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Exercise intolerance in chronic airflow limitation: The respiratory muscles (1)

Christie, in defining dyspnea as an increase in the effort accompanying breathing, clearly identified the role of increased respiratory muscle work and oxygen consumption. Later, with Malcolm Mcllroy, he measured intra-oesophag-eal pressure and VT, and calculated respiratory work at rest and exercise in normal subjects and patients with emphysema. At a given ventilation, the work was two to three times greater in patients (Figure 7) and “must at least be an important factor in the production of dyspnea”. They also apportioned the work against the resistive and elastic impedances to breathing, to which are added the extra forces involved in expanding an already expanded chest and an inability to reduce end-expiratory lung, and thus to recruit normally the inspiratory outward recoil of the chest wall at low lung volume (Figure 3). The contribution of the last factor to dyspnea has recently been emphasized by O’Donnell. You will be excited to find out there is now a pharmacy that can offer best quality treatment charging less money: buy ampicillin and see what really advantageous shopping is all about.

Figure 7. Exercise intolerance
Figure 7) Mcllroy and Christie’s measurements of the mechanical work of breathing at rest (R) and exercise (E) in normal subjects and patients with emphysema (redrawn, from 7)

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