After moving through the Vd, air reaches the respiratory bronchioles and alveoli (Fig. 26-4). Alveoli are small sacs that are the primary site of gas exchange in the lungs. The alveoli are interconnected by pores of Kohn, which allow movement of air from alveolus to alveolus (see Fig. 26-1). Deep breathing promotes air movement through these pores and assists in moving mucus out of the respiratory bronchioles. Bacteria can also move through these pores, spreading infection to previously uninfected areas. The adult lung has 300 million alveoli. Alveoli have a total volume of about 2500 mL and a surface area for gas exchange that is about the size of a tennis court.

FIG. 26-4 Scanning electron micrograph of lung parenchyma. A, Alveoli *(A)* and alveolar-capillary membrane *(arrow).* B, Effects of atelectasis. Alveoli *(A)* are partially or totally collapsed.

Gases are exchanged at the alveolar-capillary membrane where the alveoli come in contact with pulmonary capillaries (Fig. 26-5). In conditions such as pulmonary edema, excess fluid fills the interstitial space and alveoli, markedly reducing gas exchange.

FIG. 26-5 Partial pressure of respiratory gases in normal respiration. The pressures are shown in inhaled and exhaled air from the lungs and at the level of the alveoli and pulmonary venous and arterial blood vessels.

Surfactant.

The lungs are a collection of 300 million alveoli, each 0.3 mm in diameter. Because alveoli are unstable, they have a natural tendency to collapse. Alveolar cells secrete surfactant. Surfactant is a lipoprotein that lowers the surface tension in the alveoli. It reduces the amount of pressure needed to inflate the alveoli and makes them less likely to collapse. Normally, each person takes a slightly larger breath, termed a sigh, after every five or six breaths. This sigh stretches the alveoli and promotes surfactant secretion.

When not enough surfactant is present, the alveoli collapse. The term atelectasis refers to collapsed, airless alveoli (see Fig. 26-4, B). The postoperative patient is at risk for atelectasis because of the effects of anesthesia and restricted breathing with pain (see Chapter 20). In acute respiratory distress syndrome (ARDS), lack of surfactant contributes to widespread atelectasis (see Chapter 68).

Blood Supply.

The lungs have two different types of circulation: pulmonary and bronchial. The pulmonary circulation provides the lungs with blood that participates in gas exchange. The pulmonary artery receives deoxygenated blood from the right ventricle of the heart and delivers it to pulmonary capillaries that are directly connected with alveoli. Oxygen–carbon dioxide exchange occurs at this point. The pulmonary veins return oxygenated blood to the left atrium, which then delivers it to the left ventricle. This oxygenated blood is pumped by the left ventricle into the aorta, which supplies the arteries of the systemic circulation. Venous blood is collected from capillary networks of the body and returned to the right atrium by way of the venae cavae.

The bronchial circulation starts with the bronchial arteries, which arise from the thoracic aorta. The bronchial circulation provides oxygen to the bronchi and other pulmonary tissues. Deoxygenated blood returns from the bronchial circulation through the azygos vein into the superior vena cava.

Chest Wall

The chest wall is shaped, supported, and protected by 24 ribs (12 on each side). The ribs and the sternum protect the lungs and the heart from injury and are called the thoracic cage.

The chest cavity is lined with a membrane called the parietal pleura, and the lungs are lined with a membrane called the visceral pleura. The parietal and visceral pleurae join to form a closed, double-walled sac. The visceral pleura does not have any sensory pain fibers or nerve endings, whereas the parietal pleura does have sensory pain fibers. Therefore irritation of the parietal pleura causes pain with each breath.

The space between the pleural layers is called the intrapleural space. Normally this space contains 20 to 25 mL of fluid. This fluid serves two purposes: (1) it provides lubrication, allowing the pleural layers to slide over each other during breathing; and (2) it increases cohesion between the pleural layers, thereby facilitating expansion of the pleurae and lungs during inspiration.

Fluid drains from the pleural space by the lymphatic circulation. Several pathologic conditions may cause the accumulation of greater amounts of fluid, termed a pleural effusion. Pleural fluid may accumulate because of blockage of lymphatic drainage (e.g., from malignant cells) or because of an imbalance between intravascular and oncotic fluid pressures, as in heart failure. Purulent pleural fluid with bacterial infection is called empyema.

