and Perfusion
The Role of Diffusion in Respiration
Diffusion is the process by which molecules move from an area of higher concentration to an area of lower concentration. In the respiratory system, this principle...
Alterations in Respiration II
In Biot's breathing, the respiratory rate and depth are irregular, alternating between periods of deep gasping and apnea. Common causes include...
Pulmonary Ventilation: Inhalation
Boyle's law becomes particularly pertinent when examining respiratory...
Other Factors Affecting Respiration Centers
However, the ability to hold one's breath voluntarily is not limitless. When the CO2 concentration in the blood reaches a critical level,...
Hyperpnea and Hyperventilation