Figure 37-8 shows the respiratory system, demonstrating especially the respiratory passageways. The air is distributed to the lungs by way of the trachea, bronchi, and bronchioles.
One of the most important problems in all the respiratory passageways is to keep them open and allow easy passage of air to and from the alveoli. To keep the trachea from collapsing, multiple cartilage rings extend about five sixths of the way around the trachea. In the walls of the bronchi, less extensive curved cartilage plates also maintain a reasonable amount of rigidity yet allow sufficient motion for the lungs to expand and
contract. These plates become progressively less extensive in the later generations of bronchi and are gone in the bronchioles, which usually have diameters less than 1.5 millimeters. The bronchioles are not prevented from collapsing by the rigidity of their walls. Instead, they are kept expanded mainly by the same transpulmonary pressures that expand the alveoli. That is, as the alveoli enlarge, the bronchioles also enlarge, but not as much.
Muscular Wall of the Bronchi and Bronchioles and Its Control. In all areas of the trachea and bronchi not occupied by cartilage plates, the walls are composed mainly of smooth muscle. Also, the walls of the bronchioles are almost entirely smooth muscle, with the exception of the most terminal bronchiole, called the respiratory bronchiole, which is mainly pulmonary epithelium and underlying fibrous tissue plus a few smooth muscle fibers. Many obstructive diseases of the lung result from narrowing of the smaller bronchi and larger bronchioles, often because of excessive contraction of the smooth muscle itself.
Resistance to Airflow in the Bronchial Tree. Under normal respiratory conditions, air flows through the respiratory passageways so easily that less than 1 centimeter of water pressure gradient from the alveoli to the atmosphere is sufficient to cause enough airflow for quiet breathing. The greatest amount of resistance to airflow occurs not in the minute air passages of the terminal bronchioles but in some of the larger bronchioles and bronchi near the trachea. The reason for this high resistance is that there are relatively few of these larger bronchi in comparison with the approximately 65,000 parallel terminal bronchioles, through each of which only a minute amount of air must pass.
Yet in disease conditions, the smaller bronchioles often play a far greater role in determining airflow resistance because of their small size and because they are easily occluded by (1) muscle contraction in their walls, (2) edema occurring in the walls, or (3) mucus collecting in the lumens of the bronchioles.
Nervous and Local Control of the Bronchiolar Musculature— "Sympathetic" Dilation of the Bronchioles. Direct control of the bronchioles by sympathetic nerve fibers is relatively weak because few of these fibers penetrate to the central portions of the lung. However, the bronchial tree is very much exposed to norepinephrine and epineph-rine released into the blood by sympathetic stimulation of the adrenal gland medullae. Both these hormones— especially epinephrine, because of its greater stimulation of beta-adrenergic receptors—cause dilation of the bronchial tree.
Parasympathetic Constriction of the Bronchioles. A few parasympathetic nerve fibers derived from the vagus nerves penetrate the lung parenchyma. These nerves secrete acetylcholine and, when activated, cause mild to moderate constriction of the bronchioles. When a disease process such as asthma has already caused some bronchiolar constriction, superimposed parasympa-thetic nervous stimulation often worsens the condition. When this occurs, administration of drugs that block the effects of acetylcholine, such as atropine, can sometimes relax the respiratory passages enough to relieve the obstruction.
Sometimes the parasympathetic nerves are also activated by reflexes that originate in the lungs. Most of these begin with irritation of the epithelial membrane of the respiratory passageways themselves, initiated by noxious gases, dust, cigarette smoke, or bronchial infection. Also, a bronchiolar constrictor reflex often occurs when microemboli occlude small pulmonary arteries.
Local Secretory Factors Often Cause Bronchiolar Constriction.
Several substances formed in the lungs themselves are often quite active in causing bronchiolar constriction. Two of the most important of these are histamine and slow reactive substance of anaphylaxis. Both of these are released in the lung tissues by mast cells during allergic reactions, especially those caused by pollen in the air. Therefore, they play key roles in causing the airway obstruction that occurs in allergic asthma; this is especially true of the slow reactive substance of anaphylaxis.
The same irritants that cause parasympathetic constrictor reflexes of the airways—smoke, dust, sulfur dioxide, and some of the acidic elements in smog—often act directly on the lung tissues to initiate local, non-nervous reactions that cause obstructive constriction of the airways.
Mucus Lining the Respiratory Passageways, and Action of Cilia to Clear the Passageways
All the respiratory passages, from the nose to the terminal bronchioles, are kept moist by a layer of mucus that coats the entire surface. The mucus is secreted partly by individual mucous goblet cells in the epithelial lining of the passages and partly by small submu-cosal glands. In addition to keeping the surfaces moist, the mucus traps small particles out of the inspired air and keeps most of these from ever reaching the alveoli. The mucus itself is removed from the passages in the following manner.
