Pathophysiology of pulmonary edema

A force imbalance resulting in filtration rates which can no longer be accommodated by tissue fluid clearance mechanisms may be caused by the following.

1. An increased hydrostatic gradient secondary to the increased left atrial pressure of acute heart failure and fluid overload.

2. A decreased oncotic gradient which may be the result of protein dilution with crystalloid solutions or the result of increased vascular membrane permeability to protein—the 'capillary leak or injury'. In the lung, both the capillary and alveolar membrane may be injured.

These basic mechanisms are used on a daily basis to assist in the differential diagnosis, which remains one of exclusion. Pulmonary edema with normal or low pulmonary artery wedge pressure (a clinical measurement of left atrial pressure) points the diagnosis towards capillary leak. This approach can be misleading. Several hours may be required for edema to clear after the hydrostatic gradient has been normalized ( Mayers...eLal:.198Z). This is particularly likely in patients who have been acutely resuscitated with large volumes of crystalloid solutions. The hydrostatic gradients may be high due to the volume infusion. In addition, protein dilution decreases the gradient opposing edema formation and edema quickly ensues. By the time that patients are admitted to the intensive care unit for treatment of respiratory failure, the left atrial pressure may be normal but no capillary lesion may be present. Edema may resolve in 48 h. Until a direct methodology to diagnose capillary leak is developed, it is impossible to know whether such patients had a quickly resolving capillary injury or a slowly resolving hydrostatic edema.

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