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ClinE 470 > Cardiac Rehabilitation > Flashcards

Cardiac Rehabilitation Flashcards

1
Q

What is the definition of health?

A

“A state of complete physical, mental and social well-being and not merely the absence of disease or infirmity” (p 1. W.H.O., 1947)

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2
Q

What did Bouchard et al. (2007) show?

A

That there is a complex interaction between health, physical activity and physical fitness. There are important determinants from heredity, lifestyle and environment.

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3
Q

Which key studies give evidence of lower mortality in more physically active and / or higher fit people?

A

• Harvard Alumni Health Study 1986: (Paffenbarger et al., NEJM, 315) + Harvard Alumni Health Study 1995: (Lee et al., JAMA, 273) • Blair et al. 1989: aerobic centre longitudinal study • Framingham study • Baugerleuser study • Zutphen elderly study & Finnish Twin Cohort

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4
Q

What did the Harvard Alumni Health Study 1986: (Paffenbarger et al., NEJM, 315) study show?

A

Mortality ↓ with ↑ physical activity 27% less risk of mortality from expending >2000kcal per week

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5
Q

What did the Harvard Alumni Health Study 1995: (Lee et al., JAMA, 273) show?

A

Mortality ↓ with ↑ physical activity (Confirmed the 1986 HAHS results; that less risk of mortality from expending >2000kcal per week)

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6
Q

How would you expend >2000kcal per week?

A

Walking at 4mph = 400Kcal ph, thus 5hrs walking per week for 2000Kcal

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7
Q

What did the results of the Harvard Alumni Health Studies recommend?

A

less risk of mortality from expending >2000kcal per week (Walking at 4mph = 400Kcal ph, thus 5hrs walking per week for 2000Kca)

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8
Q

What did the Aerobic centre longitudinal study 1989: (Blair et al., JAMA, 262) show?

A
  1. Biggest drop in mortality moving from lowest fit (Q1) to below average fitness (Q2) 2. Low fit men have 3.3 and low fit women 4.7 X more mortality than high fit (Q5)
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9
Q

The combination of results from the Zutphen elderly study & Finnish Twin Cohort study + British regional heart study, • Harvard Alumni Health Study, aerobic centre longitudinal study and the study of osteoporotic fractures shows what?

A

That it is never too late for previously inactive patients to become more active as it has been shown to have an impact on their mortality risk ratio. Also that those with the lowest activity/fitness have the most to gain in terms of mortality risk when commencing PA.

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10
Q

What does the ACSM, 2010 evidence show?

A

A) Occupational and leisure activity: 2 X more CHD death for sedentary vs. active occupations. 2 X more CHD death for low vs. high non- occupational physical activity. B) Fitness Every 1 MET increase in aerobic fitness = 12% more survival Below 5 METs = worse prognosis

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11
Q

Below which MET level do you have a worse prognosis?

A

Below 5 METs

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12
Q

Increasing your MET by 1 improves your survival by what percentage?

A

Every 1 MET increase in aerobic fitness = 12% more survival

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13
Q

What is the best recommendation for occupation & leisure activity in terms of CHD death risk?

A

Active occupation + high PA outside occupation [2 X more CHD death for sedentary vs. active occupations. 2 X more CHD death for low vs. high non- occupational physical activity.]

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14
Q

What are the axis on the dose-response curve?

A

Y - health benefits X - activity status

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15
Q

What are the consequences of the dose-response curve?

A

The greatest health benefits are achieved when increasing physical activity levels from sedentary to moderately active + The more physical activity you do, the greater the health benefits – Each 10 minutes of MVPA results in 10% mortality risk reduction (RR) – Achieve 150 mins MVPA then 30-40% less RR – 750 mins MVPA (3 X recs) only increases RR to 50%

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16
Q

What does the dose-response curve tell us about mortality risk reduction (RR)?

A

– Each 10 minutes of MVPA results in 10% mortality risk reduction (RR) – Achieve 150 mins MVPA then 30-40% less RR – 750 mins MVPA (3 X recs) only increases RR to 50%

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17
Q

Is there truly a steeper relationship between fitness and relative risk than PA? And what are the consequences for public health initiatives?

A

–Likely due to measurement error in physical activity studies (Easier to objectively measure physical fitness) –Public health initiatives should target physical activity because that will increase fitness levels

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18
Q

What did Clarke et al, BMJ 2012 show about Olympians?

A

Olympians live 2.8 years longer on average. Thought to be due to genetics, wealth and PA throughout life. Endurance athletes had greatest benefit, but even resistance athletes benefitted.

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19
Q

Should you exercise even if unwell? What is the evidence?

A

Yes: Physically fit men with existing chronic conditions (e.g., CVD, HTN, DM) have a lower risk of mortality compared with men who are unfit. Hypertension High fit without HTN had 0.5 mortality risk reduction (RR) of low fit High fit with incidental (white coat) HTN had 0.4 RR of low fit High fit with history of HTN had 0.4 RR of low fit Diabetes High fit with DM had 0.5 RR of low fit without DM

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20
Q

For which clinical health conditions is there good evidence to suggest that being active / fit helps prevent or treat?

A

CHD, stroke, HTN, cancer, diabetes, falls, depression, dyslipidaemia. (2008 physical activity guidelines for Americans: US Dept Health and Human Services)

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21
Q

What are the key new points from the 2008 physical activity guidelines for Americans?

A

• VPA and MPA can be mixed up. VPA>MPA? • Fq: can spread over week/weekend warriors (but fq bouts better for DM, HTN, depression, hyperlipidaemia etc.) • Duration: 10min bouts currently recommended; but <10min still beneficial as avoids sedentary behaviours

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22
Q

What are the 2008 PA guidelines for American Adults?

A
  1. Inactivity should be avoided. Some is better than none, especially in low active groups. 2. 75min VPA/week 3. Or 150 MPA/week 4. Or equivalent blend 5. At least in episodes of 10min 6. Preferably spread throughout the week 7. For extensive health benefits, 5h/week MPA 8. Or 150VPA/week 9. Or equivalent combination of MPA and VPA 10. 2x strength training moderate/high intensity per week for bone density health
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23
Q

What are the 2008 PA guidelines for Children?

A
  1. Generally 1h/day MPA-VPA. 2. VPA at least 3d/wk. 3. Muscle strengthening at least 3d/wk. 4. Bone strengthening at least 3d/wk.
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24
Q

What is preload?

A

Preload–theamountof blood in the ventricles before contraction ♥ End diastolic volume About 100mL

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25
Q

What is afterload?

A

Afterload=the amount of blood left in the ventricles after contraction ♥ End systolic volume About 40mL

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26
Q

What is the ejection fraction?

A

SV/EDV x 100 = ((EDV-ESV) / EDV)) x 100 Approx at rest 70%

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27
Q

What is Q?

A

Cardiac output = HR (bpm) x SV

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28
Q

What is SV?

A

Stroke volume End Diastolic Volume – End Systolic volume Preload - afterload

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29
Q

What is shortening fraction?

A

((EDD - ESD) / EDD) x 100 Approx at rest 35%

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30
Q

What triggers the cardiovascular response?

