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Exercise & Environment > Cardiovascular and respiratory diseases > Flashcards

Cardiovascular and respiratory diseases Flashcards

1
Q

main causes of death in England

A

dementia and Alzheimer diseases 12.8%

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2
Q

Leading cause of death by gender:

A

male: ischaemic heart disease 13.2%
Female: dementia and Alzheimer disease 16.7%

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3
Q

Main cardiovascular diseases

A
  • coronary heart disease and failure
  • hypertension, vascular disease and atherosclerosis
  • thrombosis
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4
Q

main causes of CVD

A 
genetics
age
lifestyle
diet
obesity
smoking
inactivity
air pollution
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5
Q

main respiratory diseases

A
  • lung cancer
  • astham
  • chronic obstructive pulmonary disease (COPD)
  • infections
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6
Q

main causes of respiratory disease

A 
genetics
age
allergy
infectin
smoking
air pollutionn
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7
Q

no.1 world wide disease

A

cardiovascular disease

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8
Q

socioeconomic impacts of CVD and CR disease

A
  • cardiovascular disease costs the UK £19 billion p.a
  • Respiratory disease costs the UK £11 billion p.a
  • NHS costs, days off work, premature death, disability and informal care costs etc
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9
Q

dyspnoea

A

breathlessness

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10
Q

causes of dyspnoea

A 
multiple causes that are cardiac :
- heart failure
- angina with atypical features
or respiratory causes:
- COPD
-asthma
- pneumnia
-plenary embolism
- lung malignancy

other systems that effect oxygen delivery will also cause dyspnoea such as anaemia

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11
Q

Heart failure

A

when the heart is not pumping blood around the body as well as it should, most commonly when the heart muscle has been damaged e.g post heart attack

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12
Q

typical symptoms of heat attack

A

breathlessness
ankle swelling
fatigue

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13
Q

possible accompanying signs of heart failure

A
  • elevated jugular venous pressure
  • pulmoary crackles
  • peripheral oedema
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14
Q

Physiological definition of heat failure

A

inability to provide adequate cardiac output to support the needs of the tissues; or can do so but only at the expense of a raised filling pressure

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15
Q

survival of heart failure

A

It is progressive syndrome with a less than 5 year survival

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16
Q

what determines Cardiac output

A
  • heart rate and stroke volue

- preload, contractility and after load

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17
Q

enhanced heart function

A

increase contractility
increase HR
decreased after load

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18
Q

depressed heat function

A

decreased contractility
decreased HR
increased after load

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19
Q

systolic heart failure

A

impaired contractility
heart can’t pump or squeeze enough blood out to rest of body
- then weak heart muscle

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20
Q

diastolic heart failure

A

impaired filling/relaxation so heart can’t fill without enough blood
- stiff thick heart muscle

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21
Q

stiff thick heat muscle is associated with

A

diastolic heart failure

impaired filling/relaxation so heart can’t fill without enough blood

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22
Q

thin weak heart muscle is associated with

A

systolic heart failure
impaired contractility
heart can’t pump or squeeze enough blood out to rest of body

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23
Q

left heart failure

A

not pumping enough blood out of left ventricle

  • commonly caused by coronary artery disease
  • also caused by mitral/aortic valve disease or viral cardiomyopathies
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24
Q

right heart failure

A 
not pumping enough blood out of right ventricle 
caused by:
-COPD 
pulmonary hypotension
-pulmonary embolism 
- valve disease
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25
Q

congestive heart failure

A

when left heart failure leads to right heart failure

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26
Q

most common cause of heart attack is

A

coronary artery thromboembolism

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27
Q

myocardial infarction

A

heart attack

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28
Q

coronary artery thromboembolism

A

blood clot

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29
Q

thrombosis

A

inappropriate formation fo blood clots, thrombi

30
Q

types of thrombosis

A 
coronary 
deep vein (DVT)
31
Q

what does thrombosis cause

A

danger of embolisms

  • venous, DVT or right atrial thrombosis leads to pulmonary emboli
  • left arial thrombosis leads to cerebrovascular ischaemic stroke
32
Q

primary cause of DVT

A

immobility

33
Q

DVT

A

deep vein thrombosis

34
Q

primary cause of atrial thrombosis

A

status and turbulence due to atrial fibrillation

35
Q

treatment of thrombis

A

prophylaxis

arterial: anti-platelet e.g aspirin, clopidogrel
venous: anticoagulant e.g heparin, warfarin, DOAC

36
Q

examples of anticoagulants

A

heparin, warfarin, DOAC

used to prevent venous thrombisis

37
Q

examples of anti platelet drugs

A

aspirin, clopidogrel

used to prevent arterial thrombosis

38
Q

Pathophysiology of heat failure

A

fall in BP is detected but normal mechanisms don’t work

  • increased HR results in more work and more heart damage
  • vasoconstriction doesn’t work before of muscle damage
  • reabsorption of salt and water by kidneys to increase blood volume causes increased pressure and work causing more heat damage
    eabsorption of salt and water by kidneys to increase blood volume causes breathlessness and oedema
39
Q

fluid accumulation in tissue

A

peripheral oedema = right hart failure

40
Q

fluid accumulation in lungs

A

breathlessness = left heart failure

41
Q

why is heart failure progressive

A

largely caused by compensation mechanisms of the body adapting to:
exercise intolerance, weakness, breathlessness, pleural congestion, pulmonary oedema, dilated heart, peripheral oedema, pitting oedema & hepatomegaly

but, attempts at controlling cardiac output slowly cause weakness, oedema and increased work

