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Module 103: The Heart, Lungs and Blood > Theme 3: Lecture 3 - How the CVS fails > Flashcards

Theme 3: Lecture 3 - How the CVS fails Flashcards

1
Q

Stroke

A
  • rapid loss of brain function(s) due to loss of perfusion to part(s) of the brain
  • AKA a cerebrovascular accident
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2
Q

What is a haemorrhagic stroke due to

A

cerebral blood vessel rupture

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3
Q

What is an ischaemic stoke due to

A

Cerebral blood vessel blockage

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4
Q

What causes a blood vessel to burst

A
  • Stress

- Damage

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5
Q

what are causes of stress on a blood vessel

A
  • High pressure
  • Turbulent flow
  • Large diameter / high wall tension
  • Low compliance
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6
Q

What are causes of damage to a blood vessel

A
  • Trauma (eg transluminal procedures)
  • Atherosclerosis
  • Diabetes
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7
Q

What is vessel wall tension

A
  • Tension in a cylinder is the force (tangential to the circumference of the cross section) that is trying to rip the wall apart
  • The larger the vessel, the greater the wall tension
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8
Q

Vessel wall tension equation

A

Tension = Pressure x Radius

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9
Q

Compliance

A

the change in volume caused by a change in pressure (the slope of the black line in the graphs)

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10
Q

What is a highly compliant vessel

A

a stretchy vessel

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11
Q

What is a low compliant vessel

A

a stiff vessel

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12
Q

Describe laminar flow

A
  • smooth flow

- slower at the edges due to friction between blood and vessel

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13
Q

What causes turbulent flow

A
  • High speed
  • Branching and junctions
  • Low viscosity
  • Mixing
  • Obstacles (atherosclerosis and endothelial damage)
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14
Q

What activities does the endothelium do (6 things)

A
  • Blood vessel tone
  • Fluid filtration
  • Haemostasis
  • White Cell recruitment
  • Angiogenesis
  • Hormone trafficking – (transcytosis)
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15
Q

Blood vessel tone

A

How much constriction/dilation occurs at the blood vessel

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16
Q

Transcytosis

A

a type of transcellular transport in which various macromolecules are transported across the interior of a cell. Macromolecules are captured in vesicles on one side of the cell, drawn across the cell, and ejected on the other side.

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17
Q

Describe an acute myocardial infarction

A
  • A region of heart tissue that is dying or dead
  • Usually caused by a blocked coronary artery
  • Onset takes minutes – extremely painful *E
  • Reduces the capacity of the heart to pump
  • AMIs can be fatal due to arrhythmia or HF
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18
Q

What can large or multiple myocardial infarcts lead to

A

heart failure

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19
Q

What does atherosclerosis result from

A
  • hyperlipidaemia
  • immune action
  • unknown aetiology
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20
Q

Symptoms of atherosclerosis

A

asymptomatic but can lead to other disorders

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21
Q

What is atherosclerosis

A
  • A disease process that causes a build up of plaque in the blood vessels
  • Results in furring of the arteries
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22
Q

What is coronary artery disease

A

A disease process resulting in obstruction of the arteries supplying heart tissue
-AKA ischaemic heart disease or coronary heart disease

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23
Q

Symptoms of coronary artery disease

A

angina or asymptomatic

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24
Q

Primary cause of coronary artery disease

A

atherosclerosis

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25
Q

Drug treatment for coronary artery disease

A

Treat with drugs for:

  • hyperlipidaemia
  • angina
  • hypertension
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26
Q

Surgical treatment for coronary artery disease

A
  • stenting

- surgically replacing clogged vessels

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27
Q

When does a plaque rupture

A

When the fibrous cap of a plaque bursts open

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28
Q

When do atheromas become dangerous

A
  • when the plaque ruptures

- if a thrombus or embolus forms

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29
Q

Fibrous cap

A

a layer of fibrous connective tissue, which is thicker and less cellular than the normal intima, found in atherosclerotic plaques.

