Borel C O, Teitelbaum J S, Hanley D F
Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Hospital, Baltimore, MD.
Crit Care Med. 1993 Nov;21(11):1717-26. doi: 10.1097/00003246-199311000-00022.
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.
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.
Neurosciences critical care unit in a university hospital.
Seven intubated, mechanically ventilated patients with myasthenia gravis or Guillain-Barré syndrome.
Patients repeatedly performed mechanically unsupported, spontaneous breathing trials to the limits of endurance. After spontaneous breathing trials, patients underwent CO2 rebreathing studies.
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.
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.
验证以下假设,即通气驱动力降低或二氧化碳反应性降低是重症肌无力或吉兰 - 巴雷综合征患者急性通气衰竭时出现通气不足的原因。
前瞻性连续病例系列研究,评估通气衰竭患者从恢复到脱机过程中通气肌肉功能、通气驱动力和二氧化碳反应性的试验。
大学医院的神经科学重症监护病房。
7例插管并接受机械通气的重症肌无力或吉兰 - 巴雷综合征患者。
患者反复进行无机械支持的自主呼吸试验,直至耐力极限。自主呼吸试验后,患者进行二氧化碳重复呼吸研究。
对3例吉兰 - 巴雷综合征患者和4例重症肌无力患者进行了73次呼吸试验。患者在55次试验中(平均27±5分钟)无法维持自主通气。在这些试验中,平均呼气末二氧化碳分压显著升高(从41±1升至44±1托[5.6±0.1至6.0±0.1千帕]),呼吸频率显著升高(从31±1次/分钟升至35±1次/分钟,p<0.01)。通气驱动力(通过100毫秒气道阻塞压测量)从3.7±0.3厘米水柱显著升高至4.9±0.3厘米水柱(p<0.01)。这些试验后,气道阻塞压对二氧化碳重复呼吸的反应为0.33±0.07厘米水柱/秒/毫米汞柱,而分钟通气量对二氧化碳重复呼吸的反应仅为0.30±0.06升/分钟/毫米汞柱。
这些结果表明,急性通气不足时通气驱动力增加,即使分钟通气量对二氧化碳的反应较差,通气驱动力对二氧化碳的反应仍保持完整。因此,通气驱动力降低或二氧化碳反应性降低不太可能是重症肌无力或吉兰 - 巴雷综合征患者通气衰竭时通气不足的原因。