Pulmonary Edema (John West lecture)

Blood gas barrier (endothelium, ECM, Type I pneumocyte) is polarized. The thinner side is for gas exchange and the thicker side is for fluid exchange. The strength of the barrier derives from Type IV collagen in the ECM. The endothelium has looser junctions and is more permeable to ions, fluid, and proteins than the epithelial layer.

Starling forces apply. What's normal: small amount of fluid always leaving pulmonary capillaries (through thick side), and this is drained by lymphatics. Increased hydrostatic pressure (left heart failure -- most common cause, often secondary to MI, volume overload, mitral stenosis) and decreased oncotic pressure (nephrotic syndrome, cirrhosis) lead to transudate pulmonary edema. Other causes of pulmonary edema. Rapid re-expansion of collapsed lung. Lymphatic insufficiency from silicosis.

Reflection coefficient is 0.7, because some osmotic elements escape from capillary. Factors that reduce reflection coefficient (increase capillary permeability) include endotoxins (sepsis), radiation (breast carcinoma radiation -- localized pulmonary edema), and toxins (chloride gas, chronic exposure to oxygen gas) and high-altitude (uneven hypoxic pulmonary vasoconstriction). This leads to exudative (protein-rich) pulmonary edema.

If the amount of fluid leaving increases, then you get interstitial edema and then alveolar edema (alveolar epithelium becomes pathologically permeable). Interstitial edema manifests itself in perivascular and peribronchiolar spaces; septal lines (horizontal white lines) on CXR are only sign -- subtle. Alveolar edema results in shunting. Easy to see (butterfly shadow, symmetrical) on CXR.

Signs of pulmonary edema: Dyspnea, orthopnea, paroxysmal nocturnal dyspnea; pink, frothy sputum from RBCs and surfactant.