Ventilatory response to exercise in cardiopulmonary disease: the role of chemosensitivity and dead space

The lungs and heart are irrevocably linked in their oxygen (O-2) and carbon dioxide (CO2) 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 CO2 production (V'CO2) (i.e. the V'E/V'CO2 slope) is a measure of ventilatory efficiency and can be used to identify an abnormal ventilatory response to exercise. The V'E/V'CO2 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'CO2 slope is determined by two factors: 1) the arterial CO2 partial pressure (PaCO2) during exercise and 2) the fraction of the tidal volume (VT) that goes to dead space (VD) (i.e. the physiological dead space ratio (VD/VT)). An altered PaCO2 set-point and chemosensitivity are present in many cardiopulmonary diseases, which influence V'E/V'CO2 by affecting PaCO2. Increased ventilation-perfusion heterogeneity, causing inefficient gas exchange, also contributes to the abnormal V'E/V'CO2 observed in cardiopulmonary diseases by increasing VD/VT. During cardiopulmonary exercise testing, the PaCO2 during exercise is often not measured and VD/VT is only estimated by taking into account the end-tidal CO2 partial pressure (PETCO2); however, PaCO2 is not accurately estimated from PETCO2 in patients with cardiopulmonary disease. Measuring arterial gases (PaO2 and PaCO2) before and during exercise provides information on the real (and not estimated) VD/VT 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 CO2 partial pressure during exercise.