The ventilatory response to carbon dioxide in mitral disease.

As long as ventilatory studies were the only approach to the problem of dyspncea in cardiac patients, its explanation seemed to be found in pulmonary changes secondary to congestive failure (Peabody and Wentworth, 1917). Combined ventilatory and circulatory measurements in such patients showed the problem to be more complex. Reduced ventilatory capacity appears to become a significant factor in advanced left-sided failure only (West et al., 1953). In cases without gross congestive failure, the diminution of cardiac output interfering with a normal metabolic exchange to the peripheral tissue-including the respiratory centre-and the rise of pressure in the pulmonary vascular system institute an increased ventilatory demand. An increased ventilatory drive manifests itself in a raised total ventilation during rest and exercise. The sensitivity of the respiratory centre to its major stimulus (Nielsen, 1936), the arterial CO2 tension, should therefore be increased. By introducing exogenous hypercapnia under CO2 inhalation and correlating different levels of arterial PCO2 with their corresponding levels of total ventilation graphically, a stimulus response curve will be obtained. This relation has been shown to be linear within the range of physiological stimulation and response (Alexander et al., 1955; Julich, 1953; Nielsen, 1936; and Schiiffer, 1949) (Fig. 1). The responsiveness of the centre is defined by the increment in ventilation produced by a