PATHO -THE PULMONARY SYSTEM

AGING AND THE PULMONARY SYSTEM Most knowledge about pulmonary structure and function is based on norms for the middle years. Less is known about structure and function in the very young (see Chapter 36) and older adults, but a few normal physiologic (developmental and degenerative) changes are known to occur from birth to old age. An understanding of these changes is needed to provide appropriate care and to differentiate between normal alterations and disease. Normal alterations include: (1) loss of elastic recoil, (2) stiffening of the chest wall, (3) changes in gas exchange, and (4) increases in flow resistance (Figure 34-18). These changes are gradual and usually without adverse consequences in healthy individuals. They are influenced by environmental and sociocultural factors, nutritional status, respiratory disease, body size, gender, and race. 32-34 During adulthood and as age advances, the alveoli tend to lose alveoli wall tissue and capillaries. This process diminishes alveolar surface area available for gas diffusion and decreases airway support provided by normal lung tissues. Mechanical changes involve elastic properties of the lungs and chest wall. Chest wall compliance decreases with age, because the ribs become ossified (less flexible) and joints become stiffer. As a result the chest wall loses some of its ability to expand. In addition, respiratory muscle strength and endurance decrease by up to 20% by age 70. 33 These mechanical changes in the lung and chest wall, along with structural changes in the alveoli, reduce ventilatory capacity in older adults. 35 Vital capacity decreases and residual volume increases; however, total lung capacity remains unchanged. These changes decrease ventilatory reserves and lead to decreased ventilation-perfusion ratios. With advancing age there is also increased immune dysregulation, asymptomatic low-grade inflammation, and increased risk of infection. 33,36-39 Alterations in gas exchange are reflected by blood gas analysis. With advancing age, pH and Paco2 do not change much, even though it has been documented that the chemoreceptors become less sensitive to gas partial pressures with age. 40 Older adults have a decreased compensatory response to hypercapnia and hypoxemia; however, the perception of dyspnea remains intact and is even enhanced. Pao2 declines with age as a result of structural and mechanical changes, such as loss of alveolar surface area and increased ventilation-perfusion mismatch. The maximum Pao2 in an older adult at sea level can be estimated by multiplying the person’s age by 0.3 and subtracting the product from 100. For example, an 80-year-old individual would have an estimated maximum Pao2 of 76 mmHg (0.3 × 80 = 24; 100−24 = 76). 41 There is also a decrease in the capillary network. The decrease in Pao2 and diminished ventilatory reserve in an older adult lead to a decrease in exercise tolerance. Respiratory muscle strength and endurance decrease with age. 39 Furthermore, older adults are at greater risk for respiratory depression caused by medications. Changes in respiratory structure and function can vary considerably from person to person, however. Changes also are affected by activity and fitness earlier in life. A very active, physically fit individual will, all else being equal, have fewer changes in function at any age than one who has been sedentary. Conditions Caused by Pulmonary Disease or Injury Hypercapnia Hypercapnia, or increased CO2 concentration in the arterial blood (increased Paco2 ), is caused by hypoventilation of the alveoli. 12 As discussed in Chapter 34, CO2 is easily diffused from the blood into the alveolar space; thus minute volume (respiratory rate × tidal volume) determines not only alveolar ventilation, but also Paco2 . Hypoventilation is often overlooked because breathing pattern and ventilatory rate may appear normal; it is important to obtain blood gas analysis to determine the severity of hypercapnia and resultant respiratory acidosis (acid-base balance is described in Chapter 3). There are many causes of hypercapnia. 13 Most are a result of a decreased drive to breathe or an inadequate ability to respond to ventilatory stimulation. Causes include: (1) depression of the respiratory center by drugs;(2) diseases of the medulla, including infections of the central nervous system or trauma; (3) abnormalities of the spinal conducting pathways, as in spinal cord disruption or poliomyelitis; (4) diseases of the neuromuscular junction or of the respiratory muscles themselves, as in myasthenia gravis or muscular dystrophy; (5) thoracic cage abnormalities, as in chest injury or congenital deformity; (6) large airway obstruction, as in tumors or sleep apnea; and (7) increased work of breathing or physiologic dead space, as in emphysema. Hypercapnia and the associated respiratory acidosis can