A

Efferent signals: Balance between (PNS/vagus and SNS/cardiac) autonomic branches to control myocardial contraction.

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31
Q

Describe the sympathetic innervation of the myocardium.

A

• Sympathetic (CARDIAC) nerves innervate atria, SAN, AVN, myocardial muscle of ventricle. Release noradrenaline. [Also a direct link to adrenal gland leading to adrenaline response which acts on heart but is obviously slower.] • SNS exerts a chronotropic effect to increase HR and an ionotropic effect to increase strength of contraction.

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32
Q

What type of effect does the SNS have on the myocardium?

A

• SNS exerts a chronotropic effect to increase HR and an ionotropic effect to increase strength of contraction.

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33
Q

Describe the parasympathetic innervation of the myocardium.

A

Parasympathetic nerves (VAGUS NERVE) innervates the SAN and AVN and atria. PNS only exerts a chronotropic effect to decrease HR.

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34
Q

Which branch of the autonomic nervous system innervates the SAN, AVN and atria?

A

Parasympathetic nerves (VAGUS NERVE)

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35
Q

Which branch of the autonomic nervous system innervates the SAN, AVN and ventricles?

A

Sympathetic (CARDIAC) nerves

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36
Q

What effect does the PNS have on HR?

A

PNS =↓ HR

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37
Q

What effect does the SNS have on HR and contraction?

A

SNS = ↑ HR and strength of contraction

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38
Q

What bpm would a denervated heart have?

A

~100bpm (=intrinsic heart rate)

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39
Q

What is a normal HR (bpm)? Which autonomic branch dominates?

A

Normal HR ~72bpm; dominated by PNS

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40
Q

By what percentage could SNS increase HR in theory?

A

SNS could in theory increase HR by 300%

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41
Q

By what percentage could PNS increase HR in theory?

A

By 100%, to 0bpm = cardiac arrest

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42
Q

What happens to autonomic innervation of the heart during exercise?

A

At onset of exercise, PNS activity decreases before sympathetic activity increases. = massive flexibility for HR to vary during different activities +increased SNS will increase contractility. ::Therefore enhanced SV from SNS contribution.

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43
Q

What are the following abbreviations? PWT SWT LVEDD

A

PWT=posterior wall thickness; SWT=septal wall thickness; LVEDD=Left ventricular end diastolic diameter

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44
Q

If left ventricular size increases, what also increases?

A

Stroke volume. eg. in athletes

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45
Q

What is the limiting factor to myocardial stretch?

A

The pericardium –Pericardectomy allows SV to increase and hence Q

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46
Q

What is the Frank-Starling law?

A

= the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return -aided by a health myocardium

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47
Q

↑ stretching of myocardial walls will ↑ strength of contraction… is part of what principle?

A

the Frank-Starling principle as stretching the ventricles increases the pressure they can generate

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48
Q

Does the heart ever stretch to the point of the ‘inaccessible region’ on a tension-sarcomere length graph?

A

No: There is no way to get a normal heart over the peak into the downslope of tension. The heart becomes very stiff above the optimal length, and the venous filling pressure never gets high enough.

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49
Q

What is a typical blood volume in adults?

A

5L

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50
Q

What happens to blood flow distribution around the body during exercise?

A

Blood flow distribution is altered during exercise; cardiac output can increase 5x and skeletal muscle receives the majority at about 25,000mL. Blood is shunted away from non-essential organs.

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51
Q

How is blood flow distribution controlled?

A

via vasoconstriction (mediated by NE) and vasodilation (mediated by NO) NB: dilation>constriction

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52
Q

How does NO cause vasodilation?

A

It relaxes smooth muscle in response to increased shear stress

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53
Q

What are 7 things that cause vasodilation of arterioles?

A
  1. bradykinin 2. prostaglandins 3. K+ 4. CO2 5. Lactate 6. local decrease in O2. 7. NO
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54
Q

What causes vasoconstriction?

A

NE, which acts on alpha receptors in smooth muscle to cause constriction

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55
Q

What percentage of blood resides in the venous system at rest?

A

70%

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56
Q

How does exercise effect venous capitance?

A

With exercise need to return more to central circulation to increase venous return • ↑ SNS activity with exercise leads to venoconstriction

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57
Q

What percentage of blood shunting occurs through venoconstriction?

A

20%

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58
Q

What is the main system that returns venous blood to the heart?

A

Muscular pump system in conjunction with venous valves.

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59
Q

What are the 5 methods that return blood to the heart?

A
  1. Muscular pump system 2. Venoconstriction 3. Low pressure of ventricle during diastole (creates vacuum) 4. Ventricular rotation during systole and recoil during diastole sucks blood back into myocardium 5. The abdomino-thoracic pump: ↑respiratory pressure in thorax during respiration ↑blood return to heart
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60
Q

Increasing the rate and depth of inspiration would have what effect on the heart?

A

↑venous return and enhanced CO

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61
Q

What effect does the Valsalva manoeuvre have on venous return?

A

forced expiration against a closed glottis (Valsalva maneuver) impedes and therefore reduces venous return and cardiac output

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62
Q

What is afterload?

A

how much blood is left in the heart at the end of contraction (End systolic volume)

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63
Q

What 6 factors affect afterload?

A
  1. Volume of blood in the arterial circulation 2. Pressure in aorta at onset of ejection (DAP) 3. Compliance of aorta 4. Inertial component of the ejecting blood column 5. Systemic vascular resistance 6. Size of pulmonary / aorta lumen
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64
Q

What are the 3 main effects of increased afterload?

A
  1. Stroke volume will be reduced in the acute phase ::Preload will increase (which is a compensation mechanism to restore SV by Frank-Starling mechanism) 2. Reduced velocity of contraction and ejection in acute phase 3. Marked increase in myocardial O2 consumption
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65
Q

What level of arterial BP will have a contribution to afterload?

A

>200mmHg has direct impact on reducing cardiac output

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66
Q

What 5 receptors effect the cardiovascular response?

A
  1. Mechanoreceptors 2. Baroreceptors 3. Chemoreceptors 4. Metaboreceptors 5. Bainbridge reflex
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67
Q

What is a mechanoreceptor and what do they do?

A

Type III (lightly myelinated) afferent receptors a. Receptors that detect stretch and muscle contraction send afferent signals to brain to increase SNS activity

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68
Q

What is a metaboreceptor and what do they do?

A

Type IV (unmyelinated) afferent receptors a. Sensitive to >lactate, phosphate, PGs,

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69
Q

What is a baroreceptor and how do they work?

A

a. In walls of carotid sinus and aortic arch b. Sense arterial pressure; are stretch activated c. Afferent nerves IX (carotid) and X (aortic arch) to brain d. Triggers brain to decrease SNS and increase PNS i. via increased peripheral dilation and reduced HR and Q :: reduced BP ii. = INHIBITION of vasometer and cardioacceleratory centres iii. = STIMULATION of cardio inhibitory centres

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70
Q

What nerves are affected by baroreceptors?

A

Afferent nerves IX (carotid) and X (aortic arch) to brain

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71
Q

What is the baroreceptor paradox?

