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Cardiac rehabilitation > Altered exercise response of CHD patients > Flashcards

Altered exercise response of CHD patients Flashcards

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1
Q

what are the 6 components of comprehensive cardiac rehabilitation programme?

A
  • Exercise training
  • Psychological and stress counselling
  • Dietary advice
  • Advice on medications and treatments
  • Advice on risk factor modification
  • Facilitation social reintegration
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2
Q

how much does an exercise based cardiac rehabilitation programme reduce cardiac mortality?

A

10-36%

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3
Q

how much does an exercise based cardiac rehabilitation programme reduce reinfarction?

A

20-50%

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4
Q

what are the 3 main guidelines from the NICE 2013 rehabilitation guidelines?

A
  • designed to motivate people
  • being the programme as soon as possible
  • provide a range of options
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5
Q

when does post MI/PTCA rehab start?

A

2-4 weeks later

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6
Q

when does post CABG rehab start?

A

4-6 weeks later

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7
Q

what consists in stage I of cardiac rehabilitation? (4)

A
  • assessment of physical, psychological and social needs for cardiac rehabilitation
  • advice on lifestyle
  • prescription of medication
  • provision of information about cardiac rehabilitation
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8
Q

what consists in stage II of cardiac rehabilitation? (2)

A
  • comprehensive assessment of cardiac risk

- provision of lifestyle advice and psychological interventions

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9
Q

what consists in stage III of cardiac rehabilitation? (2)

A
  • structured exercise sessions

- maintain access to relevant advice and support from people trained to offer advice

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10
Q

what consists in stage IV of cardiac rehabilitation? (3)

A
  • long-term follow-up in primary care
  • offer involvement with local cardiac support groups
  • referral to specialist cardiac, behavioural pr psychological services as clinically indicate
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11
Q

what is the best single measure of an individuals cardiorespiratory fitness?

A

peak oxygen uptake

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12
Q

what is the equation for peak oxygen uptake?

A

oxygen uptake = cardiac output x aterio-venous difference

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13
Q

how much lower is the peak VO2 of cardiac patients?

A

50% lower

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14
Q

what is the relationship between VO2 and mortality?

A

inverse relationship

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15
Q

how much does 1mL.kg-1.min-1 increase in aerobic capacity reduce CV mortality risk by?

A

10%

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16
Q

how much does 1 MET increase in aerobic capacity reduce CV mortality risk by?

A

15%

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17
Q

why is peak VO2 decreased? (2)

A
  • decrease in cardiac output

- decrease in stroke volume

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18
Q

what is the core reason SV decrease in cardiac patients (2)

A

scarring/ischaemia

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19
Q

how does a decrease in SV effect TPR?

A

greater TPR

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20
Q

what is hypokinetic?

A

decreased movement due to lack of oxygen

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21
Q

what causes the myocardium to become hypokinetic in cardiac patients? (2)

A
  • subnormal production of endothelial nitric oxide

- localised overproduction of endothelin

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22
Q

how much of the blood resides in the veins at rest?

A

two thirds

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23
Q

what is the Visceral blood flow as % resting value for normal and cardiac patients?

A 
normal = 20%
cardiac = 50%
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24
Q

what 4 characteristics do cardiac patients have?

