CHAPTER 38 Pulmonary Circulation, Pulmonary Edema, Pleural Fluid

Special problems related to pulmonary hemodynamics have important implications for gas exchange in the lungs. The present discussion is concerned specifically with these features of the pulmonary circulation.

Physiologic Anatomy of the Pulmonary Circulatory System (p. 477)

The Lung Has Three Circulations: Pulmonary, Bronchial, and Lymphatic

• Pulmonary circulation. The pulmonary artery is thin-walled and distensible, giving the pulmonary arterial tree large compliance. This large compliance allows the pulmonary arteries to accommodate about two thirds of the stroke volume of the right ventricle. The pulmonary veins have distensibility characteristics similar to those of the veins in the systemic circulation.

• Bronchial circulation. Bronchial blood flow amounts to about 1% to 2% of the total cardiac output. Oxygenated blood in the bronchial arteries supplies the connective tissue, septa, and large and small bronchi of the lungs. Because the bronchial blood empties into the pulmonary veins and bypasses the right heart, the right ventricular output is about 1% to 2% less than the left ventricular output.

• Lymphatic circulation. Lymphatics are found in all the supportive tissues of the lungs. Particulate matter entering the alveoli is removed by way of lymphatic channels; plasma proteins leaking from the lung capillaries are also removed from the lung tissues, helping prevent edema.

Pressures in the Pulmonary System (p. 477)

Blood Pressures in the Pulmonary Circulation Are Low Compared with Those in the Systemic Circulation

• Pulmonary artery pressure. In the normal human being, the average systolic pulmonary arterial pressure is about 25 mm Hg, the diastolic pulmonary arterial pressure is about 8 mm Hg, and the mean pulmonary arterial pressure is about 15 mm Hg.

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• Pulmonary capillary pressure. The mean pulmonary capillary pressure has been estimated through indirect means to be about 7 mm Hg.

• Left atrial and pulmonary venous pressures. The mean pressure in the left atrium and the major pulmonary veins averages about 2 mm Hg in the recumbent human being.

The Left Atrial Pressure Can Be Estimated by Measuring the Pulmonary Wedge Pressure

Direct measurement of left atrial pressure is difficult because it requires passing a catheter retrograde through the left ventricle. The pulmonary wedge pressure can be measured by floating a balloon-tipped catheter through the right heart and pulmonary artery until the catheter wedges tightly in a smaller branch of the artery. Because all blood flow has been stopped in the blood vessels extending from the plugged artery, an almost direct connection is made through the pulmonary capillaries with the blood in the pulmonary veins. The wedge pressure is usually only 2 to 3 mm Hg higher than the left atrial pressure. Wedge pressure measurements are used often for studying changes in left atrial pressure in persons with various types of heart failure.

Blood Volume of the Lungs (p. 478)

The Lungs Provide an Important Blood Reservoir

The pulmonary blood volume is about 450 mL, or about 9% of the total blood volume. Under various physiological and pathological conditions, the quantity of blood in the lungs can vary from as little as one-half to two times normal.

Blood Shifts between the Pulmonary and Systemic Circulatory Systems as a Result of Cardiac Pathology

Left heart failure, mitral stenosis, or mitral regurgitation causes blood to dam up in the pulmonary circulation, greatly increasing pulmonary vascular pressures and volumes. Because the volume of the systemic circulation is about nine times that of the pulmonary system, a shift of blood from one system to the other affects the pulmonary system greatly but usually has only mild effects on the systemic circulation.

Blood Flow through the Lungs and Its Distribution (p. 479)

Pulmonary Blood Flow Is Nearly Equal to Cardiac Output

Under most conditions, the pulmonary vessels act as passive, distensible tubes that enlarge with increasing pressure and narrow with decreasing pressure. Blood is distributed to the segments of the lungs in which the alveoli are best oxygenated. This is achieved via the following mechanism.

