The ageing heart and lungs. Flashcards
What are the different theories of ageing?
3 functional Implications of Normal Age-Related Changes?
Telomeres get ?
Transcription ?
? stress + ? accumulation
Repeated ?
? theory
?
3 functional Implications of Normal Age-Related Changes:
- Decreased response ?
- Decreased ?
- ?
Telomeres get shorter as we get older with each successive cell division
Transcription failure
Oxidative stress + free radical accumulation
Repeated mitochondrial DNA damage
Misrepair-accumulation theory
Apoptosis
3 functional Implications of Normal Age-Related Changes:
- Decreased response to stress
- Decreased activity tolerance
- Orthostatic hypotension
What is cardiac amyloid?
Cardiac amyloidosis is the deposition of abnormal amyloid fibrils in the heart tissue. These fibrils, made up of misfolded proteins, accumulate-.
Incidence increases sharply with age.
There is also presence of senescent cells in the myocardium
Debatable whether cardiac amyloidosis is part of normal ageing.
Increased myocyte size + deposition of fibrous tissue and amyloid causes LV hypertrophy which decreases LV space
What happens to left ventricle filling as you age?
? in the early stage of ?, due to ?
So, to maintain ? the ? to ?–> ? occurs
The slow early filling can also be due to ?
LV filling in the early stage of diastole slows w age, due to altered valves
So, to maintain adequate filling the LA contracts more forcefully to push blood through the calcified, thickened valve during late diastole–> left atrial wall hypertrophy occurs
The slow early filling can also be due to conduction problems.
3 normal changes in conduction pathways?
Which cells remain constant?
- Fibrous tissue, fat & amyloid deposition interferes w conduction in ventricular walls
- Decrease in pacemaker cells w age
- Myocardium hypertrophy–> slower impulse propagation
- On the other hand, AVN cells remain constant – as they only delay the signal (to regulate the timing of electrical impulses.)
3 effects of changes to the conduction pathway?
- A slower conduction system–> premature atrial beats and ventricular ectopic beats (not super serious)
- Conduction changes put pt at a higher risk of clinically significant arrhythmias
- Myocardium irritability may result in extra systoles, along with sinus arrhythmias and sinus bradycardia
(Ventricular ectopic beats are abnormal heartbeats that originate in the ventricles rather than the SAN. They occur earlier than normal heartbeat, can disrupt sinus rhythm )
How do the arteries change with ageing?
- More ?, decreased ?, and ?. This causes ?. This increases ? –> ?
- ? also produce less ? –> ?
- arteries can become ?
- ? can become less ?
More collagen deposition, decreased elastin, and calcification thickens arterial wall. This causes stiffening (esp large arteries). This increases TPR + systolic BP–> isolated systolic hypertension
The arterial endothelial cells also produce less NO w age -> vasoconstriction of arterioles & increased atheroma formation (may cause IHD)
Arteries can become elongated and tortuous (esp aorta)
Peripheral arteries become less resilient
What are the changes in veins?
Thickening of the ?, as well as ? causes ?
The result of this is that ?, therefore we ? as effectively
Can also cause ? which increases risk of ?
Thickening of the intima and media, as well as loss of elastin causes veins to dilate & stretch
The result of this is that capacitance decreases, therefore we can’t shift blood from the veins to the heart to increase BP (via Starling’s law) as effectively
Can also cause varicose veins & blood stasis which increases risk of thrombosis & thromboembolic events
What are the changes in valves?
The most frequent valvular changes in ageing are:
- ? changes leading to ?
- ? leading to ?
? may result from ?, ? and ? valve leaflets
The most frequent valvular changes in ageing are:
- Mitral valve myxomatous changes (extra connective tissue) leading to mitral regurgitation
- Aortic valve calcification leading to aortic stenosis
Systolic and diastolic murmurs may result from thickened, calcified and maligned valve leaflets
What are the physiological heart rate changes?
Decreased cardiac responsiveness rate with exercise
Heart may take longer to return to baseline rate
Linear decrease in the max heart rate achievable during exercise. Common equation for this is 220-age=max heart rate
Generalised decrease in muscle strength with age -> decreased contractile strength & efficiency
SV and thus CO decreases, therefore HR increases to try compensate
Summarise some of the physiological changes in cardiac function with regards to pre-load and after-load
Pre-load:
- EARLY diastolic LV filling rate progressively slows with age
- LATE diastole is greater, because of increased atrial contraction
- End-diastolic volume in the supine or seated position is not usually decreased in a healthy older patient
After-load:
- Decrease in elasticity and lumen diameter within arteries–> increased sBP with age
- Small arteries and arterioles become less responsive to vasodilator cues with age–> increasing TPR
What is the difference between diastolic abnormalities, diastolic dysfunction and diastolic HF?
What are the Changes in Ejection Fraction and in the rest of the ageing heart during exersice?
Also: peak exercise capacity, aerobic capacity, 02 consumption and response to stress all decrease
There is Progressive decline in lung function from ~20yrs female and ~25yrs male.
What are the structural changes in the lungs associated w ageing?
- Increase in size of ? and ?, resulting in ?
- Loss of ? of the ? resulting in ?
- There is also ? which results in ?
- Increase in size of alveolar space and air trapping, resulting in ‘senile emphysema’.
- Loss of supporting structure of the lung parenchyma resulting in premature closure of small airways, increased air trapping and hyperinflation
- There is also decreased elasticity which results in airspace enlargement
What happens to the chest wall with ageing?
? chest wall ? due to:
? in ?, ? and ? joints –> ?
This creates a ?–>decline in ?
? of the ribs ?
? thus required for ?–> increase ?
Decreased chest wall compliance due to:
Degenerative changes/arthritis in intercostal, intervertebral and costovertebral joints –> kyphosis and vertebral fractures.
This creates a smaller chest cavity space–>decline in FEV1 and FVC
Calcification of the ribs stiffens the thoracic cage
More muscular work thus required for ventilation–> increase work of breathing
What happens to the resp muscles and resp system w ageing?
Resp. muscles become ?:
- ? & becomes less ?
- Weakened ?
- Evidence of decreased ? in ?
- Decrease in ? predisposes to ?
Age-related decline in ? to resp muscles may increase ?
Resp. muscles become weaker/atrophied:
- Diaphragm flattens & becomes less effective
- Weakened cough reflex
- Evidence of decreased ATP in resp muscle mitochondria
- Decrease in fast twitch fibres predisposes to diaphragmatic + ventilatory failure
Age-related decline in efferent neural output to resp muscles may increase vulneralbility to hypoxia and hypercapnia eg in pneumonia or acute heart failure.
Anatomical Changes With Age?
Complete this table
Respiratory Ageing and Exercise?
VO2 max (Maximum oxygen consumption), ‘an objective surrogate of fitness’ - decreases by a rate of about ?% per year
