Gwyneth A. Davies, Charlotte E. Bolton The commonly used respiratory function tests are presented in this chapter. In addition, patterns of lung function abnormality seen in some of the common types of condition are also presented. Breathing parameters include the following: The following parameters require more detailed lung physiology testing: In addition, blood gas measurements are often performed to assess acid-base balance and oxygenation. The most important measures for respiratory disease are the partial pressure of oxygen (PaO2), partial pressure of carbon dioxide (PaCO2), and the pH. A low PaO2 (hypoxemia) with a normal PaCO2 indicates type I respiratory failure. An increased PaCO2 with hypoxemia indicates type II respiratory failure. A rapidly rising PaCO2 will result in a fall in the pH—for example, that seen in an acute exacerbation of chronic obstructive pulmonary disease (COPD). Renal compensation occurs in response to a chronically high PaCO2, with correction of the pH to normal or near-normal levels, but this renal compensation takes several days to occur. Hyperventilation, associated with excess expiration of CO2, as seen in anxiety attacks but also in altered respiratory control such as Cheyne-Stokes respiration, will result in an increase in pH as a result of a drop in PaCO2. Pure anxiety-related hyperventilation will not cause hypoxemia but other causes for this altered respiratory control may cause hypoxemia. There are two main characteristic patterns of respiratory disease based on spirometric evaluation, the obstructive and restrictive patterns. An obstructive pattern is seen in several situations including in patients with asthma and COPD. It is characterized by the following: A restrictive pattern is characterized by the following: Conditions relating to both these spirometric patterns, with more detail about lung function patterns and the use of other lung physiology parameters to characterize and diagnose conditions, will be discussed elsewhere in this text. Lungs age over a lifetime but there is, in addition, an accumulation of environmental insults to which an individual has been exposed, given that the lungs have direct contact with the atmosphere. The key exposure is smoking in the form of direct smoke but also second-hand passive smoking, the impact of which has been increasingly recognized.1,2 A quantitative evaluation of a person’s smoking habit is usually classed in relation to the number of pack-years (e.g., 20 cigarettes/day =1 pack/day; for 10 years, this equates to a 10-pack-year history). Oxidative stress is an important mechanism of lung function decline, with oxidants both from cigarette smoke and other causes of airway inflammation.3,4 Oxidants and the subsequent release of reactive oxygen species (ROS) lead to the reduction and inactivation of proteinase inhibitors, epithelial permeability, and enhanced nuclear factor κB (NF-κB), which promotes cytokine production and, in a cyclic fashion, is capable of recruiting more neutrophils. There is also plasma leakage, bronchoconstriction through elevated isoprostanes levels, and increased mucus secretion. The lung has its own defensive enzymatic antioxidants, such as superoxide dismutase (SOD), which degrades superoxide anion and catalase, and glutathione (GSH), which inactivates hydrogen peroxide and hydroperoxidases. Both are found intracellularly and extracellularly. In addition there are nonenzymatic factors that act as antioxidants, such as vitamins C and E, β-carotene, uric acid, bilirubin, and flavonoids.5 There has been a renewed interest in the effect of critical early life periods determining peak lung function and the subsequent “knock-on” effect on the adult and older adult’s lungs. If peak lung function reserve is not attained, then even the natural trajectory of decline may lead to symptomatic lung impairment in midlife or later life. Such factors in early life would include premature birth, asthma, environmental exposure, nutrition, and respiratory infection.6,7 In addition, the effects of environmental pollution, nutrition, respiratory infections, and physical inactivity on lung function decline have been reported.8,9 The mechanisms affecting respiratory function are likely to be multiple and cumulative. Interestingly, in the Inuit community, where their lifestyle has gradually become more westernized—and with a reduction in fishing and hunting activities and the community developing a more sedentary lifestyle—there has been acceleration in age-related lung function decline.10 In the aging lung, there are structural and functional changes within the respiratory system and, in addition, immune-mediated and extrapulmonary alterations. These are discussed in detail in this chapter. There are three main structural changes in the aging lung—altered lung parenchyma and subsequent loss of elastic recoil, stiffening of the lung (reduced chest wall compliance), and the respiratory muscles. The main change is the loss in the alveolar surface area as the alveoli and alveolar ducts enlarge. There is little alteration to the bronchi. The small airways suffer qualitative changes far more than quantitative changes in the supporting elastin and collagen, with disruption to fibers and loss of elasticity leading to the subsequent dilation of alveolar ducts and air spaces, known as senile emphysema. The alveolar surface area may drop by as much as 20%. This leads to an increased tendency for small airways to collapse during expiration because of the loss of surface tension forces.11 In a healthy older individual, this is probably of little or no significance, but reduction in their reserve may unearth difficulties during an infection or superadded respiratory complication. Amyloid deposition in the lung vasculature and alveolar septae occurs in older adults, although its relevance is unclear. Within the large airways, with aging, there is a reduction in the number of glandular epithelial cells, resulting in a reduced production of mucus and thus impairing the respiratory defense against infection. Chest wall compliance is decreased in older adults. Contributing to this increasing stiffness of the lungs are loss of intervertebral disc space, ossification of the costal cartilages, and calcification of the rib articulatory surfaces, which combine with muscle changes to produce impaired mobility of the thoracic cage. In addition to these, additional insults from osteoporosis leading to vertebral collapse have been shown to result in a 10% reduction in FVC,12 probably through developing kyphosis and increased anterior-posterior diameter—the barrel chest. Such vertebral collapse is frequently found in older adults, increasing with age, if determined through appropriate imaging. These structural alterations lead to suboptimal force mechanics of the diaphragm and increasing chest wall stiffness. Rib fractures, again common in older adults, may further limit respiratory movements. The predominant respiratory muscle is the diaphragm, making up about 85% of respiratory muscle activity, with the intercostal, anterior abdominal, and accessory muscles also contributing. The accessory muscles are used by splinting of the arms, a feature commonly associated with the emphysematous COPD patient. Inspiration leading to chest expansion is brought about by these muscles contracting, whereas expiration is a passive phenomenon. The accessory muscles are used when there is increased ventilatory demand, such as in the COPD patient. The respiratory muscles are made up of type I (slow), type IIa (fast fatigue-resistant), and type IIx (fast fatigable) fibers. The difference in the muscle fibers is based on the aerobic capacity and adenosine triphosphate (ATP) activity of the myofibrils and confers differing physiologic properties. The major age-related change in the respiratory muscles is a reduction in the proportion of type IIa fibers, which thus impairs strength and endurance.13 An increasing reliance on the diaphragm due to loss of intercostal muscle strength and the less advantageous diaphragmatic position to generate force add to breathlessness. Globally, there is reduced muscle myosin production, and this is likely to confer a disadvantage to the respiratory muscles also. Comorbid conditions, such as COPD and congestive heart failure, are associated with altered muscle structure and function, as is poor nutrition.14–16 Physical deconditioning and sarcopenia, hormone imbalance, and vitamin D deficiency will exacerbate the age-related lung structural changes; the body becomes less adaptive to the respiratory limitations. Medications, especially oral corticosteroids, may cause problems, particularly with regard to respiratory and peripheral muscle strength. Acute infection puts added demands on the respiratory system and may expose the limited respiratory reserve.
Age-Related Changes in the Respiratory System
Respiratory Function Tests
Age-Related Changes in the Respiratory System
Structural Changes
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Age-Related Changes in the Respiratory System
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