5 - EFFECTS OF AGING ON RSPIRATORY SYSTEM Flashcards
AGING PROCESS: def & description
- Aging process alters intrinsic structure of lung & supportive extra pulmonary structures (chest wall, spine & respiratory muscles)
- Structural changes lead to unfavorable respiratory mechanics associated with decreased expiratory flows, increased air trapping & closing volume, decreased gas exchange
- Changes in lung structure & resting lung function impact exercise physiology in elderly
- Normal aging physiology synergies with pathophysiology of certain lung diseases to worsen lung function & disease manifestations in geriatric patients
- Aging like a free fall => can be delay, not stop. If you’re still alive, you’ve already jumped
What does elder mean?
- According to bible in New Testament, refers to leaders & rulers of community of heads of households
- According to WHO, subject can be considered elder when it’s 65 y.o
Comparison between 75y & 30y
- 92% of brain weight
- 84% of basal metabolism
- 70% kidney filtration rate
- 43% of maximal breathing capacity
!! We’re not people we once were !!
Mechanics breathing
- Rounding of thorax
- Calcification of costal cartilages (decreased thoracic compliance)
- Decreased space between spinal vertebrae & greater degree of spinal curvature
- Progressive enlargement of respiratory bronchioles & alveolar ducts
- Loss of functional alveolar surface area & alveolar surface tension
- 15% reduction by age of 70y
- Negative effects on forced expiratory flow
- Decreased respiratory muscle strength & endurance
- Compliance increases until 20 y.o
- After 20 y.o = free fall, lungs less compliance => easy to inflate but doesn’t deflate ==> big chest
Airways function & structure
- Increased airway reactivity
- Decreased ciliary number & activity
- Diminished airway reflexes
- Higher risk of bronchospasm
- Bronchospasms requires lesser stimulus
- Clearance of secretions impaired
- Increased propensity towards pharyngeal collapse
- With aging, preferential deposition of fat around upper airway occurs, suggesting changes in fat distribution compromise airway mechanics independent of verbal body fat
Structural properties of chest wall
- Calcification of costal ligaments
- Thoracic vertebral height loss
- Kyphosis
- Decreased chest wall compliance
- Higher residual volume (RV)
- Higher FRC
- Lower vital capacity (VC)
- Unchanged total lung capacity (TLC)
Function of respiratory muscles
- Decreased total muscle mass
- Decreased muscle strength
- Decreased proportion of fast-twitch fivers
- Decreased MIP (maximum inspiratory pressure)
- Decreased FEV1
- Decreased maximum minute ventilation
- Fatigue develops more rapidly
- Exercise capacity decreased
- Decreased diaphragmatic excursion
Lung structure & function decreasing
Structure
- “Senile emphysema”: hyperinflation
- Degeneration of elastic fibers
- Reduction in supporting tissue around small airways
- Increased lung compliance
- Decreased elastic recoil
- Increase dead space ventilation
- Increased closing volume due to premature small airway closure, increasing risk of gas trapping
Function decreasing
- FEV1 decreases with age by about 27 mL/year in men & 22mL/year in women
- Forced vital capacity (FVC) decreases by about 14 to 30 mL/year in men & 15t 24mL/year in women
- Decreases in FEV1 & FVC occurring until 40y are thought to result from changes in body weight & strength rather than tissue loss
Gas exchange: description
- Gas exchange declines at 0,5%/y
- Ventilation-perfusion ratios adversely affected by increasing age
- Increased areas of high V/Q thus causing increase in physiological dead space from 20% at 20y subject to 40% at 60y
- Increase in proportion of alveoli that have low V/Q resulting in increase in venous admixture
- No correlation between blood gas values & age in
- Series of elderly subjects, decrease in transfer capacity of lung carbon monoxide suggests that oxygen transport may be diffusion limited in aging
- Risk of hypoxemia & hypercapnia higher in patients > 70y & response to supplemental oxygen reduced
- Age-associated changes in expression, post-translational modifications & remodeling of fibrillation collagens are instrumental in progression of extra cellular matrix stiffness
- Normal lung aging characterized by increased collagen, which promotes age related changes in elasticity & airspace enlargement
Control of breathing: description
- Decrease in efferent neural output to respiratory muscles
- Elderly individuals have significantly diminished response to hypoxia & hypercapnia
- Higher incidence of apnea & periodic breathing with narcotics
- Markedly diminished response for vocal cord closure, thus increasing risk of aspiration & its consequences - During aging process, there is a progressive blunting in sensitivity to hypoxia & reduction in CO2 threshold
Airway occlusion pressure = airway pressure generated in first 100 ms of inspiration against expiratory occlusion
Immunological changes
- Increased immunoglobulin content
- Decreased alveolar macrophage population
- Increased susceptibility to bronchospasm
- Increased susceptibility to infection
- Slower recovery from infection
- Advanced age leads to immunosenescence & inflammation through effects on primary lymphoid, secondary lymphoid & target tissues
Clinical implications
- Decreased maximum breathing capacity, vital capacity & maximal O2 uptake
- Decreased mucociliary clearance, cellular & humoral lung defence mechanisms
- Increased risk for respiratory infections
- Acute & chronic respiratory conditions can have severe consequences due to hypoxemia & hypercapnia
Exercise performance & age
- VO2 max declines with age
- Likely related, in part, to physical inactivity coincident
- With advancing age: octogenarian endurance athletes maintain VO2 max close to median of those 40y younger (38mL.min-1.kg-1) & in some cases cases younger still (50mL.min-1.kg-1)
- Cross sectional studies suggest that VO2 max declines with rate between 0,2 & 0,5 mL.min-1.year-1 after age of 30y
- Longitudinal studies suggest that VO2 max decline may accelerate after 40-50y
- Mitochondrial dysfunction, characterized by damage to mtDNA, diminished energy production & increased formation of ROS, is feature of aging & important contributor to age-related lung disease
- Alterations in mitochondrial homeostasis underlie pivotal pathological changes such as premature senescence in lung cells. Another potentially important consequences of mitochondrial dysfunction is formation & release of damaged mtDNA, which act as DAMPs to drive innate immune responses
Respiratory physiology in elderly
- Decrease pulmonary elasticity
- Decrease alveolar surface area
- Increase residual volume
- Increased closing capacity
- Ventilation / mismatching
- Decreased arterial oxygen tension
- Increased chest wall rigidity
- Decreased muscle strength: decreased cough - Modified response to hypercapnia & hypoxia
Changes in pulmonary compliance
Lung & chest wall compliance decrease with advancing age
=> Dead space increases with age because larger air always increase in diameter
=> Elastic elements of lung parenchyma lost with age
=> Aging associated with reduction in number of small airways & flattening of internal surface of alveoli
=> Reduced diffusion capacity due to aging induced from a decreases in lung area owing to damage to alveoli, increase in thickness of alveolar walls & small airway. Obstruction
