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Medicine 2 > RCM Week 6 (hypertension) > Flashcards

RCM Week 6 (hypertension) Flashcards

1
Q

What are the physical laws governing pressure / flow relationships in blood vessels

A

Blood is not a simple ‘Newtonian’ fluid: red and white cells, platelets, lipids are suspended in a solution of proteins

Blood vessels are not uniform, straight, rigid tubes: vessels are multibranched with variable elasticity and variable diameters

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2
Q

How do you calculate flow

A

Flow = pressure gradient / resistance

Pressure gradient : between arteries and veins : created by pumping action of the heart

Resistance: a measure of the degree to which the tube (blood vessels) resists the flow of liquid (blood) through it

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3
Q

What is the size order of the individual vessel diameters

A

Aorta > arteries > arterioles > capillaries

capillaries < venules < veins

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4
Q

What is the size order of the total cross sectional areas

A

Aorta < arteries < arterioles < capillaries

Capillaries > venules > veins

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5
Q

What determines flow

A

Flow - directly related to pressure difference

  • inversely related to length of tube
  • inversely related to viscosity of fluid
  • directly related to radius of tube
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6
Q

How do you calculate resistance

A

Pressure difference / flow

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7
Q

How do you calculate total peripheral resistance

A

Arterial - venous P / cardiac output

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8
Q

How do you calculate renal vascular resistance

A

Arterial - venous P / renal blood flow

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9
Q

Which factors determine resistance

A

Directly related to length of vessel

Directly related to viscosity of fluid

Inversely related to vessel radius
Reduced diameter = increased resistance

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10
Q

What does blood vessel radius depend on

A

Active tension exerted by smooth muscle (vascular smooth muscle)

Passive elastic properties of wall (elastin and collagen)
Blood pressure inside vessel

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11
Q

What is the law of Laplace

A

Distending pressure = wall tension / radius

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12
Q

What happens during vasoconstriction and vasodilation

A

Vasoconstriction - increased active tension, decreased passive tension

Vasodilation - decreased active tension, increased passive tension

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13
Q

Factors affecting vascular smooth muscle contraction

A

Hormones eg catecholamines (noradrenaline, adrenaline : constrict / dilate)

Peptides :
Vasopressin, angiotensin (constrict)
Bradykinin (dilate)

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14
Q

How much of the cardiac output goes to the skin

A

4% cardiac output at rest in thermoneutral environment (can vary between 1 and 200 ml / 100g/min )

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15
Q

Describe the neuronal control of blood flow to the skin

A

Arterioles have a relatively weak innervation (a vasoconstriction) A-V anastomoses have a dense innervation (a vasoconstriction)

  • increase in core temperature causes AVAs to dilate increasing skin blood flow and hence heat loss
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16
Q

How is blood flow to the skin controlled by local mechanisms

A

Arterioles show some degree of myogenic autoregulation. A-V anastomoses show no autoregulation and no reactive hyperaemia. Endothelin may be involved in pathological states (raynauds)

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17
Q

How is blood flow to the skin controlled by hormones

A

Angiotensin, vasopressin, noradrenaline, adrenaline all cause vasoconstriction

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18
Q

Describe the special features of the skin in terms of blood flow

A

Primary function is thermoregulation. Sweat glands have sympathetic cholinergic innervation (sudomotor) which can cause vasodilation via release of eg bradykinin

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19
Q

How much of cardiac output does skeletal muscle receive

A

15% at rest ( can vary between 3 and 60 ml / 100g/ min)

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20
Q

What are the neural influences of blood flow to the skeletal muscle

A

Important a vasoconstriction, some B vasodilation, maybe sympathetic cholinergic vasodilation

Involved in systemic BP regulation. Skeletal muscle is about 40% of body mass hence vasoconstriction has large influence on TPR

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21
Q

What are the local influences of blood flow to skeletal muscle

A

Rest: neural control (baroreflexes) over-ride autoregulatory mechanisms

Exercise: local metabolites have a major influence (K+, adenosine, lactate etc)

