De Vito E L
Instituto de Investigaciones Médicas Alfredo Lanari, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Medicina (B Aires). 1993;53(4):350-6.
The mechanisms of chronic ventilatory failure in chronic obstructive pulmonary disease are complex. This paper analyses the diverse available information: mechanical factors and gas-exchange, fighter vs. non-fighter, the ventilatory pattern theory and the fatigue threshold theory. Finally we comment on the evidence supporting the new concept that hypercapnia may develop to avoid or prevent fatigue. Indeed, it is very likely that chronic CO2 retention in COPD may develop by mechanical disadvantages of the inspiratory muscles rather than impairment of ventilation-perfusion ratios. This opens a fascinating new research line on the neuromechanical control of breathing. When the respiratory effort is approaching the fatigue level, the respiratory muscles may elicit a negative feedback reflex, the muscle activity is depressed and hypercapnia develops. If this is so, chronic hypercapnia may be an index of imminent fatigue if increases in ventilation or work of breathing are required. Under this condition some degree of central diaphragm fatigue may help to protect the muscle from severe or limiting peripheral fatigue or even muscle injury. Finally, we comment on some therapeutic approaches such as ventilatory stimulants, training, rest and, specially, oxygen administration and the mechanisms involved in the PCO2 increases.
慢性阻塞性肺疾病中慢性通气衰竭的机制很复杂。本文分析了各种现有信息：机械因素与气体交换、“战斗型”与“非战斗型”、通气模式理论和疲劳阈值理论。最后，我们对支持高碳酸血症可能会发展以避免或防止疲劳这一新概念的证据进行评论。的确，慢性阻塞性肺疾病中的慢性二氧化碳潴留很可能是由吸气肌的机械劣势而非通气-灌注比受损所致。这开启了一条关于呼吸神经机械控制的迷人新研究方向。当呼吸努力接近疲劳水平时，呼吸肌可能引发负反馈反射，肌肉活动受抑制，高碳酸血症随之出现。如果是这样，当需要增加通气或呼吸功时，慢性高碳酸血症可能是即将出现疲劳的一个指标。在这种情况下，一定程度的中枢膈肌疲劳可能有助于保护肌肉免受严重或限制性外周疲劳甚至肌肉损伤。最后，我们评论了一些治疗方法，如通气兴奋剂、训练、休息，特别是氧疗以及与二氧化碳分压升高相关的机制。
