The ageing CV system Flashcards
AGE AND CVD
i) name two things that make ageing a strong RF for CVD?
ii) name three drivers of ageing > CVD
iii) name four CV conditions that are more common in older adults
i) longer exposure to classic vascular risk factors such as smoking, HTN and high cholesterol
- change in structure and function of heart and blood vessels over time even in the absence of RFs
ii) oxidative stress, chronic inflammaition, limited regenerative capacity of cardiac cells
iii) systolic hypertension, HF (disastolic - preserved EF, systolic - reduced EF), AF and IHD
OVERVIEW OF CV AGEING
i) what happens to cardiomyocytes with age?
ii) what happens to fibroblasts with age? how are collagen and elastin implicated and what does this lead to?
iii) name two other things seen in the CV system with age
iv) name four things all the above lead to? what does this ultimately lead to?
i) reduced cardiomyocytes > 1/3 lost beween age of 17 and 90 and those that persist will hypertrophy
ii) relative increase in fibroblasts with age
- increase in collagen production > increased x linking of fibres > fibrosis in atria and ventricles
- decrease in elastin production > less elasticity in cardiac tissue
iii) see calcifcation of heart and vascular structures
- accumulation of by products of ageing eg amyloid and lipofuscin
iv) leads to reduced elastic recoil, myocardial stiffness, decreased ventricular compliance, impaired LV filling
- ultimately leads to problems on sys and espec dias function
THE HEART - THE VENTRICLES
i) in the adult heart - which cells predominate? which cells predominate in the aged heart?
ii) what are the two types of LV hypertrophy? what are changes in the LV most linked to?
iii) what happens to LV mass and wall thickeness with age? does LV volume increase or decrease?
iv) what are RV changes dictated by? is RV ejection fraction affected? what happens to the RV over time?
i) adult heart - cardiomyocytes predominate
- in elderly - fibroblasts predominate (cmyos die by apop and necrotic cell death)
ii) LV hypertrophy - concentric (same change all the way round) or eccentric (different amount of hypertrophy in different areas - bigger effect)
- changes in LV are more linked to frailty than aging
iii) LV mass is the same or decreases
LV wall thickness increase > due to vascular stiffness (increases afterload)
- LV volume decreases in systole and diastole
iv) RV changes are dictated by pulmonary changes (mild increase in pul, artery pressure/vascular resis)
- RV EF is preserved but RV diastolic dysfunc develops over time
AGEING HEART AT REST
i) is resting heart rate affected by ageing?
ii) what happens to systolic function over time? (SV and LVEF)
iii) what happens to diastolic function? (rate of filling) what is this due to? what happens to calcium metabolism with age?
iv) what is preserved to maintain end diastolic volumes and pressures? how does this affect relaxation? what is the consequence of this in some people?
i) heart rate is unchanged
ii) LV systolic function is preserved
- SV is the same and LV EF is unchanged
iii) diastolic function is reduced
- rate of LV filling in early diastole is reduced - stiff ventricles decrease space and make it less able to relax
- passive filling is reduced due to stiff ventricle and delay in cmyo relaxation due to calcium metabolism (more responsive to calciu so contract for longer)
iv) atrial contraction is prolonged (maintains end dias vol and pressure) - delay in relaxation
- can cause heart failure with preserved EF
CHANGES WITH EXERCISE
i) name three general changes that occur with age that cause age related decline in aerobic capacity?
ii) what is VO2 max? how does this change with age?
iii) what happens to max heart rate? why?
iv) what happens to CO? is SV maintained?
v) in what situation does frank starling compen mechs fail? what does this lead to? (2)
vi) name four advantages of endurance exercise in elderly
i) decrease in aerobic capacity due to increased body fatt, reduced muscle mass and decline in oxygen extraction
ii) VO2 max = max amount of oxygen a person can use during exercise
- declines with age from early adulthood (in part due to compromised o2 delivery to exercising muscles with age)
iii) max HR decreases with age
- decreased intrinsic heart rate due to decreased sensitivity to symp stim
- NA/adren > B adrenergic Rs to inc HR and FOC but with age - NA levels are higher (reduced clearance) > chronic exposure > desensitisation (harder to increase HR in elderly)
iv) CO decreases due to decreased HR (CO = HRxSV)
- SV is maintained due to increased LV end dias filling volume which increases strength of FOC and SV
v) SV etc is not maintained in vigourous activity which is why people get exertional symptoms and exercise tolerance decreases over time
vi) blunts decline in VO2 max, can reduce decline in CO (max HR still declines), decreases arterial stiffness, protects from inc in fibrosis and apop, reduces risk of CVD
THE HEART - THE ATRIA
i) what happens to the atria with age? (2)
ii) why do these changes happen? (3)
iii) name a consequence of atrial ageing? what does this further cause?
i) atrial fibrosis and age dep increase in sizee (atrial dilation and vol inc)
ii) ventricles are stiff and dont relax weell > increased diastolic filling pressure > atrial dilat and hypertrophy
- forceful atrial contraction > late diastolic filling as compensation
iii) atrial fibrillation and other arrhhythmias
- impairs atrial contraction further > less ventric filling > lower SV and CO > diastolic HF
AGEING AND THE CONDUCTING SYSTEM AND VALVES
i) what % of pacemaker cells are lost from the SA node by age 50? how is innervation affected?
ii) how are number of cells in the AV node affected?
iii) what changes may be seen on ECG? name three consequences of changes in the conducting system
iv) name three things that happen to the valves with age? does valve area increase or decrease?
v) name two consequences of age changes to the valves?