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30
Q

What does the sympathetic nervous system release during an acute MI

A

adrenaline and noradrenaline

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31
Q

Why does the sympathetic nervous system release adrenaline and noradrenaline in an acute MI

A
  • in response to pain

- in response to haemodynamic abnormalities

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32
Q

What are haemodynamic abnormalities

A

abnormal or unstable blood pressure

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33
Q

How does sympathetic activity help to compensate during heart failure

A

leads to an increase in heart rate and contractility

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34
Q

What problems does sympathetic activity cause in heat failure

A
  • increases peripheral resistance making it harder for the heart to pump blood (but helps to maintain pressure if there’s a sudden pressure failure)
  • increased risk of arrhythmia (can lead to sudden death)
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35
Q

What are the 2 forces on water in the capillary

A
  • Hydrostatic pressure

- Osmotic pressure

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36
Q

How does oedema occur

A

When there is more fluid going out of the blood vessel than is being brought back in due to hydrostatic and osmotic pressures

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37
Q

What is pulmonary oedema

A

fluid accumulation in the lungs esp alveoli

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38
Q

What does pulmonary oedema lead to

A
  • impaired gas exchange

- longer O2 diffusion length

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39
Q

Symptoms of pulmonary oedema

A
  • dyspnoea
  • orthopnoea
  • leads to hypoxia
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40
Q

hypoxaemia

A

a decrease in the partial pressure of oxygen in the blood

41
Q

hypoxia

A

a reduced level of tissue oxygenation

42
Q

orthopnoea

A

shortness of breath that occurs when lying flat

43
Q

What is pulmonary oedema caused by

A

left heart failure

44
Q

Describe how left heart failure causes pulmonary oedema

A
  • Damming of the blood occurs (blood doesn’t go into left heart which causes a build up of blood in the pulmonary vasculature)
  • Leads to increased hydrostatic pressure in the pulmonary circulation
  • Net fluid leak outwards
45
Q

Ascites

A

accumulation of fluid in the peritoneal cavity

46
Q

Causes of ascites

A

many causes including heart failure

47
Q

peripheral oedema

A

swelling of tissues esp ankles

48
Q

Causes of peripheral oedema

A

many causes esp chronic low output heart failure

49
Q

What is compensation

A

Maintaining homeostasis of a physiological function despite stressors or malfunctions – happens via endogenous physiological feedback

50
Q

What does compensation do in heart failure to maintain adequate cardiac output despite damage

A

-increases plasma volume and sympathetic pathway

51
Q

What is decompensated heart failure

A
  • A medical emergency
  • The failure of the heart to maintain adequate blood circulation, after long-standing (previously compensated) vascular disease.
52
Q

What is cardiac remodelling

A
  • Growth in cardiac muscle

- Changes in shape, size and function

53
Q

What causes cardiac remodelling

A
  • Injury eg MI, hypertension, valve disease

- Response to increased afterload or preload

54
Q

What is the result of cardiac remodelling

A
  • hypertrophy

- dilation

55
Q

When is cardiac remodelling compensatory and pathological

A
  • initially compensatory

- later pathological

56
Q

Treatments for cardiac remodelling

A
  • ACE inhibitors

- Spironolactone

57
Q

What is ventricular hypertrophy a response to

A

work (a bigger athlete’s heart is normal)

58
Q

Eccentric ventricular hypertrophy

A

Dilated ventricle due to volume overload

59
Q

Concentric ventricular hypertrophy

A

Thickened ventricle due to pressure overload

60
Q

What does ADH do

A
  • Also called vasopressin
  • Causes kidneys to reabsorb more water
  • Decreases Diuresis
61
Q

Where is ADH secreted from

A

Posterior pituitary

62
Q

What type of molecule is ADH

A

peptide

63
Q

What does aldosterone do

A
  • Causes kidneys to reabsorb more NaCl (and thus more H2O)
  • Directly decreases Natriuresis
  • Which Decreases Diuresis
64
Q

Natriuresis

A

Loss of Na+ in urine

65
Q

Where is aldosterone secreted from

A

Adrenal cortex

66
Q

What type of molecule is aldosterone

A

Steroid

67
Q

Which hormones do diuretic drugs antagonise

A

ADH and aldosterone

68
Q

What does angiotensin II do

A

Increases pressure by:

  • Vasoconstriction
  • Increased fluid retention (Increases aldosterone secretion by adrenal cortex, increasing Na+ retention, Increases ADH secretion by posterior pituitary)

Contributes to ventricular hypertrophy + remodelling

69
Q

Describe the Renin Angiotensin Aldosterone System (RAAS)

A
  • Angiotensinogen is physiologically inactive
  • The enzyme Renin converts angiotensinogen into angiotensin I
  • Angiotensin I is still physiologically inactive
  • The Angiotensin Converting Enzyme (ACE) converts angiotensin I into angiotensin II
  • Angiotensin II increases blood pressure by stimulating aldosterone among doing other things
70
Q

