Theme 3: Lecture 3 - How the CVS fails Flashcards
(99 cards)
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
2
Q
What is a haemorrhagic stroke due to
A
cerebral blood vessel rupture
3
Q
What is an ischaemic stoke due to
A
Cerebral blood vessel blockage
4
Q
What causes a blood vessel to burst
A
- Stress
- Damage
5
Q
what are causes of stress on a blood vessel
A
- High pressure
- Turbulent flow
- Large diameter / high wall tension
- Low compliance
6
Q
What are causes of damage to a blood vessel
A
- Trauma (eg transluminal procedures)
- Atherosclerosis
- Diabetes
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
8
Q
Vessel wall tension equation
A
Tension = Pressure x Radius
9
Q
Compliance
A
the change in volume caused by a change in pressure (the slope of the black line in the graphs)
10
Q
What is a highly compliant vessel
A
a stretchy vessel
11
Q
What is a low compliant vessel
A
a stiff vessel
12
Q
Describe laminar flow
A
- smooth flow
- slower at the edges due to friction between blood and vessel
13
Q
What causes turbulent flow
A
- High speed
- Branching and junctions
- Low viscosity
- Mixing
- Obstacles (atherosclerosis and endothelial damage)
14
Q
What activities does the endothelium do (6 things)
A
- Blood vessel tone
- Fluid filtration
- Haemostasis
- White Cell recruitment
- Angiogenesis
- Hormone trafficking – (transcytosis)
15
Q
Blood vessel tone
A
How much constriction/dilation occurs at the blood vessel
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.
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
18
Q
What can large or multiple myocardial infarcts lead to
A
heart failure
19
Q
What does atherosclerosis result from
A
- hyperlipidaemia
- immune action
- unknown aetiology
20
Q
Symptoms of atherosclerosis
A
asymptomatic but can lead to other disorders
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
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
23
Q
Symptoms of coronary artery disease
A
angina or asymptomatic
24
Q
Primary cause of coronary artery disease
A
atherosclerosis
25
Drug treatment for coronary artery disease
Treat with drugs for:
- hyperlipidaemia
- angina
- hypertension
26
Surgical treatment for coronary artery disease
- stenting
| - surgically replacing clogged vessels
27
When does a plaque rupture
When the fibrous cap of a plaque bursts open
28
When do atheromas become dangerous
- when the plaque ruptures
| - if a thrombus or embolus forms
29
Fibrous cap
a layer of fibrous connective tissue, which is thicker and less cellular than the normal intima, found in atherosclerotic plaques.
30
What does the sympathetic nervous system release during an acute MI
adrenaline and noradrenaline
31
Why does the sympathetic nervous system release adrenaline and noradrenaline in an acute MI
- in response to pain
| - in response to haemodynamic abnormalities
32
What are haemodynamic abnormalities
abnormal or unstable blood pressure
33
How does sympathetic activity help to compensate during heart failure
leads to an increase in heart rate and contractility
34
What problems does sympathetic activity cause in heat failure
- 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)
35
What are the 2 forces on water in the capillary
- Hydrostatic pressure
| - Osmotic pressure
36
How does oedema occur
When there is more fluid going out of the blood vessel than is being brought back in due to hydrostatic and osmotic pressures
37
What is pulmonary oedema
fluid accumulation in the lungs esp alveoli
38
What does pulmonary oedema lead to
- impaired gas exchange
| - longer O2 diffusion length
39
Symptoms of pulmonary oedema
- dyspnoea
- orthopnoea
- leads to hypoxia
40
hypoxaemia
a decrease in the partial pressure of oxygen in the blood
41
hypoxia
a reduced level of tissue oxygenation
42
orthopnoea
shortness of breath that occurs when lying flat
43
What is pulmonary oedema caused by
left heart failure
44
Describe how left heart failure causes pulmonary oedema
- 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
Ascites
accumulation of fluid in the peritoneal cavity
46
Causes of ascites
many causes including heart failure
47
peripheral oedema
swelling of tissues esp ankles
48
Causes of peripheral oedema
many causes esp chronic low output heart failure
49
What is compensation
Maintaining homeostasis of a physiological function despite stressors or malfunctions – happens via endogenous physiological feedback
50
What does compensation do in heart failure to maintain adequate cardiac output despite damage
-increases plasma volume and sympathetic pathway
51
What is decompensated heart failure
- A medical emergency
- The failure of the heart to maintain adequate blood circulation, after long-standing (previously compensated) vascular disease.