The entire surface of the respiratory passages, both in the nose and in the lower passages down as far as the terminal bronchioles, is lined with ciliated epithelium, with about 200 cilia on each epithelial cell. These cilia beat continually at a rate of 10 to 20 times per second by the mechanism explained in Chapter 2, and the direction of their "power stroke" is always toward the pharynx. That is, the cilia in the lungs beat upward, whereas those in the nose beat downward. This continual beating causes the coat of mucus to flow slowly, at a velocity of a few millimeters per minute, toward the pharynx. Then the mucus and its entrapped particles are either swallowed or coughed to the exterior.
The bronchi and trachea are so sensitive to light touch that very slight amounts of foreign matter or other causes of irritation initiate the cough reflex. The larynx and carina (the point where the trachea divides into the bronchi) are especially sensitive, and the terminal bronchioles and even the alveoli are sensitive to corrosive chemical stimuli such as sulfur dioxide gas or chlorine gas. Afferent nerve impulses pass from the respiratory passages mainly through the vagus nerves to the medulla of the brain. There, an automatic sequence of events is triggered by the neuronal circuits of the medulla, causing the following effect.
First, up to 2.5 liters of air are rapidly inspired. Second, the epiglottis closes, and the vocal cords shut tightly to entrap the air within the lungs. Third, the abdominal muscles contract forcefully, pushing against the diaphragm while other expiratory muscles, such as the internal intercostals, also contract forcefully. Consequently, the pressure in the lungs rises rapidly to as much as 100 mm Hg or more. Fourth, the vocal cords and the epiglottis suddenly open widely, so that air under this high pressure in the lungs explodes outward. Indeed, sometimes this air is expelled at velocities ranging from 75 to 100 miles per hour. Importantly, the strong compression of the lungs collapses the bronchi and trachea by causing their noncartilaginous parts to invaginate inward, so that the exploding air actually passes through bronchial and tracheal slits. The rapidly moving air usually carries with it any foreign matter that is present in the bronchi or trachea.
The sneeze reflex is very much like the cough reflex, except that it applies to the nasal passageways instead of the lower respiratory passages. The initiating stimulus of the sneeze reflex is irritation in the nasal passageways; the afferent impulses pass in the fifth cranial nerve to the medulla, where the reflex is triggered. A series of reactions similar to those for the cough reflex takes place; however, the uvula is depressed, so that large amounts of air pass rapidly through the nose, thus helping to clear the nasal passages of foreign matter.
As air passes through the nose, three distinct normal respiratory functions are performed by the nasal cavities: (1) the air is warmed by the extensive surfaces of the conchae and septum, a total area of about 160 square centimeters (see Figure 37-8); (2) the air is almost completely humidified even before it passes beyond the nose; and (3) the air is partially filtered. These functions together are called the air conditioning function of the upper respiratory passageways. Ordinarily, the temperature of the inspired air rises to within 1°F of body temperature and to within 2 to 3 per cent of full saturation with water vapor before it reaches the trachea. When a person breathes air through a tube directly into the trachea (as through a tracheostomy), the cooling and especially the drying effect in the lower lung can lead to serious lung crusting and infection.
Filtration Function of the Nose. The hairs at the entrance to the nostrils are important for filtering out large particles. Much more important, though, is the removal of particles by turbulent precipitation. That is, the air passing through the nasal passageways hits many obstructing vanes: the conchae (also called turbinates, because they cause turbulence of the air), the septum, and the pharyngeal wall. Each time air hits one of these obstructions, it must change its direction of movement. The particles suspended in the air, having far more mass and momentum than air, cannot change their direction of travel as rapidly as the air can. Therefore, they continue forward, striking the surfaces of the obstructions, and are entrapped in the mucous coating and transported by the cilia to the pharynx to be swallowed.
Size of Particles Entrapped in the Respiratory Passages.
The nasal turbulence mechanism for removing particles from air is so effective that almost no particles larger than 6 micrometers in diameter enter the lungs through the nose. This size is smaller than the size of red blood cells.
Of the remaining particles, many that are between 1 and 5 micrometers settle in the smaller bronchioles as a result of gravitational precipitation. For instance, terminal bronchiolar disease is common in coal miners because of settled dust particles. Some of the still smaller particles (smaller than 1 micrometer in diameter) diffuse against the walls of the alveoli and adhere to the alveolar fluid. But many particles smaller than 0.5
A, Anatomy of the larynx.
B, Laryngeal function in phonation, showing the positions of the vocal cords during different types of phonation. (Modified from Greene MC: The Voice and Its Disorders, 4th ed. Philadelphia: JB Lippincott, 1980.)
Arytenoid cartilage ^^
Arytenoid cartilage ^^
^ Lateral cricoarytenoid muscle
Transverse arytenoid muscle
Transverse arytenoid muscle
^ Lateral cricoarytenoid muscle
Posterior cricoarytenoid muscle
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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.