The experiment was performed in order to determine the role of poor risk in cardiac insufficiency to the development of the acute pulmonary edema. The function of heart was disturbed by cardiac tamponade in the 6 normal and the 9 hypoproteinemia-induced dogs and the influences of this tamponade on the development of the acute pulmonary edema were studied with following results. 1) Femoral arterial pressure fell abruptly, pulse became rather rapid and weak, and minute tidal volume increased, but O(2) consumption decreased after the cardiac tamponade. These changes were observed without significant difference in both groups. 2) Electrocardiographically, disturbances of heart functions were of a high degree but no significant differences between the two groups. 3) Prior to the insertion of a cardiac tamponade, the mean pressure of the pulmonary artery was by 4 mg/Hg and the cardiac output by 3.39 1/m higher in the hypoproteinemia-induced groups than in the normal dogs. 4) The insertion of cardiac tamponade caused an increase in the pulmonary arterial pressure and a decrease in the cardiac output in both the normal and the hypoproteinemia-induced groups. The rate of the increase of pulmonary aterial pressure was larger in the former, while the rate of the decrease of cardiac output is greater in the latter. 5) Congestion was the prominent picture in the pathological findings of the lungs in the normal group, but the alveolar edemas were observed in over one half of the hypoproteinemia-induced dogs. 6) It is regarded from these results that hypoproteinemia sets the preparatory stage against the development of the acute pulmonary edema.