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