3. Cardiopulmonary system: age-related changes Flashcards

1
Q

CARDIOPULMONARY SYSTEM:
- composed of (3)
- works closely with what? and is controlled by which system?
- age-related changes are due to (2)

A
  • heart, vascular system and pulmonary system
  • work closely with respiratory system and is controlled by nervous system
  • not due solely to primary aging, but also due to secondary factors (physical inactivity, onset of disease)
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2
Q
  • which part of the heart wall thickens with normal aging?
  • myocytes become smaller/larger with age, alongside remodeling of WHAT (increase in (2)) –> leads to 2 things
  • ventricle myocyte number MAY increase/decline with aging due to (2)
A
  • left ventricle wall thickening!
  • become larger with age + remodeling of extracellular matrix (increase in collagen and fat deposit) –> myocyte hypertrophy + fibrosis/calcification (overall just very disorganizes)
  • MAY decline with aging due to both increase cell apoptosis and decrease regenerative ability of cardiac stem cells
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3
Q

why does myocyte hypertrophy occur in adults? (3) + sub

A
  1. driven by increased total peripheral resistance due to
    a) a reduced elasticity of blood vessels
    b) an increased resistance to blood flow in aged and often occluded arteries
  2. ventricles have to work harder to pump blood/O2 to the rest of the body
  3. increased mechanical load further exacerbated by heightened workload on fewer myocytes (lower # and lower quality)
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4
Q
  • what effect on the heart may occur (commonly around 70-80 years of age) and is EXACERBATED in the presence of (2)?
  • this effect affects what? and is associated with (4)
A
  • a slight increase in volume of left atrium! –> exacerbated in presence of diabetes and hypertension
    INCREASE in left atrial volume:
  • affects ability of L atrium to fill and increase pressure –> decrease in diastolic function
  • associated with arrhythmias, atrial fibrillation, stroke and even death
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5
Q

what are additional structural changes to the aging heart that affect its conduction system? (3)
- results in what? (3)

A
  1. decrease in number of cells in sinoatrial (SA) node
  2. decline in ion channel expression and calcium-handling proteins in the SA node/pacemaker cells –> alters force generation
  3. fat and collagen accumulate around the SA node
    RESULT:
    - electrical activity of SA node slows down (which slows down both de and repolarization)
    - decrease in max HR
    - greater susceptibility to conduction disorders (arrhythmia, atrial fibrillation)
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6
Q

structural changes of myocytes are associated with slower/longer contraction/relaxation during systole and slower/longer contraction/relaxation during diastole.
WHY? (3)

A
  • slower contraction during systole and longer relaxation during diastole
    WHY?
    1. slower calcium reuptake by sarcoplasmic reticulum pump
    2. decreased size of fast-twitch myosin heavy chain IIA fibers (change in muscle fiber type when you get older)
    3. increased fat, collagen and calcium deposits contributing to increased stiffness and decreased compliance of myocardium (= slows down cardiac cycle)
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7
Q

what is arteriosclerosis? (2)
- can be explained by (3)

A
  • age-related loss of compliance and increased stiffness of the arteries occurs
    1. proliferation and disorganization of endothelial and connective tissue cells (implication in elasticity)
    2. increased collagen/elastin ration
    3. increase in lumen size of vessel (stretching and not really returning to normal size)
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8
Q

changes in the arterial wall/arteriosclerosis appear to be driven by what environment that favors (2)
- largely mediated by (2) that do what to produce what?
- independent of what?

A
  • driven by microenvironment that favors inflammation and stress
  • largely mediated by endothelial and vascular smooth muscle cells that shift their phenotypes to produce inflammatory cytokines
    *leads to decrease vasodilation, increased vasoconstriction, increase fibrosis, vascular remodeling –> all lead to increase blood pressure
  • independent of arterial damage associated with plaque deposition (also known as atherosclerosis) and a feature of primary aging
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9
Q

AGING AND BLOOD VESSELS:
what happens to
- aorta and arteries
- capillaries
- veins and venules

A

AORTA AND ARTERIES
- progressive stiffening and thickening –> loss of distensibility –> increase systolic pressure
CAPILLARIES
- reduction in density and surface area, which may contribute to tissue hypoxia (inadequate oxygen and nutrient supply) bc not good gas exchange
VEINS AND VENULES
- become stiffer and less flexible (more connective tissue, calcium deposits) –> important for venous return
*ie varicose veins: branching/blood pooling at extremities

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10
Q

define
- arteriosclerosis
- atherosclerosis –> associated with (4)

*formation of what exactly?

