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• W2419652484 abstract "SUMMARY It is clear that no single factor can explain the pattern of respiratory control in chronic obstructive pulmonary diseases. It is a result of adaptation to the mechanical impairment, particularly to the increase in the inspiratory impedance, via neural and chemical regulatory mechanisms. An increase in inspiratory independence is usually associated with mechanical inefficiency of the muscle, and tends to reduce the gain of the carbon dioxide regulator (slope of the ventilatory response). In response to this impairment, two alternative adjustments appear to exist. One is neurally mediated augmentation of inspiratory activity. This mechanism takes place in acute external resistive load breathing and during exercise and in so called “pink puffer” or “fighter” patients. This neural mechanism, in effect, adjusts the threshold Pco2 to a lower level and augments the respiratory activity. The augmented respiratory activity thus achieved effectively prevents the development of hypercapnia, but one must pay a price in terms of efficiency of carbon dioxide load handling. Exercise performance in these patients is relatively poor. An alternative adaptive process is chemical adjustment via increased body fluid buffering capacity. This type of adaptation is prone to develop in patients with bronchitic features with chronically increased inspiratory impedance. The neurally mediated augmentation is somehow lost in this type of patient. This loss of neural compensatory mechanism plus mechanical inefficiency and increased inspiratory impedance results in a severe impairment of gain of controller and, hence, a resting hypercapnia which is followed by a compensatory increase of body fluid buffer and shift of the threshold to higher Pco2. As a result, carbon dioxide load handling and exercise performance are improved, but a price must be paid in terms of increased hypercapnia and hypoxemia. It is not known how some of the patients lose the neural compensatory mechanism, allowing the chemical adaptive mechanism to come into play. Although bronchitic patients are prone to take the latter course of adaptation, considerable individual variation appears to exist. Genetically determined and acquired hyposensitivity to chemical stimuli may modify the course of adaptation. The neural compensatory mechanism may involve information processing by central neurones perhaps at the cortical level. Individual variation may also exist in this processing. In view of the multiple factors involved, it is no surprise that considerable controversy still exists regarding the pathogenesis of carbon dioxide retention in chronic obstructive pulmonary diseases. The question of a genuine loss of central responsiveness to chemical stimuli remains unsettled." @default.
• W2419652484 created "2016-06-24" @default.
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• W2419652484 date "1980-01-01" @default.
• W2419652484 modified "2023-09-23" @default.
• W2419652484 title "RESPIRATORY CONTROL IN CHRONIC OBSTRUCTIVE PULMONARY DISEASES" @default.
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• W2419652484 doi "https://doi.org/10.1016/s0272-5231(21)00052-6" @default.
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