The respiratory system is composed of the upper and lower respiratory tracts. Together, the two tracts are responsible for ventilation (movement of air in and out of the airways). The upper tract, known as the upper airway, warms and ﬁlters inspired air so that the lower respiratory tract (the lungs) can accomplish gas exchange. Gas exchange involves delivering oxygen to the tissues through the bloodstream and expelling waste gases, such as carbon dioxide, during expiration.
ANATOMY OF THE UPPER RESPIRATORY TRACT
Upper airway structures consist of the nose, sinuses and nasal passages, pharynx, tonsils and adenoids, larynx, and trachea.
The nose is composed of an external and an internal portion. The external portion protrudes from the face and is supported by the nasal bones and cartilage. The anterior nares (nostrils) are the external openings of the nasal cavities.
The internal portion of the nose is a hollow cavity separated into the right and left nasal cavities by a narrow vertical divider, the septum. Each nasal cavity is divided into three passageways by the projection of the turbinates (also called conchae) from the lateral walls. The nasal cavities are lined with highly vascular ciliated mucous membranes called the nasal mucosa. Mucus, secreted continuously by goblet cells, covers the surface of the nasal mucosa and is moved back to the nasopharynx by the action of the cilia (ﬁne hairs).
The nose serves as a passageway for air to pass to and from the lungs. It ﬁlters impurities and humidiﬁes and warms the air as it is inhaled. It is responsible for olfaction (smell) because the olfactory receptors are located in the nasal mucosa. This function diminishes with age.
The paranasal sinuses include four pairs of bony cavities that are lined with nasal mucosa and ciliated pseudostratified columnar epithelium. These air spaces are connected by a series of ducts that drain into the nasal cavity. The sinuses are named by their location: frontal, ethmoidal, sphenoidal, and maxillary (Fig. 21-1). A prominent function of the sinuses is to serve as a resonating chamber in speech. The sinuses are a common site of infection.
Turbinate Bones (Conchae)
The turbinate bones are also called conchae (the name suggested by their shell-like appearance). Because of their curves, these bones increase the mucous membrane surface of the nasal passages and slightly obstruct the air ﬂowing through them (Fig. 21-2).
Air entering the nostrils is deﬂected upward to the roof of the nose, and it follows a circuitous route before it reaches the nasopharynx. It comes into contact with a large surface of moist, warm mucous membrane that catches practically all the dust and organisms in the inhaled air. The air is moistened, warmed to body temperature, and brought into contact with sensitive nerves. Some of these nerves detect odors; others provoke sneezing to expel irritating dust.
Pharynx, Tonsils, and Adenoids
The pharynx, or throat, is a tubelike structure that connects the nasal and oral cavities to the larynx. It is divided into three regions: nasal, oral, and laryngeal. The nasopharynx is located posterior to the nose and above the soft palate. The oropharynx houses the faucial, or palatine, tonsils. The laryngopharynx extends from the hyoid bone to the cricoid cartilage. The epiglottis forms the entrance of the larynx.
The adenoids, or pharyngeal tonsils, are located in the roof of the nasopharynx. The tonsils, the adenoids, and other lymphoid tissue encircle the throat. These structures are important links in the chain of lymph nodes guarding the body from invasion by organisms entering the nose and the throat. The pharynx functions as a passageway for the respiratory and digestive tracts.
The larynx, or voice organ, is a cartilaginous epithelium-lined structure that connects the pharynx and the trachea. The major function of the larynx is vocalization. It also protects the lower airway from foreign substances and facilitates coughing. It is frequently referred to as the voice box and consists of the following:
• Epiglottis—a valve ﬂap of cartilage that covers the opening to the larynx during swallowing
• Glottis—the opening between the vocal cords in the larynx
• Thyroid cartilage—the largest of the cartilage structures; part of it forms the Adam’s apple
• Cricoid cartilage—the only complete cartilaginous ring in the larynx (located below the thyroid cartilage)
• Arytenoid cartilages—used in vocal cord movement with the thyroid cartilage
• Vocal cords—ligaments controlled by muscular movements that produce sounds; located in the lumen of the larynx
The trachea, or windpipe, is composed of smooth muscle with C-shaped rings of cartilage at regular intervals. The cartilaginous rings are incomplete on the posterior surface and give ﬁrmness to the wall of the trachea, preventing it from collapsing. The trachea serves as the passage between the larynx and the bronchi.
