2018/02/01 by Jason Weatherald, Caroline Sattler, Gilles Garcia +1
paper · doi:10.1183/13993003.00860-2017
The lungs and heart are irrevocably linked in their oxygen (O 2 ) and carbon dioxide (CO 2 ) transport functions. Functional impairment of the lungs often affects heart function and vice versa . The steepness with which ventilation ( V ′ E ) rises with respect to CO 2 production ( V ′ CO 2 ) ( i.e. the V ′ E / V ′ CO 2 slope) is a measure of ventilatory efficiency and can be used to identify an abnormal ventilatory response to exercise. The V ′ E / V ′ CO 2 slope is a prognostic marker in several chronic cardiopulmonary diseases independent of other exercise-related variables such as peak O 2 uptake ( V ′ O 2 ). The V ′ E / V ′ CO 2 slope is determined by two factors: 1) the arterial CO 2 partial pressure ( P aCO 2 ) during exercise and 2) the fraction of the tidal volume ( V T ) that goes to dead space ( V D ) ( i.e. the physiological dead space ratio ( V D / V T )). An altered P aCO 2 set-point and chemosensitivity are present in many cardiopulmonary diseases, which influence V ′ E / V ′ CO 2 by affecting P aCO 2 . Increased ventilation–perfusion heterogeneity, causing inefficient gas exchange, also contributes to the abnormal V ′ E / V ′ CO 2 observed in cardiopulmonary diseases by increasing V D / V T . During cardiopulmonary exercise testing, the P aCO 2 during exercise is often not measured and V D / V T is only estimated by taking into account the end-tidal CO 2 partial pressure ( P ETCO 2 ); however, P aCO 2 is not accurately estimated from P ETCO 2 in patients with cardiopulmonary disease. Measuring arterial gases ( P aO 2 and P aCO 2 ) before and during exercise provides information on the real (and not “estimated”) V D / V T coupled with a true measure of gas exchange efficiency such as the difference between alveolar and arterial O 2 partial pressure and the difference between arterial and end-tidal CO 2 partial pressure during exercise.