A
  • lower peak VO2
  • lower peak work rate
  • work at a higher percentage of maximum during sub maximal exercise
  • lower VO2 during sub maximal exercise
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25
what resting SBP should be excluded from the exercise part of cardiac rehab?
>200mmHg
26
what is eccentric hypertrophy of the heart?
much greater increase in chamber dimension increase in myocyte length, increase is myocyte width
27
what is concentric hypertrophy of the heart?
much greater increase in wall thickness increase in myocyte length < increase in myocyte width
28
what is physiological hypertrophy?
proportional increase in chamber dimension and wall thickness
29
what is La Place's Law?
T = (P * R)/M
30
how do we keep the wall tension the same around the heart?
the radius and the wall thickness must be proportional
31
what 3 factors affect myocardial oxygen consumption?
- tension development - myocardial contractility - heart rate
32
what causes cardiac growth?(2)
- Hormones | - mechanical stress
33
how does NE and Epinephrine cause cardiac growth?
stimulation of alpha and beta receptors on the myocardium cause cardiac growth
34
how does RAA cause cardiac growth?
increased RAA levels stimulate cardiac myocytes to hypertrophy
35
what hormones cause cardiac growth?
- NE and Epinephrine - RAA - GH and IGF - Thyroid hormones
36
how does GH and IGF cause heart growth? (2)
- stretching of the heart muscle trigger for these muscles to activate gene expression - IGF increases myofilament sensitivity to calcium thus increase calcium forces
37
how does thyroid hormones cause cardiac growth?
Thyroxin causes myocyte hypertrophy
38
how does pressure overload lead to increase in cardiac muscle?
pressure overload = increase resistance = hypertrophy through increase cross sectional area
39
how does volume overload lead to increase in cardiac muscle?
increase volume overload = hypertrophy through increase myocyte lengthening
40
how do mechanic-sensors in myocyte increase cardiac muscle?
surface receptors and stretch activated ion channels increase calcium influx -> activate protein kinase pathways thus hypertrophy
41
what is angiogenesis?
the formation of new blood vessels
42
what is the benefit of angiogensis?
increased blood flow
43
how is contractility improved with aerobic training of cardiac patients?
improved % shortening, time to peak shortening, relaxation time
44
what is the main ion that affects contractility of the heart and how?
calcium - increased calcium binding sites in myocytes and more calcium stored in SR
45
how much does aerobic training increase stroke volume in cardiac patients?
0-18%
46
how much does aerobic training increase blood volume in cardiac patients?
6-10%
47
2 reasons why stroke volume increases in cardiac patients?
- myocardial hypertrophy | - increased ejection fraction
48
what happens to patients parasympathetic tone is cardiac patient with aerobic training?
it increases
49
how does a decrease in blood viscosity occur in cardiac patients with aerobic training?
via a reduction in fibrinogen levels and platelet activation
50
why is there a reduced endothelial dysfunction in cardiac patients undergoing aerobic training? (2)
- improved NO production promotes vasodilation | - improved production of superoxide dismutase
51
why is there an improved blood flow in cardiac patients undergoing aerobic training?
better endothelial function
52
what happens in stroke volume during exercise in cardiac patients undergoing aerobic training?
max SV increases
53
what happens in HR during exercise in cardiac patients undergoing aerobic training?
decrease in sub-maximal exercise HR
54
what happens to myocardial oxygen demand during exercise in cardiac patients undergoing aerobic training?
decreases
55
what 5 things increase in muscle in cardiac patients with aerobic training?
- arteriovenous difference - mitochondrial number - maximal muscle blood flow - muscle capillary density - muscle fibre recruitment
56
what happens to blood lactate concentrations during sub-maximal exercise in cardiac patients with aerobic training?
decreases
57
what happens to peak VO2 in cardiac patients with aerobic training?
increases 10-50%
58
what happens to total exercise capacity in cardiac patients with aerobic training?
increases 18-35%
59
what happens to angina threshold in cardiac patients with aerobic training?
increases 10-20%
60
what does RPP stand for?
rate pressure product
61
what is the equation for RPP?
RPP = SBP x HR
62
what is max exercise RPP?
25,000
63
what activities during the first 48 hr following MI or cardiac surgery should occur?
- arm and leg range of motion movement | - low resistance activities
64
Activity post-discharge: weeks 1-6. Why? (3)
- physiological benefits - increase physical self confidence - decrease dependency on others
65
Activity post-discharge: weeks 1-6. what?
walk at a comfortable pace on a flat route
66
what spray should a cardiac patient take with them when walking and what does it do?
GTN spray - coronary vasodilator

Cardiac rehabilitation (13 decks)

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