ANATOMY OF THE LOWER RESPIRATORY TRACT: LUNGS
The lower respiratory tract consists of the lungs, which contain the bronchial and alveolar structures needed for gas exchange.
The lungs are paired elastic structures enclosed in the thoracic cage, which is an airtight chamber with distensible walls (Fig. 21-3). Ventilation requires movement of the walls of the thoracic cage and of its ﬂoor, the diaphragm. The effect of these movements is alternately to increase and decrease the capacity of the chest. When the capacity of the chest is increased, air enters through the trachea (inspiration) because of the lowered pressure within and inﬂates the lungs. When the chest wall and diaphragm return to their previous positions (expiration), the lungs recoil and force the air out through the bronchi and trachea. The inspiratory phase of respiration normally requires energy; the expiratory phase is normally passive. Inspiration occurs during the ﬁrst third of the respiratory cycle, expiration during the latter two thirds.
The lungs and wall of the thorax are lined with a serous membrane called the pleura. The visceral pleura covers the lungs; the parietal pleura lines the thorax. The visceral and parietal pleura and the small amount of pleural ﬂuid between these two membranes serve to lubricate the thorax and lungs and permit smooth motion of the lungs within the thoracic cavity with each breath.
The mediastinum is in the middle of the thorax, between the pleural sacs that contain the two lungs. It extends from the sternum to the vertebral column and contains all the thoracic tissue outside the lungs.
Each lung is divided into lobes. The left lung consists of an upper and lower lobe, whereas the right lung has an upper, middle, and lower lobe (Fig. 21-4). Each lobe is further subdivided into two to ﬁve segments separated by ﬁssures, which are extensions of the pleura.
BRONCHI AND BRONCHIOLES
There are several divisions of the bronchi within each lobe of the lung. First are the lobar bronchi (three in the right lung and two in the left lung). Lobar bronchi divide into segmental bronchi (10 on the right and 8 on the left), which are the structures identiﬁed when choosing the most effective postural drainage position for a given patient. Segmental bronchi then divide into subsegmental bronchi. These bronchi are surrounded by connective tissue that contains arteries, lymphatics, and nerves.
The subsegmental bronchi then branch into bronchioles, which have no cartilage in their walls. Their patency depends entirely on the elastic recoil of the surrounding smooth muscle and on the alveolar pressure. The bronchioles contain submucosal glands, which produce mucus that covers the inside lining of the airways. The bronchi and bronchioles are lined also with cells that have surfaces covered with cilia. These cilia create a constant whipping motion that propels mucus and foreign substances away from the lung toward the larynx.
The bronchioles then branch into terminal bronchioles, which do not have mucous glands or cilia. Terminal bronchioles then become respiratory bronchioles, which are considered to be the transitional passageways between the conducting airways and the gas exchange airways. Up to this point, the conducting airways contain about 150 mL of air in the tracheobronchial tree that does not participate in gas exchange. This is known as physiologic dead space. The respiratory bronchioles then lead into alveolar ducts and alveolar sacs and then alveoli. Oxygen and carbon dioxide exchange takes place in the alveoli.
The lung is made up of about 300 million alveoli, which are arranged in clusters of 15 to 20. These alveoli are so numerous that if their surfaces were united to form one sheet, it would cover 70 square meters—the size of a tennis court.
There are three types of alveolar cells. Type I alveolar cells are epithelial cells that form the alveolar walls. Type II alveolar cells are metabolically active. These cells secrete surfactant, a phospholipid that lines the inner surface and prevents alveolar collapse. Type III alveolar cell macrophages are large phagocytic cells that ingest foreign matter (eg, mucus, bacteria) and act as an important defense mechanism.
FUNCTION OF THE RESPIRATORY SYSTEM
The cells of the body derive the energy they need from the oxidation of carbohydrates, fats, and proteins. As with any type of combustion, this process requires oxygen. Certain vital tissues, such as those of the brain and the heart, cannot survive for long without a continuing supply of oxygen. However, as a result of oxidation in the body tissues, carbon dioxide is produced and must be removed from the cells to prevent the buildup of acid waste products. The respiratory system performs this function by facilitating life-sustaining processes such as oxygen transport, respiration and ventilation, and gas exchange.