A

It is the question of how the body gets round increased BP during exercise (which you would think leads to decreased HR?) i. The baroreflex is reset to a higher operating pressure with exercise ii. Won’t kick in until a higher arterial reassure is reached iii. Thus HR and Q can increase with exercise

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72
Q

What is a chemoreceptor and how do they work?

A

a. In walls of carotid sinus and aortic arch – sense >SpCO2 b. Triggers brain to >SNS and HR

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73
Q

What is a the bainbridge reflex?

A

a. Increased cardiac filling elicits tachycardia b. ↑ right atrium filling from ↑ venous return c. Stretch receptors in right atria and vena cava stretched d. ↑ firing rate to brain e. Brain ↑ SNS tone f. ↑ HR and SV

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74
Q

How does the bainbridge reflex increase heart rate and stroke volume?

A

a. Increased cardiac filling elicits tachycardia b. ↑ right atrium filling from ↑ venous return c. Stretch receptors in right atria and vena cava stretched d. ↑ firing rate to brain e. Brain ↑ SNS tone f. ↑ HR and SV

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75
Q

What factors damage the endothelium?

A

o Normal microvascular wear and tear o Fibrinogen o Free radicals o High blood pressure o Turbulent flow o Atherosclerotic lesions often occur at artery intersections or curves o Blood flow speed and direction changes creating turbulence o Viral attack o Carbon monoxide

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76
Q

Name the common symptoms of an MI?

A

• Classic symptoms: intense, oppressive chest pressure radiating to left arm • Other symptoms: chest heaviness, burning radiation to jaw, neck, shoulder, back, arms. nausea, vomiting dysponea. Lightheadedness. Sweating (cold and clammy). Confusion.

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77
Q

Why do Q-waves develop on an ECG after an MI?

A

They are the result of absence of electrical activity. A myocardial infarction can be thought of as an elecrical ‘hole’ as scar tissue is electrically dead and therefore results in pathologic Q waves.

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78
Q

What blood tests help diagnose an MI?

A

Released from damaged myocytes. Cardiac troponins I & T (initial rise 4-6h; peak 12-24h post-MI) CK (4-6i; 12-24 peak) CK-MB (4-6h initial; peak 12-36h) Myoglobin (2h post) LDH (8-12i; 48-72p)

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79
Q

What vessels supply the anterior myocardium?

A

Branching from the ascending aorta Left coronary artery -[Circumflex; Left anterior descending / AIB] Right Coronary artery [Marginal artery]

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80
Q

What vessels supply the posterior myocardium?

A

Left coronary artery Circumflex Right Coronary artery Posterior interventricular artery

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81
Q

What is the coronary perfusion problem?

A

Pressure in the muscle tissue during systole opposes blood flow. The effect is maximal in the deeper layers.

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82
Q

What exacerbates the coronary perfusion problem?

A
  1. Tachycardia leads to decreased diastolic time. a. diastole decreases more than systole at ↑ heart rate 2. Low diastolic pressure 3. Ischaemic heart disease - large vessel or small vessel
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83
Q

In a normal subject, ↑ heart rate has what effect on coronary blood flow?

A

↑ heart rate → ↑ coronary blood flow, by autoregulatory vasodilation – In ischaemic heart disease, ability to deliver ↑ flow is limited

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84
Q

How many deaths from IHD in Britain in 2015?

A

70,000 (BHF, 2015) Biggest single killer CVD cost the country approx…. £15 billion

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85
Q

What proportion of people now survive heart attacks?

A

7 in 10 (BHF, 2015)

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86
Q

What are the macrophages trying to do to the LDL cholesterol?

A

Pro-inflammatory M2 macrophages in the vascular smooth muscle bind and transduce signals from oxLDL and thus differ from those in adipose tissue or hepatic tissue. As these macrophages ingest oxLDL to become the lipid-rich foam cells characteristic of atherosclerosis, their molecular signature changes further. Foam cells differ markedly from normal resident macrophages in healthy vessels in that foam cells are less mobile and secrete more inflammatory mediators than normal macrophages

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87
Q

What are foam cells?

A

Foam cells are the fat-laden M2 macrophages seen in atherosclerosis. … Foam cells are formed when the body sends macrophages to the location of a fatty deposit on the blood vessel walls

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88
Q

How does the body initially try to preserve the lumen width after plaque formation?

A

o Arterial enlargement around area of the stenosis can keep lumen open even with large plaque

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89
Q

What are the chain of events leading to an MI?

A

i. Atherosclerosis ii. Plaque rupture (Most likely in fatty plaques; Fibrous capped plaques more stable) iii. Platelet aggregation>Thrombus formation>Vessel occlusion iv. Vasospasm v. Distal ischaemia & Ischaemic complications

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90
Q

What did Naghavi et al. (2003) identify as the key stages of atherosclerosis?

A
  1. Endothelial damage 2. Stenosis 3. Formation of plaque
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91
Q

What is Virchow’s triad?

A

Virchow’s triad describes the three broad categories of factors that are thought to contribute to thrombosis. Hypercoagulability. Hemodynamic changes (stasis, turbulence) Endothelial injury/dysfunction.

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92
Q

What type of vessels do the majority of infarcts occur in?

A

o 85% of all infarct related lesions are in vessels that are less than 75% occluded o A fibrous cap makes the plaque more stable

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93
Q

Which coronary artery is affected with an anterior MI?

A

LAD

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94
Q

Which coronary artery is affected with a septal MI?

A

LAD

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95
Q

Which coronary artery is affected with an left lateral MI?

A

left circumflex

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96
Q

Which coronary artery is affected with an inferior MI?

A

RCA

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97
Q

Which coronary artery is affected with an right atrial MI?

A

RCA

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98
Q

Which coronary artery is affected with an posterior MI?

A

RCA

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99
Q

Which coronary artery is affected with a right ventricular MI?

A

RCA

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100
Q

If chest leads V1-4 show ST elevation, which area of the heart and coronary artery have been occluded?

A

Anterior LAD

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101
Q

If chest leads V1-2 show ST elevation, which area of the heart and coronary artery have been occluded?

A

Septum LAD

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102
Q

If chest leads I, aVL, V5, V6 show ST elevation, which area of the heart and coronary artery have been occluded?

A

left lateral left circumflex

103
Q

If chest leads II, III, aVF show ST elevation, which area of the heart and coronary artery have been occluded?

A

Inferior RCA

104
Q

What are the characteristics of stable angina?

A

Transient (<30 minutes), episodic chest discomfort resulting from myocardial ischemia Predictable, reproducible Often follows physical exertion or emotional stress Pathophysiology: fixed, stable intra-coronary lesion– no thrombus!

105
Q

What does an ECG of a patient with stable angina show?

A

ECG: normal, T-wave changes, or ST depression

106
Q

What are the characteristics of unstable angina?

A

Harbinger of myocardial infarction New-onset angina Rest angina Angina worsening in severity or occuring with less physical / emotional provocation Pathophysiology: atherosclerotic lesion +/- thrombus formation ECG: normal, T-wave changes, or ST depression

107
Q

What would you expect to see on an ECG of the following? A) Ischaemia B) Injury C) Infarction

A

Ischaemia - generally associated with inverted T waves or S-T segment depression (disappears on rest in transient ischaemia) Injury - generally associated with S-T segment elevation and t-wave inversion Infarct - generally associated with Q waves

108
Q

Why does ischaemia result in ST depression?