Where is angiotensinogen made

A

in the liver

71
Q

Where is renin made

A

in the kidneys

72
Q

Where is ACE made

A

in the lung and kidneys

73
Q

What are diuretics

A

a class of drug that lead to loss of fluid at the nephron

74
Q

Give an example of a thiazide like diuretic

A

Indapamide

75
Q

What do thiazide and thiazide like diuretics do

A

block reabsorption at distal convoluted tubule

76
Q

Give an example of a Loop diuretic

A

Furosemide

77
Q

What do loop diuretics do

A

bock reabsorption in thick loop of Henle

78
Q

Give an example of a K+ sparing diuretic

A

Spironolactone

79
Q

What do K+ sparing diuretics do

A

inhibit aldosterone receptors in cortical collecting duct

80
Q

Definition of heart failure

A

when cardiac output is insufficient for meeting the needs of the body and lungs

81
Q

Chronic low output heart failure

A
  • cardiac output is low, usually due to accumulated damage to the heart
  • Chronic condition with poor 5 year survival rate
  • Often abbreviated simply as “heart failure”
  • There is also high output heart failure
82
Q

What type of symptoms are seen in left heart failure

A

respiratory symptoms

83
Q

Describe what happens to lead to the respiratory symptoms in left heart failure

A
  • Right heart pumps into lungs but left atrium is too full
  • This leads to increased hydrostatic pressure in pulmonary circulation

This can lead to congestive heart failure:

  • pulmonary vasculature is congested
  • In extreme: Fluid leaks out of blood vessels and into lungs
84
Q

What type of symptoms are seen in right heart failure

A

systemic symptoms

85
Q

Describe what happens to lead to the systemic symptoms seen in right heart failure

A

increased central venous pressure leads to peripheral oedema and ascites

86
Q

How does sympathetic activity compensate in heart failure

A

it increases heart rate and peripheral resistance

87
Q

Signs and symptoms of heart failure

A
  • Fatigue (esp during exercise)
  • Peripheral oedema
  • Dyspnoea
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
88
Q

Paroxysmal nocturnal dyspnoea

A

Shortness of breath that occurs at night and wakes the person up

89
Q

Fluid retention in heart failure

A
  • A form of compensation

- Eventually does more harm than good

90
Q

Cardiogenic shock

A
  • Critically low perfusion due to low cardiac output
  • Medical emergency, usually fatal
  • Insufficient perfusion of tissues, esp. the heart
  • Progresses by positive feedback
  • Definition of shock includes SBP < 90 mmHg *E
91
Q

How is cardiogenic shock treated

A
  • Aggressive intravenous fluid AND Oxygen

- Airway maintained

92
Q

Treatments for chronic heart failure

A
  • ACE Inhibitors (increase fluid loss)
  • Diuretics (increase fluid loss)
  • Beta blockers (decrease sympathetic activity)
93
Q

Why does the body make so much trouble for itself during heart failure - all of the homeostatic responses (fluid retention, sympathetic activity) to heart failure make it worse

A
  • Heart failure is a low output state
  • Haemorrhage is a low volume state
  • The kidney can’t tell the difference between these two states and was evolved to cope with haemorrhage (useful back when we were cavemen) not heart failure
94
Q

The kidneys in decompensated heart failure

A
  • The kidney increases plasma volume
  • To compensate for poor perfusion of renal tissue
  • The kidney responds as if it is a haemorrhage
  • This leads to Fluid Overload
95
Q

The heart in decompensated heart failure

A
  • The heart is unable to pump the extra fluid retained by kidneys
  • Fluid damming leads to increased venous hydrostatic pressures
  • Increased back pressure further damages heart
  • Positive feedback loop —> rapid deterioration
96
Q

The capillaries in decompensated heart failure

A

leak fluid into tissues

97
Q

The lungs in decompensated heart failure

A

Can’t exchange O2 and CO2

98
Q

What are the treatment goals for low output heart failure

A
  • Prevent acute decompensated heart failure
  • Counteract cardiac remodelling
  • Minimize symptoms
99
Q

What is the kidney’s homeostatic response to low output heart failure

A
  • Decrease Glomerular Filtration Rate
  • Which increases central venous pressure
  • And increases venous return and preload

Module 103: The Heart, Lungs and Blood (51 decks)

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