The diaphragm is the major muscle of respiration. During inspiration the diaphragm contracts, increasing intrathoracic volume and pushing the abdominal contents downward. At the same time the external intercostal muscles and scalene muscles contract, increasing the lateral and anteroposterior (AP) dimension of the chest. This causes the size of the thoracic cavity to increase and intrathoracic pressure to decrease, so air enters the lungs.

The diaphragm is made up of two hemidiaphragms, each innervated by the right and left phrenic nerves. The phrenic nerves arise from the spinal cord between C3 and C5, the third and fifth cervical vertebrae. Injury to the phrenic nerve results in hemidiaphragm paralysis on the side of the injury. Complete spinal cord injuries above the level of C3 result in total diaphragm paralysis and dependence on a mechanical ventilator.

Physiology of Respiration

TABLE 26-1

NORMAL ARTERIAL AND VENOUS BLOOD GAS VALUES *

Arterial Blood Gases			Venous Blood Gases
Laboratory Value	Sea Level BP 760 mm Hg	1 Mile Above Sea Level BP 629 mm Hg	Mixed Venous Blood Gases
pH	7.35-7.45	7.35-7.45	pH	7.32-7.43
PaO₂†	80-100 mm Hg	65-75 mm Hg	PvO₂	38-42 mm Hg
SaO₂†	>95%‡	>95%‡	SvO₂	60%-80%‡
PaCO₂	35-45 mm Hg	35-45 mm Hg	PvCO₂	38-55 mm Hg
HCO₃⁻	22-26 mEq/L (mmol/L)	22-26 mEq/L (mmol/L)	HCO₃⁻	22-26 mEq/L (mmol/L)

BP, Barometric pressure; HCO₃⁻, bicarbonate; PaCO₂, partial pressure of arterial CO₂; PvCO₂, partial pressure of CO₂ in venous blood; PaO₂, partial pressure of O₂ in arterial blood; PvO₂, partial pressure of O₂ in venous blood; SaO₂, arterial O₂ saturation; SvO₂, venous O₂ saturation.

^*Assumes patient is ≤60 yr of age and breathing room air.

^†Values decrease with age.

^‡The same normal values apply when SpO₂ and SvO₂ are obtained by oximetry.

Blood for ABG analysis can be obtained by arterial puncture or from an arterial catheter, usually in the radial or femoral artery. Both techniques allow only intermittent analysis. Continuous intraarterial blood gas monitoring is also possible via a fiberoptic sensor or an oxygen electrode inserted into an arterial catheter. An arterial catheter permits ABG sampling without repeated arterial punctures.

The normal PaO₂ decreases with advancing age. It also varies in relation to the distance above sea level. At higher altitudes the barometric pressure is lower, resulting in a lower inspired oxygen pressure and a lower PaO₂ (see Table 26-1).

Mixed Venous Blood Gases.

For the patient with a normal or near-normal cardiac status, an assessment of PaO₂ or SaO₂ is usually sufficient to determine the level of oxygenation. The patient with impaired cardiac output or hemodynamic instability may have inadequate tissue oxygen delivery or abnormal oxygen consumption.³

The amount of oxygen delivered to the tissues or consumed can be calculated. A catheter positioned in the pulmonary artery, termed a pulmonary artery (PA) catheter, is used for mixed venous sampling (see Chapter 66). Blood drawn from a PA catheter is termed a mixed venous blood gas sample because it consists of venous blood that has returned to the heart and “mixes” in the right ventricle. Normal mixed venous values are given in Table 26-1. When tissue oxygen delivery is inadequate or when inadequate oxygen is transported to the tissues by the hemoglobin, the PvO₂ and SvO₂ fall.

Oximetry.

Arterial oxygen saturation can be monitored noninvasively and continuously using a pulse oximetry probe on the finger, toe, ear, or bridge of the nose ⁴ (see eFig. 26-2 available on the website). The abbreviation SpO₂ is used to indicate the oxygen saturation of hemoglobin as measured by pulse oximetry. SpO₂ and heart rate are displayed on the monitor as digital readings (see eFig. 26-2).