result in several important clinical manifestations. Of greatest concern are electrolyte abnormalities that occur in response to the low pH that may cause dysrhythmias. Individuals also may have somnolence and even be in a coma because of changes in intracranial pressure associated with high levels of arterial carbon dioxide, which causes cerebral vasodilation. Alveolar hypoventilation with increased alveolar carbon dioxide limits the amount of alveolar oxygen available for diffusion into the blood, leading to secondary hypoxemia. Hypoxemia Hypoxemia, or reduced oxygenation of arterial blood (reduced Pao2 ), is caused by respiratory alterations, whereas hypoxia, or reduced oxygenation of cells in tissues, may be caused by alterations of other systems as well. Although hypoxemia can lead to tissue hypoxia, tissue hypoxia can result from other abnormalities, such as low cardiac output or cyanide poisoning. Hypoxemia results from problems with one or more Hypoxemia results from problems with one or more of the major mechanisms of oxygenation: 1. Oxygen delivery to the alveoli a. Oxygen content of the inspired air (Fio2 ) 2. Ventilation of the alveoli 3. Diffusion of oxygen from the alveoli into the blood a. Balance between alveolar ventilation and perfusion (V/ ˙ Q˙ mismatch) b. Diffusion of oxygen across the alveolocapillary membrane 4. Perfusion of pulmonary capillaries Table 35-1 lists some of the common clinical causes of these problems. The amount of oxygen in the alveoli is called the Pao2 and is dependent on two factors. The first factor is the presence of adequate oxygen content of the inspired air. The amount of oxygen in inspired air is expressed as the percentage or fraction of air that is composed of oxygen, called the Fio2 . The Fio2 of air at sea level is approximately 21% or 0.21. Anything that decreases the Fio2 (such as high altitude) decreases the Pao2 . The second factor is the amount of alveolar minute ventilation (tidal volume × respiratory rate). Hypoventilation results in an increase in Paco2 and a decrease in Pao2 such that there is less oxygen available in the alveoli for diffusion into the blood. This type of hypoxemia can be completely corrected if alveolar ventilation is improved by increases in the rate and depth of breathing. Hypoventilation causes hypoxemia in unconscious persons; in people with neurologic, muscular, or bone diseases that restrict chest expansion; and in individuals who have COPD. Diffusion of oxygen from the alveoli into the blood is also dependent on two factors. The first is the balance between the amount of air getting into alveoli (V˙ ) and the amount of blood perfusing the capillaries around the alveoli (Q˙ ). An abnormal ventilation-perfusion ratio (V/ ˙ Q˙ ) is the most common cause of hypoxemia (Figure 35-2). Normally, alveolocapillary lung units receive almost equal amounts of ventilation and perfusion. The normal V/ ˙ Q˙ is 0.8 to 0.9 because perfusion is somewhat greater than ventilation in the lung bases and because some blood is normally shunted to the bronchial circulation. V/ ˙ Q˙ mismatch refers to an abnormal distribution of ventilation and perfusion. Hypoxemia can be caused by inadequate ventilation of well perfused areas of the lung (low V/ ˙ Q˙ ). Mismatching of this type, called shunting, occurs in atelectasis, in asthma as a result of bronchoconstriction, and in pulmonary edema and pneumonia when alveoli are filled with fluid. When blood passes through portions of the pulmonary capillary bed that receive no ventilation, right-to-left shunt occurs, resulting in decreased systemic Pao2 and hypoxemia. Hypoxemia also can be caused by poor perfusion of well-ventilated portions of the lung (high V/ ˙ Q˙ ), resulting in wasted ventilation. The most common cause of high V/ ˙ Q˙is a pulmonary embolus that impairs blood flow to a segment of the lung. An area where alveoli are ventilated but not perfused is termed alveolar dead space. The second factor affecting diffusion of oxygen from the alveoli into the blood is the alveolocapillary barrier. Diffusion of oxygen through the alveolocapillary membrane is impaired if the alveolocapillary membrane is thickened or the surface area available for diffusion is decreased. Abnormal thickness, as occurs with edema (tissue swelling) and fibrosis (formation of fibrous lesions), increases the time required for diffusion across the alveolocapillary membrane. If diffusion is slowed enough, the oxygen in the alveolar gas (Pao2 ) and capillary blood does not have time to equilibrate during the fraction of a second that blood remains in the capillary. Destruction of alveoli, such as that which occurs in emphysema, decreases the surface area available for diffusion. Hypercapnia is rarely produced by impaired diffusion, because carbon dioxide diffuses so easily from capillary to alveolus that the individual with impaired diffusion