Exchange of gases between the alveolar air and the pulmonary capillary blood is discussed in the next chapter. However, it is important to note here that the alveolar walls are lined with so many capillaries that, in most places, the capillaries almost touch one another side by side. Therefore, it is often said that the capillary blood f lows in the alveolar walls as a “sheet of flow,” rather than in individual capillaries.

Pulmonary Capillary Pressure. No direct measurements of pulmonary capillary pressure have ever been made. However, “isogravimetric” measurement of pulmonary capillary pressure, using a technique described in Chapter 16, has given a value of 7 mm Hg. This measurement is probably nearly correct because the mean left atrial pressure is about 2 mm Hg and the mean pulmonary arterial pressure is only 15 mm Hg, so the mean pulmonary capillary pressure must lie somewhere between these two values.

Length of Time Blood Stays in the Pulmonary Capillaries. From histological study of the total cross sectional area of all the pulmonary capillaries, it can be calculated that when the cardiac output is normal, blood passes through the pulmonary capillaries in about 0.8 second. When the cardiac output increases, this time can shorten to as little as 0.3 second. The shortening would be much greater were it not for the fact that additional capillaries, which normally are collapsed, open up to accommodate the increased blood flow. Thus, in only a fraction of a second, blood passing through the alveolar capillaries becomes oxygenated and loses its excess carbon dioxide.

CAPILLARY EXCHANGE OF FLUID IN THE LUNGS AND PULMONARY INTERSTITIAL FLUID DYNAMICS

 The dynamics of fluid exchange across the lung capillary membranes are qualitatively the same as for peripheral tissues. However, quantitatively, there are important differences, as follows:

 1. The pulmonary capillary pressure is low, about 7 mm Hg, in comparison with a considerably higher functional capillary pressure in the peripheral tissues of about 17 mm Hg.

2. The interstitial fluid pressure in the lung is slightly more negative than that in peripheral subcutaneous tissue. (This pressure has been measured in two ways: by a micropipette inserted into the pulmonary interstitium, giving a value of about −5 mm Hg, and by measuring the absorption pressure of fluid from the alveoli, giving a value of about −8 mm Hg.)

3. The colloid osmotic pressure of the pulmonary interstitial fluid is about 14 mm Hg, in comparison with less than half this value in the peripheral tissues.

4. The alveolar walls are extremely thin, and the alveolar epithelium covering the alveolar surfaces is so weak that it can be ruptured by any positive pressure in the interstitial spaces greater than alveolar air pressure (>0 mm Hg), which allows dumping of fluid from the interstitial spaces into the alveoli. Now let us see how these quantitative differences affect pulmonary fluid dynamics.

Interrelations Between Interstitial Fluid Pressure and Other Pressures in the Lung. Figure 1 shows a pulmonary capillary, a pulmonary alveolus, and a lymphatic capillary draining the interstitial space between the blood capillary and the alveolus. Note the balance of forces at the blood capillary membrane, as follows:

Fig1. Hydrostatic and osmotic forces in mm Hg 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.

Thus, the normal outward forces are slightly greater than the inward forces, providing a mean filtration pressure at the pulmonary capillary membrane that can be calculated as follows:

This filtration pressure causes a slight continual flow of fluid from the pulmonary capillaries into the interstitial spaces and, except for a small amount that evaporates in the alveoli, this fluid is pumped back to the circulation through the pulmonary lymphatic system.

Negative Pulmonary Interstitial Pressure and the Mechanism for Keeping the Alveoli “Dry.” What keeps the alveoli from filling with fluid under normal conditions? If one remembers that the pulmonary capillaries and the pulmonary lymphatic system normally maintain a slight negative pressure in the interstitial spaces, it is clear that whenever extra fluid appears in the alveoli, it will simply be sucked mechanically into the lung interstitium through the small openings between the alveolar epithelial cells. The excess fluid is then carried away through the pulmonary lymphatics. Thus, under normal conditions, the alveoli are kept “dry,” except for a small amount of fluid that seeps from the epithelium onto the lining surfaces of the alveoli to keep them moist.

Pulmonary Edema

 Pulmonary edema occurs in the same way that edema occurs elsewhere in the body. Any factor that increases fluid filtration out of the pulmonary capillaries or that impedes pulmonary lymphatic function and causes the pulmonary interstitial fluid pressure to rise from the negative range into the positive range will cause rapid filling of the pulmonary interstitial spaces and alveoli with large amounts of free fluid.

The most common causes of pulmonary edema are as follows:

1. Left-sided heart failure or mitral valve disease, with consequent great increases in pulmonary venous pressure and pulmonary capillary pressure and flooding of the interstitial spaces and alveoli.

 2. Damage to the pulmonary blood capillary mem branes caused by infections such as pneumonia or by breathing noxious substances such as chlorine gas or sulfur dioxide gas. Each of these mechanisms causes rapid leakage of both plasma proteins and fluid out of the capillaries and into both the lung interstitial spaces and the alveoli.

“Pulmonary Edema Safety Factor.” Experiments in animals have shown that the pulmonary capillary pressure normally 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 2 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.

Fig2. 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.)

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 Persons with 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 may ensue in less than 30 minutes as a result of acute pulmonary edema.

اخر الاخبار

اخبار العتبة العباسية المقدسة

قسم الشؤون الفكرية يصدر عددين جديدين من نشرتي الكفيل والخميس

متحف الكفيل يستعرض حاملَ شموعٍ يعود إلى العصر القاجاري

ذوو شهداء مدرسة ميناب الإيرانية يتشرفون بزيارة مرقد أبي الفضل العباس (عليه السلام)

قسم الصناعات ينجز 75‎%‎ من أعمال إنشاء سور حديدي في شركة عين الحياة

المزيد

الآخبار الصحية

السجائر الإلكترونية والإقلاع عن التدخين.. نتائج متباينة تثير الجدل العلمي

مصر تحقق إنجازاً دولياً جديداً في منظمة الصحة العالمية

دراسة: السباحة فعّالة أكثر من الجري في الحفاظ على صحة القلب

عامل خطر في بداية الحمل يؤخر تطور الكلام والمهارات الحركية لدى الرضع

المزيد

الآخبار التكنلوجية

أحلامك ليست عشوائية.. إليك ما يفعله دماغك أثناء نومك

روسيا.. العلماء يضاعفون الاستقرار الحراري للألواح الشمسية ثلاث مرات

علماء يكشفون سر سرعة الدلافين في السباحة

سلمي أو دموي.. هكذا تنتقل السلطة في مجتمع الجرذان

المزيد

مواضيع ذات صلة

Effect of Hydrostatic Pressure Gradients in the Lungs on Regional Pulmonary Blood Flow

Blood Flow Through the Lungs and its Distribution

Conversion of Prothrombin to Thrombin

Formation of the Platelet Plug

Hemoglobin Formation

Erythropoietin Regulates Red Blood Cell Production

Stages of Differentiation of Red Blood Cells

Genesis of Blood Cells

Role of the Nervous System in Rapid Control of Arterial Pressure

Special Features of Nervous Control of Arterial Pressure

The Lymphatic System Plays A Key Role in Controlling Interstitial Fluid Protein Concentration, Volume, and Pressure

Formation of Lymph