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22
Q

Special features of skeletal muscle in terms of blood flow

A

Capacity to increase flow in exercise (20-fold)- active hyperaemia. Large increase in flow post occlusion- reactive hyperaemia

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23
Q

What is hyperaemia

A

Increased blood flow

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24
Q

How much of the cardiac output does the kidney receive

A

25%

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25
Q

What is the neural role of blood flow to the kidney

A

Important a vasoconstriction; some B vasodilation. Renin secreting cells have a sympathetic innervation (B adrenoceptors)

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26
Q

What is the hormonal influence on blood flow to the kidneys

A

Noradrenaline, adrenaline, angiotensin can cause constriction. Vasopressin may cause vasodilation via prostaglandin / NO release. Dopamine causes vasodilation

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27
Q

What are the special features of the kidney in regard to blood flow

A

Excretory function of the kidney depends on well maintained flow (autoregulation). Vascular connections provide for capacity to regulate afferent / efferent resistances

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28
Q

How much cardiac output do the lungs receive

A

100%

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29
Q

What are the local influences on blood flow to the lungs

A

Unlike elsewhere, hypoxia causes vasoconstriction which is augmented by hypercapnia - possibly mediated by endothelin. NO causes dilation - may be used therapeutically

Pulmonary hypertension - possible therapeutic strategies include endothelin receptor antagonism and NO inhalation

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30
Q

What are the mechanical influences on blood flow to the lungs

A

Flow is affected by changes in alveolar pressure and lung volume. Increase in flow (cardiac output) associated with recruitment and distension of micro vessels and a decrease in vascular resistance

If alveolar pressure > intravascular pressure, flow is reduced. Lung inflation reduces resistance in extra- alveolar vessels (traction) and increases resistance in intra-alveolar vessels (compression)

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31
Q

Special feature of the lungs in relation to blood flow

A

Thin walled vessels with low resistance, low vasoconstrictor capacity. Hydrostatic pressure < colloid osmotic pressure which favours reabsorption

Hydrostatic pressure = 10mmHg
Colloid osmotic pressure = 25 mmHg

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32
Q

What is white coat hypertension

A

There is good evidence that the stress of visiting the GP can increase blood pressure leading to false diagnosis

Home monitoring and ambulatory devices are now more widely used to give a more realistic picture

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33
Q

What is systolic BP determined by

A

Stroke volume - increase StV, increase SBP

Aortic elasticity - decrease elasticity, increase SBP

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34
Q

Why does decreased elasticity increase systolic BP

A

Because normally elastic aorta take up kinetic energy from blood during systole and dampens the rise in pressure. Inelastic aorta may cause systolic hypertension in the elderly

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35
Q

What is diastolic BP determined by

A

Peripheral resistance: increase TPR, increase DBP

Aortic elasticity : decrease elasticity, decrease DBP

Heart rate: decrease HR, decrease DBP

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36
Q

Why does decreased aortic elasticity decrease diastolic BP

A

Kinetic energy taken up during systole is given back in diastole, adding to the pressure. If less is taken up there is less to give back, causing wide pulse pressure in the elderly

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37
Q

How do you calculate mean arterial BP

A

Cardiac output x total peripheral resistance

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38
Q

What are the estimates for mean arterial blood pressure, cardiac output and total peripheral resistance in systemic circulation

A

MAP- 100mmHg
CO- 5 L/min
TPR- 20 units (mmHg / litre / min)

39
Q

What are the estimates of mean arterial blood pressure, cardiac output and total peripheral resistance in pulmonary circulation

A

Mean pulmonary arterial pressure - 10mmHg

CO (right heart) - 5 L/min

Pulmonary vascular resistance - 2 units

40
Q

Why is control of arterial blood pressure important

A 
Because it provides a pressure head to drive blood flow, permits activity, postural changes - protects against effects of gravity. 
This is achieved by: 
Pressure sensors (in circulation) 
Integration centres (in CNS) 
Effector mechanisms (via autonomic nervous system)
41
Q

