Determinants And Consequences Of Exertional Ventilatory Inefficiency In Patients With Ild

Excessive exertional ventilation is commonly observed in chronic cardiopulmonary diseases being associated with relevant clinical outcomes such as dyspnoea and exercise intolerance. The underlying physiological determinants of the increased ventilatory response to the metabolic demand (⇑ V̇E/V̇CO2) and its implication to exercise intolerance in interstitial lung disease (ILD) remain unclear. Twenty-seven subjects with chronic fibrosing ILD (62.3±10.1yrs; 18♂; FVC=63±15; DLCO=39±14%pred) and 11 matched controls (58.4±8.4yrs; 6♂) underwent incremental cardiopulmonary exercise test with serial measurements of inspiratory capacity and dyspnoea. Resting arterial or capillary blood samples were obtained in patients. Patients presented with ⇓ peak O2 uptake (75±17 vs 120±27%pred) and ⇑ V̇E/V̇CO2NADIR (39±9 vs 27±3L/L) (p<0.01).They also developed earlier ventilatory constraints to tidal volume (VT) expansion ( Panel A) and reported higher dyspnoea scores (Panel B) than controls. The resting factors predicting exercise V̇E/V̇CO2NADIR in a multivariate linear regression analysis were: the fraction of VT/dead space and alveolar-arterial O2 pressure difference (Panel C). Arterial/capillary pressure of CO2, however, did not remain in the final. Exertional ventilatory inefficiency in ILD is consequence of increased “wasted” ventilation and a high hypoxic drive, leading to early mechanical ventilatory constraints and intolerable dyspnoea.