Elastic behavior of lungs

In a healthy individual, the lungs are very distensible; in other words, they can be inflated with minimal effort. Furthermore, during normal, quiet breathing, expiration is passive. The lungs inherently recoil to their prein-spiratory position. These processes are attributed to the elastic behavior of the lungs. The elasticity of the lungs involves the following two interrelated properties:

• Elastic recoil

• Pulmonary compliance

The elastic recoil of the lungs refers to their ability to return to their original configuration following inspiration. It may also be used to describe the tendency of the lungs to oppose inflation. Conversely, pulmonary compliance describes how easily the lungs inflate. Compliance is defined as the change in lung volume divided by the change in transpulmonary pressure:

A highly compliant lung is one that requires only a small change in pressure for a given degree of inflation; a less compliant lung requires a larger change in pressure for the same degree of inflation. For example, during normal, quiet breathing, all adults inhale a tidal volume of about 500 ml per breath. In an individual with healthy, compliant lungs, the transpul-monary pressure gradient needed to be generated by the inspiratory muscles is very small (approximately 2 to 3 cmH2O). The patient with less compliant, or "stiff," lungs must generate a larger transpulmonary pressure to inflate the lungs with the same 500 ml per breath. In other words, more vigorous contraction of the inspiratory muscles is required. Therefore, the work of breathing is increased. The elastic behavior of the lungs is determined by two factors:

• Elastic connective tissue in the lungs

• Alveolar surface tension

The elastic connective tissue in the lungs consists of elastin and collagen fibers found in the alveolar walls and around blood vessels and bronchi. When the lungs are inflated, the connective tissue fibers are stretched, or distorted. As a result, they have a tendency to return to their original shape and cause the elastic recoil of the lungs following inspiration. However, due to the interwoven mesh-like arrangement of these fibers, the lungs remain very compliant and readily distensible.

The alveoli are lined with fluid. At an air-water interface, the water molecules are much more strongly attracted to each other than to the air at their surface. This attraction produces a force at the surface of the fluid referred to as surface tension (ST). Alveolar surface tension exerts two effects on the elastic behavior of the lungs. First, it decreases the compliance of the lungs. For example, inflation of the lung would increase its surface area and pull the water molecules lining the alveolus apart from each other. However, the attraction between these water molecules, or the surface tension, resists this expansion of the alveolus. Opposition to expansion causes a decrease in compliance; the alveolus is more difficult to inflate and the work of breathing is increased. The greater the surface tension, the less compliant are the lungs.

The second effect of surface tension is that it causes the alveolus to become as small as possible. As the water molecules pull toward each other, the alveolus forms a sphere, which is the smallest surface area for a given volume. This generates a pressure directed inward on the alveolus, or a collapsing pressure. The magnitude of this pressure is determined by the Law of LaPlace:

The collapsing pressure (P) is proportional to the alveolar surface tension (ST) and inversely proportional to the radius (r) of the alveolus. In other words, the greater the surface tension and the smaller the radius, the greater the collapsing pressure.

Due to this collapsing pressure, alveoli are inherently unstable. For example, if two alveoli of different sizes have the same surface tension, the smaller alveolus has a greater collapsing pressure and would tend to empty into the larger alveolus (see Figure 17.2, panel a). Air flows from an area of higher pressure to an area of lower pressure. As a result, the air within the smaller alveolus flows into the larger one and an area of atelectasis (airway collapse) develops. Therefore, if alveolar surface tension were to remain the same throughout the lungs, it would have the potential to cause widespread alveolar collapse.

Normal lungs, however, produce a chemical substance referred to as pulmonary surfactant. Made by alveolar type II cells within the alveoli, surfactant is a complex mixture of proteins (10 to 15%) and phospholipids (85 to 90%), including dipalmitoyl phosphatidyl choline, the predominant constituent. By interspersing throughout the fluid lining the alveoli, surfactant disrupts the cohesive forces between the water molecules. As a result, pulmonary surfactant has three major functions:

• Decreases surface tension

• Increases alveolar stability

• Prevents transudation of fluid

Pulmonary surfactant decreases surface tension of alveolar fluid. Reduced surface tension leads to a decrease in the collapsing pressure of the alveoli, an increase in pulmonary compliance (less elastic recoil), and a decrease in the work required to inflate the lungs with each breath. Also, pulmonary surfactant promotes the stability of the alveoli. Because the surface tension is reduced, the tendency for small alveoli to empty into larger ones is decreased (see Figure 17.2, panel b). Finally, surfactant inhibits the transudation of fluid out of the pulmonary capillaries into the alveoli. Excessive surface tension would tend to reduce the hydrostatic pressure in the tissue outside the capillaries. As a result, capillary filtration would be promoted. The movement of water out of the capillaries may result in interstitial edema formation and excess fluid in the alveoli.