Oxygen is supplied to, and carbon dioxide is removed from, cells by way of the circulating blood. Cells are in close contact with capillaries, whose thin walls permit easy passage or exchange of oxygen and carbon dioxide. Oxygen diffuses from the capillary through the capillary wall to the interstitial ﬂuid. At this point, it diffuses through the membrane of tissue cells, where it is used by mitochondria for cellular respiration. The movement of carbon dioxide occurs by diffusion in the opposite direction—from cell to blood.
After these tissue capillary exchanges, blood enters the systemic veins (where it is called venous blood) and travels to the pulmonary circulation. The oxygen concentration in blood within the capillaries of the lungs is lower than in the lungs’ air sacs (alveoli). Because of this concentration gradient, oxygen diffuses from the alveoli to the blood. Carbon dioxide, which has a higher concentration in the blood than in the alveoli, diffuses from the blood into the alveoli. Movement of air in and out of the airways (ventilation) continually replenishes the oxygen and removes the carbon dioxide from the airways in the lung. This whole process of gas exchange between the atmospheric air and the blood and between the blood and cells of the body is called respiration.
During inspiration, air ﬂows from the environment into the trachea, bronchi, bronchioles, and alveoli. During expiration, alveolar gas travels the same route in reverse.
Physical factors that govern air ﬂow in and out of the lungs are collectively referred to as the mechanics of ventilation and include air pressure variances, resistance to air ﬂow, and lung compliance.
AIR PRESSURE VARIANCES
Air ﬂows from a region of higher pressure to a region of lower pressure. During inspiration, movement of the diaphragm and other muscles of respiration enlarges the thoracic cavity and thereby lowers the pressure inside the thorax to a level below that of atmospheric pressure. As a result, air is drawn through the trachea and bronchi into the alveoli.
During normal expiration, the diaphragm relaxes and the lungs recoil, resulting in a decrease in the size of the thoracic cavity. The alveolar pressure then exceeds atmospheric pressure, and air ﬂows from the lungs into the atmosphere.
Resistance is determined chieﬂy by the radius or size of the airway through which the air is ﬂowing. Any process that changes the bronchial diameter or width affects airway resistance and alters the rate of air ﬂow for a given pressure gradient during respiration (Chart 21-1). With increased resistance, greater-than-normal respiratory effort is required by the patient to achieve normal levels of ventilation.
The pressure gradient between the thoracic cavity and the atmosphere causes air to ﬂow in and out of the lungs. When pressure changes are applied in the normal lung, there is a proportional change in the lung volume. A measure of the elasticity, expandability, and distensibility of the lungs and thoracic structures is called compliance. Factors that determine lung compliance are the surface tension of the alveoli (normally low with the presence of surfactant) and the connective tissue (ie, collagen and elastin) of the lungs.
Compliance is determined by examining the volume–pressure relationship in the lungs and the thorax. In normal compliance (1.0 L/cm H2O), the lungs and thorax easily stretch and distend when pressure is applied. High or increased compliance occurs when the lungs have lost their elasticity and the thorax is overdistended (ie, in emphysema). When the lungs and thorax are “stiff,” there is low or decreased compliance. Conditions associated with this include pneumothorax, hemothorax, pleural effusion, pulmonary edema, atelectasis, pulmonary fibrosis, and acute respiratory distress syndrome (ARDS), all of which are discussed in later chapters in this unit. Measurement of compliance is one method used to assess the progression and improvement in ARDS. Lungs with decreased compliance require greater-than-normal energy expenditure to achieve normal levels of ventilation. Compliance is usually measured under static conditions.
Lung Volumes and Capacities
Lung function, which reﬂects the mechanics of ventilation, is viewed in terms of lung volumes and lung capacities. Lung volumes are categorized as tidal volume, inspiratory reserve volume, expiratory reserve volume, and residual volume. Lung capacity is evaluated in terms of vital capacity, inspiratory capacity, functional residual capacity, and total lung capacity. These terms are described in Table 21-1.
Diffusion and Perfusion
Diffusion is the process by which oxygen and carbon dioxide are exchanged at the air–blood interface. The alveolar–capillary membrane is ideal for diffusion because of its large surface area and thin membrane. In the normal healthy adult, oxygen and carbon dioxide travel across the alveolar–capillary membrane without difﬁculty as a result of differences in gas concentrations in the alveoli and capillaries.
