Pulmonary edema is one of the most serious consequences of left ventricular cardiac failure. When the left ventricle fails or when the mitral valve fails, left atrial pressure (LAP) may increase substantially. The resulting increase in pulmonary capillary pressure (Pc) forces excess fluid filtration through the pulmonary capillary walls and into the lung tissue. At first, the fluid collects within the lung interstitial space. If LAP exceeds a critical level of ~25 mmHg, the volume of edema fluid will overwhelm the capacity of the interstitial spaces and fluid will flood the airways and alveoli (8). This airway edema directly interferes with gas exchange, and it can kill the patient. However, many people live for months or years with modestly elevated LAP (<25 mmHg). We believe that sustained, subcritical LAP elevations lead to two phases of change in the lungs. The first phase is the acute edema that develops in the first few hours of elevated LAP. The second phase concerns the effect of long-term (7 days or more) increases in LAP below the critical level. This review deals with the acute phase and long-term phase changes in the lung caused by modestly elevated LAP. The acute phase of pulmonary edema has been the subject of intense investigation for many years. In 1896, Starling (7) laid the foundation for our current understanding of pulmonary edema with his famous fluid filtration equation. The equation relates the rate of fluid filtration through the capillary wall (Jv) to the pressures across the capillary wall and to the filtration characteristics of the capillary membrane Ref: guyton and hall textbook of medical physiology 12 edition