A

ARTERIOSCLEROSIS
- generic hardening/stiffening or loss of compliance of an artery
- age-related!
- thickening of inner wall and central wall of artery
ATHEROSCLEROSIS
- very specific type of artery stiffening due to cardiovascular disease that is associated with the following, distinctive pathological processes:
a) endothelial damage
b) formation of plaque
c) stenosis (reduction of internal section of the vessel)
d) thrombosis or embolism (build up of plaque might break off)
- formation of atheromas (plaques of lipid material)

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11
Q

blood pressure and aging:
- aging causes increase in WHAT? (define)
- age related changes in WHAT affect (3)

A
  • increase in vascular tone! (degree of constriction in a blood vessel relative to its maximally dilated state)
  • age-related changes in vascular tone affect
    a) resting and exercising blood pressure
    b) ability to cope with hemodynamic challenges (ie changes in blood flow)
    c) ability to deliver O2 to the tissues
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12
Q

what are the 4 layers of a blood vessel/artery? –> these are critical determinants of (2)

A
  1. tunica externa (collagen fibers)
  2. tunica media (smooth muscle cells)
  3. tunica intima (endothelium)
  4. basement membrane
  • critical determinant of vascular tone and mechanics of blood flow
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13
Q
  • what happens to SNS when aging? results in what?
  • what happens to PSNS when aging?
  • ___________ in both result in what?
A

SNS activity and NE concentrations in blood at rest INCREASE with aging
- result: arterial stiffening, increase peripheral vascular tone, increased risk of hypertension

PSNS tone at rest DECREASES with aging

imbalance in the autonomic nervous system is a common feature of aging, BUT it is most severe in the presence of age-related disease

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14
Q
  • what (2) result in increases/decreases in resting and exercising blood pressure?
  • chronic/acute exposure to increased/decreased systolic/diastolic BP contributes to WHAT, causing a further rise in what?
  • what happens to diastolic BP with age? why?
A
  • structural alterations in vascular tone + stiffening of aortic and arterial walls —> increase in resting and exercising BP
  • chronic exposure to increased systolic BP contributes to left ventricle hypertrophy! causing further rise in myocardial O2 demand
  • diastolic BP tends to DECLINE with age –> reduction in aorta elasticity and reduced elastic recoil of arterial wall during diastole (heart doesn’t fill as quickly = decrease DBP)
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15
Q
  • systolic hypertension and lower diastolic BP result in increased/decreased O2 supply despite higher/lower oxygen demand
  • healthy BP = what?
  • hypertension = WHAT?
  • ___% of canadian adults aged 60-79 yo have hypertention
A
  • decreased O2 supply despite higher O2 demand
  • 120/80 mm Hg
  • > =130/>=80 mmHg
  • 53%
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16
Q

(2), especially in the presence of WHAT may lead to myocardial ischemia and potentially myocardial infarction
define myocardial ischemia VS infrrction

A
  • coronary atherosclerosis and remodeling of myocardial microvasculature, especially with chronic hypertension (drives incidence of CV event)
    MYOCARDIAL ISCHEMIA
  • occurs when blood flow to the heart muscle is obstructed by a partial or complete blockage of a coronary artery (build up of plaque) –> injury to tissue (lack of O2)/death of cells ish –> plaque builds up and can rupture (infarction)

MYOCARDIAL INFARCTION:
- necrosis of cardiac myocytes resulting from prolonges ischemia caused by complete vessel occlusion
- further perpetuates lack of O2 delivery

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17
Q

define cerebrovascular disease
- 3 examples
- if (2) prevent brain cells from getting enough _______, what can occur?
- develops due to variety of causes including (4)
- stroke can happen at any age but stroke prevalence rises sharply after what age?

