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concentration and cerebrospinal fluid hydrogen ion concentration

Sometimes a person who is emotionally upset may hyperventilate, become dizzy, and lose consciousness. This is due to a lowered carbon dioxide concentration followed by a rise in pH (respiratory alkalosis) and a localized vasoconstriction of cerebral arterioles, decreasing blood flow to nearby brain cells. Hampered oxygen supply to the brain causes fainting. A person should never hyperventilate to help hold the breath while swimming, because the person may lose consciousness under water and drown.

U Describe the inflation reflex.

^9 Which chemical factors affect breathing?

^9 How does hyperventilation decrease respiratory rate?

Alveolar Gas Exchanges

The tubelike parts of the respiratory system move air in and out of the air passages. The alveoli are the sites of the vital process of gas exchange between the air and the blood.

Exercise and Breathing

Moderate to heavy exercise greatly increases the amount of oxygen skeletal muscles use. A young man at rest utilizes about 250 milliliters of oxygen per minute, but may require 3,600 milliliters per minute during maximal exercise. While oxygen utilization is increasing, carbon dioxide production increases also. Since decreased blood oxygen and increased blood carbon dioxide concentration stimulate the respiratory center, it is not surprising that exercise is accompanied by increased breathing rate. However, studies reveal that blood oxygen and carbon dioxide concentrations usually do not change during exercise — this reflects the respiratory system's effectiveness in obtaining oxygen and releasing carbon dioxide to the outside.

The cerebral cortex and the p. 456). The cortex transmits stimulat-

proprioceptors associated with mus- ing impulses to the respiratory center cles and joints are also implicated in whenever it signals the skeletal muscles the increased breathing rate associ- to contract. At the same time, muscular ated with exercise (see chapter 12, movements stimulate the propriocep tors, triggering a joint reflex. In this reflex, sensory impulses are transmitted from the proprioceptors to the respiratory center, and breathing accelerates.

The increase in breathing rate during exercise requires increased blood flow to skeletal muscles. Thus, exercise increases demand on both the respiratory and the circulatory systems. If either of these systems fails to keep pace with cellular demands, the person will begin to feel out of breath. This sensation, however, is usually due to the inability of the heart and circulatory system to move enough blood between the lungs and the cells, rather than to the inability of the respiratory system to provide enough air. ■

Alveoli

Alveoli (al-ve'o-li) are microscopic air sacs clustered at the distal ends of the finest respiratory tubes—the alveolar ducts. Each alveolus consists of a tiny space surrounded by a thin wall that separates it from adjacent alveoli. Tiny openings, called alveolar pores, in the walls of some alveoli may permit air to pass from one alveolus to another (fig. 19.32). This arrangement provides alternate air pathways if the passages in some portions of the lung become obstructed.

Phagocytic cells called alveolar macrophages are in alveoli and in the pores connecting the air sacs. These macrophages phagocytize airborne agents, including bacteria, thereby cleaning the alveoli.

Respiratory Membrane

The wall of an alveolus consists of an inner lining of simple squamous epithelium (type I cells, see fig. 19.16) and a dense network of capillaries, which are also lined with simple squamous epithelial cells (fig. 19.33). Thin basement membranes separate the layers of these flattened cells, and in the spaces between them are elastic and col-lagenous fibers that help support the alveolar wall. At least two thicknesses of epithelial cells and basement

Figure

Alveolar pores (arrow) allow air to pass from one alveolus to another (300x).

membranes separate the air in an alveolus and the blood in a capillary. These layers make up the respiratory membrane (alveolar-capillary membrane), through which gas exchange occurs between the alveolar air and the blood (figs. 19.34 and 19.35).

Cell of Surfactant- Fluid with alveolar wall secreting cell surfactant Macrophage

Cell of Surfactant- Fluid with alveolar wall secreting cell surfactant Macrophage

Surfactant Secreting Cell

Cell of capillary wall

Figure

The respiratory membrane consists of the walls of the alveolus and the capillary.

Cell of capillary wall

Figure

The respiratory membrane consists of the walls of the alveolus and the capillary.

Diffusion Through the Respiratory Membrane

Molecules diffuse from regions where they are in higher concentration toward regions where they are in lower concentration. Thus, in determining the direction of diffusion of a solute, we must know the concentration gradient. In the case of gases, it is more convenient to think in terms of a partial pressure gradient, such that a gas will diffuse from an area of higher partial pressure to an area of lower partial pressure.

1 Reconnect to chapter 3, Diffusion, page 82.

When a mixture of gases dissolves in blood, the resulting concentration of each dissolved gas is proportional to its partial pressure. Each gas diffuses between blood and its surroundings from areas of higher partial pressure to areas of lower partial pressure until the partial pressures in the two regions reach equilibrium. For example, the PCo2 of blood entering the pulmonary capillaries is 45 mm Hg, but the PCO2 in alveolar air is 40 mm Hg. Because of the difference in these partial pressures, carbon dioxide diffuses from blood, where its partial pressure is higher, across the respiratory membrane and into alveolar air. When blood leaves the lungs, its PCO2 is 40 mm Hg, which is the same as the PCO2 of alveolar air. Similarly, the PO2 of blood entering the pulmonary capillaries is 40 mm Hg, but that of alveolar air reaches 104 mm Hg as oxygen diffuses from alveolar air into blood. Thus, since equilibrium is reached, blood leaves the alveolar capillaries with a PO2 of 104 mm Hg.

