Experimental Studies on the Post-operative Acute Pulmonary Edema Part 2 On the Influence of Hypoxia and Hypercapnia on the Development of the Post-operative Acute Pulmonary Edema

Eighteen normal adult dogs were divided into 5 groups and inhalated, for 30 minutes, the following gas mixtures, respectively; (Group Ⅰ, O(2) 15%, N(2) 85%; Group Ⅱ, O(2) 10%, N(2) 90%; Group Ⅲ, O(2) 5%, N(2) 95%; Group Ⅳ, O(2) 20%, CO(2) 5%, N(2) 75%; Group Ⅴ, O(2) 20%, CO(2) 10%, N(2) 70%). The results are as follow: 1) In the cases of slight hypoxia, O(2) consumption did not alter, while cardiac output increased and respiration became exaggerated. The cardiac output abruptly began to decrease, when O(2) concentrations were below 10%. 2) Pulmonary arterial pressure increased as hypoxia became more marked. This was caused by the increased diastolic pressure. It was obvious from these findings that the resistence of the pulmonary blood vessels had been augmented by an increase of the blood circulating in the lungs. 3) As the hypoxia became severer, changes on the lung tissues became more pronounced. These changes were interstitial congestion, hemorrhage, congestion and dilatation of the pulmonary capillaries, narrowing of the alveolar cavities, bleeding into the alveoli and the partial breakdown of the alveolar structures. 4) In the group of severe anoxia, the changes of ST and T were marked, which show the disturbances of the heart muscles. 5) As the severity of anoxia advances, the respiration became exaggerated, pulmonary ventilation insufficient, signs of heart muscle disturbances appear, and the cardiac output became smaller causing the congestion of pulmonary circulation and an increase of pulmonary arterial pressure. Histologically, pronnounced congestion and hemorrhage were observed but pulmonary edemas were never found. Therefore, lung edema was thought not to be caused by anoxia only. 6) In the case of hypercapnia, CO(2) in the arterial blood markedly increased and pulmonary arterial pressure rose, because effective ventilation was not available in spite of the increased tidal volume. Histologically, only moderate congestions were observed, but not pulmonary edema. Therefore, hypercapnia alone was perhaps not responsible to the lung edema, as in the case of anoxia