52
What is cardiac remodelling
- Growth in cardiac muscle
| - Changes in shape, size and function
53
What causes cardiac remodelling
- Injury eg MI, hypertension, valve disease
| - Response to increased afterload or preload
54
What is the result of cardiac remodelling
- hypertrophy
| - dilation
55
When is cardiac remodelling compensatory and pathological
- initially compensatory
| - later pathological
56
Treatments for cardiac remodelling
- ACE inhibitors
| - Spironolactone
57
What is ventricular hypertrophy a response to
work (a bigger athlete's heart is normal)
58
Eccentric ventricular hypertrophy
Dilated ventricle due to volume overload
59
Concentric ventricular hypertrophy
Thickened ventricle due to pressure overload
60
What does ADH do
- Also called vasopressin
- Causes kidneys to reabsorb more water
- Decreases Diuresis
61
Where is ADH secreted from
Posterior pituitary
62
What type of molecule is ADH
peptide
63
What does aldosterone do
- Causes kidneys to reabsorb more NaCl (and thus more H2O)
- Directly decreases Natriuresis
- Which Decreases Diuresis
64
Natriuresis
Loss of Na+ in urine
65
Where is aldosterone secreted from
Adrenal cortex
66
What type of molecule is aldosterone
Steroid
67
Which hormones do diuretic drugs antagonise
ADH and aldosterone
68
What does angiotensin II do
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
Describe the Renin Angiotensin Aldosterone System (RAAS)
- 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
Where is angiotensinogen made
in the liver
71
Where is renin made
in the kidneys
72
Where is ACE made
in the lung and kidneys
73
What are diuretics
a class of drug that lead to loss of fluid at the nephron
74
Give an example of a thiazide like diuretic
Indapamide
75
What do thiazide and thiazide like diuretics do
block reabsorption at distal convoluted tubule
76
Give an example of a Loop diuretic
Furosemide
77
What do loop diuretics do
bock reabsorption in thick loop of Henle
78
Give an example of a K+ sparing diuretic
Spironolactone
79
What do K+ sparing diuretics do
inhibit aldosterone receptors in cortical collecting duct
80
Definition of heart failure
when cardiac output is insufficient for meeting the needs of the body and lungs
81
Chronic low output heart failure
- 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
What type of symptoms are seen in left heart failure
respiratory symptoms
83
Describe what happens to lead to the respiratory symptoms in left heart failure
- 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
What type of symptoms are seen in right heart failure
systemic symptoms
85
Describe what happens to lead to the systemic symptoms seen in right heart failure
increased central venous pressure leads to peripheral oedema and ascites
86
How does sympathetic activity compensate in heart failure
it increases heart rate and peripheral resistance
87
Signs and symptoms of heart failure
- Fatigue (esp during exercise)
- Peripheral oedema
- Dyspnoea
- Orthopnoea
- Paroxysmal nocturnal dyspnoea
88
Paroxysmal nocturnal dyspnoea
Shortness of breath that occurs at night and wakes the person up
89
Fluid retention in heart failure
- A form of compensation
| - Eventually does more harm than good
90
Cardiogenic shock
- 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
How is cardiogenic shock treated
- Aggressive intravenous fluid AND Oxygen
| - Airway maintained
92
Treatments for chronic heart failure
- ACE Inhibitors (increase fluid loss)
- Diuretics (increase fluid loss)
- Beta blockers (decrease sympathetic activity)
93
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
- 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
The kidneys in decompensated heart failure
- 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
The heart in decompensated heart failure
- 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
The capillaries in decompensated heart failure
leak fluid into tissues
97
The lungs in decompensated heart failure
Can't exchange O2 and CO2
98
What are the treatment goals for low output heart failure
- Prevent acute decompensated heart failure
- Counteract cardiac remodelling
- Minimize symptoms
99
What is the kidney's homeostatic response to low output heart failure
- Decrease Glomerular Filtration Rate
- Which increases central venous pressure
- And increases venous return and preload