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Pulmonary Blood Flow Distribution Is Controlled by Alveolar Oxygen

When the alveolar oxygen concentration decreases below normal, the adjacent blood vessels constrict. This is opposite to the effect normally observed in systemic vessels. This vasoconstrictor effect of a low oxygen level distributes blood flow away from poorly ventilated alveoli.

The Autonomic Nervous System Does Not Have a Major Function in Normal Control of Pulmonary Vascular Resistance

However, sympathetic stimulation has a significant effect in constricting the large pulmonary capacitative vessels, especially the veins. This constriction of large pulmonary veins provides a means by which sympathetic stimulation can displace much of the extra blood in the lungs into other segments of the circulation when needed to combat low blood pressure.

Effect of Hydrostatic Pressure Gradients in the Lungs on Regional Pulmonary Blood Flow (p. 479)

In the normal adult, the distance between the apex and base of the lungs is about 30 cm, which creates a 23 mm Hg difference in blood pressure. This pressure gradient has a marked effect on blood flow in the various regions of the lung.

Hydrostatic Pressure Gradients in the Lung Create Three Zones of Pulmonary Blood Flow

Under normal and various pathologic lung conditions, any one of three possible zones of pulmonary blood flow can be found:

• Zone 1 (top of the lung) has no blood flow because the capillary pressure never rises higher than the alveolar pressure. In this zone, alveolar pressure > artery pressure > venous pressure; thus the capillaries are pressed flat. Zone 1 does not occur during normal conditions; it can occur when pulmonary artery pressure is decreased following hemorrhage and when alveolar pressure is increased during positive-pressure ventilation.

• Zone 2 (middle of the lung) has an intermittent blood flow that occurs during systole (when the arterial pressure is greater than the alveolar pressure) but not during diastole (when the arterial pressure is less than the alveolar pressure). Zone 2 blood flow is thus determined by the difference between arterial and alveolar pressures.

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• Zone 3 (bottom of the lung) has a high, continuous blood flow because the capillary pressure remains greater than the alveolar pressure during the entire cardiac cycle.

Pulmonary Vascular Resistance Decreases During Heavy Exercise

During exercise the blood flow through the lungs increases fourfold to sevenfold. This extra flow is accommodated in the lungs in two ways: (1) by increasing the number of open capillaries, sometimes as much as threefold, and (2) by distending the capillaries and increasing the flow through each capillary by more than twofold. In the normal person, these two changes together decrease the pulmonary vascular resistance so much that the pulmonary arterial pressure rises very little, even during maximum exercise.

Pulmonary Capillary Fluid Dynamics (p. 481)

The alveolar walls are lined with so many capillaries that the capillaries almost touch one another; therefore, the capillary blood flows in the alveolar walls as a “sheet” rather than through individual vessels.

Capillary Exchange of Fluid in the Lungs; Pulmonary Interstitial Fluid Dynamics (p. 481)

The Dynamics of Fluid Exchange through the Lung Capillaries Are Qualitatively the Same as Those for Peripheral Tissues

Quantitatively, however, there are several important differences:

• Pulmonary capillary pressure is low (about 7 mm Hg) compared with a higher functional capillary pressure in the peripheral tissues (about 17 mm Hg).

• Interstitial fluid pressure is slightly more negative than in the peripheral subcutaneous tissue; values range from about −5 to −8 mm Hg.

• Capillary permeability is high, allowing extra amounts of protein to leak from the capillaries; therefore, the interstitial fluid colloid osmotic pressure is also high, averaging about 14 mm Hg, compared with an average of less than 7 mm Hg in many peripheral tissues.

• The alveolar walls are thin. The alveolar epithelium covering the alveolar surfaces is so weak it ruptures when the interstitial pressure becomes greater than atmospheric pressure (i.e., more than 0 mm Hg), which allows dumping of fluid from the interstitial spaces into the alveoli.

