Question

DIscuss age-related changes that affect respiration. What do these changes mean for the health and well-being of older patients?

Answer 1

Since the 1950s the median age of the US population increased by 20 years. Increased life expectancy reflects, in part, a better understanding of the disease states, newer interventions, and the success of public health programs. The number of persons aged 65 and over is projected to increase from 35 million in 2000 to an estimated 71 million in 2030, with the largest increase in individuals age 80 and above (US Census 2005). Differentiating a disease state from “normal” aging is vital when encountering this population in the clinical setting. Respiratory system undergoes various structural, physiological, and immunological changes with age. There is a large variation in different physiologic measures among older adults, making it difficult to construct “normal” limits to differentiate a disease from a normal state. The current review explores age-related structural, physiological, and immunological changes of the respiratory system. These changes may in part explain older individuals’ clinical presentation and/or aberrant diagnostic studies, avoiding unnecessary interventions, and how these changes may predispose these vulnerable individuals to increased risk for respiratory diseases. Moreover, these changes may in part be responsible for variable response to currently available drugs to treat pulmonary diseases in older adults.

Respiratory system mechanics

The respiratory system comprises primarily the thoracic cage, lungs, and diaphragm. Total respiratory system compliance includes lung and chest wall compliance. Compliance is change in volume relative to change in pressure. Lung compliance determines the rate and force of expiration and the thoracic compliance determines the elastic load during inspiration. With aging there are structural changes to the thoracic cage causing reduction in chest wall compliance. Age-related osteoporosis results in reduced height of the thoracic vertebrae. Stiffening of the thoracic cage from calcification of the rib cage and age-related kyphosis from osteoporosis reduces the ability of the thoracic cage to expand during inspiration and places the diaphragm at a mechanical disadvantage to generate effective contraction. Mittman et al (1965) studied total respiratory compliance in 42 healthy male subjects, ages 24 to 78 yrs, with 5 subjects being age ≥70 years. Lung compliance was similar, but the chest wall compliance was lower in older subjects. Moreover, subjects with lower chest wall compliance had higher residual volume (RV), suggesting an impediment to complete emptying of the lungs from stiff chest wall (Mittman et al 1965).

Respiratory muscle function

The diaphragm is the most important respiratory muscle and plays an essential role during inspiration. Exact measurement of diaphragmatic strength can only be done in vivo. There is very little information on the effect of aging on the contractile properties of the diaphragm. Respiratory muscle strength can be measured by transdiaphragmatic pressure (Pdi), maximum voluntary ventilation (MVV), and maximum inspiratory pressure (MIP). MIP is an index of strength of the diaphragm measured using a mechanical pressure gauge with a closed valve at the mouth during an inspiration. MIP is an indicator of inspiratory muscle strength and a determinant of vital capacity. Decline in MIP can lead to inadequate ventilation and impaired clearance of airway secretions, as seen in patients with neuromuscular disease. Studies measuring MIP have been cross-sectional, and their primary objective has been to establish reference values rather than to evaluate the longitudinal impact of age on diaphragmatic function. MIP is 30% higher in men compared with women at all age groups and decreases by 0.8 cm to 2.7 cm of H20/year between the ages of 65 and 85 years, with larger age-related declines seen in men (Enright et al 1994). Tolep et al (1995) showed a 25% lower Pdi measured using Mueller maneuver in healthy older subjects (age 65–75, n=10) compared with young healthy adults (age 19–28, n=9). Similar results were seen in a study by Polkey et al (1997). The degree of reduction in Pdi in healthy older compared with healthy young controls was less (13%) in the latter study, partly explained by different measurement techniques . Maximum voluntary ventilation is also reduced with age, and one longitudinal study showed a 12% decline over 6 years in older trained athletes (McClaran et al 1995). Likely explanation for reduced diaphragmatic strength with age is related to muscle atrophy and age-related decrease in fast twitch fibers, responsible for generating higher peak tensions. This age-related decline in diaphragmatic strength may predispose older individuals to diaphragmatic fatigue and ventilatory failure during increased ventilatory load on the respiratory system.

Anatomical changes

Senile hyperinflation of the lungs is a well known entity in the medical literature. It is not clear whether it reflects aging-associated destruction of lung parenchyma or loss of supporting structures within the lung parenchyma. Gillooly and Lamb (1993) studied 38 (age ≥65 yrs, n=14) autopsy or surgical lung resection specimens in lifelong nonsmokers and showed increase in airspace size with advancing age. There is homogeneous degeneration of the elastic fibers around the alveolar duct starting around 50 years of age resulting in enlargement of airspaces. Reduction in supporting tissue results in premature closure of small airways during normal breathing and can potentially cause air trapping and hyperinflation, hence “senile emphysema”.

Immunologic changes

Bronchoalveolar lavage (BAL) fluids in healthy older subjects have consistently shown an increased proportion of neutrophils and lower percentage of macrophages compared with younger adults. There is age-associated increase in immunoglobins IgA and IgM in the BAL fluid. Ratio of CD4+/CD8+ lymphocyte increases with age in the BAL fluid, suggesting the presence of primed T-cell from repeated antigenic stimuli of the lower respiratory tract mucosa (Meyer et al 1996). Moreover, there is increased ability of alveolar macrophages to release superoxide anion in response to stimuli in the elderly. These changes likely represent the combined affect of repetitive antigenic stimuli from environmental exposure and age-related decline in down regulatory response to antigenic exposure. Persistent low grade inflammation in the lower respiratory tract can cause proteolytic and oxidant-mediated injury to the lung matrix resulting in loss of alveolar unit and impaired gas exchange across the alveolar membrane seen with aging. The clinical implication of immune dysregulation with age is yet to be determined.

The cellular profile of epithelial lining fluid (ELF) changes with age. The ELF is rich in antioxidant defenses and minimizes oxidative injury to the respiratory epithelium following toxic exposure. ELF is rich in superoxide dismutase, catalase, metal binding proteins, glutathione, and vitamins C and E. In vitro and in vivo studies showed reduction in antioxidant levels in the ELF on exposure to ozone, nitrous oxide, and particulate matter. Composition of ELF changes with age, increasing susceptibility of older individuals to environmental toxic exposure (Kelly et al 2003)

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