Lung Fluid Balance

The pulmonary capillaries are extremely thin and contain pores that allow fluid to move across their walls. Starling's law describes the forces that govern fluid flux across capillary walls (see Chapter 16), and an understanding of these forces is necessary to understand both normal and pathologic lung fluid balance. Starling's law states that the net fluid flux across the capillary depends on a balance of hydrostatic forces (P) and colloid osmotic (or oncotic) forces (n):

Net fluid flux = Kfc[(Pc - Pt)- a(nc - O], where Kfc is a filtration coeff icient that depends on the total surface area of the capillary and on the number and size of pores in the capillary. Hydrostatic pressure in the capillary (Pc) tends to move fluid out, and interstitial pressure (Pi) tends to move fluid into the capillary. Conversely, capillary osmotic pressure (nc) tends to hold fluid in the capillary, and interstitial osmotic pressure (n) tends to draw fluid out of the capillary. The osmotic reflection coefficient (a) describes the effectiveness of osmotic pressure at moving fluids, and it can range from 0 to 1. Conceptually, a compares the size of the pore to the osmotically active solute: a = 0 if the solute can move freely through the pore, and a = 1 if the solute cannot move through the pore.

Normally, the balance of forces results in net filtration, or the movement of a few milliliters per hour of fluid out of the capillaries. Normal Pc & 10 mm Hg and normal Pi in the lungs is subatmospheric so there is a positive hydrostatic force moving fluid out of the capillaries. The interstitial space around alveolar capillaries is not compliant, so filtration in this region tends to increase local interstitial pressure. This local pressure increase is thought to provide a gradient moving filtrate toward the interstitium around the extra-alveolar vessels. Filtrate in this extra-alveolar region can be reabsorbed by the bronchial circulation or collected by lymphatics, which also return the fluid to the vascular system.

Normal plasma protein concentration is about 7.5 g/dL (mainly albumin); this exerts an osmotic pressure of about 28 mm Hg. The interstitium contains only about 5 g/dL of protein with an osmotic pressure of 15-20 mm Hg. Therefore, the osmotic forces promote absorption. Also, osmotic forces provide a natural feedback system, in which increased filtration dilutes the interstitial space. This reduces the osmotic gradient pulling fluid out of the capillaries. Recall that the osmotic pressure depends on the number of molecules in solution.

When this normal balance of forces is disturbed, filtration can exceed the capacity of reabsorption, and lymphatic drainage and fluid accumulates in the inter-stitium. Edema is the accumulation of excess filtrate outside the capillaries. Pulmonary edema fluid accumulates first in the peribronchiolar and perivascular spaces; this is called interstitial edema. Interstitial edema can alter local ventilation and perfusion and make gas exchange inefficient (Chapter 21). Alveolar edema, or flooding of excess filtrate into the alveolar spaces, is more serious because it can totally block ventilation and cause blood flow shunts in affected lung regions (Chapter 21). The exact mechanisms resulting in alveolar edema are not known, but they involve exceeding the lung's capacity for lymphatic drainage and changes in solute and fluid transport across airway epithelial cells. Alveolar type II epithelial cells normally transport NaCl to the basolateral surface, and water follows, keeping the alveoli dry.

Edema fluid can have a low or high protein concentration. Hydrostatic edema, which may occur with elevated pulmonary capillary pressures in congestive heart failure, results in filtrate with low protein concentrations. Other lung injuries, such as adult respiratory distress syndrome, may alter the permeability of the capillary endothelium (i.e., changes) and produce a protein-rich edema fluid.

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