C. P. Patil

Transient, steady-state and rebreathing responses to carbon dioxide in man, at rest and during light exercise.

1. The transient ventilatory response to CO2, measured using short pulses at constant inflow, was compared with the steady‐state response at rest and during exercise at 50 W, and with the rebreathing response at rest, in nine healthy subjects. At rest CO2 was given at flow rates of 0.2 and 0.4 l min‐1 and during exercise, to compensate for the smaller inhaled CO2 fraction as ventilation increased, at flow rates of 0.4 and 0.8 l min‐1. 2. We calculated two indexes of gain for the transient response: the ratio of the peaks of the ventilation and PCO2 pulses, and the ratio of their integrals. 3. The steady‐state response was greater than the transient response at rest and during exercise, but there was no correlation between the two. The rebreathing response was greater than both. Both the transient and the steady‐state responses were greater during exercise than at rest. 4. To assess alinearity, the steady‐state responses to the two CO2 flow rates were compared. At rest, there was no significant difference. During exercise, the response was greater to 0.4 than 0.8 l min‐1, indicating alinearity concave downwards. 5. We conclude that the transient response as we calculate it is not representative of steady‐state gain, and that the CO2 response in light exercise is steeper, and concave downwards in shape. The rebreathing technique overestimates CO2 sensitivity near the control point.

Immediate ventilatory response to sudden changes in venous return in humans.

We changed venous return transiently by postural manoeuvres, and by lower body positive pressure, to see what happened simultaneously to ventilation. Cardiac output was measured by a Doppler technique. In seven subjects, after inflation of a pressure suit to 80 and 40 mmHg at 30 deg head‐up tilt, both cardiac output and ventilation increased. Ventilation increased rapidly to a peak in the first 5 s, cardiac output more slowly to a steady state in about 20 s, at 80 mmHg inflation. After inflation to 80 mmHg in six subjects at 12.5 deg head‐up and 30 deg head‐down tilt, cardiac output did not change in the first, and fell in the second case. There were no significant changes in ventilation. On release of pressure there were transient increases in both cardiac output and ventilation, with ventilation lagging behind cardiac output, in contrast to (2) above. In five subjects, elevation of the legs at 30 deg head‐up tilt caused a rise in both cardiac output and ventilation, but in two subjects neither occurred. In all seven subjects there was a transient increase in cardiac output and ventilation when the legs were lowered. Ventilation and cardiac output changes were approximately in phase. We were therefore unable to dissociate entirely increasing cardiac output from increasing ventilation. The relation between them was certainly not a simple proportional one.

Modelling the Ventilatory Response to Pulses of Inhaled Carbon Dioxide in Exercise

Recent computer-assisted techniques permit experimental inhaled CO2 stimuli to be precisely shaped, for example to a square wave, while alveolar PO2 (PAO2) is held constant. The respiratory control mechanisms sensitive to CO2 have then been modelled as a two-compartmental first order system, with central and peripheral components, each with a defined time delay (mainly circulatory), time constant and gain1.