Pulmonary edema results from transudation of fluid, first from pulmonary capillaries into intersti-tial spaces and then from the interstitial spaces into alveoli. Fluid within the interstitial space and alveoli is collectively referred to as extravascular lung water. The movement of water across the pulmonary cap-illaries is similar to what occurs in other capillary beds and can be expressed by the Starling equation:
Q = K × [(πc′ − Pi) − σ(πc′ − πi)]
where Q is net flow across the capillary; πc′ and Pi are capillary and interstitial hydrostatic pressures, respectively; πc′ and πi are capillary and interstitial oncotic pressures, respectively; K is a filtration coef-ficient related to effective capillary surface area per mass of tissue; and σ is a reflection coefficient that expresses the permeability of the capillary endothe-lium to albumin. Albumin is particularly important in this context because water loss to the intersti-tium will increase when albumin is also lost to the interstitium. A σ with a value of 1 implies that the endothelium is completely impermeable to albumin, whereas a value of 0 indicates free passage of albu-min and other particles/molecules. The pulmonary endothelium normally is partially permeable to albumin, such that interstitial albumin concentra-tion is approximately one half that of plasma; there-fore, under normal conditions πi must be about 14 mm Hg (one half that of plasma). Pulmonary capillary hydrostatic pressure is dependent on verti-cal height in the lung (gravity) and normally varies from 0 to 15 mm Hg (average, 7 mm Hg). Because Pi is thought to be normally about –4 to –8 mm Hg, the forces favoring transudation of fluid (πc′, Pi, and πi) are usually almost balanced by the forces favoring reabsorption (πc′). The net amount of fluid that normally moves out of pulmonary capillaries is small (about 10–20 mL/h in adults) and is rapidly removed by pulmonary lymphatics, which return it into the central venous system.The alveolar epithelial membrane is usually per-meable to water and gases but is impermeable to albu-min (and other proteins). A net movement of water from the interstitium into alveoli occurs only when the normally negative Pi becomes positive (rela-tive to atmospheric pressure). Fortunately, because of the lung’s unique ultrastructure and its capacity to increase lymph flow, the pulmonary interstitium usu-ally accommodates large increases in capillary transu-dation before Pi becomes positive. When this reserve capacity is exceeded, pulmonary edema develops.
Pulmonary edema is often divided into four stages:
Stage I: Only interstitial pulmonary edema ispresent. Patients often become tachypneic as pulmonary compliance begins to decrease. The chest radiograph reveals increased interstitial markings and peribronchial cuffing.
Stage II: Fluid fills the interstitium and beginsto fill the alveoli, being initially confined to the angles between adjacent septa (crescentic filling). Near-normal gas exchange may be preserved.
Stage III: Many alveoli are completely flooded and no longer contain gas. Flooding is most prominent in dependent areas of the lungs. Blood flow through the capillaries of flooded alveoli results in a large increase in intrapulmonary shunting. Hypoxemia and hypocapnia (the latter due to dyspnea and hyperventilation) are characteristic.
Stage IV: Marked alveolar flooding spillsinto the airways as froth. Gas exchange is compromised due to both shunting and airway obstruction, leading to progressive hypercapnia and severe hypoxemia.
Pulmonary edema usually results from either an increase in the net hydrostatic pressure across the capillaries (hemodynamic or cardiogenic pulmo-nary edema) or an increase in the permeability of the alveolar–capillary membrane (increased permeabil-ity edema or noncardiogenic pulmonary edema). If a pulmonary artery catheter is present, the distinc-tion can be based on the pulmonary artery occlusion pressure, which if greater than 18 mm Hg indicates that hydrostatic pressure is involved in forcing fluid across the capillaries into the interstitium and alveoli. The protein content of the edema fluid can also help differentiate the two. Fluid due to hemo-dynamic edema has a low protein content, whereas that due to permeability edema has a high protein content.
Less common causes of edema include pro-longed severe airway obstruction (negative pres-sure pulmonary edema), sudden reexpansion of a collapsed lung, high altitude, pulmonary lymphatic obstruction, and severe head injury, although the same mechanisms (ie, changes in hemodynamic parameters or capillary permeability) also account for these diagnoses. Pulmonary edema associated with airway obstruction may result from an increase in the transmural pressure across pulmonary capil-laries associated with a markedly negative interstitial hydrostatic pressure. Neurogenic pulmonary edema appears to be related to a marked increase in sympa-thetic tone, which causes severe pulmonary hyper-tension. The latter can disrupt the alveolar–capillary membrane.
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