When air is inhaled into the respiratory system, it first enters the nasal passages, passing over the conchae or turbinates, where it is warmed and moistened by the highly vascular mucosa. Foreign material is filtered out by the mucous secretions and hairs before the air enters the delicate lung tissue. Opening off the nasal cavity through small canals are four pairs of paranasal sinuses, which are small cavities in the skull bones (Fig. 13-1). The presence of the hollow sinuses reduces the weight of the facial bones and adds resonance to the voice. They are named according to the bones in which they are located—the frontal, ethmoid, sphenoid, and maxillary sinuses.

The airflow continues through the nasopharynx and larynx into the trachea. On the posterior wall of the nasopharynx are located the pharyngeal tonsils or adenoids, which consist of lymphoid tissue, another defense against the inhalation of foreign material. If these tonsils become enlarged owing to infection, they can obstruct the flow of air through the nasopharynx, leading to mouth breathing. When air passes through the mouth directly into the respiratory tract, it is not warmed, moistened, and filtered properly before it reaches the delicate lung tissue. The tissues of the mouth become dry and irritated, and there is a risk of increased dental caries as normal salivary cleansing function is lost. The palatine tonsils, popularly called the tonsils, are lymphoid tissue located in the posterior portion of the oral cavity (see Fig. 17-2 in Chapter 17). Also opening off the nasopharynx are the two auditory (eustachian) tubes, which connect to the middle ear cavities. The continuation of the respiratory mucosa into the sinuses and middle ear creates a predisposition to the spread of infection from the upper respiratory tract. The upper respiratory tract has a resident flora, whereas the lungs are sterile, containing no microorganisms.

The pharynx, where the nasopharynx joins the oropharynx, serves as a common passage for air and food and descends to the point of separation of the esophagus and trachea. When infection is present, the inflammation and swelling in the area causes sore throat and painful swallowing. In the airway, the cartilaginous epiglottis protects the opening into the larynx, or voice box, by flipping up or down during swallowing or ventilation.

The larynx consists of various cartilages and their associated muscles. The largest is the thyroid cartilage, which forms the “Adam’s apple,” a structure that may protrude in the anterior neck area. There are two pairs of vocal cords, which are infoldings of the mucous membrane: the upper, or “false,” pair, and the lower pair, comprising the true vocal cords. The glottis refers to the true vocal cords and the space between them. When air is expired through the larynx, the true vocal cords vibrate, producing the sound of the voice. Other structures affect the characteristics of this sound, including the mouth, tongue, pharynx, and sinuses. The vocal cords, when approximated, prevent food from entering the trachea and lungs.

As inspired air is tracked downward through the larynx, it flows into the trachea, or windpipe. The wall of the trachea contains 16 to 20 hyaline cartilage rings, fibroelastic tissue, and smooth muscle tissue. The trachea is flexible enough to allow bending and elongation. The cartilage rings prevent the collapse of the trachea and keep the airway open even with the pressure changes. The posterior wall of the trachea is not rigid, thus allowing the esophagus to expand as swallowed food moves through it.

Air in the bronchioles then flows into the alveolar ducts and alveoli, or air sacs, which resemble a cluster of grapes. The alveoli are formed by a single layer of simple squamous epithelial tissue, which promotes the diffusion of gases into the blood, the end-point for inspired air (see Fig. 13-5). The respiratory membrane is the combined alveolar and capillary wall, a very thin membrane, through which gas exchange takes place. There are millions of alveoli, and the capillaries of the pulmonary circulation are in close contact, providing a very large surface area for the diffusion of gases. The alveoli contain macrophages (alveolar macrophages), whose function is to remove any foreign material that penetrates to this level. However some substances can escape any action by macrophages.

The inside surfaces of the alveoli are coated with a very small amount of fluid containing surfactant, produced by specialized cells in the alveolar wall. Surfactant has a detergent action that reduces surface tension of the alveolar fluid (the tendency for fluid to reduce its surface area by forming droplets), facilitating inspiration and preventing total collapse of the alveoli during expiration. When inspiration is complete, the process of expiration reverses airflow in the passageways, forcing air out of the alveoli and up the bronchi, trachea, and nose.