A
  • refers to a group of vascular diseases that affect the blood supply to the brain
  • stroke, transient ischemic attack (TIA), aneurysm
  • if a blockage (ischemic) or rupture (hemorrhagic/brain bleed) prevents brain cells from getting enough O2, loss of brain function can occur
  • atherosclerosis, thrombosis, embolic arterial or venous blood clots –> vascular changes!
  • 55!
18
Q
  • ability to cope with hemodynamic perturbations during movement is increased/reduced with aging –> increase susceptibility to (2)
  • define orthostatic or ________ hypotension
  • WHY? (2)
A
  • reduced with aging! –> increase susceptibility to dizziness and fainting
  • orthostatic/postural hypotension: low BP after rapid posture changes (standing up from bed, abrupt exercise cessation, Valsalva maneuver)
    WHY
    a) impaired ability of blood vessels to dilate in response to an increased metabolic demand from the tissues (decrease muscle pump)
    *inadequate venous return
    b) impaired ability to deliver O2 to the tissues
19
Q
  • blood volume is increased/reduced by ___% with aging –> contributes to what?
  • what disease ish has been reported in 11% of >65 yo and in 20% of those >85 yo. what are the cut-offs to be diagnosed?
  • causes of that disease (3)
A
  • reduced by 10% –> contributes to a reduction in preload at the end of diastole
    ANEMIA!
  • <12.2g/dL in women and <13.2 g/dL in men
    CAUSES
  • idiopathic (unknown)
  • chronic disease or inflammation
  • caloric or nutritional deficiency
20
Q

Summary: age-related changes to CV system
- age-related structural and functional changes in CV system contribute to a linear increase/decline in (2)
- even though some age-related deteriorations are virtually ________, there are several age-related limitations that can be ________ by participating in what?

A
  • linear decline in aerobic capacity and exercise tolerance
  • unavoidable –> reversed by participating in regular exercise
21
Q

What age- and disease-related changes are taking place in the structure and function of Shirley’s heart? (4)

A
  1. left ventricle wall thickens (due to chronic systolic hypertension): increased collagen relative to elastin within the myocardial cells (less flexible/distensible) + ventricle myocyte number decline
  2. Slower contraction during systole and slower relaxation during diastole (fat/calcific deposits, calcium pump dysfunction, decrease in FT fibers)
  3. Left atrial size/volume increases (affects filling) + decrease in the number of cells in the SA node/pacemaker -> increased risk for arrhythmias/conduction disorders
  4. Heart attack – myocardial ischemia and infarction secondary to coronary atherosclerosis (endothelial dysfunction, thrombosis or embolism)
22
Q

What age- and disease-related changes are taking place in the structure and function of Shirley’s blood vessels? (4)

A
  • Loss of compliance and increased stiffness (greater collagen relative to elastin) of the connective tissue in arteries, also known as arteriosclerosis
  • Reduction in the density and surface area of the capillaries, resulting in a reduced delivery of O2 at rest and to working muscles during exercise
  • Coronary atherosclerosis – stiffening of arteries leading to plaque deposition/break off and occlusion of blood vessels – could be linked to heart attack
  • Uncontrolled hypertension due to increased sympathetic nervous activity, increased vascular tone, endothelial dysfunction/vascular smooth muscle apoptosis (inflammation)
23
Q

which pulmonary mechanisms (2) are altered by normal aging, typically starting after age of ____
- BUT limiting factor for exercise?

A
  • mechanisms by which pulmonary system can achieve adequate delivery of oxygen and removal of carbon dioxide are altered by normal aging, typically starting after age of 30.
    BUT pulmonary system does so without becoming the primary limiting factor for exercise –> pulmonary system is typically thought of as being over-engineered!!!
24
Q

resting pulmonary function peaks around age ____, and then declines ______, with a steeper decline after ages ___-____
- can be explained by (3)

A
  • age 30, declines linearly, steeper decline after ages 50-60
    1. resistance to air flowing out of airways –> decrease rate of expiratory airflow
    2. structural changes that occur in the airways, lungs, chest wall and respiratory muscles –> decrease strength = decrease capacity
    3. alterations in lung volumes and capacities
25
Q

what happens to airway diameter, lung elastic recoil and airway tethering after age of 40? increase or decrease?
- results (3)

A

AIRWAY NARROWING
- decrease airway diameter
- decrease lung elastic recoil
- decrease airway tethering –> small airways of older adults are more susceptible to dynamic compression and collapse –> alveoli share walls together –> if 1 collapses, the other one will also collapses

RESULTS:
- greater volume of air left in the lungs at the end of a complete exhalation (increase residual volume)
- residual volume increase by 250mL per decade
- less functional or usable lung volume

26
Q

age-related decrease in lung elastic recoil leads to increase/decrease lung compliance –> WHY?
- what happens to chest wall compliance with age? WHY? (2)
RESULT?

