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

Abstract

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 andvice versa. The steepness with which ventilation (V′E) rises with respect to CO2production (V′CO2) (i.e.theV′E/V′CO2slope) is a measure of ventilatory efficiency and can be used to identify an abnormal ventilatory response to exercise. TheV′E/V′CO2slope is a prognostic marker in several chronic cardiopulmonary diseases independent of other exercise-related variables such as peak O2uptake (V′O2). TheV′E/V′CO2slope is determined by two factors: 1) the arterial CO2partial 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 alteredPaCO2set-point and chemosensitivity are present in many cardiopulmonary diseases, which influenceV′E/V′CO2by affectingPaCO2. Increased ventilation–perfusion heterogeneity, causing inefficient gas exchange, also contributes to the abnormalV′E/V′CO2observed in cardiopulmonary diseases by increasingVD/VT. During cardiopulmonary exercise testing, thePaCO2during exercise is often not measured andVD/VTis only estimated by taking into account the end-tidal CO2partial pressure (PETCO2); however,PaCO2is not accurately estimated fromPETCO2in patients with cardiopulmonary disease. Measuring arterial gases (PaO2andPaCO2) before and during exercise provides information on the real (and not “estimated”)VD/VTcoupled with a true measure of gas exchange efficiency such as the difference between alveolar and arterial O2partial pressure and the difference between arterial and end-tidal CO2partial pressure during exercise.