A

The ischaemic myocardium is slow to repolarise and remains more positively charged than the surrounding areas

109
Q

Why does myocardial injury result in ST segment elevation and tall T waves.

A

Delayed depolarisation + tall T waves due to potassium leakage from dead cells

110
Q

What is the coronary artery blockage associated with the best prognosis? And worst?

A

Proximal LAD = 25% 1-yr mortality Small inferior = 7%

111
Q

Why do blood tests help diagnose an MI?

A

With cell death • Holes develop in cell membrane • Contents leak dependent on size, solubility • Small, cytoplasmic markers leak quickly • Larger, complex markers released slowly • These markers are not released during ischaemia • Direct relationship between concentration of these markers and size of infarct

112
Q

What is the therapy triad for an MI?

A
  1. Anti-ischaemics (O2, B-blockers, Nitrates, morphine) 2. Anti-thrombotics (streptokinase, tpa, heparin) 3. Reperfusion (t-PA, PTCA, CABG)
113
Q

What is the pathology post-MI?

A

In first 4-6h – acute ischemia Poor contraction, loses systolic power – floppy bag Infarct dilation and remolding – 7 days Inflammation bruising thinning of ventricular wall and enlargement of infarct site Necrosis during first 6-12 weeks May develop congestive heart failure Scarring Scar tissue leads to increased stiffness Partially resolves with time

114
Q

What pharmacological treatment is given to MI patients after recovery?

A
  • Blood thinners (Aspirin / Heparin / Warfarin) - β-Blockers (Atenolol [Reduce heart work] - Calcium channel blockers (Diltiazem) [Decrease peripheral resistance = less heart work] - ACE inhibitors (Lisonopril) [Decrease peripheral resistance = reduces BP and less heart work + Aids fibrin dissolving] - Diuretics (Frusemide) [Reduce blood volume = reduces BP and heart work reduces] - Cholesterol lowering drugs (Statins)
115
Q

What treatment path should a stable MI survivor take?

A

Medical therapy + exercise stress test + cardiac rehab & GP (risk factors, medication, risk stratification)

116
Q

What treatment path should an unstable MI survivor take?

A

Angiogram + CABG/PTCA + cardiac rehab + GP

117
Q

What are the interventions for an unstable MI patient?

A
  1. Angiogram with or without PTCA (balloon angioplasty) o alternatives include laser angioplasty and atherectomy 2. CABG o Saphenous vein graph or left internal mammalian artery graph
118
Q

What are the 4 stages of cardiac rehab?

A

Phase I: before discharge from hospital (assessment, advice, medication) Phase II: early post-discharge period (assessment + lifestyle advice) Phase III: As early post-discharge period plus (exercise sessions, access to trained support) Phase IV: long term maintenance of changed behaviour (1’ care follow up, local cardiac support groups, referral to specialists)

119
Q

What are benefits of an exercise based cardiac rehab programme?

A

• 13–26 per cent reduction in all-cause mortality • 26–46 per cent reduction in cardiac mortality • 23–56 per cent reduction in hospital re-admission • Cost-effective • Improved quality of life • Improved functional capacity • Supports early return to work

120
Q

What framework recommended an exercise based cardiac rehab programme post-MI?

A

CHD: National Service Framework 200 • NSF, published in March 2000 • Standard 12

121
Q

What is the equation for peak oxygen uptake?

A

VO2 = Q x (a-v)O2

122
Q

What percentage lower peak VO2 for CAD patients have?

A

50% lower than normal: 20 mL.kg-1.min-1 males 15 mL.kg-1.min-1 females

123
Q

What is the relationship between mortality and peak VO2?

A

Inverse relationship

124
Q

What are the VO2 values for highest and lowest survival

A

• Highest survival = pVO2 >18mL.kg-1.min-1 • Lowest survival = pVO2 <10mL.kg- 1.min-1 • Holds true for MI and Surgery patients

125
Q

What percentage of CV risk reduction does each 1mL.kg-1.min-1 give?

A

Each 1mL.kg-1.min-1increase in aerobic capacity reduces CV mortality risk by 10%

126
Q

What percentage of CV risk reduction does each 1 MET increase give?

A

Each 1 MET increase in aerobic capacity reduces CV mortality risk by 15%

127
Q

Why do CAD patients have a lower peak VO2?

A

Due to lower CO/Q. Rest = SV (75 ml) x HR (60 bpm) = Q (4.5L.min-1)

128
Q

How is Q affected during submaximal exercise in CAD patients?

A

Normal

129
Q

How is Q affected during heavy/maximal exercise in CAD patients?

A

Q drops & reduced maximal Q

130
Q

How is SV affected in CAD patients?

A

↑ with exercise intensity • levels off after approx. 50% peak VO2 • Dictated by – Venous return (EDV = Preload) – TPR (ESV =afterload) – Myocardial contractility

131
Q

How does the lower SV impact Q?

A

• Stroke volume is reduced after approx 60% PVO2 • TPR is higher at all work levels than in healthy persons – Poorer sympathovagal regulation – blunted NO production • This increases afterload

132
Q

How is TPR affected in cardiac patients and why? What affect does this have on Q?

A

• TPR is higher at all work levels than in healthy persons – Poorer sympathovagal regulation – blunted NO production • This increases afterload

133
Q

How do CAD pts compensate for reduced SV and Q?

A

• Higher submaximal exercise HR – ↓ SV – ↑ sympathetic activation • Lower peak HR

134
Q

How could the body successfully compensate for reduced SV and Q?

A

• Higher submaximal exercise HR – ↓ SV – ↑ sympathetic activation • Lower peak HR

135
Q

Why do cardiac pts unsuccessfully compensate for reduced SV?

A

They fail to increase HR so CO remains low. This is due to a blunted HR response: – Right coronary stenosis – ↓ sympathetic sensitivity

136
Q

How does coronary vasoconstriction affect cardiac output?

A

• Exercise may cause localised coronary vasoconstriction • This reduces blood supply to myocardium making it hypokinetic • Why? – Subnormal production of endothelial nitric oxide – Localised overproduction of endothelin

137
Q

Summarise the causes of reduced pVO2 in cardiac patients?

A

• ↓ submaximal and peak Q (SV x HR) – Major factor is ↓↓SV – ↑or↓HR Ultimately a lower SV will mean a reduced max Q

138
Q

What effects does exercise have on the vascular systems of CAD pts?

A

• body has excess blood needed for rest – two-thirds of blood resides in veins at rest • body has insufficient blood needed for maximal exercise – blood is shunted away from non-working and towards working muscles • Cardiac patients do not redistribute blood as effectively around the body – Visceral blood flow as % resting value • Normal = 20% • Cardiac = 50% • Therefore less delivered to the muscles

139
Q

List some key points of cardiac patients issues with exercise

A

Lower peak VO2 Lower peak work rate Work at a higher % of maximum during submaximal exercise Lower VO2 during submaximal exercise Slower oxygen kinetics Greater reliance on anaerobic system to fuel the exercise

140
Q

How does training benefit healthy individuals?

