In the externally pipped chicken embryo, oxygen consumption through the chorioallantoic membrane (VO2CAM) ranged between 2 and 55% (mean approximately 24%) of that through the lungs (VO2lung). Hypercapnia (5'-10' of 2, 5, or 8% CO2) or mild hypoxia (15% O2) had minor effects on VO2, whereas moderate or severe hypoxia (10-5% O2) caused large drops of VO2. Hypoxia or hypercapnia delivered through the lungs increased pulmonary ventilation (VE), largely through increases in tidal volume (VT). Exposures of the whole embryo provoked VE responses either similar, or significantly higher, than with exposures of the lungs alone, because of greater increases in VT. The larger the VO2CAM, the smaller were the VE and VT responses when hypoxia or hypercapnia were delivered through the lungs. Hypoxic or hypercapnic exposures for longer periods of time (30'-40') gave qualitatively similar results. We conclude that in the externally pipped chick embryo (1) the increase in VT is the primary means of expressing the hypoxic or hypercapnic VE chemosensitivity, (2) hypometabolism contributes to the hypoxic hyperventilation, and (3) CAM gas exchange lowers the ventilatory effects of lung hypoxia or hypercapnia.