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The Mean Filtration Pressure at the Pulmonary Capillaries Is +1 mm Hg

This value is derived as follows:

• Total outward force (29 mm Hg). Forces tending to cause movement of fluid out of the capillaries include the capillary pressure (7 mm Hg), interstitial fluid colloid osmotic pressure (14 mm Hg), and interstitial fluid pressure (−8 mm Hg).

• Total inward force (28 mm Hg). Only the plasma colloid pressure (28 mm Hg) tends to cause absorption of fluid into the capillaries.

• Net mean filtration pressure (+1 mm Hg). Because the total outward force (29 mm Hg) is slightly greater than the total inward force (28 mm Hg), the net mean filtration pressure is slightly positive (29 − 28 = +1 mm Hg). This net filtration pressure causes a continual loss of fluid from the capillaries.

Pulmonary Edema (p. 482)

Pulmonary Edema Develops in the Same Way Peripheral Edema Does

The most common causes of pulmonary edema are as follows:

• Left-sided heart failure or mitral valvular disease causes a great increase in pulmonary capillary pressure with subsequent flooding of the interstitial spaces and alveoli.

• Damage to the pulmonary capillary membrane caused by infections or breathing of noxious substances produces rapid leakage of plasma proteins and fluid out of the capillaries.

When the Pulmonary Interstitial Fluid Volume Increases by More than 50%, Fluid Pours into the Alveoli

Therefore, except in the mildest cases of pulmonary edema, the edema fluid enters the alveoli.

Acute Safety Factors Tend to Prevent Edema in the Lungs

All the following factors must be overcome before edema can occur: (1) normal negativity of the interstitial fluid pressure, (2) lymphatic pumping of fluid out of the interstitial spaces, and (3) decreased colloid osmotic pressure of the interstitial fluid caused by “washout” resulting from increased loss of fluid from the pulmonary capillaries.

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The Pulmonary Capillary Pressure Normally Must Rise to Equal the Plasma Colloid Osmotic Pressure before Significant Pulmonary Edema Occurs

In the human being, who normally has a plasma colloid osmotic pressure of 28 mm Hg, 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 about 21 mm Hg.

The Lymphatic System Provides a Chronic Safety Factor against Pulmonary Edema

The lymph vessels can expand greatly and proliferate over a period of several weeks to months, increasing their ability to carry fluid away from the interstitial spaces by perhaps as much as 10-fold. In a patient with chronic mitral stenosis, a pulmonary capillary pressure of 40 to 45 mm Hg has been measured without the development of significant pulmonary edema.

Lethal Pulmonary Edema Can Occur within Hours

When the pulmonary capillary pressure does rise even slightly above the safety factor level, lethal pulmonary edema can occur within minutes to hours. With acute left-sided heart failure, in which the pulmonary capillary pressure occasionally rises to 50 mm Hg, death often ensues within less than 30 minutes from the onset of acute pulmonary edema.

Fluid in the Pleural Cavity (p. 483)

The Lungs Slide Back and Forth in the Pleural Cavity as They Expand and Contract During Normal Breathing

Small amounts of interstitial fluid transudate continually across the pleural membranes into the pleural space. These fluids contain proteins, which give the pleural fluid a mucoid character, allowing easy slippage of the moving lungs. The total amount of fluid in the pleural cavities is only a few milliliters. The pleural space—the space between the parietal and visceral pleurae—is called a potential space because it normally is so narrow it is not obviously a physical space.

Pleural Effusion—The Collection of Large Amounts of Free Fluid in the Pleural Space—Is Analogous to Edema Fluid in the Tissues

The possible causes of effusion are the following:

• Blockage of lymphatic drainage from the pleural cavity allows excess fluid to accumulate.

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• Cardiac failure causes excessively high peripheral and pulmonary capillary pressures, leading to excessive transudation of fluid into the pleural cavity.

• Decreased plasma colloid osmotic pressure allows excessive transudation of fluid from the capillaries.

• Increased capillary permeability caused by infection or any other source of inflammation of the pleural surfaces allows rapid dumping of both plasma proteins and fluid into the pleural cavity.