A

↑ Stroke volume – ↑ contractile function • ↑ calcium handling proteins in cell wall and SR – ↑ LV chamber volume (eccentric) • Myocyte elongation as sarcomeres added in series: occurs after 5 weeks – ↑ LV muscle mass (concentric) • More myocytes added in parallel (hypertrophy) – ↑ in plasma volume • 10% PV expansion may occur in just 10 days

141
Q

What is La Place’s Law?

A

T=(PR)/M • Where T is the tension in the walls • P is the pressure difference across the wall • R is the radius of the cylinder • M is the thickness of the wall To keep wall tension the same, the radius and the wall thickness must be proportional

142
Q

What are the 3 determinants of myocardial oxygen consumption?

A

HR Myocardial contractility Tension development

143
Q

So if the LV volume increases, what must also happen?

A

Wall thickness must increase or else wall tension increases.

144
Q

What mechanisms cause myocardial growth in response to training?

A

Hormones & mechanical stress

145
Q

Which hormones cause cardiac growth?

A

Cortisol, growth hormone, thyroxine, renin, angiotensin, IGF, testosterone show acute ↑ with exercise (all potentially anabolic) 1. NE and epinephrine stimulation of alpha and beta receptors in the myocardium cause cardiac growth 2. RAAS – ↑ SNS activity reduces renal blood flow during exercise, ↑ renin release, thus ↑ RAA levels – ↑ RAA levels stimulate cardiac myocytes to hypertrophy 3. GH and IGF – Cardiac myocytes have receptors for both GH and IGF – Stretching of heart muscle is trigger for these hormones to activate gene expression – IGF increases myofilament sensitivity to Ca++ thus ↑ contractile force 4. Thyroid hormones – Exercise stimulates TSH, thus thyroxin production – Thyroxin causes myocyte hypertrophy

146
Q

How does mechanical stress cause cardiac growth?

A

• Pressure overload = ↑ resistance = hypertrophy through ↑ cross sectional area (Concentric) • ↑ volume overload = hypertrophy through ↑ myocyte lengthening (Eccentric) • Mechano-sensors in myocyte activated by stress: – Surface receptors (integrins) and stretch activated ion channels ↑ CA++ influx → activate protein kinase pathways → hypertrophy

147
Q

What are the physiological cardiac adaptations to aerobic training in healthy individuals?

A

Improved contractility & Angiogenesis Improved contractility • Improved % shortening, time to peak shortening, relaxation time – ↑ calcium binding sites in myocytes – ↑ Na+ - Ca++ exchanger pumps speed removal of Ca back into SR – ↑ Ca stored in SR = more Ca = more contractile force – ↑ Ca sensitivity of myofilaments • Increased ATPase expression • Angiogensis – Myocyte hypertrophy comes with angiogensis to increase blood flow • Increased arterial size to be equal or greater than increase in cardiac mass (over adaptation!) • Increased capillarisation

148
Q

Explain La Place’s law in simple terms

A

states that wall tension (T) is proportionate to the pressure (P) times radius (r) for thin-walled spheres or cylinders

149
Q

Why should people with uncontrolled hypertension be excluded from Cardiac rehab?

A

Due to La Place’s law: if pressure in the myocardium is raised due to HTN, and left ventricle volume overload is caused by exercise, concentric and eccentric hypertrophy develop in response.

150
Q

What’s difference between eccentric and concentric myocardial hypertrophy?

A

Pressure overload = ↑ resistance = hypertrophy through ↑ cross sectional area (Concentric) • ↑ volume overload = hypertrophy through ↑ myocyte lengthening (Eccentric)

151
Q

What causes the different types of hypertrophy (Ecc / Con) and why?

A

Pressure overload = ↑ resistance = hypertrophy through ↑ cross sectional area (Concentric) • ↑ volume overload = hypertrophy through ↑ myocyte lengthening (Eccentric)

152
Q

What mechano-sensors in the myocyte are activated by stress?

A

Surface receptors (integrins) and stretch activated ion channels ↑ CA++ influx → activate protein kinase pathways → hypertrophy

153
Q

Explain pathological hypertrophy of the left ventricle, and explain the negative consequences

A

LV hypertrophy may occur through chronic overload due to high BP (afterload stressor) and through a greater preload as heart stays full of blood • This hypertrophy is not good because: – Preload / afterload engorgement and increased resistance to arterial flow causes hypertrophy in both series and parallel of myocytes to compensate – Reduced contractile function • No increase in SR Ca pumps – Reduced SR uptake of Ca lengthens relaxation time – Reduced Ca reservoir for contraction initiation – No increase in Ca sensitivity by myofilaments

154
Q

By what percentage does cardiovascular training in cardiac pts increase stroke volume? By which mechanisms?

A

↑ Stroke volume 0 - 18% – ↑ blood volume 6-10% – Myocardial hypertrophy – Improved contractile force - ↓ ESV – ↑ ejection fraction – ↑ Heart rate variability

155
Q

How many kcal of activity must be done each week to cause a partial regression of vascular stenosis?

A

• Partial regression of vascular stenosis (>2200kcal/wk)

156
Q

What are the benefits of exercise in a cardiac patient?

A
  • increased SV - decreased blood viscosity (reduced fibrinogen) - angiogenesis of coronary collaterals - Partial regression of vascular stenosis (>2200kcal/wk) - Increase in cardiac capillary blood flow - Reduced endothelial dysfunction - exercise training may reduce myocyte length to normal (aids contractile fx)
157
Q

Does exercise cause myocardial hypertrophy in CAD pts?

A

No, the reverse. Their hearts are already hypertrophied due to the stress they are under; Paradoxically exercise training may reduce myocyte length to “normal”, but this helps contractile function • Contractile function – Normal length myocytes contract better – Improvements occur due to same reasons as for healthy people

158
Q

What benefits does exercise training have for cardiac patients at rest?

A

• Small ↓ in resting HR • Resting Q remains the same

159
Q

Summarise the benefits of physiological adaptation to exercise in the cardiovascular system of cardiac patients

A

• ↑inmaxSV • ↓ In sub-maximal exercise heart rate - but this may arise without increase in SV • ↓ Systolic blood pressure response – ↑ Nitric oxide production, ↑ vasodilation thus ↓ TPR • ↓ In myocardial oxygen demand (measured by RPP) • Small ↓ in Submax exercise Q • Improvement in max cardiac output • ↑ Arteriovenous difference - more O2 extracted

160
Q

What are the benefits to the muscles in response to exercise training in cardiac pts?

A

↑ Arteriovenous difference - V. important as may cause ↑ in peak VO2 without ↑ in Q. ↑ Mitochondrial number and quantity of aerobic enzymes Shift towards a more aerobic muscle fibre type profile ↓ submaximal exercise muscle blood flow because of ↑ usage of delivered O2 ↑ Maximal muscle blood flow ↑ Muscle capillary density ↑ Muscle fibre recruitment ↓ Blood lactate concentration during sub-maximal exercise

161
Q

What papers showed that exercise training can cause reduced blood lactate in cardiac pts training?

