Heart failure (HF) is a clinical syndrome caused by structural or functional cardiac abnormalities, characterized by symptoms like shortness of breath and wheezing due to fluid accumulation in the lungs. Acute lung injury (ALI) is an inflammation-driven condition that increases lung permeability, leading to respiratory failure. ALI can coexist with HF, and the underlying lung injury involves endothelial dysfunction and increased vascular permeability. Acute respiratory distress syndrome (ARDS) is an advanced form of ALI, defined by severe respiratory failure, hypoxia, and bilateral lung opacities. The pathophysiology of both HF and ALI/ARDS involves complex interactions between mechanical injury, inflammatory responses, and oxidative stress, with disruption of the alveolar-capillary barrier. No reliable biomarkers currently distinguish between pulmonary oedema from HF and ALI/ARDS, but surfactant proteins like SP-B may hold potential for diagnosis. Understanding these mechanisms is crucial for developing therapeutic strategies targeting both conditions.