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

The lungs and heart are irrevocably linked in their oxygen (O₂) 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 O₂ uptake (V'O₂ ). 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 O₂ partial pressure and the difference between arterial and end-tidal CO₂ partial pressure during exercise.