ABSTRACT
The main function of the respiratory control system is to maintain constant the value of blood gases during daily activities. Many patients affected by respiratory disease are able to maintain blood gases within substantial normal values, indicating that the respiratory control system has efficacious adaptive capacities. However, in some patients these adaptive capacities are not sufficient, and impairment of arterial blood gases ensues. In particular, the elevation of arterial carbon dioxide partial pressure (Paco2) indicates that ventilatory control system is not able to maintain an adequate alveolar ventilation (V˙ a). Paco2 is determined by the ratio of metabolic CO2 production (V˙ co2) to alveolar ventilation according the following equation:
Paco2 K V˙ co2
V˙ e 1 VdVt (1)
where K is a constant of proportionality, V˙ e is minute ventilation, Vt is tidal volume, and Vd is the physiological deadspace. This equation indicates that hypercapnia will develop when: a) CO2 production increases at a constant V˙ a; b) Minute ventilation
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decreases; c) alveolar ventilation decreases because of a rise in Vd or a decrease in Vt; and d) a combination of the above factors takes place. From Eq. (1) it clearly appears that for a given V˙ e, the lower the Vt the higher the Paco2. Nonetheless, the reason as to why some patients are able to maintain blood gases within normal limits whereas others do not remains to be defined. Many years ago COPD patients with no CO2 retention were defined as ‘‘fighters’’ as opposed to patients with increased level of Paco2, defined as ‘‘nonfighters’’ (1). The former were thought to be able to increase their neuromuscular drive to compensate for their impaired ventilatory function; the latter were thought to choose not to increase their neuromuscular drive (NMD) with consequent CO2 retention. However, successive studies clearly demonstrated that the neuromuscular drive is not low in hypercapnic COPD patients (2,3). Sorli et al. (3) showed that there is no difference in P0.1, an index of neuromuscular drive (4), between hypercapnic and normocapnic COPD patients, both exhibiting high values compared to normal subjects. The smaller Vt in hypercapnic patients compared to normocapnic ones, according to the Eq. (1), resulted in a decreased Vd/Vt ratio and thereby hypoventilation. These results were later confirmed in a larger group of patients (5). Later studies by Scano et al. investigated the NMD in terms of electromyographic activity of the diaphragm (EMGd) and the parasternal muscles in COPD patients (6-8). Compared to normal subjects both normocapnic and hypercapnic COPD patients showed an increased NMD during both room air breathing and hypercapnic stimulation. Also, hypercapnics exhibited lower Vt and inspiratory muscle strength than both normocapnics and controls. These studies have shown that chronic CO2 retention is associated with normal or increased NMD, lower inspiratory muscle force, and rapid and shallow breathing. Thus, several lines of evidence (6-12) indicate that derangement in respiratory muscle function and development of hypercapnia are closely related in COPD patients. An increased mechanical load faced with a reduced inspiratory muscle force (1315) leads to impending respiratory muscle fatigue (16). In order to avoid fatigue, respiratory control system resets breathing pattern reducing Vt and the pressure developed, but the inescapable consequence is CO2 retention (16,17).