Pulse oximetry is particularly valuable in intensive care and perioperative situations, in which sedation or decreased consciousness might mask hypoxia (Table 26-2). SpO₂ is assessed with each routine vital sign check in many inpatient areas. Changes in SpO₂ can be detected quickly and treated (Table 26-3). Oximetry is also used during exercise testing and when adjusting flow rates during long-term oxygen therapy.

TABLE 26-2

MANIFESTATIONS OF INADEQUATE OXYGENATION

	Onset
Manifestations	Early	Late
Central Nervous System
Unexplained apprehension	X
Unexplained restlessness or irritability	X
Unexplained confusion or lethargy	X	X
Combativeness		X
Coma		X
Respiratory
Tachypnea	X
Dyspnea on exertion	X
Dyspnea at rest		X
Use of accessory muscles		X
Retraction of interspaces on inspiration		X
Pause for breath between sentences, words		X
Cardiovascular
Tachycardia	X
Mild hypertension	X
Dysrhythmias	X	X
Hypotension		X
Cyanosis		X
Cool, clammy skin		X
Other
Diaphoresis	X	X
Decreased urine output	X	X
Unexplained fatigue	X	X

TABLE 26-3

CRITICAL VALUES FOR PaO₂ AND SpO₂ *

PaO₂ (%)	SpO₂ (%)	Significance
≥70	≥94	Adequate unless patient is hemodynamically unstable or hemoglobin (Hgb) has difficulty releasing O₂ to the tissues.
60	90	Adequate in almost all patients. Provides adequate oxygenation but with less margin for error than above.
55	88	Adequate for patients with chronic hypoxemia if no cardiac problems occur. These values are also used as criteria for prescription of continuous O₂ therapy.
40	75	Inadequate but may be acceptable on a short-term basis if the patient also has CO₂ retention. In this situation, respirations may be stimulated by a low PaO₂. Thus the PaO₂ cannot be raised rapidly.
<40	<75	Inadequate. Tissue hypoxia and cardiac dysrhythmias can be expected.

^*The same critical values apply for SpO₂ and SaO₂. Values pertain to rest or exertion.

Values obtained by pulse oximetry are less accurate if the SpO₂ is less than 70%. At this level the oximeter may display a value that is ±4% of the actual value. For example, if the SpO₂ reading is 70%, the actual value can range from 66% to 74%. Pulse oximetry is also inaccurate if hemoglobin variants (e.g., carboxyhemoglobin, methemoglobin) are present. Other factors that can alter the accuracy of pulse oximetry include motion, low perfusion, anemia, cold extremities, bright fluorescent lights, intravascular dyes, thick acrylic nails, and dark skin color. If there is doubt about the accuracy of the SpO₂ reading, obtain an ABG analysis to verify the results.

Oximetry can also be used to monitor SvO₂ via a PA catheter. A decrease in SvO₂ suggests that less oxygen is being delivered to the tissues or that more oxygen is being consumed. Changes in SvO₂ provide an early warning of a change in cardiac output or tissue oxygen delivery. Normal SvO₂ is 60% to 80%.

Carbon Dioxide Monitoring.

Carbon dioxide can be monitored using transcutaneous CO₂ (PTCCO₂) and end-tidal CO₂ (PETCO₂) (capnography). Transcutaneous measurement of CO₂ is a noninvasive method of estimating arterial pressure of CO₂ (PaCO₂) using an electrode placed on the skin.

PETCO₂ is the noninvasive measurement of alveolar CO₂ at the end of exhalation when CO₂ concentration is at its peak. It is used to monitor and assess trends in the patient’s ventilatory status. Expired gases are sampled from the patient’s airway and are analyzed by a CO₂ sensor that uses infrared light to measure exhaled CO₂. The sensor may be attached to an adaptor on the endotracheal tube or the tracheostomy tube. A nasal cannula with a sidestream capnometer can be used in patients without an artificial airway. Capnography is usually presented as a graph of expiratory CO₂ plotted against time.

In the past, capnography was used mainly intraoperatively, postoperatively, and in critical care units. Today’s monitors are portable and practical for use on inpatient units and emergency departments.

Measurement of oxygen saturation (oximetry) is primarily used to assess for hypoxia. CO₂ monitoring assesses for hypoventilation. The use of both measures together is important in determining patients’ oxygenation and ventilatory status.