Pulmonary perfusion is the actual blood ﬂow through the pulmonary circulation. The blood is pumped into the lungs by the right ventricle through the pulmonary artery. The pulmonary artery divides into the right and left branches to supply both lungs. These two branches divide further to supply all parts of each lung. Normally about 2% of the blood pumped by the right ventricle does not perfuse the alveolar capillaries. This shunted blood drains into the left side of the heart without participating in alveolar gas exchange.
The pulmonary circulation is considered a low-pressure system because the systolic blood pressure in the pulmonary artery is 20 to 30 mm Hg and the diastolic pressure is 5 to 15 mm Hg. Because of these low pressures, the pulmonary vasculature normally can vary its capacity to accommodate the blood ﬂow it receives. When a person is in an upright position, however, the pulmonary artery pressure is not great enough to supply blood to the apex of the lung against the force of gravity. Thus, when a person is upright, the lung may be considered to be divided into three sections: an upper part with poor blood supply, a lower part with maximal blood supply, and a section in between the two with an intermediate supply of blood. When a person lying down turns to one side, more blood passes to the dependent lung.
Perfusion also is inﬂuenced by alveolar pressure. The pulmonary capillaries are sandwiched between adjacent alveoli. If the alveolar pressure is sufﬁciently high, the capillaries will be squeezed. Depending on the pressure, some capillaries completely collapse, whereas others narrow.
Pulmonary artery pressure, gravity, and alveolar pressure determine the patterns of perfusion. In lung disease these factors vary, and the perfusion of the lung may become very abnormal.
Ventilation and Perfusion Balance and Imbalance
Ventilation is the ﬂow of gas in and out of the lungs, and perfusion is the ﬁlling of the pulmonary capillaries with blood. Adequate gas exchange depends on an adequate ventilation–perfusion ratio. In different areas of the lung, the ratio varies.
Alterations in perfusion may occur with a change in the pulmonary artery pressure, alveolar pressure, and gravity. Airway blockages, local changes in compliance, and gravity may alter ventilation.
A ventilation–perfusion V /Q imbalance occurs from inadequate ventilation, inadequate perfusion, or both. There are four possible V /Q states in the lung: normal V /Q ratio, low V /Q ratio (shunt), high V/Q ratio (dead space), and absence of ventilation and perfusion (silent unit) (Chart 21-2).
Ventilation and perfusion imbalance causes shunting of blood, resulting in hypoxia (low cellular oxygen level). Shunting appears to be the main cause of hypoxia after thoracic or abdominal surgery and most types of respiratory failure. Severe hypoxia results when the amount of shunting exceeds 20%. Supplemental oxygen may eliminate hypoxia, depending on the type of V/Q imbalance.
The air we breathe is a gaseous mixture consisting mainly of nitrogen (78.62%) and oxygen (20.84%), with traces of carbon dioxide (0.04%), water vapor (0.05%), helium, and argon. The atmospheric pressure at sea level is about 760 mm Hg. Partial pressure is the pressure exerted by each type of gas in a mixture of gases. The partial pressure of a gas is proportional to the concentration of that gas in the mixture. The total pressure exerted by the gaseous mixture is equal to the sum of the partial pressures.
PARTIAL PRESSURE OF GASES
Based on these facts, the partial pressures of nitrogen and oxygen can be calculated. The partial pressure of nitrogen is 79% of 760 (0.79 × 760), or 600 mm Hg; that of oxygen is 21% of 760 (0.21 × 760), or 160 mm Hg. Chart 21-3 spells out terms and abbreviations related to partial pressure of gases.
Once the air enters the trachea, it becomes fully saturated with water vapor, which displaces some of the gases so that the air pressure within the lung remains equal to the air pressure outside (760 mm Hg). Water vapor exerts a pressure of 47 mm Hg when it fully saturates a mixture of gases at the body temperature of 37°C (98.6°F). Nitrogen and oxygen are responsible for the remaining 713 mm Hg (760 - 47) pressure. Once this mixture enters the alveoli, it is further diluted by carbon dioxide. In the alveoli, the water vapor continues to exert a pressure of 47 mm Hg. The remaining 713 mm Hg pressure is now exerted as follows: nitrogen, 569 mm Hg (74.9%); oxygen, 104 mm Hg (13.6%); and carbon dioxide, 40 mm Hg (5.3%).