What are baroreceptors

A

Pressure sensors

1) arterial (high pressure) baroreceptors- located in walls of carotid sinus and aortic arch

42
Q

What are effector mechanisms

A

Autonomic control of the circulation

Heart:

  • parasympathetic (acetylcholine, muscarinic receptors, decrease HR)
  • sympathetic (noradrenaline, B1-adrenoceptors, increase HR and force (StV)
43
Q

What are cardiopulmonary receptors

A

Low pressure baroreceptors located in pulmonary vasculature, atrial-vena caval junctions, ventricular walls

Increase in transmural pressure- increase in afferent nerve discharge (vagus)

44
Q

Describe blood flow velocity in capillaries

A

It is not uniform- depends on contractile state of arterioles / pre-capillary vessels
Can vary from 0 to 8mm/sec (average 1mm/sec)

45
Q

Describe solute / solvent movement across capillaries

A

Is not uniform

  • depends on the permeability which can vary between tissues, within tissues at different times and along the capillary bed
  • determined by diffusion ; filtration ; pinocytosis
46
Q

What is fick ‘s law

A

J = -PS (Co-Ci)

J- quantity moved per unit time
P - capillary permeability to the substance
S- capillary surface area
C- concentration outside (o) and inside (i)

47
Q

What are filtration and reabsorption favoured by

A

Filtration:

1) capillary hydrostatic pressure (Pc)
2) interstitial fluid colloid osmotic pressure

Reabsorption

1) capillary (plasma) colloid osmotic pressure
2) interstitial fluid hydrostatic pressure

48
Q

What is capillary hydrostatic pressure (Pc)

A

Major determinant of fluid movement

Depends on: pre / post capillary resistances 
Venous pressure (arterial pressure)

If an arteriole constricts :
Increase pressure upstream, decrease pressure downstream so precapillary constriction reduced Pc

49
Q

What is interstitial fluid colloid osmotic pressure

A

Normally a minor determinant of fluid movement depends on the presence of protein in interstitium hence capillary permeability to protein - normally very low

50
Q

What is capillary colloid osmotic pressure

A

Major determinant of fluid movement depends upon:

Synthesis / breakdown of protein (liver)
Capillary permeability to protein
Abnormal protein loss (kidney damage)

51
Q

What is interstitial fluid hydrostatic pressure

A

Normally a minor determinant of fluid movement

Depends upon:
Interstitial fluid volume
Compliance of organ
Effective drainage

52
Q

Describe lymphatic system and vessels

A

Lymphatic system provides drainage
Lymphatic vessels are valves and highly permeable to protein

Lymph flow rate - 2-4 litres / day - returns excess filtered fluid and 95% of protein lost from vascular system back to the circulation (subclavian vein)

53
Q

What is an oedema

A

Excessive tissue fluid formation that will result in swelling

54
Q

What are possible causes of oedema

A

Lymphatic obstruction (reduced drainage)
Increased venous pressure (congestion)
Hypoproteinaemia (eg renal damage)
Hypervolaemia
Inflammation (vasodilation and increased permeability)

55
Q

Define hypertension

A

A blood pressure which is associated with significant cardiovascular risk

56
Q

What can secondary hypertension be due to

A
  • renal disease
  • renovascular disease
  • conns syndrome (too much aldosterone)
  • Cushing’s syndrome
  • hyperthyroidism
  • phaeochromocytoma - catecholamine secreting tumour
  • pregnancy
  • drugs (eg NSAIDs, corticosteroids, sympathomimetics)
57
Q

Causes of essential hypertension

A

Thought to be due to interaction of a range of causes

  • obesity : production of angiotensin from adipocytes
  • insulin resistance (‘metabolic syndrome’)
  • excessive alcohol consumption
  • genetics
  • environment ?
  • fetal programming : low birth weight?
  • salt sensitivity
  • ethnicity
  • age
58
Q

Goals of treatment of hypertension.

