Pulmonary edema occurs in the same way that edema occurs elsewhere in the body. Any factor that causes the pulmonary interstitial fluid pressure to rise from the negative range into the positive range will cause rapid filling of the pulmonary interstitial spaces and alveoli with large amounts of free fluid.

The most common causes of pulmonary edema are as follows:

Experiments in animals have shown that the pulmonary capillary pressure normally must rise to a value at least equal to the colloid osmotic pressure of the plasma inside the capillaries before significant pulmonary edema will occur.

Everytime the left atrial pressure rises to high values, the pulmonary capillary pressure rises to a level 1 or 2 mmHg grater than the left atrial pressure.

In the human being, whose normal plasma colloid osmotic pressure is 28mmHg, once can predict that the pulmonary capillary pressure must rise from the normal level of 7mmHg to more than 28mmHg to cause pulmonary edema, giving an acute safety factor against pulmonary edema of 21mmHg.

When the pulmonary capillary pressure remains elevated chronically (for at least 2 weeks), the lungs become even more resistant to pulmonary edema because the lymph vessels expand greatly, increasing their capability of carrying fluid away from the interstitial spaces perhaps as much as 10-fold. Therefore, in patients with chronic mitral stenosis, pulmonary capillary pressures of 40 to 45 mmHg have been measured without the development of lethal pulmonary edema.

When the pulmonary capillary pressure rises even slightly above the safety factor level, lethal pulmonary edema can occur within hours, or even within 20 to 30 minutes if the capillary pressure rises 25 to 30 mmHg above the safety factor level. Thus, in acute left-sided heart failure, in which the pulmonary capillary pressure occasionally does rise to 50 mmHg, death frequently ensues in less than 30 minutes from acute pulmonary edema.