PARTIAL PRESSURE IN GAS EXCHANGE
When a gas is exposed to a liquid, the gas dissolves in the liquid until an equilibrium is reached. The dissolved gas also exerts a partial pressure. At equilibrium, the partial pressure of the gas in the liquid is the same as the partial pressure of the gas in the gaseous mixture. Oxygenation of venous blood in the lung illustrates this point. In the lung, venous blood and alveolar oxygen are separated by a very thin alveolar membrane. Oxygen diffuses across this membrane to dissolve in the blood until the partial pressure of oxygen in the blood is the same as that in the alveoli (104 mm Hg). However, because carbon dioxide is a byproduct of oxidation in the cells, venous blood contains carbon dioxide at a higher partial pressure than that in the alveolar gas. In the lung, carbon dioxide diffuses out of venous blood into the alveolar gas. At equilibrium, the partial pressure of carbon dioxide in the blood and in alveolar gas is the same (40 mm Hg).
EFFECTS OF PRESSURE ON OXYGEN TRANSPORT
Oxygen and carbon dioxide are transported simultaneously dissolved in blood or combined with some of the elements of blood. Oxygen is carried in the blood in two forms: ﬁrst as physically dissolved oxygen in the plasma, and second in combination with the hemoglobin of the red blood cells. Each 100 mL of normal arterial blood carries 0.3 mL of oxygen physically dissolved in the plasma and 20 mL of oxygen in combination with hemoglobin. Large amounts of oxygen can be transported in the blood because it combines easily with hemoglobin to form oxyhemoglobin:
O2+ Hgb ↔ HgbO2
The volume of oxygen physically dissolved in the plasma varies directly with the partial pressure of oxygen in the arteries (PaO2). The higher the PaO2, the greater the amount of oxygen dissolved. For example, at a PaO2 of 10 mm Hg, 0.03 mL of oxygen is dissolved in 100 mL of plasma. At 20 mm Hg, twice this amount is dissolved in plasma, and at 100 mm Hg, 10 times this amount is dissolved. Therefore, the amount of dissolved oxygen is directly proportional to the partial pressure, regardless of how high the oxygen pressure rises.
The amount of oxygen that combines with hemoglobin also depends on PaO2, but only up to a PaO2 of about 150 mm Hg. When the PaO2 is 150 mm Hg, hemoglobin is 100% saturated and will not combine with any additional oxygen. When hemoglobin is 100% saturated, 1 g of hemoglobin will combine with 1.34 mL of oxygen. Therefore, in a person with 14 g/dL of hemoglobin, each 100 mL of blood will contain about 19 mL of oxygen associated with hemoglobin. If the PaO2 is less than 150 mm Hg, the percentage of hemoglobin saturated with oxygen is lower. For example, at a PaO2 of 100 mm Hg (normal value), saturation is 97%; at a PaO2 of 40 mm Hg, saturation is 70%.
OXYHEMOGLOBIN DISSOCIATION CURVE
The oxyhemoglobin dissociation curve (Chart 21-4) shows the relationship between the partial pressure of oxygen (PaO2) and the percentage of saturation of oxygen (SaO). The percentage of saturation can be affected by the following factors: carbon dioxide, hydrogen ion concentration, temperature, and 2,3-diphosphoglycerate. A rise in these factors shifts the curve to the right so that more oxygen is then released to the tissues at the same PaO2. A reduction in these factors causes the curve to shift to the left, making the bond between oxygen and hemoglobin stronger, so that less oxygen is given up to the tissues at the same PaO2. The unusual shape of the oxyhemoglobin dissociation curve is a distinct advantage to the patient for two reasons:
1. If the arterial PO2 decreases from 100 to 80 mm Hg as a result of lung disease or heart disease, the hemoglobin of the arterial blood remains almost maximally saturated (94%) and the tissues will not suffer from hypoxia.
2. When the arterial blood passes into tissue capillaries and is exposed to the tissue tension of oxygen (about 40 mm Hg), hemoglobin gives up large quantities of oxygen for use by the tissues.
