title: Ventilatory drive and carbon dioxide response in ventilatory failure due to myasthenia gravis and Guillain-Barré syndrome.
abstract: OBJECTIVE
  To test the hypothesis that either decreased ventilatory drive or decreased CO2 responsiveness accounts for the hypoventilation observed in patients during acute ventilatory failure from myasthenia gravis or Guillain-Barré syndrome.
  
  
  METHODS
  Prospective, consecutive case series evaluating trials of ventilatory muscle performance, ventilatory drive, and CO2 response in patients during recovery from ventilatory failure until they were weaned from mechanical ventilation.
  
  
  METHODS
  Neurosciences critical care unit in a university hospital.
  
  
  METHODS
  Seven intubated, mechanically ventilated patients with myasthenia gravis or Guillain-Barré syndrome.
  
  
  METHODS
  Patients repeatedly performed mechanically unsupported, spontaneous breathing trials to the limits of endurance. After spontaneous breathing trials, patients underwent CO2 rebreathing studies.
  
  
  RESULTS
  Seventy-three breathing trials were performed in three patients with Guillain-Barré syndrome and four patients with myasthenia gravis. Patients were unable to sustain spontaneous ventilation in 55 trials averaging 27 +/- 5 mins. In these trials, significant increases occurred in mean end-tidal CO2 (41 +/- 1 to 44 +/- 1 torr [5.6 +/- 0.1 to 6.0 +/- 0.1 kPa]) and respiratory rate (31 +/- 1 to 35 +/- 1 breaths/min, p < .01). Ventilatory drive (as measured by airway occlusion pressure for 100 msecs) increased significantly p < .01 from 3.7 +/- 0.3 to 4.9 +/- 0.3 cm H2O. The response of airway occlusion pressure to CO2 rebreathing after these trials was 0.33 +/- 0.07 cm H2O/sec/mm Hg, while the minute ventilation response to CO2 rebreathing was only 0.30 +/- 0.06 L/min/mm Hg.
  
  
  CONCLUSIONS
  These results suggest that ventilatory drive increases during acute hypoventilation, and the ventilatory drive response to CO2 remains intact, even when the minute ventilation response to CO2 is poor. Therefore, a decrease in ventilatory drive or CO2 response is unlikely to account for hypoventilation during ventilatory failure in patients with myasthenia gravis or Guillain-Barré syndrome.
authors.affiliation: Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Hospital, Baltimore, MD.
authors.forename: C O
authors.initials: CO
authors.lastname: Borel
authors.forename: J S
authors.initials: JS
authors.lastname: Teitelbaum
authors.forename: D F
authors.initials: DF
authors.lastname: Hanley
mesh_terms: D000208:Acute Disease; D000368:Aged; D002245:Carbon Dioxide / Q000502:physiology*; D005260:Female; D006801:Humans; D007040:Hypoventilation / Q000209:etiology / Q000503:physiopathology; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009157:Myasthenia Gravis / Q000150:complications / Q000453:epidemiology / Q000503:physiopathology*; D011129:Polyradiculoneuropathy / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology*; D016016:Proportional Hazards Models; D012119:Respiration / Q000502:physiology; D012129:Respiratory Function Tests / Q000706:statistics & numerical data; D012131:Respiratory Insufficiency / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology*; D015656:Respiratory Mechanics; D012132:Respiratory Muscles / Q000503:physiopathology
chemical_list: D002245:Carbon Dioxide