Blood Vessels Figures

Figure

Electron micrograph of a capillary located between alveoli (7,000x). (AS, alveolar space; RBC, red blood cell; BM, basement membrane; IS, interstitial connective tissue; EP, epithelial nucleus.)

Figure

Electron micrograph of a capillary located between alveoli (7,000x). (AS, alveolar space; RBC, red blood cell; BM, basement membrane; IS, interstitial connective tissue; EP, epithelial nucleus.)

(Some venous blood draining the bronchi and bronchioles mixes with this blood before returning to the heart, so the PO2 of systemic arterial blood is 95 mm Hg.) Because of the large volume of air always in the lungs, as long as breathing continues, alveolar PO2 stays relatively constant at 104 mm Hg. Clinical Application 19.5 examines illnesses that result from impaired gas exchange.

The respiratory membrane is normally quite thin (about 1 micrometer thick), and gas exchange is rapid. However, a number of factors may affect diffusion across the respiratory membrane. More surface area, shorter distance, greater solubility of gases, and a steeper partial pressure gradient all favor increased diffusion. Thus, diseases that harm the respiratory membrane, such as pneumonia, or reduce the surface area for diffusion, such as emphysema, impair gas exchange. These conditions may require increased PO2 for treatment.

The respiratory membrane is normally so thin that certain soluble chemicals other than carbon dioxide may diffuse into alveolar air and be exhaled. This is why breath analysis can reveal alcohol in the blood, or acetone can be smelled on the breath of a person who has untreated diabetes mellitus. Breath analysis may also detect substances associated with kidney failure, certain digestive disturbances, and liver disease.

Alveolus

Diffusion of CO,

Diffusion of O,

Diffusion of CO,

Diffusion of O,

Alveolar

(from body tissues)

Blood flow (to body tissues)

Figure 19.35

Gas exchanges occur between the air of the alveolus and the blood of the capillary as a result of differences in partial pressures.

Describe the structure of the respiratory membrane. What is partial pressure?

What causes oxygen and carbon dioxide to move across the respiratory membrane?

Exposure to high oxygen concentration (hyperoxia) for a prolonged time may damage lung tissues, particularly capillary walls. Excess fluid may escape the capillaries and flood the alveolar air spaces, interfering with gas exchange, which can be lethal. Similarly, hyperoxia can damage the retinal capillaries of premature infants, causing retrolental fibroplasia (RLF), a condition that may lead to blindness.

Gas Transport

The blood transports oxygen and carbon dioxide between the lungs and the body cells. As these gases enter the blood, they dissolve in the liquid portion, the plasma, or combine chemically with other atoms or molecules.

Oxygen Transport

Almost all the oxygen (over 98%) is carried in the blood bound to the protein hemoglobin (he"mo-glo'bin) in red blood cells. The iron in hemoglobin provides the color of these blood cells. The remainder of the oxygen is dissolved in the blood plasma.

Hemoglobin consists of two types of components called heme and globin (see chapter 14, p. 549). Globin is a protein that contains 574 amino acids in four polypep-tide chains. Each chain is associated with a heme group, and each heme group contains an atom of iron. Each iron atom can loosely combine with an oxygen molecule. As oxygen dissolves in blood, it rapidly combines with hemoglobin, forming a new compound called oxyhemoglobin (ok"se-he'mo-glo'bin). Each hemoglobin molecule can combine with a maximum of four oxygen molecules.

The PO2 determines the amount of oxygen that combines with hemoglobin. The greater the PO2, the more oxygen will combine with hemoglobin, until the hemoglobin molecules are saturated with oxygen (fig. 19.36). At normal arterial PO2 (95 mm Hg) hemoglobin is essentially completely saturated.

Each year, about 100,000 mountain climbers and high-altitude exercisers experience varying degrees of altitude sickness. This is because at high altitudes, the proportion of oxygen in air remains the same (about 21%), but the PO2 decreases. Consequently, if a person breathes high-altitude air, oxygen diffuses more slowly from the alveoli into the blood, and the hemoglobin is less saturated with oxygen. The body's efforts to get more oxygen—increased breathing and heart rate and enhanced red blood cell and hemoglobin production — cannot keep pace with the plummeting oxygen supply.

Symptoms of oxygen deficiency (hypoxia) may ensue at high altitudes. For example, at 8,000 feet, a person may experience anxiety, restlessness, increased breathing rate, and rapid pulse. At 12,500 feet, where the PO2 is only 100 mm Hg rather than 160 mm Hg at sea level, symptoms include drowsiness, mental fatigue, headache, and nausea. Above 13,000 feet, the brain swells (cerebral edema), producing severe headache, vomiting, loss of coordination, and hallucinations. Finally, at about 23,000 feet, the person may lose consciousness and die.

