cardiovascular System Flashcards
myocardium changes with age
reduced myocyte numner
increase LV wall thickness
increased fibrous component
increased cardiac muscle contraction and relaxation time
amyloid fat deposits
myocyte number
- myocytes enlarge and reduce in number, through apoptosis and necrosis- due to lack of o2
- myocardium valves being replaced by fibrous/calcified tissue
- partially compensated by hypertrophy of remaining myocutes
LV wall thickness
may increase by ~30%
heart is pumping against higher pressure– reduced ventricular dimensions but some pathologies may result in ventricular atrophy
increased fibrous component
fibrous componentincreased collagen in tissue, cross linking= myocardial fibrosis (less contractile and functional)
myofilament binding to ca2+ combines with fibrous alterations of heart to increase myocardial stiffening which prlongs early diastolic filling.
amyloid deposits
amyloid deposits found in atria and ventricles (endocardium and pericardium)- produce inflammatory markers. Senule amylouidosis associated with atrophied myocardial fibres- results in arrythmia.
ageing of valves and aorta
- Collagen crosslinking (made of fibrous tissue)
- Reduced elastin – stiffer and less elastic
- Increases inflammatory markers reduced elasticity + stiffening of the valves
- Less effective closing of valves- leaky valves (backflow of blood)
arterial stiffness
reduced ability of an artery to expand and contract in response to pressure changes
.Independent predictor of mortality after CV event. AS may contribute to resetting baroreceptor response in carotid arteries increasing systolic pressure. AS increases in post menopausal women on HRT.
pulse wave velocity
Pulse wave velocity- in younger people the aorta will bounce back when blood enters causing another pulse of pressure but with ageing there is an increase in pressure which can’t be absorbed by the enlargement of the arteries.
- therefore greater peaks in blood pressure and slower contractions means it takes longer to reach peak blood pressure
conducting system ageing
SA node, electrical impulses by AV node- coordinating the contraction of the heart
- Decrease in number of SA node pacemaker cells- slightly less sympathetic response
- Increases chances of arrythmia- irregular heartbeat
- Axonal degeneration- compromises sympathetic innervation
innervation of heart and ageing
s§ympathetic- releases NE (norepinephrine) + heart rate increases (in response to stimulation)
Parasympathetic- releases Ach + heart rate slows (at rest)
- Sympathetic stimulation declines
- Response to stimulation declines- lowers HR in response to stimulation
changes in ventricular function with age
Heart rate- resting is maimtaind but maximal is consistently lower with age
- HRmax= 220-age
- HRmax=210-(0.65xage)- more accurate
Stroke volume
- Maintained (rest) or may increase to compensate reduced heart rate during submaximal exercise
Cardiac output
- Submaximal cardiac output maintained but maximal is reduced as max HR is reduced
SV and contributing factors
- Ventricular relaxed during diastole= filling
- Preload- how much blood enters heart depends on how quickly the ventricles stretch
- EDV- how much blood is in the heart at its maximum
- ESV- amount of blood left in heart after a beat
SV with ageing
Reduced early diastolic filling
- Sustained Ca2+ activation (to compensate for reduced contractile function) causes residual Ca2+ activation from previous contraction
- Delayed ventricular relaxation – slower relaxation will result in slower filling of the ventricles
- Increased late diastolic filling in men – makes up for the loss of early filling
- Maintained end diastolic volume
- Maintained dist fraction in healthy people (Frank starling principle)- more stretching of ventricles stimulates greater contraction
baroreceptors reflexes
- Baroreceptor sensitivity declines- partly due to reduced arterial compliance + less sensitivity
- Neural transmission time increases- postural (orthostatic) hypotension (feeling dizzy when you stand up due to lower blood pressure)
- Responses are slower to change in sensation
changes in blood vessels with age
muscle fibre numbers
collagen content and cross linkage
fat deposition
increased wall thickness due to calcification of vessel walls
reduced number of b adregernic receptors
endothelial becomes flatter
smooth musle fibre
number and strength declines
reduced ability for vasoconstriction
collagen
cross linkage- degradation of elastin= reduced elasticity
blood vessel walls become stiffer and more prone to damage
fat deposition
lumen of blood vessels- vessel Xsection reduced- reducing blood flow and increasing blood pressure
B adrenergic receptors
reduced number in response to sympathetic stimulation
reduced vasodilation in response to catecholamines
endothelial cells
become flatter and less continuous, reduced proliferation and metabolism
contributes to atherosclerosis
consequences of changes to blood vessels
- Reduced compliance; pulse wave returns in systole rather than diastole
- Increased large vessel and peripheral resistance
- Increased blood pressure
- Increased risk of damage to blood vessel walls
development of atherosclerosis
- Fat building up on inside of blood vessels – less continuous endothelium with macrophages building up and causing foam cells
- Foam cells- activity contributes to fibrous cap + atheroma
- Plaque can break off and travel around the blood vessels, which can block / narrow the whole blood vessel
effects of atheroscelrotic plaque
- Provides less blood to the heart which in turn will provide less oxygen to heart contributing to certain diseases
consequences of atherosclerotic plaque
depends on the location of the affected vessels
- Brain- stroke – death of brain tissue, loss of speech/movement
- Coronary circulation- angina pectoris (pain in heart on exertion- due to lack of o2), myocardial infarction – heart attack
- Major arteries- aneurism – stretching of blood vessels which is weaker and may give way, leading to a large loss of blood
- Peripheral circulation- gangrene – localised death and decomposition of body tissue due to obstructed circulation
factors infleuncing variability
- Telomere length
- Sex steroids (HRT)- linked with increased risk of CVD
- Inactivity- can accelerate negative effects of CVD/exercise- can help to treat and prevent
- Smoking
- Nutrition- has a large effect on atherosclerosis - fat, fish oils, fruit and vegetables
- Obesity (particularly abdominal)
- Disease – T2D and other chronic disease
CVD diseases and ageing
congestive heart failure
- systolic dysfunction- heart doesn’t eject enough blood so will get a backup
- diastolic dysfunction – effects filling of the heart
- Fluid may build up in lungs or tissues, reduction in function
Arrythmias- irregular heart rate, due to loss of SA node cells
malignant disease eg acute leukaemia