The lungs are cone-shaped structures positioned on either side of the heart. The mediastinum is the region in the center of the chest, which contains the heart, the major blood vessels, the esophagus, and the trachea. The dome-shaped muscular diaphragm forms the inferior boundary. The right lung is divided into three lobes and the left lung into two lobes because of the position of the heart, and each lobe is then divided into segments. The lung tissue (lungs, bronchi, and pleurae) is nourished by the bronchial arteries, which branch from the thoracic aorta.

Each lung is covered by its own double-walled sac, the pleural membrane. The visceral pleura is attached to the outer surface of the lung and then doubles back to form the parietal pleura, which lines the inside of the thoracic cavity, adhering to the chest wall and the diaphragm. The visceral pleura lies closely against the parietal pleura, separated only by very small amounts of fluid in the pleural cavity or space, which is considered only a potential space. The slightly negative pressure (less than atmospheric pressure) in the pleural cavity also assists in holding the pleura in close approximation and promoting lung expansion. The pleural fluid provides lubrication during respiratory movements and a force that provides cohesion, or “sticking together” (high surface tension), between the two pleural layers during inspiration.

The thorax, consisting of ribs, vertebrae, and sternum (breastbone) provides a rigid protective wall for the lungs. The upper seven pairs of ribs (true ribs) articulate with the vertebrae and are attached to the sternum by costal (hyaline) cartilage. The next three pairs of ribs are “false” ribs, which are connected to the costal cartilage of the seventh rib, not directly to the sternum. The last two ribs (also false), the eleventh and twelfth pairs, are attached only to vertebrae and are therefore called floating ribs. Between the ribs are located the external and internal intercostal muscles, which move the thoracic structures during ventilation.

A sequence of events is responsible for the change in size of the thorax and the changes in airflow with inspiration and expiration:

Changes in ventilation occur during pregnancy (see Chapter 22) and with aging (see Chapter 24).

Pulmonary volumes are a measure of ventilatory capacity in that they measure the air moving in and out of the lungs with normal or forced inspiration and expiration (Fig. 13-3). Pulmonary volumes can change with disease processes and are helpful in monitoring a patient’s progress or response to treatment. For example, impaired expiration can cause an increase in residual volume and therefore increased carbon dioxide levels in body fluids. Some of the basic volumes are summarized in Table 13-1.

Chemical factors are most important in respiratory control. Chemoreceptors sense changes in the levels of carbon dioxide, hydrogen ions, and oxygen in blood or cerebrospinal fluid (Fig. 13-4).

When carbon dioxide levels in the blood increase (hypercapnia), the gas easily diffuses into the cerebrospinal fluid, lowering pH and stimulating the respiratory center, resulting in an increased rate and depth of respirations (hyperventilation). Hypercapnia causes respiratory acidosis, and acidosis depresses the nervous system. Hypocapnia, or low PCO₂, may be caused by hyperventilation after excessive amounts of carbon dioxide have been expired. Hypocapnia causes respiratory alkalosis. To review the conditions of respiratory acidosis and alkalosis and the role of arterial blood gases, refer to Chapter 2.

Other major factors in gas exchange are the total surface area available for diffusion and the thickness of the alveolar membranes. The alveoli are the only structures that provide such a surface area, and both ventilation and perfusion must be adequate for diffusion to occur (see Fig. 13-20). If part of the alveolar wall is destroyed, as in emphysema, or fibrosis occurs in the lungs, the surface area is greatly reduced. If airflow into the alveoli is obstructed or the capillaries are damaged, the involved surface area becomes nonfunctional.

This imbalance is measured by the ventilation-perfusion ratio (). An autoregulatory mechanism in the lungs can adjust ventilation and blood flow in an attempt to produce a good match. For example, if PO₂ is low because of poor ventilation in an area, vasoconstriction occurs in the pulmonary arterioles, shunting the blood to other areas of the lungs where ventilation may be better. If airflow is good, the pulmonary arterioles dilate to maximize gas exchange.