Pharmacy application: infant respiratory distress syndrome

Infant respiratory distress syndrome (IRDS), also known as hyaline membrane disease, is one of the most common causes of respiratory disease in premature infants. In fact, it occurs in 30,000 to 50,000 newborns per year in the U.S. — most commonly in neonates born before week 25 of gestation. IRDS is characterized by areas of atelectasis, hemorrhagic edema, and the formation of hyaline membranes within the alveoli. IRDS is caused by a deficiency of pulmonary surfactant. Alveolar type II cells, which produce surfactant, do not begin to mature until weeks 25 to 28 of

Radius=1 Surface tension=1 Pa=2ST

Radius=2 Surface tension=1 Pb=1ST

Radius=1 Surface tension=1 Pa=2ST

Radius=2 Surface tension=1 Pb=1ST

Radius=1

Surface tension=1/2 Pa=1ST

Radius=2 Surface tension=1 Pb=1ST

Radius=1

Surface tension=1/2 Pa=1ST

Radius=2 Surface tension=1 Pb=1ST

Figure 17.2 Effects of surface tension and surfactant on alveolar stability. (a) Effect of surface tension. According to the law of LaPlace (P = 2ST/ r), if two alveoli have the same surface tension (ST), the alveolus with the smaller radius (r), and therefore a greater collapsing pressure (P), would tend to empty into the alveolus with the larger radius. (b) Effect of surfactant. Surfactant decreases the surface tension and thus the collapsing pressure in smaller alveoli to a greater extent than it does in larger alveoli. As a result, the collapsing pressures in all alveoli are equal. This prevents alveolar collapse and promotes alveolar stability.

gestation. Therefore, premature infants may have poorly functioning type II cells and insufficient surfactant production.

At birth, the first breath taken by the neonate requires high inspiratory pressures to cause the initial expansion of the lungs. Normally, the lungs will retain a portion of this first breath (40% of the residual volume), so subsequent breaths require much lower inspiratory pressures. In infants lacking surfactant, the lungs collapse between breaths and their airless portions become stiff and noncompliant. Therefore, every inspiration is as difficult as the first. In fact, a transpulmonary pressure of 25 to 30 mmHg is needed to maintain a patent airway (compared to the normal 5 mmHg). This results in a significant increase in the work of breathing and a decrease in ventilation. The inability of the neonate to ventilate adequately leads to progressive atelectasis, hypoxia, hy-percarbia (increased carbon dioxide), and acidosis. Furthermore, formation of the hyaline membranes impairs gas exchange, which exacerbates these conditions.

The therapy for IRDS includes mechanical ventilation with continuous positive airway pressure. This maintains adequate ventilation and prevents airway collapse between breaths with the formation of atelectasis. Therapy also includes administration of exogenous pulmonary surfactant. Two types of surfactants are used to prevent and treat IRDS in the U.S. These include surfactants prepared from animal sources as well as synthetic surfactants. Exogenous pulmonary surfactants are administered as a suspension (in saline) through the endotracheal tube used for mechanical ventilation.

Many exogenous pulmonary surfactants are derived from bovine extracts. For example, Infasurf® contains the active ingredient calfactant, which is an unmodified calf lung extract that includes mostly phospholipids and hydrophobic surfactant-specific proteins. Other exogenous pulmonary surfactants derived from bovine lung extracts include Survanta® (active ingredient, beractant) and Bovactant® (active ingredient, alveofact). Exosurf® is a synthetic surfactant. It contains colfosceril palmitate, which is a phos-pholipid and an important constituent of natural and many synthetic pulmonary surfactant compounds.

Essentials of Human Physiology

Essentials of Human Physiology

This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.

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