A

Wasserman & Whipp (1975); Sullivan et al (1991)

162
Q

What is the mean and range of VO2 peak increase in cardiac patients in response to aerobic training?

A

↑PeakVO2 10 to 50% with mean @ 20%

163
Q

What is the range of TTE/distance increase in cardiac patients in response to aerobic training?

A

• ↑ Total exercise capacity (exercise time and / or distance): 18-35%

164
Q

What is the difference in angina threshold in cardiac patients in response to aerobic training?

A

• ↑Angina threshold: 10- 20%

165
Q

What did the Janssen & Jolliffe, MSSE, 38(3), 2006 paper show?

A

Looked at all cause mortality in CAD patients with change in EE. All cause mortality greater in people whose EE level had decreased • Irrespective of age or sex • Mortality risk 24% higher if EE ↓ by 1000Kcal.wk, but 19% lower if EE ↑ by 1000 Kcal.wk

166
Q

What figures did the Janssen & Jolliffe, MSSE, 38(3), 2006 paper give for reduction or increase in EE and all cause mortality relative risk?

A

Mortality risk 24% higher if EE ↓ by 1000Kcal.wk but 19% lower if EE ↑ by 1000 Kcal.wk

167
Q

What percentage of oxygen in the coronary blood is extracted at rest by the myocardium? What implications does this have for exercise?

A

70-80% If MVO2 ↑ during exercise ⇒ little scope to ↑ extraction ⇒ must ↑ coronary blood flow

168
Q

In what oxygen circumstances is angina present?

A

When myocardial oxygen (either blood flow or oxygen extraction) cannot meet demands.

169
Q

What is RPP and what is its equation and maximal value?

A

Rate pressure product is used in cardiology and exercise physiology to determine the myocardial workload RPP = SBP X HR Max exercise RPP >25,000mmHg.bt.min

170
Q

What effect does exercise training have on the RPP? What implication does this have for the angina threshold?

A

Submax exercise ↓SBP(froma↓inQ and TPR) ↓ HR ↑ in angina threshold

171
Q

What activities are allowed within 48h of cardiac surgery?

A

* Self Care Activities * Arm and leg range of motion movement * Low Resistance activities * Minimal activities - active remodelling of myocardium occurring. Don’t want to exacerbate damaged area.

172
Q

What activity would you prescribe to a cardiac patient in the weeks 1-6 post-discharge?

A

Walking. 1 1/4 mile 4 days / week 2 1/2 mile 4 days / week 3 3/4 mile 4-5 days / week 4 3/4 mile 4-5 days / week 5 1 mile 5 days / week 6 1 mile 5 days / week • Walk at a comfortable pace (RHR + 20bpm) • Take GTN spray • Know rules of chest pain • Choose flat route • Go with someone at first • Once solo, let others know the route

173
Q

What does an exercise stress test allow you to measure?

A

– Clinical maximum – Peak HR, VO2 – Exercise capacity – Angina threshold

174
Q

What are the 6 stage VO2 requirements of the Bruce protocol?

A
  1. 16 2. 23 3. 34 4. 46 5. 57 6. 68
175
Q

Give 5 reasons why you might stop an exercise test as the clinician?

A

• Reaching estimated max HR ± 10bts.min-1 • Light headedness, confusion, ataxia, cyanosis, dysponea, nausea • Onset of angina • Symptomatic SVT • ST depression >2mm • VT • Exercise induced LBBB Why • Onset of 2nd or 3rd degree heart block • One R on T PVC • PVC’s accounting for >30% of all complexes • Hypotension (>20mmHg drop in BP) • Hypertension (>220 mmHg SBP : >110mmHg DBP) • Inappropriate bradycardia (drop in HR >10 beats / min) with increase or no change in work load

176
Q

How do you determine what HR to prescribe exercise at?

A

Determine peak HR from test data [The highest HR achieved before problems (Angina etc)] Calculate training heart rate zone: 40-80% of the peak HR value recommended – some studies suggest 70-85% as intensity threshold – Use common sense

177
Q

What is a MET equivalent to?

A

1 MET =resting oxygen uptake (3-4mL.kg- 1.min-1)

178
Q

What are the MET requirements of each stage of the Bruce protocol?

A

3-4 (stage 1 etc) 5-7 7-9 9-11 11-13

179
Q

What METS are each of the following activities? Walking Cycling Dancing Golf Jogging Football Tennis Swimming

A

W: 3 - 10 METS C: 3 - 8 METS D: 4 - 8 METS G: 4 - 7 METS J: 8 - 16 METS F: 5 - 12 METS T: 4 - 9 METS S: 4 - 8 METS

180
Q

How do you calculate heart rate reserve?

A

(HRR = predicted max HR - resting HR) + resting HR

181
Q

What level of HR reserve should a cardiac patient exercise at?

A

40-80%

182
Q

How would you calculate the recommended HRR exercise level for a cardiac patient with a max HR of 200bpm, and resting HR of 60bpm?

A

(6 x (200-60)) + 60 = 84 + 60 = 144 bts.min-1 (HRR = predicted max HR - resting HR) + resting HR

183
Q

How would you predict peak HR for an ELDERLY cardiac patient? What research supports this?

A

β-blocked = 203-1.49(age) Non β-blocked = 252-1.91(age) Brodie et al., (1998)

184
Q

At what RPE should a cardiac patient exercise?

A

12-16 (fairly light-upper hard limit)

185
Q

How much training is needed for a significant change in a cardiac pt life to be seen?

A

Regular training (3d.wk-1) for minimum of 3 months needed for significant changes to be seen

186
Q

A 55 year-old woman who has been a smoker for 35 years has recently suffered a myocardial infarction (MI). She is determined to start making changes in her life and so wishes to stop smoking and start an exercise programme. She has been signed off work for 3 months, giving her plenty of time to attend a cardiac rehabilitation programme. Her discharge exercise test results were; Total treadmill time - 9 min Peak exercise intensity - 5.4km.hr–1 @ 14% gradient ECG changes - ST depression in V3 + V4 Peak attained HR - 130 bts.min-1 Peak oxygen consumption - 34 mL.kg-1.min-1 Peak MET intensity - 11 METS Peak RPE score - 20 Resting HR - 60bpm What starting exercise intensity would you prescribe?

A

You could use peak HR, or HRR, or METS, or RPE!

187
Q

What particular exercise recommendations would you give to post-MI patients?

A

• Long warm up period of at least 10 minutes • A mixture of aerobic exercise and resistance exercise can be used • Exercise intensity should be set at an intensity of 50-80% of peak HR, 50-70% HRR, 12-16 / 4-6 RPE, or 5-8 METS. • Intermittent exercise (work / rest) is often better tolerated • Start with 10-15 minutes total exercise time, increasing to 30-60 minutes • Exercise all major muscle groups - at least 10min cool down

188
Q

What particular exercise recommendations would you give to post-CABG patients?

