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'_CO ) (i.e. the V'_E/V'_CO slope) is a measure of ventilatory efficiency and can be used to identify an abnormal ventilatory response to exercise. The V'_E/V'_CO slope is a prognostic marker in several chronic cardiopulmonary diseases independent of other exercise-related variables such as peak O₂ uptake (V'_O ). The V'_E/V'_CO slope is determined by two factors: 1) the arterial CO₂ partial pressure (P_aCO ) 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 set-point and chemosensitivity are present in many cardiopulmonary diseases, which influence V'_E/V'_CO by affecting P_aCO Increased ventilation-perfusion heterogeneity, causing inefficient gas exchange, also contributes to the abnormal V'_E/V'_CO observed in cardiopulmonary diseases by increasing V_D/V_T During cardiopulmonary exercise testing, the P_aCO during exercise is often not measured and V_D/V_T is only estimated by taking into account the end-tidal CO₂ partial pressure (P_ETCO ); however, P_aCO is not accurately estimated from P_ETCO in patients with cardiopulmonary disease. Measuring arterial gases (P_aO and P_aCO ) 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 O₂ partial pressure and the difference between arterial and end-tidal CO₂ partial pressure during exercise.