i) by age 50 around 75% of pacemaker cells are lost
- reduced atrial sympathetic innervation
ii) number of cells in AV node are unchanged
iii) see prolongation of PR, QRS, QT interval on ECG
- cause arrhythmia > AF and sinus node disease (sinus brady, sinus arrest, AV block, tachy brady syndrome)
iv) fibrosis, calcification, degeneration (superadded effects of athero > degen aortic valve)
- valve area increases with age
v) calcification (aortic sclerosis) but non significant valve defects > murmurs
- valvular heart disease with haaemodynamic compromise > HF, angina, syncope
SUMMARY OF CARDIAC CHANGES WITH AGEING
i) what happens to the atria? why?
ii) how is epicardial fat affected?
iii) which system is preserved at the expense of the other?
iv) what happens to the aortic valve?
v) what happens to cardiomyocytes
i) atria dilate as they need to pump against the stiff LV
ii) increase in epicardial fat
iii) systolic func (EF) is preserved at the expense of diastolic function
iv) calcification of the aortic valve
v) cmyos hypertrophy and fibroblasts increase
BLOOD VESSEL REMODELLING
i) what happens to central elastic arteries with age?
ii) name two changes to the intimal later? what does this lead to?
iii) name two changes to the media
iv) what happens to the endothelium? how is NO production affected - what does this lead to?
v) how is vascular smooth muscle relaxation affected? what does this lead to?
i) central elastic arteries eg aorta, carotid, pulmonary > dilate/ increase lumen size
ii) intima - thickens, increased collagen/decreased elastin > infiltrat smooth muscle > stiff arteries
iii) media - decrease in smooth muscle cells, hypertrophy of remaining cells (unclear if func is affected)
iv) endothelial dysfunction > decreased NO prod (less vdil/responsiveness) > inc free radicals and dec endothelial NO synthase
v) decrease vasc smooth muscle relaxation > adds to arterial stiffness and increesaes risk of CVD
= large lumens and stiff walls
VASCULAR STIFFNESS
i) what do the aorta and large arteries normally do when systolic pressure is high?
ii) what causes stiff arteries? how does this affect function?
iii) what happens to pulse pressure? explain. what does this lead to?
i) buffer and smooth pulsatile pressre when systolic pressure is high
ii) increased collagen and decreased elastin > stiff
- reduced elastic recoil - cant bugger pressure well so pressure remains high and can consequently cause microvascular problems
iii) widened pulse pressure - inc systolic BP, decreased dias BP
- leads to isolated systolic hypertension - inc risk of CVD and peripheral organ damage
- not much elastic recoil so lumen size doesnt change much in sys and dias > bigger diffs in sys and dias BP
ISOLATED SYSTOLIC HYPERTENSION
i) what is it defined aas?
ii) what % of HTN in adults does this account for?
i) systolic BP > 160 and dias <90
ii) accounts for 60-80% of HTN in older adults
TREATMENT TARGETS IN OLDER ADULTS
i) what does it depend on?
ii) which BP can reflect poor health status in an individual?
iii) what % of patients with isolated systolic HTN also have orthostatic hypertension?
iv) what are the NICE guidlines for ISH?
i) depends on level of frailty
ii) low diastolic BP can reflect poor health status and its linked to adverse outcomes
iii) 20% of ISH have orthostatic HTN
iv) treat ISH as you would general HTN
ORTHOSTATIC HYPOTENSION - NORMAL
i) what is it defined as?
ii) where does blood pool when you stand up? (2) what does this lead to? (3)
iii) what responds to the change? what happens to symp and psym responses?
i) 20mmHg drop in SBP within 3 minutes of standing
ii) blood pools in extremities (legs) and splanchnic circulation
- leads to decrease venous return to heart, reduced BP and CO
iii) baroreceptors respond to the change (stretch R in carotid sinus and aortic arch via medulla)
- increase symp and decrease psymp response
- inc symp > increase vasc resis by v constric, inc venous return, inc cardiac contractility and output
> compensation limits BP drop
ORTHOSTATIC HYPOTENSION IN ELDERLY
i) what happens to the ANS with age? name three things that can cause this
ii) name two things that decrease baroreptor response with age?
iii) name the most common cause of inhibition of compensation (inc symp) mechs in elderly?
iv) what does inhibition of compensation lead to? (3)
i) primary autonomic failure - PD, multiple system atrophy, lewy body dementia, diabetes
ii) chronic HTN, arterial stiffness and drugs can decrease baroreceptor response
iii) drugs can inhibit compen mechs (inhibit symp sys > symptoms)
- volume depletion can also inhibit symp responses
iv) compensation failure > cerebral hypoperfusion, symptoms and transient loss of conciousness
DRUG CAUSES OF POSTURAL HYPOTENSION
i) name two diuretics? by what mech do they cause PH?
ii) name four vasodilators? by what mech do they cause PH?
iii) how do beta blockers cause PH?
iv) name two centrally acting anti hypertensives? by what mech do they cause PH?
v) name three drugs that have CNS effects causing hypotension?
vi) how do opioids cause PH?
i) furosemide and thizaides > volume depletion
ii) ACEi, CCBs, nitrates, alpha adrenergic blockers
- reduce systemic vascular resistance and venodilation
iii) negative inotropic (alterr FOC) and chronotropic (alter HR) effect plus some vasodilation
iv) clonidine and monoxidine - central CNS effects on BP
v) antidepressants (tricyclics, SSRIs, MAOi), anti psychotics and alcohol
vi) opioids reducee vascular resistance