The normal value of PaO2 is 80 to 100 mm Hg (95% to 98% saturation). With this level of oxygenation, there is a 15% margin of excess oxygen available to the tissues. With a normal hemoglobin level of 15 mg/dL and a PaO2 level of 40 mm Hg (oxygen saturation 75%), there is adequate oxygen available for the tissues but no reserve for physiologic stresses that increase tissue oxygen demand. When a serious incident occurs (eg, bronchospasm, aspiration, hypotension, or cardiac dysrhythmias) that reduces the intake of oxygen from the lungs, tissue hypoxia will result.
An important consideration in the transport of oxygen is cardiac output, which determines the amount of oxygen delivered to the body and which affects lung and tissue perfusion. If the cardiac output is normal (5 L/min), the amount of oxygen delivered to the body per minute is normal. If cardiac output falls, the amount of oxygen delivered to the tissues also falls. Under normal conditions, most of the oxygen delivered to the body is not used. In fact, only 250 mL of oxygen is used per minute. Under normal conditions, this is approximately 25% of available oxygen. The rest of the oxygen returns to the right side of the heart, and the PaO2 of venous blood drops from 80 to 100 mm Hg to about 40 mm Hg.
Carbon Dioxide Transport
At the same time that oxygen diffuses from the blood into the tissues, carbon dioxide diffuses in the opposite direction (ie, from tissue cells to blood) and is transported to the lungs for excretion. The amount of carbon dioxide in transit is one of the major determinants of the acid–base balance of the body. Normally, only 6% of the venous carbon dioxide is removed, and enough remains in the arterial blood to exert a pressure of 40 mm Hg. Most of the carbon dioxide (90%) enters the red blood cells; the small portion (5%) that remains dissolved in the plasma (PCO2) is the critical factor that determines carbon dioxide movement in or out of the blood.
In summary, the many processes involved in respiratory gas transport do not occur in intermittent stages; rather, they are rapid, simultaneous, and continuous.
Neurologic Control of Ventilation
Resting respiration is the result of cyclical excitation of the respiratory muscles by the phrenic nerve. The rhythm of breathing is controlled by respiratory centers in the brain. The inspiratory and expiratory centers in the medulla oblongata and pons control the rate and depth of ventilation to meet the body’s metabolic demands.
The apneustic center in the lower pons stimulates the inspiratory medullary center to promote deep, prolonged inspirations. The pneumotaxic center in the upper pons is thought to control the pattern of respirations.
Several groups of receptor sites assist in the brain’s control of respiratory function. The central chemoreceptors are located in the medulla and respond to chemical changes in the cerebrospinal ﬂuid, which result from chemical changes in the blood. These receptors respond to an increase or decrease in the pH and convey a message to the lungs to change the depth and then the rate of ventilation to correct the imbalance. The peripheral chemoreceptors are located in the aortic arch and the carotid arteries and respond ﬁrst to changes in PaO2, then to PaCO2 and pH. The Hering–Breuer reﬂex is activated by stretch receptors in the alveoli. When the lungs are distended, inspiration is inhibited; as a result, the lungs do not become overdistended. In addition, proprioceptors in the muscles and joints respond to body movements, such as exercise, causing an increase in ventilation. Thus, range-of-motion exercises in an immobile patient stimulate breathing. Baroreceptors, also located in the aortic and carotid bodies, respond to an increase or decrease in arterial blood pressure and cause reﬂex hypoventilation or hyperventilation.
A gradual decline in respiratory function begins in early to middle adulthood and affects the structure and function of the respiratory system. The vital capacity of the lungs and respiratory muscle strength peak between ages 20 and 25 and decrease thereafter. With aging (40 years and older), changes occur in the alveoli that reduce the surface area available for the exchange of oxygen and carbon dioxide. At approximately age 50, the alveoli begin to lose elasticity. A decrease in vital capacity occurs with loss of chest wall mobility, thus restricting the tidal ﬂow of air. The amount of respiratory dead space increases with age. These changes result in a decreased diffusion capacity for oxygen with age, producing lower oxygen levels in the arterial circulation. Elderly people have a decreased ability to move air rapidly in and out of the lungs. Gerontologic changes in the respiratory system are summarized in Table 21-2. Despite these changes, in the absence of chronic pulmonary disease, elderly people are able to carry out activities of daily living, but they may have decreased tolerance for and require additional rest after prolonged or vigorous activity.
REFERENCES AND SELECTED READINGS
Bickley, L. S. (2003). Bates’ guide to physical examination and history taking (8th ed.). Philadelphia: Lippincott Williams & Wilkins.