A
  • decrease lung elastic recoil = increase lung compliance (ability for lungs to stretch and expand) in older adults
    BC alteration in collagen and elastin fiber network in lung tissue –> can stretch well but don’t return to normal size = bad
  • chest wall compliance decreases with age
    BC 1) calcification of costal cartilage (chest is stiffer, less able to stretch)
    2) greater kyphosis, postural change –> reduced intervertebral spaces, loss of vertebral height, more hunched over
    RESULT: reduced expiratory airflow with aging
27
Q
  • what happens to respiratory muscle strength starting at age 40?
  • driven by increase/decrease in what strength? due to (3)
A
  • decrease by 8-10% per decade
  • driven by DECREASE in diaphragm strength due to
    1) age-associated muscle weakness and atrophy (+ change in muscle type)
    2) decrease in force generation
    3) reduced chest wall compliance
28
Q

what is
- TIDAL VOLUME (VT)
- INSPIRATION RESERVE VOLUME (IRV)
- EXPIRATION RESERVE VOLUME (ERV)
- RESIDUAL VOLUME (RV)

  • INSPIRATORY CAPACITY (IC)
  • FUNCTIONAL RESIDUAL CAPACITY (FRC)
  • VITAL CAPACITY (VC)
  • TOTAL LUNG CAPACITY (TLC)
A
  • VT: volume that moves during a respiratory cycle (air that gets in/out during normal breathing) (kinda like stroke volume)
  • IRV: additional volume above tidal volume (when you use neck muscles)
  • ERV: forcefully exhaled after end of normal expiration (when you use abs and internal intercostal muscles)
  • RV: volume of air in respiratory system after maximal exhalation
  • IC = IRV + VT
  • FRC = ERV + RV
  • VC = IRV + VT + ERV
  • TLC = IRV + VT + ERV + RV
29
Q

what happens to lung volumes with aging?
- TLC
- RV
- VC
- ERV
- IRV
- FRV
*think of schéma!

  • forced expiratory volume
  • FEV1
A
  • total lung capacity is either unchanged or increases slightly (bc more compliant lungs, can stretch more)
  • residual volume increases by 30-50%
  • by 70 yo, vital capacity is reduced by 40-50%
  • after age 65, expiratory reserve volume is decreased by 10-20%
  • inspiratory reserve volume remains steady
  • functional reserve capacity increases slightly
  • forced expiratory volume at 75% of vital capacity is reduced by 64% from age 25 to 65 yo in men and by 69% in women
  • forced expiratory volume in 1sec (FEV1) also declines with age –> prediction equations demonstrate that FEV1 is reduced by 25-30% from age 25-65 in both men and women
30
Q

why are there age-related changes in lung volumes and capacities? (3)

A
  1. structural changes in pulmonary system
  2. increase in lung compliance
  3. decrease in airway tethering
31
Q
  • is minute ventilation at rest altered during aging?
  • what about during exercise? can be explained by (3)
  • consequence?
A
  • does not appear to be altered with age
  • VE responses to exercise are consistently higher in healthy older adults versus young adults (particularly at >65-85% peak VO2)
    1. increase physiological dead space (unusable air volume + matching ventilation and perfusion)
    2. decrease ventilatory threshold (acidotic effect, lactate)
    3. decrease contractile respiratory muscle strength
  • LEADS to progressive increase in exertional breathlessness with advancing age! + greater awareness of it!
32
Q
  • dead space volume is ___-___mL greater/smaller in older adults vs younger
  • proportion of tidal volum made up by dead space volume (VD/VT) is greater/smaller) in older adults compared to younger
  • RESULT?
A
  • 30-40mL greater in older
  • proportion is greater in older (24 vs 17%)
  • RESULT: ventilation is less efficient –> VE/VCO2 is higher for a given exercise intensity and workload in older adults –> breathing more bc less effective removal of CO2
33
Q

what is work of breathing?
- what happens to it when aging? particularly when?
- at modest exercise intensities eliciting a minute ventilation of 50-60L/min, older adults have a WoB that is ____% greater/smaller than younger adults, even more pronounced in which populations?

