Pulmo Hazzard.docx

Structural changes associated with age occur most notably in the alveoli rather than the large airways. Alveoli are where gas exchange takes place. All the environmental lung insults. accumulated over a lifetime affect the alveoli and change their structure. For example, alveoli lose their elastic recoil and enlarge with age, a phenomenon referred to as “senile emphysema.” Unlike what occurs in other pathologic processes, “senile emphysema” results in alveolar dilatation without any destructive changes to the alveolar walls. Moreover, there is no reduction in the production of elastin, collagen, or surfactant. These characteristics lead us to believe that the increase in surface area is probably a result of changes to the structures surrounding the alveoli that accumulate over time, and result in reduced surface tension forces on the alveolar walls and in turn reduced lung recoil. The next important change in lung function with age is attributed to the chest wall rather than the lung itself. The lungs are suspended within the chest wall which plays a crucial role in maintaining function. As noted in other chapters within this text, structural changes to bone are a common phenomenon of aging. Calcification of the articulating surfaces of the ribs and ossification of the cartilage make the chest wall stiffer. The vertebrae are also affected by a loss of intervertebral space and a compression of the vertebral bodies resulting in reduced vertebral height. These changes modify the shape of the thorax and result in kyphosis and a barrel-shaped chest. Such reshaping affects the outward force needed to keep the lung in shape during respiration and the next section addresses how spirometry readings reflect these changes. Aging also affects muscle strength throughout the body, and the respiratory muscles are not spared. Expiration is largely a passive process, while inspiration depends mostly on the diaphragm. Compared to young adults, healthy older persons have approximately 25% lower diaphragmatic strength. Due to the age-related decline in muscle strength, there is a decline in the maximum inspiratory and expiratory pressures in the normal population. Further, as a result of the changes in the chest wall there is also an increased load on accessory muscles of respiration. The vital capacity is reduced when the diaphragm is weak and expiratory muscles of the abdomen and thorax cannot fully compensate to empty the lungs before reaching the resting respiratory position. Respiratory muscle strength is higher in men, but declines with age in both sexes. The mean MIP for healthy 85-year-old men is approximately 30% lower than that for 65-year-old men. A lower MIP is associated with many factors, including decreased handgrip strength, lower body mass index, and current smoking. A low MIP often causes a low functional vital capacity. LUNG VOLUMES AND LUNG CAPACITIES Total lung capacity (TLC) is the volume of air within the respiratory system when a subject makes a maximal voluntary inspiratory effort. It is a sum of RV, the volume of air remaining in the lungs when subjects have exhaled as much air as possible, and VC, the amount of air that a person can slowly exhale after inhaling maximally. TLC is determined by the balance of forces between the maximally activated inspiratory muscles and the elastic recoil of the lung and chest wall. As we discussed, the elastic recoil of lung tissue decreases with aging, which makes it easier for the lungs to expand with less effort, increasing TLC. However, the increased stiffness of the chest wall and the loss of motor power together decrease TLC. Thus, the two together result in an almost unchanged TLC with age. Because lung recoil decreases with age and the muscles that oppose outward chest wall recoil weaken, RV and the ratio of RV to TLC increase from young adulthood to older age. Collapse of the alveoli with aging, which results in air trapping, also contributes to the increase in RV. Abnormally high RV/TLC is called hyperinflation, which can often be seen on a chest x-ray, and occurs with both asthma and COPD as well as advanced age. Because TLC is relatively constant while RV

increases with age, the VC decreases with age. Functional residual capacity (FRC) is the volume of air left at the end of normal respiration. This again is determined by the opposing factors of lung recoil and chest wall compliance. The increase in FRC with age, roughly 1% to 3% per decade, is a direct result of losing more lung recoil than chest wall compliance at the end of normal tidal expiration. Both FRC and RV increase with age, but RV increases more than FRC. Expiratory reserve volume (ERV) is the difference between RV and FRC. Both FRC and RV increase with age, as discussed above, but RV increases more than FRC. With aging, expiratory airflow is impaired, and air is often trapped in the dependent alveoli. This is due to changes in the pressure dynamics across alveolar openings discussed earlier. Thus, there is a