Pulmonary edema

Pulmonary edema, also known as pulmonary congestion, is excessive liquid accumulation in the tissue and air spaces (usually alveoli) of the lungs. It leads to impaired gas exchange and may cause hypoxemia and respiratory failure. It is due to either failure of the left ventricle of the heart to remove oxygenated blood adequately from the pulmonary circulation (cardiogenic pulmonary edema), or an injury to the lung tissue directly or blood vessels of the lung (non-cardiogenic pulmonary edema). Treatment is focused on three aspects: firstly improving respiratory function, secondly, treating the underlying cause, and thirdly preventing further damage and assuring full recovery to the lung. Pulmonary edema, especially when sudden (acute), can lead to respiratory failure or cardiac arrest due to hypoxia. It is a cardinal feature of congestive heart failure. The term edema is from the Greek οἴδημα (oidēma, "swelling"), from οἰδέω (oidéō, "(I) swell"). Classically it is cardiogenic (left ventricular) but fluid may also accumulate due to damage to the lung. This damage may be from direct external injuries or injuries mediated by high pressures within the pulmonary circulation. When directly or indirectly caused by increased left ventricular pressure, pulmonary edema may form when mean pulmonary pressure rises from the normal average of 15 mmHg to above 25 mmHg, where pulmonary fluid may form. Broadly, the causes of pulmonary edema can be divided into cardiogenic and non-cardiogenic. By convention, cardiogenic specifically refers to left ventricular causes. Congestive heart failure which is due to the heart's inability to pump the blood out of the pulmonary circulation at a sufficient rate resulting in elevation in pulmonary wedge pressure and edema – this usually is due to left ventricular failure, but may also be from arrhythmias, or fluid overload, (e.g. from kidney failure or intravenous therapy). Hypertensive crisis can cause pulmonary edema as the elevation in blood pressure and increased afterload on the left ventricle hinders forward flow in blood vessels and causes the elevation in wedge pressure and subsequent pulmonary edema.