A
  • energetic cost of breathing
  • age-related changes in energetic cost of breathing can occur, particularly when ventilation is high (ie during exercise) –> increase ventilation = increase E cost
  • that is 40% greater than younger adults, more pronounced in older women –> less efficient breathing
34
Q
  • what happens to pulmonary vascular resistance with age? leads to increase in what? during exercise
  • WHY (3)
A
  • increase in pulmonary vascular resistance, and therefore, increase in mean pulmonary artery pressure (MAP)
    1. decrease pulmonary vascular compliance
    2. decrease elastin fiber concentration in pulmonary circulation
    3. decrease left ventricular compliance
35
Q
  • with aging, there is a well-described increase/reduction in diffusing capacity at rest. WHY (4)
  • however, older adults can do what?

*Recall: what is Fick’s law of diffusion?

A
  • reduction in diffusing capacity at rest
    1. decrease surface area of diffusion (fewer, larger alveoli)
    2. decrease number of pulmonary capillaries
    3. decrease hemoglobin (O2 carrying component) due to anemia
    4. less ideal matching of airflow and blood flow!
  • however, older adults can increase diffusing capacity during exercise without reaching a plateau
  • Vgas = Diffusion coefficient x (P1-P2) x surface area/thickness of barrier
36
Q

Resting PaO2 increases/decreases with aging, possibly due to greater what?
- the difference btw PAO2 and PaO2 is increased/decreased slightly at rest and during exercise, but arterial _______ rarely occurs during aging. WHY?

A
  • decreases with aging! bc greater ventilation/perfusion mismatch
  • difference (what drives O2 delivery) is increased slightly at rest and during exercise –> but arterial hypoxemia rarely occurs during aging
    WHY? over-engineered lungs allow for normal oxygenation of blood at rest and during exercise in both the young and older adult!

PAO2 = alveolar
PaO2 = arterial

37
Q

are older adults limited by lungs during exercise?
- what is a symptom they can feel? describe?
- however, what happens to fit older adults?

A
  • Healthy older adults can perform their activities of daily living and most physical exertion uninhibited by the lungs
  • Shortness of breath (or dyspnea) often causes older adults to voluntarily end exercise sessions
  • SoB = Subjective feeling of breathing discomfort that varies in intensity; pathological when it occurs in unexpected situations –> have to think about it and manage!
  • However, highly fit older adults can reach the limits of their lungs during performance events –> decrease pulmonary transit time (blood flow is going too fast) –> can lead to exercise induced arterial hypoxemia (not present in general healthy elders)
38
Q
  • respiratory illnesses like ___A_____ are significant contributors to (2) in older adults –> incidence of ___A____ are ___x greater than in younger adults
  • 3 causes ish
  • RESULT? (3)
A

pneumonia! –> contributor to morbidity and mortality in older adults
- incidence is 3x greater
1. reduced epithelial lining fluid and ciliary action (remove toxic waste and unhealthy agents)
2. lead to persistent low-grade inflammation –> damage to lung matrix, impaired gas exchange
3. may be explained by age-associated weakening of respiratory muscles, which may cause less productive coughing (defence mechanism) and impaired ability to dislodge harmful particles
RESULT:
- greater frequency, incidence and severity of illness

39
Q

what is COPD? characterized by (2)
- what is a risk factor for COPD? why?
- what can also affect development of COPD (3)

A
  • chronic obstructive pulmonary disease –> respiratory disease characterized by airflow obstruction due to chronic bronchitis (inflammation, excess mucus) or emphysema (decrease membrane surface area of alveoli)
  • Older age! –> due to age-related changes in lung structure and function
  • smoking, air pollution or occupational exposures = 2° factors
40
Q

SUMMARY: age-related pulmonary changes
- lungs are considered ________ for the demands of exercise in both young and older adults
- with aging, significant physiological deterioration occurs to pulmonary and respiratory systems including (2 main thing)
- what are the primary limitations to exercise performance in older adults? same for younger?

A
  • over-engineered!
    1. structural alterations in airways and vasculature –> resulting in smaller, collapsible airway and fewer, stiffer pulmonary vessels (trapping of air = increase reserve volume)
    2. alterations in lung volumes and lower ventilatory efficiency –> less functional lung capacity (increase dead space, weaker muscles) and greater exertional breathlessness (subjectively!)
  • primary limitations = cardiovascular and musculoskeletal! same as in young adults!
41
Q
  • How might aging affect Shirley’s lung volumes/capacities?
  • How does aging affect her expiratory flow and minute ventilation during exercise?
A
  1. increase residual volume
  2. decrease expiratory reserve volume
  3. decrease minute ventilation at higher workloads –> increase WoB + dyspnea/breathlessness