Control of Respiration

The respiratory center in the medulla (located in the brainstem) responds to chemical and mechanical signals. Impulses are sent from the medulla to the respiratory muscles through the spinal cord and the phrenic nerves.

Chemoreceptors.

A chemoreceptor is a receptor that responds to a change in the chemical composition (PaCO₂ and pH) of the fluid around it. Central chemoreceptors are located in the medulla and respond to changes in the hydrogen ion (H⁺) concentration. An increase in the H⁺ concentration (acidosis) causes the medulla to increase the respiratory rate and tidal volume (Vt). A decrease in H⁺ concentration (alkalosis) has the opposite effect. Changes in PaCO₂ regulate ventilation primarily by their effect on the pH of the cerebrospinal fluid. When the PaCO₂ level is increased, more CO₂ is available to combine with H₂O and form carbonic acid (H₂CO₃). This lowers the cerebrospinal fluid pH and stimulates an increase in respiratory rate. The opposite process occurs with a decrease in PaCO₂ level.

Peripheral chemoreceptors are located in the carotid bodies at the bifurcation of the common carotid arteries and in the aortic bodies above and below the aortic arch. The peripheral chemoreceptors respond to decreases in PaO₂ and pH and to increases in PaCO₂. These changes also stimulate the respiratory center.

In a healthy person an increase in PaCO₂ or a decrease in pH causes an immediate increase in the respiratory rate. The PaCO₂ does not vary more than about 3 mm Hg if lung function is normal. Conditions such as COPD alter lung function and may result in chronically elevated PaCO₂ levels. In these instances the patient is relatively insensitive to further increases in PaCO₂ as a stimulus to breathe and may be maintaining ventilation largely because of a hypoxic drive from the peripheral chemoreceptors (see Chapter 29).

Mechanical Receptors.

Mechanical receptors (juxtacapillary and irritant) are located in the lungs, upper airways, chest wall, and diaphragm. They are stimulated by a variety of physiologic factors, such as irritants, muscle stretching, and alveolar wall distortion. Signals from the stretch receptors aid in the control of respiration. As the lungs inflate, pulmonary stretch receptors activate the inspiratory center to inhibit further lung expansion. This is termed the Hering-Breuer reflex, and it prevents overdistention of the lungs. Impulses from the mechanical sensors are sent through the vagus nerve to the brain. Juxtacapillary (J) receptors are believed to cause the rapid respiration (tachypnea) seen in pulmonary edema. These receptors are stimulated by fluid entering the pulmonary interstitial space.

Respiratory Defense Mechanisms

Respiratory defense mechanisms are efficient in protecting the lungs from inhaled particles, microorganisms, and toxic gases. The defense mechanisms include filtration of air, the mucociliary clearance system, the cough reflex, reflex bronchoconstriction, and alveolar macrophages.

Filtration of Air.

Nasal hairs filter inspired air. In addition, the abrupt changes in direction of airflow that occur as air moves through the nasopharynx and larynx increase air turbulence. This causes particles and bacteria to contact the mucosa lining these structures. Most large particles (greater than 5 µm) are less dangerous because they are removed in the nasopharynx or bronchi and do not reach the alveoli.

The velocity of airflow slows greatly after it passes the larynx, facilitating the deposition of smaller particles (1 to 5 µm). They settle out the way sand does in a river, a process termed sedimentation. Particles less than 1 µm in size are too small to settle in this manner and are deposited in the alveoli. An example of small particles that can build up is coal dust, which can lead to pneumoconiosis (see Chapter 28).

Mucociliary Clearance System.

Below the larynx, the movement of mucus is accomplished by the mucociliary clearance system, commonly referred to as the mucociliary escalator. This term is used to indicate the relationship between the secretion of mucus and the ciliary activity. Mucus is continuously secreted at a rate of about 100 mL/day by goblet cells and submucosal glands. It forms a mucous blanket that contains the impacted particles and debris from distal lung areas (see Fig. 26-1). The small amount of mucus normally secreted is swallowed without being noticed. Secretory immunoglobulin A (IgA) in the mucus helps protect against bacteria and viruses.