Blair, K. A. (1999). The aging pulmonary system. In M. Stanley & P. G. Bear (Eds.), Gerontological nursing (2d ed.). Philadelphia: F. A. Davis.
Levitzky, M. G. (1999). Pulmonary physiology (4th ed.). New York: McGraw Hill.
Sole, M. L., & Byers, J. F. (2001). Ventilatory assistance. In M. L. Sole, J. C. Hartshorn, & M. L. Lamborn (Eds.), Introduction to critical care nursing (3rd ed.). Philadelphia: W. B. Saunders.
West, J. B. (2000). Respiratory physiology: The essentials. Philadelphia: Lippincott Williams & Wilkins.
West, J. B. (2001). Pulmonary physiology and pathophysiology: An integrated, case-based approach. Philadelphia: Lippincott Williams & Wilkins.
Wilkins, R. L., Sheldon, R. L., & Knider, S. J. (2000). Clinical assessment in respiratory care (4th ed.). St. Louis: Mosby-Year Book.
Asterisks indicate nursing research articles. Boyle, A. H., & Waters, H. F. (2000). Issues in respiratory nursing:
Focus on prevention: recommendations of the National Lung Health Education Program. Heart & Lung, 29(6), 446–449.
Camhi, S. L., & Enright, P. L. (2000). How to assess pulmonary function in older persons. Journal of Respiratory Diseases, 21(6), 395–399.
Coleman, R. E. (1999). PET in lung cancer. Journal of Nuclear Medicine, 40(5), 814–820.
Graeber, G. M., Gupta, N. C., & Murray, G. F. (1999). Positron emission tomographic imaging with ﬂuorodeoxyglucose is efﬁcacious in evaluating malignant pulmonary disease. Journal of Thoracic and Cardiovascular Surgery, 117(4), 719–727.
Horne, C., & Derrico, D. (1999). Mastering ABGs. The art of arterial blood gas measurement. American Journal of Nursing, 99(8), 26–32.
Janssens, J. P., de Muralt, B., & Titelion, V. (2000). Management of dyspnea in severe chronic obstructive pulmonary disease. Journal of Pain and Symptom Management, 19(5), 378–392.
Johnson, B. D., Beck, K. C., Zeballos, R. J., & Weisman, I. M. (1999). Advances in pulmonary laboratory testing. Chest, 116(5), 1377–1387.
Kauczor, H. U., & Kreitner, K. E. (2000). Contrast-enhanced MRI of the lung. European Journal of Radiology, 34(3), 196–207.
Lowe, V. J., Fletcher, J. W., Gobar, L., Lawson, M., et al. (1998). Prospective investigation of positron emission tomography in lung nodules. Journal of Clinical Oncology, 16(3), 1075–1084.
Martin, B., Llewellyn, J., Faut-Callahan, M., & Meyer, P. (2000). The use of telemetric oximetry in the clinical setting. MedSurg Nursing, 9(2), 71–76.
*Nield, M. (2000). Dyspnea self-management in African Americans with chronic lung disease. Heart & Lung, 29(1), 50–55.
Salzman, S. (1999). Pulmonary function testing: Tips on how to interpret the results. Journal of Respiratory Diseases, 20(12), 809–812.
Shortall, S. P., & Perkins, L. A. (1999). Interpreting the ins and outs of pulmonary function tests. Nursing, 29(12), 41–47.
Shuster, D. P. (1998). The evaluation of lung function with PET. Seminars in Nuclear Medicine, 28(4), 341–351.
Wong, F. W. H. (1999). A new approach to ABG interpretation. American Journal of Nursing, 99(8), 34–36.
RESOURCES AND WEBSITES
American Lung Association, 1740 Broadway, New York, NY 10019; (212) 315-8700; 1-800-LUNG USA; http://www.lungusa.org .
American Association for Respiratory Care, 11030 Ables Lane, Dallas, TX 75229; (972) 243-2272; http://www.aarc.org .
National Heart, Lung, and Blood Institute/National Institutes of Health, Rockville Pike, Bldg. 31, Bethesda, MD 20892; (301) 4965166; http://www.nhlbi.nih.gov/nhlbi/index.htm .
National Lung Health Education Program: http://www.nlhep.org. Has easy-to-read teaching resources for patients