would die from hypoxemia before hypercapnia could occur. Hypoxemia most often is associated with a compensatory hyperventilation and resultant respiratory alkalosis (i.e., decreased Paco2 and increased pH). However, in individuals with associated ventilatory difficulties, hypoxemia may be complicated by hypercapnia and respiratory acidosis. Hypoxemia results in widespread tissue dysfunction and, when severe, can lead to organ infarction. In addition, hypoxic pulmonary vasoconstriction can contribute to increased pressures in the pulmonary artery (pulmonary artery hypertension) and lead to right-sided heart failure and cor pulmonale (see p. 1276). Clinical manifestations of acute hypoxemia may include cyanosis, confusion, tachycardia, edema, and decreased renal output. Acute Respiratory Failure Respiratory (lung) failure is defined as inadequate gas exchange, that is, hypoxemia, in which Pao2 is≤50 mmHg, or hypercapnia, in which Paco2 is≥50 mmHg with a pH of ≤7.25. Respiratory failure can result from direct injury to the lungs, airways, or chest wall or indirectly because of injury to another body system, such as the brain or liver. 14 It can occur in individuals who have an otherwise normal respiratory system or in those with underlying chronic pulmonary disease. Most pulmonary diseases can cause episodes of acute respiratory failure. If the respiratory failure is primarily hypercapnic, it is the result of inadequate alveolar ventilation (see Hypercapnia, p. 1251) and the individual must receive ventilatory support, such as with a bag-valve mask, noninvasive positive pressure ventilation, or intubation and placement on mechanical ventilation. If the respiratory failure is primarily hypoxemic, it is the result of inadequate exchange of oxygen between the alveoli and the capillaries (see Hypoxemia, p. 1251) and the individual must receive supplemental oxygen therapy. Many individuals have a combined hypercapnic and hypoxemic respiratory failure and require both kinds of support. Respiratory failure is an important potential complication of any major surgical procedure, especially those that involve the central nervous system, thorax, or upper abdomen. Smokers are at risk, particularly if they have preexisting lung disease. Limited cardiac reserve, chronic renal failure, chronic hepatic disease, and infection also increase the tendency to develop postoperative respiratory failure. The most common postoperative pulmonary problems are atelectasis, pneumonia, pulmonary edema, and pulmonary emboli (these conditions are discussed later in this chapter). Prevention of postoperative respiratory failure includes frequent turning and position changes, deep breathing exercises, and early ambulation to prevent atelectasis and accumulation of secretions. Humidification of inspired air can help loosen secretions. Incentive spirometry gives individuals immediate feedback about tidal volumes, which encourages them to breathe deeply. Supplemental oxygen is given for hypoxemia, and antibiotics are given as appropriate to treat infection. If respiratory failure develops, the individual may require conventional mechanical ventilation, high-frequency ventilation, or extracorporeal membrane oxygenation. 15 Pleural Abnormalities Pneumothorax Pneumothorax is the presence of air or gas in the pleural space caused by a rupture in the visceral pleura (which surrounds the lungs) or the parietal pleura and chest wall (see Chapter 34). As air separates the visceral and parietal pleurae, it destroys the negative pressure of the pleural space. This disrupts the state of equilibrium that normally exists between elastic recoil forces of the lung and chest wall. No longer held in check by the recoil forces of the chest wall, the lung fulfills its tendency to recoil by collapsing toward the hilum. Primary (spontaneous) pneumothorax ,which occurs unexpectedly in healthy individuals (usually men) between ages 20 and 40 years, is most often caused by the spontaneous rupture of blebs (blister-like formations) on the visceral pleura, although there may be underlying pleural disease with emphysemalike changes. 16 Approximately 10% of affected individuals have a significant family history of primary pneumothorax that has been linked to mutations in the folliculin gene (Birt-Hogg-Dubé- syndrome), which influences cell–cell adhesion. 17 Bleb rupture can occur during sleep, rest, or exercise. The ruptured bleb or blebs are usually located in the apexes of the lungs. Secondary (traumatic) pneumothorax can be caused by chesttrauma,such as a rib fracture, stab or bullet wounds, or a surgical procedure that tears the pleura; rupture of a bleb or bulla (larger vesicle) as occurs in COPD; or mechanical ventilation, particularly if it includes positive end-expiratory pressure (PEEP). 18 Iatrogenic pneumothorax is most commonly caused by transthoracic needle aspiration. 19