Disorders that Impair Gas Exchange

Five-year-old Carly had what her parents at first thought was just a "bug" that was passing through the family. But after twelve hours of flulike symptoms, Carly's temperature shot up to 105° F, her chest began to hurt, and her breathing became rapid and shallow. Later that day, a chest radiograph confirmed what the doctor suspected — Carly had pneumonia. Apparently, the bacteria that had caused a mild upper respiratory infection in her parents and sisters had taken a detour in her body, infecting her lower respiratory structures instead.

Antibiotics successfully treated Carly's bacterial pneumonia. A viral infection, or, as is often the case in people with AIDS, Pneumocystis carinii infection, can also cause pneumonia. For all types of pneumonia, the events within the infected lung are similar: alveolar linings swell with edema and become abnormally permeable, allowing fluids and white blood cells to accumulate in the air sacs. As the alveoli fill, the surface area available for gas exchange diminishes. Breathing becomes difficult. Untreated, pneumonia can kill.

Tuberculosis is a different type of lung infection, caused by the bacterium Mycobacterium tuberculosis (fig. 19D). Fibrous connective tissue develops around the sites of infection, forming structures called tubercles. By walling off the bacteria, the tubercles help stop their spread. Sometimes this protective mechanism fails, and the bacteria flourish throughout the lungs and may even spread to other organs. In the later stages of infection, other types of bacteria may cause secondary infections. As lung tissue is destroyed, the surface area for gas exchange decreases. In addition, the widespread fibrous tissue thickens the respiratory membrane, further restricting gas exchange. A variety of drugs are used to treat tuberculosis, but in recent years, strains resistant to drugs have arisen, and these can be swiftly deadly.

Another type of condition that impairs gas exchange is atelectasis. This is the collapse of a lung, or some part of it, together with the collapse of the blood vessels that supply the affected region. Obstruction of a respiratory tube, such as by an inhaled foreign object or excess mucus secretion, may cause atelec-tasis. The air in the alveoli beyond the obstruction is absorbed, and as the air pressure in the alveoli decreases, their elastic walls collapse, and they can no longer function. Fortunately, after a portion of a lung collapses, the functional regions that remain are often able to carry on

The chemical bonds that form between oxygen and hemoglobin molecules are relatively unstable, and as the Po2 decreases, oxygen is released from oxyhemoglobin molecules (fig. 19.36). This happens in tissues, where cells have used oxygen in their respiratory processes. The free oxygen diffuses from the blood into nearby cells, as figure 19.37 shows.

Increasing blood concentration of carbon dioxide (Pco2), acidity, and temperature all increase the amount of oxygen that oxyhemoglobin releases (figs. 19.38, 19.39, and 19.40). These influences explain why more oxygen is released from the blood to the skeletal muscles during periods of exercise. The increased muscular activity

Figure 19.36

Hemoglobin is completely saturated at normal systemic arterial PO,, but readily releases oxygen at the PO, of the body tissues.

Cal Damage Human
0 10 20 30 40 50 60 70 80 90 100110120130140 Po2 (mm Hg) Oxyhemoglobin dissociation at 38°C

Shier-Butler-Lewis: Human Anatomy and Physiology, Ninth Edition

V. Absorption and Excretion

19. Respiratory System

© The McGraw-Hill Companies, 2001

enough gas exchange to sustain the body cells.

Adult respiratory distress syndrome (ARDS) is a special form of atelectasis in which alveoli collapse. It has a variety of causes, all of which damage lung tissues. These include pneumonia and other infections, near drowning, aspiration of stomach acid into the respiratory system, or physi-

cal trauma to the lungs from an injury or surgical procedure. Anesthetics can suppress surfactant production, causing postsurgical difficulty breathing for twenty-four to forty-eight hours, or until surfactant production returns to normal. This damage disrupts the respiratory membrane that separates the air in the alveoli from the blood in the pulmonary capillaries, allowing protein-rich fluid to escape from the capillaries and flood the alveoli. They collapse in response, and surfactant is nonfunctional. Blood vessels and airways narrow, greatly elevating blood pressure in the lungs. Delivery of oxygen to tissues is seriously impaired. ARDS is fatal about 60% of the time. ■

Alveolus Blood Flood

Figure 19D

Healthy lungs

Tuberculosis

Figure 19D

Healthy lungs

Tuberculosis

Healthy lungs appear dark and clear on a radiograph. Lungs with tuberculosis have cloudy areas where fibrous tissue grows to wall off infected areas.

Blood

Oxyhemoglobin molecule

Blood

Capillary

Hemoglobin molecules

Net diffusion of oxygen

Capillary

Hemoglobin molecules

Tissue cells Tissue

Oxyhemoglobin molecule

Tissue cells Tissue

Blood flow

(to lungs) Blood

Hemoglobin molecules

Blood flow -7/ N,et diffusion

Figure 19.37

(a) Oxygen molecules, entering the blood from the alveolus, bond to hemoglobin, forming oxyhemoglobin. (b) In the regions of the body cells, oxyhemoglobin releases oxygen. Note that much oxygen is still bound to hemoglobin at the PO2 of systemic venous blood (see fig. 19.36).

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