Bubbles of either He, N2 or SF6 were infused intravenously into anesthetized dogs at a rate of 0.2 ml/kg/min. Alterations in pulmonary gas exchange were quantitated by the invert gas elimination method during control, steady state infusion and resolution phases. The hypoxemia produced was predominantly due to regions of low VA/Q rather than pure shunt, and the increase in physiological dead space was due to the addition of high VA/Q regions rather than 'pure' dead space. The VA/Q distribution returned to normal within 30 minutes of stopping the He or N2 bubbles, but remained abnormal for longer periods with SF6 bubbles. The net elimination of insoluble gases (such as He or N2) was only slightly impaired by bubble emboli, provided the cardiac output remained constant. Early pulmonary edema from bubble embolization was documented by increased wet weight/dry weight ratio, but the increased lung water was not apparent on histological examination. This form of pulmonary embolus is unique in that there is a constant fraction of the vasculature blocked although any given region with embolus is undergoing continuous resportion of the bubble. This produced a partial obstruction of the affected gas exchange units which manifests as regions of high VA/Q rather than pure dead space.