Cilia cover the airways from the level of the trachea to the respiratory bronchioles (see Fig. 26-1). Each ciliated cell contains approximately 200 cilia, which beat rhythmically about 1000 times per minute in the large airways, moving mucus toward the mouth. The ciliary beat is slower further down the tracheobronchial tree. As a consequence, particles that penetrate more deeply into the airways are removed less rapidly. Ciliary action is impaired by dehydration; smoking; inhalation of high oxygen concentrations; infection; and ingestion of drugs such as atropine, anesthetics, alcohol, or cocaine. Patients with COPD and cystic fibrosis have repeated lower respiratory tract infections. Cilia are often destroyed during these infections, resulting in impaired secretion clearance; a chronic productive cough; and chronic colonization by bacteria, which leads to frequent respiratory tract infections.

Cough Reflex.

The cough is a protective reflex action that clears the airway by a high-pressure, high-velocity flow of air. It is a backup for mucociliary clearance, especially when this clearance mechanism is overwhelmed or ineffective. Coughing is only effective in removing secretions above the subsegmental level (large or main airways). Secretions below this level must be moved upward by the mucociliary mechanism before they can be removed by coughing.

Reflex Bronchoconstriction.

Reflex bronchoconstriction is another defense mechanism. In response to the inhalation of large amounts of irritating substances (e.g., dusts, aerosols), the bronchi constrict in an effort to prevent entry of the irritants. A person with hyperreactive airways, such as a person with asthma, may experience bronchoconstriction after inhalation of triggers such as cold air, perfume, or other strong odors.

Alveolar Macrophages.

Because ciliated cells are not found below the level of the respiratory bronchioles, the primary defense mechanism at the alveolar level is alveolar macrophages. Alveolar macrophages rapidly phagocytize inhaled foreign particles such as bacteria. The debris is moved to the level of the bronchioles for removal by the cilia or removed from the lungs by the lymphatic system. Particles (e.g., coal dust, silica) that cannot be adequately phagocytized tend to remain in the lungs for indefinite periods and can stimulate inflammatory responses (see Chapter 28). Because alveolar macrophage activity is impaired by cigarette smoke, the smoker who is employed in an occupation with heavy dust exposure (e.g., mining, foundries) is at an especially high risk for lung disease.

Gerontologic Considerations

Effects of Aging on Respiratory System

Age-related changes in the respiratory system can be divided into alterations in structure, defense mechanisms, and respiratory control (Table 26-4). Structural changes include calcification of the costal cartilages, which can interfere with chest expansion. The outward curvature of the spine is marked, especially with osteoporosis, and the lumbar curve flattens. Therefore the chest may appear barrel shaped, and the older person may need to use accessory muscles to breathe. Respiratory muscle strength progressively declines after age 50. Overall, the lungs in the older adult are harder to inflate.⁵

TABLE 26-4

GERONTOLOGIC ASSESSMENT DIFFERENCES
Respiratory System

Changes	Differences in Assessment Findings
Structures
Chest wall stiffening Costal cartilage calcification ↓ Elastic recoil ↓ Chest wall compliance ↑ Anteroposterior diameter ↓ Functioning alveoli ↓ Respiratory muscle strength	Barrel chest appearance, kyphotic posture, ↓ chest wall movement, ↓ deep breathing; mucus thickened ↓ Vital capacity, ↑ residual volume, ↑ functional residual capacity Diminished breath sounds, particularly at lung bases; ↓ PaO₂ and SaO₂, normal pH and PaCO₂
Defense Mechanisms
↓ Cell-mediated immunity ↓ Specific antibodies ↓ Cilia function ↓ Cough force ↓ Alveolar macrophage function ↓ Sensation in pharynx	↓ Cough effectiveness, ↓ secretion clearance ↑ Risk of upper respiratory aspiration, infection, influenza, pneumonia Respiratory infections may be more severe and last longer
Respiratory Control
↓ Response to hypoxemia ↓ Response to hypercapnia	Greater ↓ in PaO₂ and ↑ in PaCO₂ before respiratory rate changes ↓ Ability to maintain acid-base balance Significant hypoxemia or hypercapnia may develop from relatively small incidents Retained secretions, excessive sedation, or positioning that impairs chest expansion may substantially alter PaO₂ or SpO₂ values