A
  • reduction in cardiovascular damage
  • preservation of renal function
  • limitation or reversal of left ventricular hypertrophy
  • prevention of ischaemic heart disease
  • reduction in mortality
59
Q

How do you calculate blood pressure

A

Cardiac output x total peripheral resistance

60
Q

What is the role of ACEIs

A

By inhibiting the ACE, they lead to reductions in angiotensin II which leads to:

  • reductions in arterial and venous vasoconstriction
  • reduced aldosterone production leads to reductions in salt and water retention
  • also potentiate bradykinin - cough
  • may increase potassium
  • best at decreasing nephropathy in pts with diabetes
61
Q

Why should ACEIs be avoided in renovascular disease

A

Renin- dependent hypertension, ACEIs lead to renal underperfusion and severe hypotension

62
Q

What are vasodilators

A

Calcium channel inhibitors

- inhibit voltage operated Ca2+ channels on vascular smooth muscle (leading to vasodilation and a reduction in BP)

63
Q

What is the role of diuretics

A

Inhibit Na+ / Cl- in distal convoluted tubule
- reduction in circulating volume

Important side effects:

  • hypokalaemia
  • postural hypotension
  • impaired glucose control
64
Q

What is the role of alpha-blockers

A

These are competitive receptor antagonists of a1- adrenoceptors

  • last choice antihypertensives due to widespread side effects
65
Q

Adverse effects of ACEIs

A
  • cough
  • severe first dose hypotension
  • renal damage
66
Q

Adverse effects of calcium channel blockers

A
  • peripheral oedema (swollen ankles)
  • postural hypotension
  • constipation (some)
67
Q

Adverse effects of thiazides

A
  • diabetogenic
  • alter lipid profile
  • hypokalaemia
  • postural hypotension
68
Q

Adverse effects of beta blockers

A

Bronchospasm

69
Q

Adverse effects of alpha blockers

A

Widespread side effects

Postural hypotension

70
Q

How to decide which antihypertensive should be used

A

Choose ACE inhibitors in diabetes / diabetic nephropathy

  • avoid ACE inhibitors in renovascular disease
  • choose ACE inhibitors with CHF
  • avoid B blockers in asthma
  • choose B blockers in ischaemic heart disease
71
Q

Define infarction

A

An area of ischaemic necrosis (death of tissue due to lack of oxygen) due to abrupt cessation of the arterial supply or venous draining

  • the process of formation of an infarct
72
Q

Factors affecting development of infarction

A

Vascular occlusion - from minimal effect to death of patients

Rate of development of occlusion - abrupt Vs gradual

Nature of vascular supply- end artery Vs dual blood supply

Type of tissue: vulnerability to hypoxia (irreversible damage)
Neuron: 2-3mins
Myocardium: 20-40mins
Fibroblasts: many hours

73
Q

Examples of different infarctions

A

Myocardial and cerebral infarction: one of the most common cause of death

Pulmonary infarction: variable outcome

Bowel infarction is frequently fatal

Gangrene: life threatening condition

74
Q

What do the different colours of infarction indicate

A

Colour is based on amount of haemorrhage

  • pale of white infarct: solid organs such as heart and spleen
  • red or haemorrhagic infarct: loose spongy tissue rich in blood supply or has due allergies blood supply such as lung
75
Q

Describe morphology of an infarct

A

Usually wedge shaped with occluded artery at apex and base at periphery

Margins: early poorly defined slightly haemorrhagic but later well defined

Inflammatory response followed by reparative response - finally scar tissue

76
Q

Causes of arterial infarction

A

Occlusion by embolus

Occlusion by atheroma and thrombosis

Occlusion by atheroma with plaque fissure

Occlusion by atheroma alone

Arterial spasm or arterial trauma

77
Q

Define myocardial infarction

A

Necrosis of heart muscle due to occlusion of the supplying coronary artery

78
Q

Outcomes of myocardial infarction

A

Sudden death due to cardiac dysrhythina or acute left ventricular failure

Rupture of myocardium > haemopericardium

Rupture of papillary muscle > acute valve failure

Survival with infarct replaced by granulation tissue and ultimately fibrous scar

Death due to complications during the infarct healing process

79
Q

Stages in myocardial infarction

A

0-12 hours: early stages of cell death
12-24 hours: necrotic muscle fibres apparent microscopically
24-72 hours: acute inflammatory reaction to dead muscle
3-14 days: macrophagic removal of debris and vascular granulation tissue formation
14-21 days : fibrous granulation tissue formation
21-56 days: scar formation and cicatrisation

