Acute left ventricular failure after a myocardial infarction causes venous congestion in the pulmonary capillary bed and increased hydrostatic pressure, which leads to pulmonary edema by transudation in the alveolar space. Neutrophils and fibrin would be found in cases of acute
inflammation of the lung (i.e., pneumonia). Fibrosis and hemosiderin-filled macrophages (heart failure cells) would be found in long-standing, not acute, left ventricular failure. Purulent exudate in the pleural space (empyema) or draining from bronchi results from bacterial infection, not heart failure. No pleural effusions are present in this radiograph.
Fluid collections are likely to be transudates (few cells and minimal protein) in noninflammatory conditions.