VENTILATORY DRIVE AND CARBON-DIOXIDE RESPONSE IN VENTILATORY FAILURE DUE TO MYASTHENIA-GRAVIS AND GUILLAIN-BARRE-SYNDROME

Citation
Co. Borel et al., VENTILATORY DRIVE AND CARBON-DIOXIDE RESPONSE IN VENTILATORY FAILURE DUE TO MYASTHENIA-GRAVIS AND GUILLAIN-BARRE-SYNDROME, Critical care medicine, 21(11), 1993, pp. 1717-1726
Citations number
33
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
00903493
Volume
21
Issue
11
Year of publication
1993
Pages
1717 - 1726
Database
ISI
SICI code
0090-3493(1993)21:11<1717:VDACRI>2.0.ZU;2-X
Abstract
Objective: To test the hypothesis that either decreased ventilatory dr ive or decreased CO2 responsiveness accounts for the hypoventilation o bserved in patients during acute ventilatory failure from myasthenia g ravis or Guillain-Barre syndrome. Design: Prospective, consecutive cas e series evaluating trials of ventilatory muscle performance, ventilat ory drive, and CO2 response in patients during recovery from ventilato ry failure until they were weaned from mechanical ventilation. Setting : Neurosciences critical care unit in a university hospital. Patients: Seven intubated, mechanically ventilated patients with myasthenia gra vis or Guillain-Barre syndrome. Interventions: Patients repeatedly per formed mechanically unsupported, spontaneous breathing trials to the l imits of endurance. After spontaneous breathing trials, patients under went CO2 rebreathing studies. Measurements and Main Results: Seventy-t hree breathing trials were performed in three patients with Guillain-B arre 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). Ven tilatory 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 H 2O. 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 ven tilation response to CO2 rebreathing was only 0.30 +/- 0.06 L/min/mm H g. Conclusions: These results suggest that ventilatory drive increases during acute hypoventilation, and the ventilatory drive response to C O2 remains intact, even when the minute ventilation response to CO2 is poor. Therefore, a decrease in ventilatory drive or CO2 response is u nlikely to account for hypoventilation during ventilatory failure in p atients with myasthenia gravis or Guillain-Barre syndrome.