Experimental Unilobar Pulmonary Edema †

In medical literature there are early accounts of what was probably acute pulmonary edema. In these early descriptions, however, it was confused with other catastrophic states manifested by acute cardio-respiratory symptoms. It was not until the eighteenth century that Albertini,1 a student of Malpighi, made the first clinico-pathological correlations. He grouped chronic pulmonary congestion and pulmonary edema together but differentiated obvious right heart failure, hydrothorax, pneumothorax, and bronchial asthma. The belief that acute pulmonary edema was but a severe manifestation of congestive failure prevailed until the late 1930's when Farber,' Luisada,9 Sir Thomas Lewis,8 and others began to question this identity. Today, it is suspected by numerous workers that there are fundamental differences between acute pulmonary edema and chronic pulmonary congestion; however, the elements are obscure and often they blend into one another. The differences which exist may be considered under several headings: First, as to cause, the pulmonary congestion seen as part of congestive heart failure is invariably due to heart disease, whereas acute pulmonary edema may result from numerous causes other than heart disease-toxic gases, drowning, uremia, central nervous system disorders, infections, thyroid storm, and allergy. Second, in regard to the clinical picture, acute pulmonary edema is characterized by a very rapid onset and a severely cyanotic individual with copious, frothy, blood-tinged sputum who usually lacks the hepatic engorgement and peripheral edema which are seen in the patient with congestive heart failure, in whom also the onset is usually slower and the clinical picture not as severe. The latter usually makes a slow recovery only after treatment such as bed rest, digitalis, and mercurials, whereas the acute pul-