80
Q

Late complications of MI

A

Chronic LVF

Ventricular aneurysm

81
Q

What is a renal infarct

A

Usually due to emboli from L side of heart

Wedge shaped

Pale area with hyperaemia around

Heals by scar formation

82
Q

What is arterial infarction caused by

A

Atherothrombotic in extra-cerebral arteries

Embolic

83
Q

What is gangrene

A

Type of necrosis caused by vascular insufficiency following injury or infection.

Gangrene is a complication of necrosis. Tissue becomes black and malodorous. Bacteria decompose dead tissue- release of hydrogen sulphide and iron -> iron sulphide is black

84
Q

What is the difference between dry gangrene and wet or moist gangrene

A

Dry gangrene occurs when the arterial blood supply to an area is occluded but the venous drainage is intact

Wet or moist gangrene is caused by occlusion or impairment of venous drainage plus putrefaction or caused by a bacterial infection

85
Q

Define gangrene

A

Localised death and decomposition of body tissue, resulting from obstructed circulation or bacterial infection. Dry, wet / infected and gas (caused by clostridia). Extremities, bowel and internal

86
Q

What is venous infarction

A

Can occur when the entire venous drainage from an organ or tissue is, and remains, completely obstructed

2 common examples:
Bowel infarction eg Volvus, hernial strangulation

Testis infarction due to torsion

Ovarian infarction due to torsion

87
Q

Sequence of events of venous infarction

A

1) veins become obstructed, usually by extrinsic pressure
2) tissues become congested with blood, venules and capillaries being engorged with blood which cannot escape
3) pressure in capillaries and venules rises so that:
- many of them rupture with leakage of blood
- arterial blood cannot enter so hypoxia ensues
4) tissues become congested, hypoxia and necrotic

88
Q

What is venous infarction: torsion of testis

A

Spermatic cord has twisted, thus compressing plexus of veins. Blood cannot drain out of testis or epididymis. Venous infarction occurs

89
Q

What is LO salt

A

A KCL salt substitute - advocated for a low salt diet
Has a severe reaction with ACE inhibitors
Can cause hyperkalaemia so would worsen ACE inhibitor induced hyperkalaemia

90
Q

What is alteplase

A

Clot busting drug. Activates plasminogen to form plasmin (an enzyme that breaks down fibrin to break up a clot)

91
Q

Describe blood flow to the renal system

A

25% of cardiac output goes to kidneys
Renin secreting cells have a sympathetic innervation
Local: good autoregulation of flow over a wide pressure range
Hormones: noradrenaline, adrenaline, angiotensin can cause constriction. Vasopressin may cause vasodilation via prostaglandin / NO release. Dopamine causes vasodilation

92
Q

What are the special features of renal blood flow

A

Excretory function of the kidney depends on well maintained flow. Vascular connections provide for capacity to regulate afferent / efferent resistances

93
Q

What do centrally acting antihypertensives do eg alpha-methyl dopa, moxonidine

A

Decrease sympathetic output from central cardiovascular control centres in the medulla
- alpha -methyl dopa is a false substrate resulting in an analogue of noradrenaline acting at central a2-adrenoceptors
- moxonidine: an imidazoline which activates central imidazoline receptors
These agents are not widely used due to widespread side effects and no advantages over other antihypertensive agents

94
Q

Factors affecting the development of infarction

A

Vascular occlusion - minimal effect to death of patients

  • nature of vascular supply: end artery Vs dual blood supply
  • rate of development of occlusion: abrupt Vs gradual
  • type of tissue: vulnerability to hypoxia (irreversible damage)

Medicine 2 (16 decks)

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