42
Q

how to treat heat failure

A

reduce symptoms to improve QoL and prolong survival but doesn’t cure

  • beta blockers
  • diuretics
  • ACE inhibitor
43
Q

COPD

A

Chronic obstructive pulmonary disease

44
Q

what is COPD

A

Chronic obstructive pulmonary disease
a common preventable and treatable disease
characterised by:
– persistant respiratory symptoms and air flow limitation
due to:
- airway or alveolar abnormalities

45
Q

common cause of COPD

A

significant exposure to noxious particles or gases:

  • tobacco smoking, active and passive
  • biomass fuel exposure from poorly ventilated dwellings
  • occupational exposure e.g dust, chemical agents, fumes
  • rare inherited alpha anti-trypsin deficiency
46
Q

common symptoms of COPD

A

Dyspnea
coughing
sputum production

47
Q

clinical feats of COPD

A
  • Barrel chested
  • difficult to locate cardiac apex beat
  • reduced chest wall expansion on inspiration
48
Q

pathophysiology of airways in COPD

A
  • hypertrophy and hyperplasia of bronchial submucuocal glands
  • increased no. goblet cells = hyper secretion of mucus
  • destruction of cillia
  • narrowing of airways from remodelling
  • increased airway resistance
49
Q

pathophysiology of parenchyma in COPD

A
  • proteolytic enzymes destroy alveolar tissue
  • elastin an collage are destroyed =reduced elasticity and structural integrity of lungs
  • reduced surface area for gas exchange
50
Q

COPD pathophysiology

A
  • impaired gas exchange causes hyperaemia
  • airways poorly supported & collapsible
  • reduced driving pressure for expiratory flow
51
Q

what drives movement of air through airways

A

pressure gradient between mouth and alveoli

52
Q

what is turbulence

A

when laminar flow is disrupted. causes by high velocity, sharp edges and branching points in airways

53
Q

what is the effect of turbulence

A

significant increase in resistance and causes vibrations = wheezing noice as air tries to move through narrowed airways at high velocity

54
Q

why is a silent chest ominous for an asthmatic

A

wheezing only occurs if air flow is present, If obstruction worsens such that there is no airflow then there will be no wheezing

55
Q

resistance is inversely proportionate to

A

r^4

R = 1/r^4

if radius is hated, resistance increases 16 fold with same pressure gradient so flow is reduced to 1/16th

56
Q

two main factors causing variations in airway resistance

A

factors within the airways

pressure across airway wall

57
Q

RAW

A

airway resistance

58
Q

factors within the airways

A
  • bronchial smooth muscle tone
  • inflammation of epithelium
  • hypertrophy of glands and secretion like mucus
59
Q

what affects airway smooth muscle tone

A
  • prostaglandins
  • arenaline
  • co2
  • sympathetic stimulation
  • parasympathetic stimulation
60
Q

negative intrapleural pressure in normal breathing =

A

airways held open

61
Q

positive intrapleural pressure in normal breathing =

A

collapsing force on airways

62
Q

which airways are most likely to collapse

A
  • bronchi around generation 3 or 4 which is site of maximum resistance
    this is because here the pressure within the airways falls below Ppl during forced expression
63
Q

why is expiratory airflow limited for everyone

A

because of dynamic compression of airways.
At low lung volume, expiratory airflow will not increase no matter how hard you try
It is effort independent

64
Q

difference in airflow in normal and COPD

A 
high airway resistant increases the limitation of airflow.
Slow expiration =
- slow expiratory flow rate
- air trapping 
- expiratory wheezes
65
Q

summary of COPD

A
  • Air flow obstruction
  • loss of lung elasticity
  • loss of alveoli
  • # airway inflammation
  • expiratory flow limitation
  • reduced elastic recoil of lungs
  • reduced gas exchange
  • hyperinflation
  • sputum production
  • chest infections
66
Q

Diagnosing COPD

A

use of to measure how fast and how much air you breath out.

use FEV1 and FVC to distinguish between Obstructive disease and Restrictive lung disease

67
Q

FEV1

A

forced expiratory volume in 1 second

68
Q

FVC

A

forced vital capacity

69
Q

normally FEV1/FVC >

A

75%

70
Q

COPD

A

significantly reduced FEV1
reduced or normal FVC
Reduced FEV1/FVC

71
Q

Restrictive disease

A
  • reduced FEV1
  • reduced FVC
  • normal FEV1/Fvc
72
Q

spiral of disability of cardiorespiratory disease

A

reduced breathlessness leads to inactivity leads to muscle deconditioning which leads to excess lactate and co2 production which leads to breathless ness :(

muscle deconditioning also adds to leg fatigue and weakness which increases inactivity

importance of exercise training pulmonary rehab

Exercise & Environment (14 decks)

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