reduction in ERV over the normal process of aging. Spirometry is easily performed on 9 of 10 older adults and measures dynamic lung function. Modern office spirometers use a flow sensor, connected to a microprocessor that determines the forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and FEV1/FVC from the best maneuver, as well as the predicted values. FEV1 is the most important value, representing the volume of air (in liters) exhaled during the first second. Guidelines for spirometry methods and instrument accuracy are available from the American Thoracic Society. The presence of airways obstruction is indicated by a low FEV1/FVC ratio and visualized on the flow-volume (F-V) curve as concavity toward the volume axis or tail at the end of the maneuver. The descending limb of the F-V curve of healthy young adults is a straight line at about a 45 degree angle until the end of the maneuver (shaped like a sail), corresponding to exponential emptying of the lungs. The shape of the F-V curve becomes progressively more curvilinear as a healthy adult becomes older, corresponding to decreases in expiratory flows at low lung volumes. The reduced flow at low lung volumes, even in healthy older adults, is a result of a decrease in the mean diameter of small airways. Adults normally experience a loss in FEV1 of about one-third liter per decade. The decline in FEV1 with aging is greater than the decline in FVC, so that the FEV1/FVC also declines with age. Values below 0.65 usually indicate airway obstruction in patients aged 65 years and older. Many nonpulmonary factors contribute to the decline in the FEV1 in older adult persons. The strongest factors are cigarette smoking; a diagnosis of COPD or asthma; workplace exposure to dust, chemicals, or smoke; and wheezing symptoms—all of which are known to cause airway obstruction (a low FEV1/FVC ratio). The inability to take a deep breath (restriction) also reduces the FEV1, a symptom seen in obesity, malnutrition, heart disease, and chest wall abnormalities. Lung volume restrictions can also be associated with ECG abnormalities, pitting angle edema, diabetes and past history of chest surgery. Further, for a given height, gender, and age, the FVC and FEV1 of healthy older African Americans is approximately 12% lower than that of healthy older Caucasians, thus spirometry reference equations, which are race/ethnicity specific (as from the NHANES III study), are used to calculate predicted values. Since spirometry tests require athletic-type breathing maneuvers, poorly trained technologists in outpatient settings often do not obtain maximal patient effort during one or more of the three phases of the maneuver, causing misclassification of the results. It is also important to note that maximal expiratory flow, as seen during spirometry tests, varies as a function of lung volume because higher flows are possible at a higher lung volume. For forced exhalation beginning from a deep inhalation (the first phase of a spirometry maneuver), the initial (peak) flow (phase 2) is determined by the recoil of the lung and chest wall and the degree of effort expended by the patient, as well as by the speed with which the patient’s respiratory muscles can generate positive pleural pressure. Once maximal flow is achieved, maximal flow throughout the remainder of the VC (phase 3) is determined by the intrinsic properties of

the lung. Another important change to be studied in aging is the effect on closing volume (CV). It is measured at the point where basal airways close during normal expiration and is determined as the volume of gas that can be exhaled starting from the point of sharp change in alveolar concentration of the tracer gas after the alveolar plateau. This volume combined with RV from closing capacity (CC), which increases linearly with age from approximately 10% of TLC in young adults to approximately 30% of TLC by the age of 70. Increased CV is likely a result of reduced elastic recoil in the lung, which results in the collapse of the small airways. RESPIRATORY MECHANICS The ventilation of a respiratory zone must match its perfusion (V/Q matching) for optimal gas exchange. However, even in normal conditions, the ventilation of lung is not uniform and there is increased perfusion of the base of the lung, resulting in a low V/Q ratio in the sitting position. This difference is not significant enough to cause a disturbance in gas exchange under normal conditions. This equilibrium is even more disturbed in aging. As discussed, the increased rigidity of the chest walls combined with reduced elastic recoil of the lung leads to an airflow limitation. This is seen as a decreased FEV1/FVC, increased FRC, increased CV and increased RV. All of this combines and further reduces the ventilation at the bases of the lungs in comparison to perfusion, resulting in a much lower V/Q ratio in older adults. The lungs, however, are still capable of a large physiologic reserve and therefore these changes are not evident in older adults unless