Читать книгу Pathy's Principles and Practice of Geriatric Medicine - Группа авторов - Страница 78

With age, mucus glands decrease in large airways, thus reducing mucus production. Tracheal cartilage becomes ossified and stiff, and bronchial cilia movement reduces with age. Vocal cord elasticity is impaired with age, making the voice thinner and harder to project. Small airway changes in the ageing lung include loss of elastic recoil, reduced lung compliance, increased fibrosis of lung parenchyma, and loss of alveolar surface area. Collagen and elastin structures are impaired with age, leading to alveoli and alveolar duct enlargement. Enlargement of these small airways causes easy collapse during expiration, causing senile emphysema.^88‐89 Lung compliance (chest wall compliance) decreases with age because of degenerated intervertebral disks, kyphosis, ossified cartilage ribs, weak respiratory muscles, and sarcopenia. This causes a decrease in forced vital capacity (FVC), which is a sign of restrictive pathology. Along with the destruction of small airways and weakness in the diaphragm and intercostal muscles, forced expiratory volume in 1 second (FEV1) also decreases with age. The FEV1/FVC ratio decreases, as the reduction in FEV1 is more prominent than the reduction in FVC, leading to a pattern of obstructive pathology. Residual volume (RV) increases due to decreased elastic recoil and decreased chest wall compliance.^90‐91

Older people tend to breathe more deeply, which demands excessive respiratory muscle performance. The total lung capacity (TLC) does not change significantly with age. Structural changes in lung parenchyma result in an impaired capacity to diffuse oxygen more so than is the case for carbon dioxide, leading to a lower arterial partial pressure of oxygen without resulting in desaturation of haemoglobin. An impaired response to the sympathetic nervous system is seen in the respiratory system as well as the cardiovascular system, resulting in bronchoconstriction, hypoxia, and delayed acceleration of respiratory rate with stress such as exercise. In addition, the coughing reflex is impaired in the elderly. As a result, aspiration of food into the airway and related complications (like pneumonia) are more commonly experienced with age.⁹² Decreased mucus secretion impairs the immune defence system of the respiratory system, further predisposing elderly people to lung infections.

Cigarette smoke is the primary extrinsic factor causing parenchymal damage of the lungs. Smoking causes inflammation, immune response, and oxidative damage to the alveoli epithelium. Cigarette smoke also leads to increased vascular permeability; neutrophils migration to the alveolar interstitium; production of proinflammatory cytokines like IL1, IL6, and TNF alpha; exaggerated immune response; increased metalloproteinase activity; and degraded collagen and elastin in the alveoli interstitium, eventually resulting in alveolar structural damage. Lymphocytes and NK cells contribute to these damaging mechanisms as well. Impaired elastic recoil and decreased alveolar surface are the main properties of emphysema triggered by smoking. In addition, mucociliary clearance of chemicals is impaired with smoking. Tobacco is responsible for 50% of laryngeal and lung cancers.^93‐95