Respiratory System

Alterations in control of respiration, lung structure, mechanics, and pulmonary blood flow place the elderly at increased risk for perioperative pulmonary complications (also see Chapter 17 ). Ventilatory responses to hypoxia, hypercapnia, and mechanical stress are impaired secondary to reduced central nervous system activity.^[15] In addition, the respiratory depressant effects of benzodiazepines, opioids, and volatile anesthetics are exaggerated.^{[15] [16]} These changes compromise the usual protective responses against hypoxemia after anesthesia and surgery in the elderly.

Structural changes in the lung with aging include the loss of elastic recoil after reorganization of collagen and elastin in lung parenchyma. This loss of recoil, combined with altered surfactant production, leads to an increase in lung compliance. Loss of elastic elements within the lung is associated with enlargement of the respiratory bronchioles and alveolar ducts and a tendency for early collapse of the small airways on exhalation. In addition, a progressive loss of alveolar surface area occurs secondary to increases in size of the interalveolar pores of Kohn. The functional results of these pulmonary changes are increased anatomic dead space, decreased diffusing capacity, and increased closing capacity.

Loss of height and calcification of the vertebral column and rib cage lead to a typical barrel chest appearance with diaphragmatic flattening. The flattened diaphragm is mechanically less efficient, and function is further impaired by a significant loss of muscle mass associated with aging. Functionally, the chest wall becomes less compliant.

The combination of decreased elastic recoil and increased chest wall stiffness causes an elevation in intrapleural pressure by 2 to 4 cm H₂ O. However, total lung capacity is relatively unchanged. Residual volume increases by 5% to 10% per decade. Therefore, vital capacity decreases. Closing capacity, the volume at which small dependent airways start to close, increases with age. Change in the relationship between functional residual capacity and closing capacity causes an increased ventilation-perfusion mismatch and represents the most important mechanism for the increase in alveolar-arterial gradient for oxygen observed in aging. ^[17] In younger individuals, closing capacity is below functional residual capacity.

At 44 years of age, closing capacity equals functional residual capacity in the supine position and, at 66 years of age, equals functional residual capacity in the upright position.^[17] When closing capacity encroaches on tidal breathing, ventilation-perfusion mismatch occurs. When functional residual capacity is below closing capacity, shunt will increase and arterial oxygenation will fall. This effect is observed in the decreased resting arterial oxygen tension with aging ( Table 62-3 ) and results in impairment of preoxygenation. Another effect of increasing closing capacity in concert with depletion of muscle mass is a progressive decrease in forced expiratory volume in 1 second by 6% to 8% per decade.

Increases in pulmonary vascular resistance and pulmonary artery pressure occur with age and may be secondary to decreases in cross-sectional area of the

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