Class 19 Flashcards
Aging in the CV System (Changes to Blood Vessels)
There is difference between cardiovascular aging & cardiovascular disease. While accumulation of cardiovascular events & disorders is part of their lifespan challenges for many individuals, following list speaks to CV developments that are consistent with normal, healthy aging, not disease
● Degree of generalized thickening & stiffening, loss of suppleness in blood vessels
● Infiltration of elastin fibres with calcium ions, making them more “stretched out” & less elastic (“from balloon to bicycle tire”)
● Resulting reduced expansion & ↓’d elastic recoil of large arteries; a less compliant aorta ↑’s speed at which blood flows through arterial tree & back to heart, altering fill cycle speed & increasing ventricular afterload. This results in increased systolic BP but decreased diastolic pressure.
● Stretch-sensitive baroreceptors become less effective, esp. with getting up or changing positions quickly (↑’d incidence of orthostatic hypotension, dizziness with movement).
● ↓’d arterial compliance ↑’s TPR, meaning LV must work harder to push blood into aorta; arterial compliance is more problematic during exercise, adding to LV workload
● Normal growth factors that promote vessel wall
maintenance & repair are less prevalent.
● Endothelial stem cell numbers decline, & with them angiogenesis (new blood vessel formation in tissue). In smaller vessels normal growth factors that can promote angiogenesis around narrow spots or blockages decline with age.
● There is some thickening of capillary walls &
therefore tissue health compromise, edema.
● ↑’d oxidative stress/low-grade inflammation in tissues promote weakening of membranes between intima & media layers, as well as general increase in fibrosis (collagen content) of wall; such changes promote endothelial stress & susceptibility to atheroma development.
● Some loss of smooth muscle cells in tunica media layers results in increased workload & hypertrophy of remaining cells; stress on these cells may signal for remodelling processes in walls that add to fibrosis & calcium deposition.
The more severe the effects of aging are on blood vessels, the _________ it is for atherosclerosis, hypertension, & other processes to _____________ & have an effect on rate of aging in vessels. Smoking, lack of exercise, a poor diet, and obesity also can ________________ these effects.
- easier
- do damage
- exacerbate
Aging in the CV System (Changes to Myocardial Cells)
● ↑ in cell size (hypertrophy) in response to ↑’d workload, esp. in LV.
● Some degenerative changes with deposits of lipofuscin (“aging pigment”)
● Some loss of cell population (permanent cell type)
● Adaptive changes in cellular calcium dynamics occur to improve contractility, slowing both contraction & relaxation times, they make it harder for heart to speed up when needed.
● Inherent capacity of these cells to resist damage during short bursts of ischemic conditions (high activity) is reduced as heart ages.
● Changes in calcium-electrochemical gradient inside cells can promote dysrhythmia.
● As in BV’s, there is ↑’d fibrosis of intercellular spaces, which can affect synchronous contraction.
Aging in the CV System (Myocardial Hypertrophy/Enlargement, esp. in LV)
Aging & CCHF are not synonymous, changes associated with normal aging, esp. if there’s reduced physical activity, create degree of heart adaptation that’s CHF-like & combines with any other CHF-promoting elements in person’s body.
● Myocardial cell hypertrophy results in thickened heart wall.
● Increased septum bulk makes heart less flexible/contractile.
● Myocardium becomes harder to perfuse.
● Chamber capacity is reduced.
● Heart fills more slowly & less effectively; LA works harder to complete fill (↑’d active LA contribution to end-diastolic volume) may undergo some hypertrophy as result.
● To maintain cardiac output, compensating mechanism is to increase stretch of chamber wall to add end-diastolic volume (Frank-Starling mechanism), wall thickening reduces chamber expansibility & therefore lowers EDV & SV, ↓’ing maximal cardiac output.
Aging in the CV System (Changes to the Conduction System)
● Gradual loss of SA & AV cell populations, esp. in SA node, can lose 50-75% of cells over time, slowing intrinsic heart rate & making nodes less responsive to autonomic signals.
● Accumulation of fatty tissue around SA node, can impede its action potentials.
● Conduction system pathways, esp. in bundle of His, develop fibrous, fat & calcium deposits, & may lose some cells, slowing transmission.
● Dysrhythmias & atrial fibrillation are also more common as result of ↓’d synchrony in propagation of action potentials through myocardium.
Aging in the CV System (Altered Sympathetic Responsiveness)
● Overall ↓’d heart responsiveness to autonomic directives; particularly of adrenergic (sympathetic) receptors, esp. in SA node.
● ↓’d effectiveness of baroreceptor & chemoreceptor (for O2, CO2) reflexes, on afferent side in arterial walls & on effector side in conduction
system.
● ↓’d maximal heart rate, ↓’d myocardium contractility, reduced ability of heart to respond to high intensity situations (physical exertion, emotional stress, illness, injury, some meds, etc.).
● Longer cardiorespiratory recovery time from stress or shock.
Aging in the CV System (Valves)
● Overall, can thicken & become stiffer, open/close less completely (mild heart murmur common in elderly).
● Tendency to calcification, esp. at base of aortic valve & in mitral valve.
● Overuse of ventricular stretch/dilation (Frank-Starling mechanism) adaptation can promote valve regurgitation.
Aging in the CV System (Blood)
● Some reduction of total body fluid, meaning blood more viscous, tissues (& person) are more easily dehydrated.
● ↓’d speed of rbc production, esp. when depleted by stress, illness; overall tendency to more easily develop anemia, which adds to heart’s workload.
● Most wbcs remain at usual level, circulating neutrophil population goes down, reducing ability to resist infection.
Aging in the CV System (Blood Pressure)
● ↑’d systolic pressure stresses heart, esp. LV.
● ↓’d diastolic pressure reduces effectiveness of wall perfusion, which occurs during diastole.
● Higher pulse pressure is associated with heart responding to increased arterial wall thickening stiffness; some suggest pulse pressure size is better indicator of decline in CV health than specific systolic or diastolic pressure values.
● Because heart is less responsive to symp ns signals, more catecholamines (adrenalin & norepinephrine) are released; ↑’d circulating catecholamines and angiotensin 2 cause
generalized arteriolar vasoconstriction, which ↑’s TPR and also ↓’s body tissue perfusion.
● With ↑’d blood pressure larger volumes of blood are held in the venous system, which ↑’s
hydrostatic pressure in veins (promotes varicosities) and in capillary beds (promotes edema).
Aging in the CV System (Other Related Changes)
● Body tissues can exert some autonomous controls over their blood supply, usually dilating their local arterioles; this can help reduce TPR, their insistence on their nutritional demands can add to heart’s workload.
● Some degree of heart enlargement is consistent with aging-related changes over time; can impinge on lungs/respiration.
● There is ↑’d stiffness of chest wall, diminished blood flow efficiency through lungs.
● Decrease in oxygen consumption during exercise (↓’d maximal aerobic capacity), along with
↓’d maximum heart rate, produce faster dyspnea & tissue ischemia during activity.
● Changes (parenchymal or vascular) that may cause some slowing/resistance of blood flow through kidneys &/or liver are common.
