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Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.
Cardiogenic Pulmonary Edema
Cardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to back up into the pulmonary circulation, raising venous pressure. This disrupts the balance between hydrostatic and oncotic forces, allowing fluid to move from capillaries into interstitial and alveolar spaces. Fluid-filled alveoli cannot participate in gas exchange, leading to hypoxemia and dyspnea.
Noncardiogenic Pulmonary Edema
Noncardiogenic edema occurs with normal hydrostatic pressure but increased capillary permeability due to injury or inflammation of the alveolar-capillary membrane. Conditions such as acute respiratory distress syndrome (ARDS), sepsis, aspiration, and inhalational injury damage endothelial and epithelial barriers, allowing protein-rich fluid to leak into alveoli. The high protein content of this fluid draws in additional water osmotically, worsening the edema.
Effects on Lung Function
Regardless of the cause, fluid accumulation disrupts surfactant, increases surface tension, and reduces lung compliance, impairing alveolar expansion. Increased diffusion distance and ventilation–perfusion mismatch further worsen hypoxemia.
Severe Outcomes and Management
In severe cases, pulmonary edema can progress to acute respiratory failure, characterized by respiratory distress, hypercapnia, and refractory hypoxemia. Prompt identification of the underlying cause is critical, as cardiogenic and noncardiogenic pulmonary edema require distinct treatment strategies to reverse the pathophysiologic processes and restore adequate gas exchange.