Only about 1% of total oxygen is dissolved in plasma because oxygen is relatively insoluble in water. This factor also limits the ease with which oxygen can diffuse. The dissolved form of the gas is that which diffuses from the alveolar air into the blood in the pulmonary capillaries and also diffuses into the interstitial fluid and the cells during the process of internal respiration. Most oxygen is transported reversibly bound to hemoglobin by the iron molecules and is called oxyhemoglobin (see Fig. 10-16A for a diagram of hemoglobin and attachments). When all four heme molecules in hemoglobin have taken up oxygen, the hemoglobin is termed fully saturated (measurement expressed as SaO₂).

As oxygen diffuses out of the blood into the interstitial fluid and the cells, hemoglobin releases oxygen to replace it, so dissolved oxygen is always available in the plasma, ready to diffuse into the cells. The rate at which hemoglobin binds or releases oxygen depends on factors such as PO₂ (the partial pressure of dissolved oxygen), PCO₂ temperature, and plasma pH (Fig. 13-6). Normally approximately 25% of the bound oxygen is released to the cells for metabolism during an erythrocyte’s trip through the systemic circulation, leaving 75% of the hemoglobin in the venous blood still saturated with oxygen. This provides a good safety margin of oxygen that is available to meet increased cell demands.

Carbon dioxide, a waste product from cell metabolism, is transported in several forms. Approximately 7% is dissolved in the plasma and can easily diffuse across membranes. Roughly 20% is loosely and reversibly bound to hemoglobin, attached to an amino group on the globin portion (not the heme). This is termed carbaminoglobin. The majority of carbon dioxide resulting from cell metabolism diffuses into the red blood cells (RBCs), where, under the influence of the enzyme carbonic anhydrase, it transitions very briefly as carbonic acid, then is immediately converted into bicarbonate ions (see the following equation). These bicarbonate ions can then diffuse back into the plasma to function in the buffer pair (see Chapter 2).

    CO2+H2O←→H2CO3←→   H+    +  HCO3−carbon dioxide  +  water   ←  →carbonic acid   ←  →hydrogen ions+bicarbonate ions                  (in presence of enzyme, carbonic anhydrase)

A ratio of 20 parts bicarbonate ion to 1 part carbonic acid maintains blood pH at 7.35. Thus, carbon dioxide plays a major role in control of blood pH through this buffer system.

Treatment is symptomatic, consisting of acetaminophen for fever and headache and decongestants (vasoconstrictors) to reduce the edema and congestion in the respiratory passages. A cold is a self-limiting infection. Antihistamines reduce secretions but may cause excessive drying of tissues and cough. Humidifiers aid in keeping the secretions liquid and easily drained. The role of vitamin C in prevention and therapy remains controversial. Antibiotics do not cure viral infections and are usually reserved for secondary bacterial infections such as sinusitis, otitis media (see Chapter 15), or tracheitis, or for prophylactic use in high-risk patients (such as those with chronic illnesses). Proper handwashing and disposal of tissues as well as avoidance of crowded areas reduce the risk of transmission to others.

Secondary bacterial infections, for example, pharyngitis or “strep throat,” are usually caused by streptococcus invading inflamed and necrotic mucous membranes (Fig. 13-8). A purulent exudate forms and systemic signs such as fever develop. These bacteria should be identified by culture and treated quickly with antimicrobial drugs to reduce the risk of rheumatic fever or acute glomerulonephritis arising from group A beta-hemolytic Streptococcus pneumoniae.

Sinusitis is usually a bacterial infection secondary to a cold or an allergy that has obstructed the drainage of one or more of the paranasal sinuses into the nasal cavity (see Fig. 13-1). Common causative organisms include pneumococci, streptococci, or Haemophilus influenzae. As the exudate accumulates, pressure builds up inside the sinus cavity, causing severe pain in the facial bone. The pain may be confused with headache (ethmoid sinus) or toothache (maxillary sinus). Other signs, such as nasal congestion, fever, or sore throat, may already be present. Diagnosis may be confirmed by radiograph or transillumination. Decongestants and analgesics are recommended until the sinuses are draining well, and a course of antibiotics is often required to eradicate the infection totally.

