Pulmonary oedema is characterised by the accumulation of an abnormal amount of fluid in the lung interstitium and/or the terminal air spaces. Broadly, pulmonary oedema may be divided into two categories based on the pathophysiology of fluid accumulation. Transudative pulmonary oedema occurs when the balance between the components of Starling equation (hydrostatic pressure, oncotic pressure) within the pulmonary capillaries and alveoli is disturbed. In such cases, the intercellular capillary junctions are intact, and the oedema fluid is therefore a transudate. Instances of transudative pulmonary oedema are most usually due to cardiac causes (cardiogenic pulmonary oedema). Alternatively, pulmonary oedema may be the result of disruption of pulmonary capillary junctions by a variety of conditions, whereupon a protein-rich exudate leaks into the alveolar spaces. Such exudative pulmonary oedema is typical of the conditions leading to the acute respiratory distress syndrome (ARDS). In this chapter, both cardiogenic and noncardiogenic pulmonary oedema have been discussed: their definitions, pathophysiology, criteria for diagnosis, along with the clinical, radiological and other means whereby they may be discriminated have been elucidated. The specific causes of pulmonary oedema have been explored along with the distinguishing characteristics of each condition that might be responsible. The caveats associated with the role of selected investigations like brain natriuretic peptide that might be used to distinguish cardiogenic from noncardiogenic causes have been outlined. A discussion on the relatively rare unilateral pulmonary oedema has been included.