3. Cardiopulmonary system: age-related changes Flashcards
CARDIOPULMONARY SYSTEM:
- composed of (3)
- works closely with what? and is controlled by which system?
- age-related changes are due to (2)
- 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)
- 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)
- 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
why does myocyte hypertrophy occur in adults? (3) + sub
- 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 - ventricles have to work harder to pump blood/O2 to the rest of the body
- increased mechanical load further exacerbated by heightened workload on fewer myocytes (lower # and lower quality)
- 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 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
what are additional structural changes to the aging heart that affect its conduction system? (3)
- results in what? (3)
- decrease in number of cells in sinoatrial (SA) node
- decline in ion channel expression and calcium-handling proteins in the SA node/pacemaker cells –> alters force generation
- 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)
structural changes of myocytes are associated with slower/longer contraction/relaxation during systole and slower/longer contraction/relaxation during diastole.
WHY? (3)
- 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)
what is arteriosclerosis? (2)
- can be explained by (3)
- 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)
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?
- 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
AGING AND BLOOD VESSELS:
what happens to
- aorta and arteries
- capillaries
- veins and venules
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
define
- arteriosclerosis
- atherosclerosis –> associated with (4)
*formation of what exactly?
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)
blood pressure and aging:
- aging causes increase in WHAT? (define)
- age related changes in WHAT affect (3)
- 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
what are the 4 layers of a blood vessel/artery? –> these are critical determinants of (2)
- tunica externa (collagen fibers)
- tunica media (smooth muscle cells)
- tunica intima (endothelium)
- basement membrane
- critical determinant of vascular tone and mechanics of blood flow
- what happens to SNS when aging? results in what?
- what happens to PSNS when aging?
- ___________ in both result in what?
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
- 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?
- 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)
- 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
- decreased O2 supply despite higher O2 demand
- 120/80 mm Hg
- > =130/>=80 mmHg
- 53%
(2), especially in the presence of WHAT may lead to myocardial ischemia and potentially myocardial infarction
define myocardial ischemia VS infrrction
- 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