they are affected by a pathologic process. Curiously enough, there are also areas with an increased V/Q ratio in older adults due to the changes in perfusion of the lung. Under normal conditions, the area where such a mismatch happens is minimal. They have impaired clearance of CO2 and are called “alveolar dead spaces,” one of the components of physiologic dead space. This reduced perfusion results in an increased PaCO2 (arterial partial pressure of carbon dioxide) and is thus an alternate form of peripheral alveolar hypoventilation. With age, there is an increase in the pulmonary vascular resistance and decline in the density of lung capillaries. These changes result in increased pulmonary vascular pressure with aging, causing a heterogeneous pattern of lung perfusion with reduced flow to some areas that exhibit an increased V/Q ratio. Lung perfusion can also be reduced with aging because of lower cardiac output. Reduction in lung capillary density, along with the reduction in the alveolar surface area leads to decline in other measurable lung functions, for example, the diffusion lung capacity for carbon monoxide (DLCO). DLCO is the amount of carbon monoxide (from a test gas containing 0.3% CO) that is absorbed into the blood during a 10-second breath-hold and a measure of the transfer capacity of the lungs across the alveolar-capillary interface. The test can be performed using a single-breath DLCO technique available at all hospital-based pulmonary function laboratories. A 15-minute noninvasive DLCO test is more expensive and skillintensive, but may be clinically valuable for differentiating airway obstruction and restriction of lung volumes. In healthy persons, the absolute value of DLCO in adults varies with height, age, gender, and race. As with spirometry, 1238 AGING OF THE RESPIRATORY SYSTEMCHAPTER 83 reference values from the healthy subset of large population studies are used to obtain percent predicted values for individual patients. DLCO is higher in very obese persons and lower in patients with anemia. The DLCO declines about 5% per decade after age 40 years, even in healthy adults. Acid-base balance is tightly controlled, and therefore, normal values for arterial pH and PaCO2 do not change throughout adult life in healthy persons. However, because of increased nonuniformity of ventilation

with aging, mean arterial oxygen tension (PaO2 [partial pressure arterial oxygen]) declines during middle life even in healthy never-smokers. Mean PaO2 remains relatively constant at about 80 mm Hg from age 65 to 90 years in healthy older persons at sea level. This is probably because hemoglobin/ oxygen (HbO2) dissociation curve levels off at PaO2 values greater than 60 mm Hg. So in areas with high V/Q ratio, there is no change in the O2 content of the blood while the areas with decreased V/Q ratio will have a reduced O2 content. This results in a combined reduction in PO2 which becomes significant only when it falls below 60 mm Hg. However, CO2 is linear in its relationship, therefore areas with increased V/Q ratio will have decreased PaCO2 and areas with low V/Q ratio will have high PaCO2 resulting in a net unchanged PaCO2. AGING IN IPF AND COPD Aging is associated with an increased incidence of a number of diseases affecting all organ systems, from atherosclerosis to osteoporosis. Similarly, aging lungs are prone to diseases, and we know that COPD and IPF, two common chronic disorders of the lungs, are seen more frequently in older adults. What is interesting is that even though COPD and IPF are distinct disease entities, they share some similarities with each other and the normal process of aging. Both COPD and IPF occur late in life and are associated with enhanced deposition of collagen and subsequent fibrosis. Collagen deposition is seen in the small airways in COPD versus the lung parenchyma in IPF. In both diseases, there is a loss of alveolar parenchyma that leads to impaired respiratory function. IPF and COPD, which can occur in the same person, are associated with an increased incidence of lung cancer and most studies suggest that this is unrelated to the risk for cancer posed by smoking cigarettes. It is widely believed that abnormal regulation of the aging process contributes to the pathophysiology of these diseases. Further, many think that abnormal regulation, rather than aging acceleration, is responsible for both illnesses. CONCLUSION Healthy adults experience a number of changes in the structure of the lung and chest wall, lung volume, capacity, and mechanics. Although aging is pathologically distinct from a number of disease entities common in older adults (eg, IPF and COPD), aging reduces reserve in the respiratory system and confounds the diagnosis of numerous disease processes. COPD and IPF exhibit abnormal regulation of the natural aging process, the exact results of which become clearer when contrasting the respiratory system of a healthy, nonsmoking adult and that of an older adult exhibiting a chronic respiratory disease.