Aging and the Lungs

Geriatric Essentials

• Lung function gradually declines after age 20. In the absence of respiratory insults (eg, smoking, exposure to environmental toxins, prior respiratory infections), most elderly people have sufficient respiratory reserve to avoid symptoms.
• Aging's reduction of respiratory reserve, which tends to cause only minimal symptoms in healthy people, often increases the risk and severity of pulmonary disorders.

The effects of aging on the lungs are physiologically and anatomically similar to those that occur during the development of mild emphysema. After about age 20, the number of alveoli and the number of lung capillaries gradually begin to decrease. Although aging affects compliance, lung volumes, airflow, diffusing capacity, and other parameters of lung function, purely age-related changes do not lead to clinically significant symptoms or changes in nonsmokers. However, in smokers, former smokers, and those exposed to environmental toxins, injury due to inflammation is superimposed on and accelerates the effects of aging, resulting in dyspnea. Other serious risk factors for pulmonary symptoms in the elderly include deconditioning, obesity, and heart disease.

Compliance and Lung Volumes

Pulmonary compliance is the change in lung volume per unit change in elastic recoil pressure. Chest wall compliance is the change in thoracic volume per unit change in intrathoracic pressure. Changes in lung and chest wall compliance are primarily responsible for age-related decreases in ventilation and the corresponding decreases in gas distribution that result from collapse of small airways.

Beginning at about age 30, there is a decrease in the number and elasticity of parenchymal elastic fibers, which causes gradual loss of elastic recoil of the lungs (increasing compliance). Airway size also decreases.

At about age 55, respiratory muscles begin to weaken, and the chest wall gradually becomes stiffer (decreasing compliance). These changes likely result from age-associated kyphoscoliosis, calcification of intercostal cartilage, and arthritis of the costovertebral joints. The increased outward pull of the stiffer chest wall combined with the reduced ability of the lung to pull inward result in a small increase in functional residual capacity (FRC--ie, lung volume at the end of a quiet expiration) and residual volume (RV--ie, lung volume after a maximal expiration). Total lung capacity (TLC--ie, lung volume after maximal inspiration) remains fairly constant.

Airflow

Airway collapse is prevented by intra-alveolar pressure generated by the elastic recoil of the lung. Age-related loss of this elastic recoil results in easy collapse of poorly supported peripheral airways, which in turn may result in decreased flow at low lung volumes.

The forced expiratory volume in 1 sec (FEV₁) begins to decrease after age 20. The annual decline is small at first but accelerates with aging. The forced vital capacity (FVC) decreases as well, by about 14 to 30 mL/yr in men and 15 to 24 mL/yr in women.

Until age 40, decreases in FEV₁ and FVC are thought to result from changes in body weight and strength rather than from loss of tissue. After age 40, decreases in FEV₁ and FVC are due to aging itself and superimposed cumulative effects of inflammatory injury from respiratory illness, smoking, and exposure to environmental toxins. For example, cigarette smoking repeatedly induces inflammatory mediators, humoral protection (elastase and antielastase, oxidant and antioxidant), neutrophil recruitment, and tissue repair, culminating in inflammatory lung destruction and airway obstruction. Accumulated environmental oxidant injuries produce similar damage.

Diffusing Capacity

Diffusing capacity peaks in people in their early 20s and then declines; from middle age onward, it declines at a rate of about 17% (2.03 mL/min/mm Hg) per decade in men and at a rate of about 15% (1.47 mL/min/mm Hg) per decade in women. This decline results from decreased alveolar-capillary surface area caused by inflammation-induced destruction of alveoli and by thickening and inflammation-induced destruction of capillary-containing alveolar walls. The loss of alveolar-capillary surface area decreases venous blood oxygenation, particularly under conditions of high pulmonary blood flow (eg, exercise). The rate of decline in diffusing capacity among women may be lower because endogenous estrogen may slow the destruction of alveolar-capillary tissue in women between ages 25 and 46; destruction slows presumably because of preserved vascular integrity.

Partial Pressure of Arterial Oxygen

Partial pressure of arterial oxygen (PaO₂) declines linearly with aging (about 0.3%/yr) until age 75, at which time it stabilizes at about 80 mm Hg in healthy nonsmokers. This gradual decline is mostly attributable to ventilation/perfusion (V/Q) mismatch caused by age-related collapse of peripheral airways, leading to shunting of blood through nonventilated alveoli. PaO₂ at any age can be roughly estimated by the equation PaO₂ = 109 - (0.43 x age).

Autonomic Response

Heart rate and ventilatory responses to hypoxia and hypercapnia diminish with aging because peripheral and central chemoreceptor responses diminish, as do their integration of CNS pathways. Aging also decreases neural output to respiratory muscles and lowers chest wall and lung mechanical efficiency. As a result, the ventilatory response to hypoxia is reduced by 51% in healthy men aged 64 to 73 compared with healthy men aged 22 to 30; the ventilatory response to hypercapnia is reduced by 41%. These reductions increase the risks of developing hypoxia and hypercapnia if elderly people acquire disorders that produce low O₂ levels (eg, pneumonia, COPD, obstructive sleep apnea). Effects are greater in people who are deconditioned.

With aging, the diaphragm weakens by up to 25%. This weakening is not usually clinically relevant in healthy people, but in the presence of a disorder that requires sustained increases in ventilation (eg, pneumonia), it predisposes the elderly to hypoxemia and hypercapnia, and thus possibly the need for mechanically assisted ventilation.

Oxygen Consumption

Maximal O₂ consumption (VO_2max) is the body's ability to maximally deliver O₂ to the tissues. It is the standard measurement of physical work (exercise) capacity. VO_2max increases during childhood (from growth of muscle, heart, and lungs), peaks in the late teens, plateaus until the mid-20s, then gradually declines each decade by 7.6% (32 mL/min/yr) in men and 5.3% (14 mL/min/yr) in women due to age-related reductions in maximal heart rate, muscle mass, and cardiovascular deconditioning associated with lower levels of physical activity or from changes in cardiovascular function. VO_2max and exercise capacity tend to be higher in people who undergo regular aerobic training than in people of similar age and health who do not; however, exercise does not seem to slow the age-related decline in VO_2max and exercise capacity.

Immunity

The rate of mucociliary transport declines with aging, although effects on clinical infection are unproven. More than 70% of elderly patients with community-acquired pneumonia develop a blunted cough reflex (compared with only 10% of age-matched controls), probably due to accompanying hypoxia, drug-induced sedation, and neurologic disorders. Dysphagia and other swallowing difficulties and impaired esophageal motility occur more often in the elderly and increase risk of aspiration.

Antibody responses to some vaccines that can decrease risk of pneumonia (eg, pneumococcal, influenza) decline with aging, but precise implications for challenges with natural antigens are unknown. Cellular immunity also declines with aging. Elderly people produce fewer helper T cells and the ones they do have are often less effective than they were earlier in life. Among the elderly who have been exposed to TB, T cells may have surrounded TB organisms in a granuloma for many years, inactivating the organisms; cellular immune senescence may result in reactivation of TB.

This topic was last updated April 2006.