Laryngotracheobronchitis is a common viral infection, particularly in children between 1 and 2 years of age, although adults may also contract laryngitis, tracheitis, or bronchitis. Common causative organisms are parainfluenza viruses and adenoviruses (Table 13-3). The infection begins as an upper respiratory condition with nasal congestion and cough. In the young child, the larynx and subglottic area become inflamed with swelling and exudate, leading to obstruction and a characteristic barking cough (croup), hoarse voice, and inspiratory stridor. The condition often becomes more severe at night. Cool, moisturized air from a humidifier or shower or croup tent often relieves the obstruction. The infection is usually self-limited, and full recovery occurs in several days. In some children with allergic tendencies, smooth muscle spasm may exacerbate the obstruction, requiring additional medical treatment.

Influenza is a viral infection that may affect both the upper and the lower respiratory tracts. As indicated in the discussion of this topic at the end of Chapter 6 (influenza is presented as an example of infection), there are three groups of the influenza virus—type A, the most prevalent pathogen, and types B and C. These viruses mutate constantly, preventing effective immune defense for prolonged time periods.

Flu differs from a common cold in that it usually has a sudden, acute onset with fever, marked fatigue, and aching pains in the body. It may also cause a viral pneumonia. Similarly to the common cold, a mild case of influenza can be complicated by secondary problems such as bacterial pneumonia. Most deaths during flu epidemics result from pneumonia.

Treatment is symptomatic and supportive unless bacterial infection occurs. Antiviral drugs, such as amantadine (Symmetrel, Endantadine), zanamivir (Relenza inhaler), or oseltamivir (Tamiflu) taken by adults in the first 2 days, may reduce the symptoms and duration as well as reduce the risk of infecting others. These drugs are useful in the control of flu outbreaks in hospitals or nursing homes. The incubation period for the virus is 1 to 4 days, with an average of 2, but the individual can pass the virus on a day before symptoms develop and for up to 5 days after.

Prevention of influenza by vaccination is highly recommended for all individuals. If flu does develop following immunization, it is a mild infection. A period of 2 to 3 weeks after vaccination is required before immunity develops.

An upper respiratory infection caused by group A β-hemolytic streptococcus (Streptococcus pyogenes). Incubation period is generally 1 to 2 days. Symptoms usually begin with a fever and sore throat; chills, vomiting, abdominal pain, and malaise may occur as well. The typical “strawberry” tongue (Fig. 13-9) is caused by the exotoxin produced by the bacteria. A fine rash on the chest, neck, groin, and thighs are characteristic also. Once a serious childhood disease, upper respiratory infection is now generally treatable with antibiotics.

Bronchiolitis is a common infection in young children 2 to 12 months of age and is caused by the respiratory syncytial virus (RSV), a myxovirus. It is transmitted directly by oral droplet and occurs more frequently in the winter months. Predisposing factors include a familial history of asthma and the presence of cigarette smoke. Bronchiolitis varies in severity. The virus causes necrosis and inflammation in the small bronchi and bronchioles, with edema, increased secretions, and reflex bronchospasm leading to obstruction of the small airways. Signs include wheezing and dyspnea; rapid, shallow respirations; cough; rales; chest retractions; fever; and malaise. There may be areas of hyperinflation with air trapping due to partial obstruction (see Fig. 13-19C) or areas of atelectasis or nonaeration resulting from total obstruction (see Fig. 13-24). Treatment is supportive and symptomatic, with monitoring of blood gases in severe cases to ensure that oxygen levels are adequate. Respiratory syncytial virus-immunoglobulin serum or palivizumab, an RSV monoclonal antibody, may be administered to reduce the severity of infection, particularly in premature infants.