p. -8 (Surface tension at pore)

Net pressure

V Lymphatic pump

Hydrostatic and osmotic forces at the capillary (left) and alveolar membrane (right) of the lungs. Also shown is the tip end of a lymphatic vessel (center) that pumps fluid from the pulmonary interstitial spaces. (Modified from Guyton AC, Taylor AE, Granger HJ: Circulatory Physiology II: Dynamics and Control of the Body Fluids. Philadelphia: WB Saunders, 1975.)

Figure 38-6

Figure 38-6

Figure 38-7

Rate of fluid loss into the lung tissues when the left atrial pressure (and pulmonary capillary pressure) is increased. (From Guyton AC, Lindsey AW: Effect of elevated left atrial pressure and decreased plasma protein concentration on the development of pulmonary edema. Circ Res 7:649, 1959.)

Left atrial pressure (mm Hg)

mally 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. To give an example, Figure 38-7 shows how different levels of left atrial pressure increase the rate of pulmonary edema formation in dogs. Remember that every time the left atrial pressure rises to high values, the pulmonary capillary pressure rises to a level 1 to 2 mm Hg greater than the left atrial pressure. In these experiments, as soon as the left atrial pressure rose above 23 mm Hg (causing the pulmonary capillary pressure to rise above 25 mm Hg), fluid began to accumulate in the lungs. This fluid accumulation increased even more rapidly with further increases in capillary pressure. The plasma colloid osmotic pressure during these experiments was equal to this 25 mm Hg critical pressure level. Therefore, in the human being, whose normal plasma colloid osmotic pressure is 28 mm Hg, one can predict that the pulmonary capillary pressure must rise from the normal level of 7 mm Hg to more than 28 mm Hg to cause pulmonary edema, giving an acute safety factor against pulmonary edema of 21 mm Hg.

Safety Factor in Chronic Conditions. 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 mm Hg have been measured without the development of lethal pulmonary edema.

Rapidity of Death in Acute 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 mm Hg above the safety factor level. Thus, in acute left-sided heart failure, in which the pulmonary capillary pressure occasionally does rise to 50 mm Hg, death frequently ensues in less than 30 minutes from acute pulmonary edema.

Fluid in the Pleural Cavity

When the lungs expand and contract during normal breathing, they slide back and forth within the pleural cavity. To facilitate this, a thin layer of mucoid fluid lies between the parietal and visceral pleurae.

Figure 38-8 shows the dynamics of fluid exchange in the pleural space. The pleural membrane is a porous, mesenchymal, serous membrane through which small amounts of interstitial fluid transude continually into the pleural space. These fluids carry with them tissue proteins, giving the pleural fluid a mucoid characteristic, which is what allows extremely easy slippage of the moving lungs.

The total amount of fluid in each pleural cavity is normally slight, only a few milliliters. Whenever the quantity becomes more than barely enough to begin flowing in the pleural cavity, the excess fluid is pumped away by lymphatic vessels opening directly from the pleural cavity into (1) the mediastinum, (2) the superior surface of the diaphragm, and (3) the lateral surfaces of the parietal pleura. Therefore, the pleural space—the space between the parietal and visceral pleurae—is called a potential space because it normally is so narrow that it is not obviously a physical space.

"Negative Pressure" in Pleural Fluid. A negative force is always required on the outside of the lungs to keep the lungs expanded. This is provided by negative pressure in the normal pleural space. The basic cause of this negative pressure is pumping of fluid from the space by the lymphatics (which is also the basis of the negative pressure found in most tissue spaces of the body). Because the normal collapse tendency of the lungs is about -4 mm Hg, the pleural fluid pressure must always be at

Figure 38-8

Dynamics of fluid exchange in the intrapleural space.

least as negative as -4 mm Hg to keep the lungs expanded. Actual measurements have shown that the pressure is usually about -7 mm Hg, which is a few millimeters of mercury more negative than the collapse pressure of the lungs. Thus, the negativity of the pleural fluid keeps the normal lungs pulled against the parietal pleura of the chest cavity, except for an extremely thin layer of mucoid fluid that acts as a lubricant.

Pleural Effusion. Pleural effusion means the collection of large amounts of free fluid in the pleural space.The effusion is analogous to edema fluid in the tissues and can be called "edema of the pleural cavity." The causes of the effusion are the same as the causes of edema in other tissues (discussed in Chapter 25), including (1) blockage of lymphatic drainage from the pleural cavity; (2) cardiac failure, which causes excessively high peripheral and pulmonary capillary pressures, leading to excessive transudation of fluid into the pleural cavity;

(3) greatly reduced plasma colloid osmotic pressure, thus allowing excessive transudation of fluid; and (4) infection or any other cause of inflammation of the surfaces of the pleural cavity, which breaks down the capillary membranes and allows rapid dumping of both plasma proteins and fluid into the cavity.

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Essentials of Human Physiology

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