A

6 week post-surgery. Make sure leg and sternal wounds are well healed. • Warm up • Commence with a programme of aerobic exercise • Flexibility exercises for the pectorals, shoulder and legs • Exercise intensity should be set at an intensity of 50-80% of HRR, 12-16 / 4-6 RPE, or 5-8 METS. • Start with 10-15 minutes total exercise time, increasing to 30-60 minutes • Upper body resistance exercises should be included with patient agreement, but under close supervision - cool down

189
Q

What are the benefits of circuit interval training for cardiac pts?

A

– Better tolerated by patients – accumulation of exercise allows a greater total amount of work to be performed per session – Rest allows HR and SBP to ↓, thus MVO2

190
Q

What advice would you give about circuit interval training for cardiac pts?

A

• Work periods ∝ 2-3 minutes • May start with 5 reps of 30 seconds • 1:1 work:rest ratio • Supine & upright exercises not interspersed – ↑ preload = ↑ MVO2 – Orthostatic hypotension

191
Q

How should you progress exercise prescription for the patient?

A

• Ask the person!!! • 10% every 2 weeks • Durationthenintensity • Don’t be afraid to↓ work load

192
Q

What advice would you give about walking for cardiac pts?

A

• Walkingspeedshould achieve HR in training zone • Pleasurable

193
Q

What advice would you give about golf for cardiac pts?

A

• METS 4-7 • Aerobic/anaerobic • Flatcourse • 9 Holes at first,↑ number slowly • 3/4swing • Half set of clubs • Pull or carry clubs • Chest pain rules

194
Q

What advice would you give about bowls for cardiac pts?

A

• Bowls has NO cardiovascular benefit • But will improve co- ordination, flexibility and confidence in physical activity

195
Q

What advice would you give about swimming for cardiac pts?

A

• No swimming until sure of arrhythmia / angina / wound status • METS4-8 • Is HR in training zone? • Vary stroke • Chest pain rules • Cold water

196
Q

Which cardiac patients might strength training not be appropriate for?

A

• Congestive Heart Failure • Severe Valvular Disease • Low ejection fractions • Uncontrolled Arrhythmias • Significant left ventricular dysfunction

197
Q

What advice would you give about strength training for cardiac pts?

A

Safe CV responses seen if load is < 60%1RM Keep RPP below trigger point • Can exercise > 5 MET • Circuits of 6-10 exercises • 8-20 repetitions • 2-3 d.wk-1 • Light weight (30-80% 1RM) • Alternate arm / legs • Alternate arms or legs • Controlled breathing • Sitting or standing (Ehrman, 2013)

198
Q

What is the BP response to isotonic type resistance exercise like in comparison to aerobic exercise?

A

Similar (i.e. increase in SBP and HR)

199
Q

What is the BP response to isometric type resistance exercise like?

A

• Muscle develops tension but does not shorten • Note how both SBP and DBP increase

200
Q

What is the BP response to isometric type resistance exercise like?

A

• Muscle develops tension but does not shorten • Note how both SBP and DBP increase

201
Q

What are the key responses of BP during resistance training?

A

> intra muscular pressure BP >>TPR >intrathoracic pressure

202
Q

What are the acute effects of strength training on BP, HR and VO2?

A

– ↑ BP ⇒ ↑ RPP (HR X SBP∴MVO2) not problematic if < 80% 1RM – ↑ HR; 60-80% HR max during circuit weights – ↑ VO2; 30-50% VO2max during circuit weights

203
Q

What does the response to strength training depend on?

A

Type (isotonic / isometric) Weight lifted (% 1RM) Duration of rest intervals Starting CV fitness of person Medications

204
Q

What are chronic effects of strength training?

A

Muscular strength: ↑ 20-30% in cardiac patients ↑ efficiency of movement Small ↑ in peak VO2 Improved blood lipid profile ? Improvement in body composition ?

205
Q

What increase in muscular strength do cardiac patients see with chronic strength training?

A

20-30% increase

206
Q

When should you use resistance training?

A

4-6weeks into supervised cardiorespiratory endurance exercise program • Use elastic bands, light handweights, or resistive tubing to add variety • Monitor heart rate and ECG continually • >? Ask the person !!! • 10 % every 2 weeks • > Reps then intensity • Don’t be afraid to ↓ work load

207
Q

What are the advantages of water based exercise?

A

Buoyancy, water resistance and temperature ↓ joint compression forces Stimulus for muscular development Useful for people with orthopaedic limitations Weight management due to greater EE

208
Q

What are the effects of water submersion on circulation at rest?

A

Hydrostatic pressure forces blood back into the central circulation ↑ venous return ↑ heart blood volume 200ml ↑ SV 30-50% HR same or ↓ ↑ Q 25% ↑ Mean BP 12mmHg - vasoconstriction in cold water, dilation in warm Diuretic effect - dehydration, ↓ blood volume

209
Q

What are the effects of water submersion on arrhythmias?

A

↑ incidence of Ventricular arrythmias (esp Ventricular ectopic beats) ↑ ST depression But why? Unclear Breath holding = ↑ SNS tone to heart especially after taking a breath prior to holding∴ more arrhythmia risk This is different from the breath hold dive reflex which works after facial immersion in cold water (<20°C) which causes bradycardia No increase in angina

210
Q

What are the effects of water submersion on ventilation at rest?

A

Hydrostatic pressure squeezes the thoracic cavity • ↓vitalcapacity5-10% • ↓gasexchange • ↓PaO2 • ↑loadonrespiratory muscles

211
Q

During sub maximal exercise, how much more do CHD patients have to work?

A

– CHD patients work at higher % of maximum (50-80%) – Yet RPE similar between groups - feels easier than it is, safety issue!

212
Q

What order or difficult do swimming, cycling and running come for CHD pts and normal ones?

A

TM>CE>W for both CHD and healthy people

213
Q

What advice would you give about water based exercise for cardiac pts?

A

Should be restricted to low risk patients - 10 beats off training HR to be safe Limited evidence as yet

214
Q

What MET capacity should you aim for in order for a pt to return to a white collar job?

A

7 METs

215
Q

What year were the current British activity guidelines published?

A

2004

216
Q

ABC of activity for health O’Donovan JSS 2010: What does the paper recommend for the three groups - ABC?

A

All health adults: >150min MPA/ 75min VPA/ equivalent mix (aerobic) + weight training/ resistance (8-10 exercises) 2d/week at a weight that brings muscle fatigue after 8-10 reps Beginners: work steadily towards meeting the PA levels recommended Conditioned individuals: meeting recommendations for >6months may gain additional benefits by 300min MPA/ 150min VPA/ week

217
Q

ABC of activity for health O’Donovan JSS 2010: What does the paper recommend for children?

A

5-16y: at least 60min MVPA per day, including VPA activities that improve bone density and muscle strength

218
Q

ABC of activity for health O’Donovan JSS 2010: What does the paper recommend for CVD/diabetics?

A

To go beyond the recommended ‘healthy’ adult levels and progress towards conditioned individual recommendations. (300min MPA/ 150min VPA)

219
Q

ABC of activity for health O’Donovan JSS 2010: What does the paper recommend for obese patients?

