Lung mechanics and neuromuscular output during CO2 inhalation after airway anesthesia.
Airway anesthesia with aerosolized lidocaine has been associated with an increase in minute ventilation (VE) during CO2 inhalation. The increase in VE may be due to increased neuromuscular output or decreased mechanical load on breathing. To evaluate this we measured VE, breathing pattern, mouth occlusion pressure, and lung mechanics in 20 normal subjects during room-air breathing and then inhalation of 6% CO2-94% O2, before and after airway anesthesia. Measurements of lung mechanics included whole-lung resistance, dynamic and static compliance, and functional residual capacity. Airway anesthesia had no detectable effect on any measurements during room-air breathing. During CO2 inhalation, airway anesthesia produced increases in VE and mean inspiratory flow rate (VT/TI) and more negative inspiratory pleural pressure but had no detectable effect on lung mechanics or mouth occlusion pressure. Pleural pressure was more negative during the latter 25% of inspiration. We concluded that airway receptors accessible to airway anesthesia play a role in determining neuromuscular output during CO2 inhalation.
D000328:Adult; D000769:Anesthesia, Inhalation; D002245:Carbon Dioxide; D005260:Female; D005652:Functional Residual Capacity; D006801:Humans; D008012:Lidocaine / Q000494:pharmacology*; D008168:Lung / Q000187:drug effects / Q000502:physiology; D008170:Lung Compliance; D008297:Male; D009469:Neuromuscular Junction / Q000502:physiology*; D012123:Pulmonary Ventilation; D012119:Respiration
D002245:Carbon Dioxide; D008012:Lidocaine