Pulmonary edema

Pulmonary edema (British English: oedema), also known as pulmonary congestion, is excessive fluid accumulation in the tissue or air spaces (usually alveoli) of the lungs. This leads to impaired gas exchange, most often leading to shortness of breath (dyspnea) which can progress to hypoxemia and respiratory failure. Pulmonary edema has multiple causes and is traditionally classified as cardiogenic (caused by the heart) or noncardiogenic (all other types not caused by the heart).

Various laboratory tests (CBC, troponin, BNP, etc.) and imaging studies (chest x-ray, CT scan, ultrasound) are often used to diagnose and classify the cause of pulmonary edema.

Treatment is focused on three aspects:

Pulmonary edema can cause permanent organ damage, and when sudden (acute), can lead to respiratory failure or cardiac arrest due to hypoxia. The term edema is from the Greek οἴδημα (oidēma, "swelling"), from οἰδέω (oidéō, "(I) swell").

The amount of fluid in the lungs is governed by multiple forces and is visualized using the Starling equation. There are two hydrostatic pressures and two oncotic (protein) pressures that determine the fluid movement within the lung air spaces (alveoli). Of the forces that explain fluid movement, only the pulmonary wedge pressure is obtainable via pulmonary artery catheterization. Due to the complication rate associated with pulmonary artery catheterization, other imaging modalities and diagnostic methods have become more popular. Imbalance in any of these forces can cause fluid movement (or lack of movement) causing a buildup of fluid where it should not normally be. Although rarely clinically measured, these forces allow physicians to classify and subsequently treat the underlying cause of pulmonary edema.

Pulmonary edema has a multitude of causes, and is typically classified as cardiogenic or noncardiogenic.

Cardiogenic pulmonary edema is caused by increased hydrostatic pressure causing increased fluid in the pulmonary interstitium and alveoli.

Noncardiogenic causes are associated with the oncotic pressure as discussed above causing malfunctioning barriers in the lungs (increased microvascular permeability).