Table 601

Changes in structure and function of the aging human respiratory system

Structural changes in the lung

Structural disruption and possible loss of elastin Altered cross-linking of elastin and collagen Loss of alveolar surface area Enlargement of terminal airspaces Decreased number of capillaries per alveolus Decreased diameter of small bronchioles Increased interalveolar pores (pores of Kohn)

Other respiratory system changes Decreased chest wall compliance Decline in respiratory muscle function

Changes in measures of lung function

Diminished lung elastic recoil (increased lung compliance) Decreased vital capacity (FVC) and forced expiratory flows

(FEVi, FEF25-75) Increased residual volume (RV) and functional residual capacity (FRC)

Decreased inspiratory capacity (IC)

Decreased diffusion capacity for carbon monoxide (DLCO) Decreased partial pressure of arterial oxygen (PaO2) Decreased maximal oxygen consumption during maximal exercise

However, biochemical analysis of the lung suggests that the total content of elastin and collagen does not change significantly with aging (Lang et al., 1994), and changes in the spatial arrangement or cross-linking of elastic fiber networks rather than measurable elastin loss may be the cause of the observed decline in elastic recoil (Crapo, 1993). The number of capillaries per alveolus also declines and is accompanied by loss of alveolar surface area as terminal airspaces (alveolar ducts and alveoli) increase in volume and the diameter and number of interalveolar pores increase (Thurlbeck, 1991). The causes of age-associated changes in lung matrix remain elusive. Although the loss of elastic recoil and distal airspace enlargement is somewhat similar to smoke-induced emphysema, the airspace enlargement is quite homogeneous, in contrast to the irregular distribution of airspace enlargement in emphysematous lungs that is accompanied by alveolar wall destruction.

Loss of elastic recoil and tethering of airways leads to small airway closure at identical lung volumes in older compared to younger subjects. This causes gradual reduction in forced expiratory flows (FEVi, FEF25-75), and early airway closure causes more gas to be trapped in the chest such that RV increases while FVC and IC decrease (Janssens et al., 1999). These alterations in measurement of pulmonary function are attributed to diffuse emphysema-like changes in the lung (senile emphysema), which differs in appearance from emphysema induced by tobacco smoke or other environmental exposures (Thurlbeck, 1991; 1999). In addition to altered expiratory flow rates and lung volumes, the loss of alveolar surface area and alveolar capillaries with aging correlates with a gradual reduction of DLCO.

The ability of the lung to facilitate gas exchange also declines with advancing age. The PaO2 begins to decline in the third decade of life, and the average PaO2 may approach 70 mm Hg in the eighth decade but then tends to stabilize (Sorbini et al., 1968; Cerveri et al., 1995). The gradually widening alveolar to arterial oxygen gradient that is associated with advancing age is considered to be a consequence of ventilation-perfusion mismatching due to closure of small airways as lung matrix tissue is lost or disrupted and elastic recoil declines. The elderly tend to breathe with a greater frequency but with smaller tidal volume compared to young normal subjects while maintaining a similar minute ventilation (Krumpe et al., 1985), but resting ventilatory responses to both hypoxia and hypercapnea become blunted (Peterson et al., 1981). In contrast to the decline in arterial oxygen tension, PaCO2 is maintained at approximately 40 mm Hg despite the blunted response to hypercapnea.

Other age-associated phenomena that affect respiratory function include changes in the chest wall, impaired respiratory muscle function, and altered breathing patterns during sleep. Chest wall compliance progressively decreases and is presumed to be due to diminished mobility of the costovertebral joints, calcification of intercostal cartilage, narrowing of intervertebral disc spaces, and the appearance of varying degrees of kyphoscoliosis (Peterson and Fishman, 1982). Maximal inspiratory and expiratory pressures in the elderly appear to correlate quite well with peripheral muscle strength (Enright et al., 1994). With advancing age the contribution of thoracic muscles (intercostals) to ventilation declines as the chest cage becomes less compliant (Mizuno, 1991). Diaphragmatic muscle mass tends to be preserved, but intercostal muscles display a decline in mean cross-sectional area after the fifth decade. Although diaphragmatic mass is preserved, respiratory muscle performance is reduced by the increase in RV and FRC, and the ability of the diaphragm to develop maximal force becomes impaired (Polkey et al., 1997). Other factors such as poor nutritional status and low body mass index have a deleterious effect on respiratory muscle strength and can confound the age-associated changes in respiratory muscle function (Arora and Rochester, 1982). Respiratory muscle function is also linked to cardiac performance, as reflected by cardiac index or maximal oxygen consumption, and maximal inspiratory pressures can fall as a consequence of cardiac dysfunction (Nishimura et al., 1994; Mancini et al., 1992).

Changes in the control of breathing in both the awake and sleep state are associated with aging. Blunted ventilatory and cardiac responses to both hypoxia and hypercapnia have been observed in the wakeful state (Peterson et al., 1981; Kronenberg and Drage, 1973), and attenuated responses to these stimuli when measured by mouth occlusion pressure (Peterson et al., 1981) suggest that this decline in respiratory drive may be caused by diminished ability to process information from mechanoreceptors and chemoreceptors. Indeed, responses to resistive loads are also diminished in the elderly (Tack et al., 1982). When compared to middle-aged individuals, ventilatory dysfunction during sleep is quite prevalent in the elderly. Significant upper airway obstruction during sleep affects up to 75% of elderly individuals, and the prevalence of sleep apnea has been reported to approach 50% (Ancoli-Israel and Coy, 1994). Additionally, ventilatory responses to upper airway occlusion is attenuated in elderly subjects compared to younger control subjects (Krieger et al., 1997). Despite these changes in the control of breathing in the resting state, ventilatory responses to CO2 are maintained or even increased in the elderly during exercise (Poulin et al., 1994).

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