A

Reduce sedentary time, reduce energy intake, + 300min MPA/ 150min VPA

220
Q

ABC of activity for health O’Donovan JSS 2010: When might the health of conditioned individuals suffer by increasing the amount of activity they are doing?

A

A large volume of resistance training may lead to overreaching and overtraining if the balance between training and recovery is inappropriate [over- reaching refers to a decrease in performance that may last several days to several weeks and overtraining refers to a decrease in performance that may last several weeks to several months and may be accompanied by greater fatigue, performance decline, and mood disturbance (Halson & Jeukendrup, 2004)].

221
Q

ABC of activity for health O’Donovan JSS 2010: Why is it suggested that the relationship between activity and health is only moderately strong and may actually be an underestimate?

A
  1. The reductions in morbidity and mortality associated with physical activity might sound modest, but they are the most conservative of estimates obtained by statistically isolating physical activity from potential confounders, such as age, smoking habit, cholesterol profile, and blood pressure. (Mora, Cook, Buring, Ridker, & Lee, 2007). 2. It is also possible that the relationship between physical activity (exposure) and health (outcome) has been underestimated because it has been difficult to measure accurately people’s exposure to physical activity (Lee & Paffenbarger, 1996)
222
Q

ABC of activity for health O’Donovan JSS 2010: What health conditions may not benefit if the activity is ¨packed¨ into the week on 1 / 2 days rather than being spread out

A

Obesity, depression, hypertension, diabetes, hyperlipidaemia.

223
Q

ABC of activity for health O’Donovan JSS 2010: What’s the evidence that bout length can be less than 10 mins?

A

Although more research is required, there is some evidence that bouts of less than 10 min may also be beneficial to health (Miyashita, Burns, & Stensel, 2008; Strath et al., 2008). There is also growing evidence that it is beneficial to avoid sitting and other sedentary behaviours (Hamilton, Hamilton, & Zderic, 2007; Levine, 2007).

224
Q

ABC of activity for health O’Donovan JSS 2010: What’s the evidence that bout length can be less than 10 mins?

A

Although more research is required, there is some evidence that bouts of less than 10 min may also be beneficial to health (Miyashita, Burns, & Stensel, 2008; Strath et al., 2008). There is also growing evidence that it is beneficial to avoid sitting and other sedentary behaviours (Hamilton, Hamilton, & Zderic, 2007; Levine, 2007).

225
Q

ABC of activity for health O’Donovan JSS 2010: What are the MET ratings for moderate and vigorous activity?

A

Moderate: 4-6 METs Vigorous: >6 METs

226
Q

ABC of activity for health O’Donovan JSS 2010: What are some of the key issues about the Built environment’s impact on activity?

A

• Walking for transport • Public spaces for recreation • Neighbourhood design • Safety of routes for school commutes

227
Q

• Which infections have been linked with atherosclerosis?

A

Chlamydia pneumonia Herpes family viruses Cytomegalovirus

228
Q

• Why might anti-inflammatories be useful against CHD?

A

Cyclosporine + sirolimus (immunosuppressive drugs) block the activation of T cells, inhibit intimal lesions and at high doses inhibit smooth muscle proliferation. COX-2 inhibitors eg. Rofecoxib Lipid-lowering statins Vaccination

229
Q

What swimming pool temperature has the least effect on the heart of cardiac patients?

A

26-33oC Public pools about 29C

230
Q

What effect can pools that are too hot or too cold have on the heart?

A

Hot: vasodilation; vasovagal syncope Cold: arrhythmias

231
Q

How do saunas and jacuzzis affect cardiac patients? How should they be used?

A

Gradually increase time up to 10 mins. Drink plenty of water. NEVER use the plunge pool before/afterwards.

232
Q

How long should you wait after cardiac surgery before swimming?

A

6 weeks after MI to allow myocardial tissue to recover 12 weeks after CABG to allow sternal healing

233
Q

What recommendations would you give to someone swimming with a pacemaker?

A

• If your device has recently been put in you should wait at least six weeks to allow the wires to settle • You are advised only to use breaststroke. Front crawl, backstroke and fly can potentially damage the leads due to repeated strain on them • With an ICD you should always have someone with you or be in a lifeguard supervised pool, in case the device activates and you need help

234
Q

Explain the process of atherosclerosis (flow diagram)

A
235
Q

Explain A-F

A

A. Normal ECG

B. Hyperacute T wave changes - increased T wave amplitude and width, may also see ST elevation

C. Marked ST elevation with hyperacute T wave changes (transmural injury)

D. Patholigic Q waves, less ST elevation, terminal T wave inversion (necrosis)

E. Pathologic Q waves, T wave inversion (necrosis and fibrosis)

F. Pathologic Q waves, upright T waves

236
Q

Complete the table

A
237
Q

What does the increase of HR with exercise look like in graphical form? What are the autonomic responses?

A
  • Curvilinear  in HR with  exercise intensity
  • Initially withdrawal of PNS and then activation of SNS
238
Q

Above what bpm does Q drop as a result of reduced filling time?

A

180bpm

239
Q

What are the 4 factors that influence SV?

A
  • Venous return (EDV = Preload)
  • TPR (ESV =afterload)
  • Myocardial contractility
  • HR
240
Q

What is the SV response to exercise? At what percentage of pVO2 does SV level off?

A
  •  with exercise intensity
  • levels off after approx. 50% peak VO
241
Q

By what percentage does SV increase from resting to maximal when supine?

And when upright?

A

Supine ~ SV > 7% rest – max

Upright ~ SV > 33% rest - max

242
Q

At rest, is SV greater in the supine or upright position and why?

A

Supine > upright. As in upright position there is reduced venous return due to gravity and blood pooling.

243
Q

At submaximal and maximal exercise intensities, is SV greater in the supine or upright position and why?

A

They are equal, as the muscle pump & venoconstriction mechanisms increase venous return in the upright position.

244
Q

What is the equation for stroke volume?

A

SV = EDV - ESV

245
Q

Draw the patterns of SV, end diastolic volume and end systolic volume on a graph with ventricular diameter (mm) as the y axis.

A
246
Q

What are the haemodynamic factors determining venous return?

A
247
Q

During what phase does the heart experience improvements in contractility?

A

Only in the first phase

248
Q

What percentage is EF at rest? And what does it increase to at peak exercise?

A

EF increases from approx 65% at rest to 80% at peak exercise

249
Q

To what peak VO2 does end diastolic volume increase to?

A

40%

250
Q

What happens to TPR during exercise and why? Give values of mmHg that TPR begins and ends at with increasing exercise intensity.

A

TPR decreases as a result of dominating vasodilation. 22mmHg at rest to 6mmHg heavy exercise.

251
Q

What is resting Q? By how much does Q increase with each 1L VO2?

A

Resting Q = 5L/min

During exercise +1L VO2 = +5L Q

252
Q

At <50% pVO2 (rest-submax), which of the following are increasing: SV or HR?

A

Both SV and HR increase at below 50% pVO2 to accomodate exercise

253
Q

> 50% pVO2, how does the body accomodate the need for an increase in Q?

A

SV is maximised, so increase in Q is down to increase in HR

-during exercise SV only increases 25%, but HR increases 300%

ClinE 470 (9 decks)

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