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Cardiovascular system > Properties of special circulations > Flashcards

Properties of special circulations Flashcards

1
Q

What are the three characteristics that special circulations have to consider?

A
  1. Special requirements met by the circulation
  2. Special structural or functional features of the circulation
  3. Specific problems relating to that circulation
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2
Q

What are examples of special circulations with unique requirements?

A
  • Cerebral
  • Pulmonary
  • Skeletal muscle
  • Renal
  • Gastrointestinal
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3
Q

Where do the two coronary arteries originate from?

A

The two coronary arteries originate from the left side of the heart at the beginning (root) of the aorta, just after it exits the left ventricle

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4
Q

What is the role of the cardiac veins?

A

The cardiac veins carry blood with a poor level of oxygen, from the myocardium to the right atrium.

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5
Q

Where does most of the blood from the coronary veins return through?

A

The coronary sinus

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6
Q

What are the special requirements of coronary circulation?

A
  • Needs a high basal supply of O2: 2 times that of the supply of O2 in the resting skeletal muscle
  • Increase in O2 supply is proportional to an increased demand/cardiac work
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7
Q

What are the special structural features of coronary circulation?

A
  • High capillary density
  • Large surface area: needed for O2 transfer
  • Together these reduced diffusion distance to myocytes: diffusion
  • Time is proportional to distance required: so O2 transport is fast
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8
Q

What does the higher numbers of fibers and capillaries in the cardiac muscles give rise to?

A

Shorter diffusion distances

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9
Q

Fibre diameter in the skeletal muscles

A

50 um

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10
Q

Capillaries in skeletal muscle

A

400 /mm^2

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11
Q

Fibre diameter in the cardiac

A

18 um

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12
Q

Capillaries in the cardiac muscle

A

3000 /mm2

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13
Q

Describe normal activity in the coronary circulation:

A
  • High blood flow: 10x the flow per weight of the rest of the body
  • Relatively sparse sympathetic innervation
  • High nitric oxide concentration released during vasodilation
  • High O2 extraction (75%), whereas the average in the rest of the body is 25%
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14
Q

Describe what occurs during increased demand in the coronary circulation

A
  • Coronary blood flow increases in proportion to demands
  • Production of vasodilators (adenosine, K+, acidosis) out-compete relatively low sympathetic vasoconstriction
  • Circulating adrenaline dilates coronary vessels due to abundance of B2-adrenoreceptors
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15
Q

What are the effects of the curve shifting left (for the curve plotted for Oxyhaemoglobin against PO2)?

A
  • Decreased temperature
  • Decreased 2-3 DPG
  • Decreased [H+]
  • CO
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16
Q

What are the effects of the curve shifting right (for the curve plotted for Oxyhaemoglobin against PO2)?

A
  • Reduced affinity
  • Increased temperature
  • Increased 2-3 DPG
  • Increased [H+]
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17
Q

Describe the blood in the coronary sinus when it is returning to the right atrium from the myocardial tissue:

A

The blood has a greater carbon dioxide content due to high capillary density, surface area and small diffusion difference

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18
Q

Describe the effect of the Bohr shift

A
  • blood in the coronary sinus has high CO2 content
  • High CO2 and low pH means that the haemoglobin has less affinity for oxygen
  • This means that more O2 is given up to the myocardial tissues
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19
Q

What is unique about the myocardium?

A

It is able to extract 75% of oxygen as opposed to typically 25% in other tissues

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20
Q

What is metabolic hyperaemia?

A

Increase in organ blood flow due to metabolic activity

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21
Q

How does metabolic hyperaemia occur?

A

Myocardium metabolism generates metabolites to produce vasodilation, which then increases blood flow

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22
Q

What is the need for metabolic hyperaemia (increasing blood flow)?

A
  • O2 extraction is near maximum during normal activity

- To provide more O2 during demand, must increase the blood flow

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23
Q

Example of metabolic hyperaemia

A

Adenosine is produced by ATP metabolism and is released from cardiac myocytes

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24
Q

What are the effects of metabolic hyperaemia?

A

Increased pCO2, H+ and K+ levels

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25
Q

Why is it important that the coronary arteries function correctly?

A

Coronary arteries are functional-end arteries and therefore decreased perfusion produces major problems, such as Ischaemic heart disease

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26
Q

What is the heart susceptible to?

A

Sudden and slow obstruction

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27
Q

Sudden Ischaemic heart disease

A

Acute thrombosis, produce myocardial infarction

28
Q

Slow Ischaemic heart disease

A

Atheroma (sub-endothelium lipid plaques) chronic narrowing of lumen, produces angina

29
Q

Role of systole in coronary blood flow

A

Systole obstructs coronary blood flow

30
Q

What are human coronary arteries?

A

Functional end-arteries

31
Q

What are arterio-arterial anastomoses?

A

Low numbers of cross-branching collateral vessels

32
Q

What does the atheromatous plaque do?

A

Obstructs flow

33
Q

What does the zone of necrosis do?

A

INFARCTION: obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus, causing local death of the tissue.

34
Q

What is an example of thrombosis?

A

Total occlusion of left anterior descending coronary artery

35
Q

What does occlusion lead to?

A

Occlusion leads to obstruction of blood flow to the anterior (front) ventricle: leads to myocardial infarction

36
Q

Possible physiological symptoms of Thrombosis

A
  • Ischaemic tissue, acidosis, pain stimulation (of C-fibres)
  • Impaired contractility
  • Sympathetic activation
  • Arrythmias
  • Cell death (necrosis)
37
Q

What is Stenosis?

A

Partial occlusion due to plaque formation

38
Q

What is an angiography?

A

X-ray after opaque dye has been injected into the vessels

39
Q

When does angina become more of a problem?

A

During increased activity

40
Q

What happens in the normal heart at rest and during exercise?

A

AT REST:

  • Resistances in series: add together
  • In the large coronary arteries resistance is low but in the arterioles resistance is high

DURING EXERCISE:

  • Metabolic vasodilation of the arterioles reduces the total resistance
  • Therefore there is increased blood flow to meet the increased O2 demands
41
Q

What happens at rest and during exercise for a person with Angina?

A

AT REST:

  • Stenosis in the large coronary artery increases resistance
  • Metabolic hyperaemia occurs at rest, so blood flow meets needs

DURING EXERCISE:

  • The arterioles further dilate to reduce resistance, but total resistance is still too high due to dominance of stenosis
  • O2 demand cannot be met and so therefore angina develops
42
Q

What are three mechanical factors that reduce coronary flow?

A
  1. Shortening diastole, e.g. high heart rate
  2. Increased ventricular end-diastolic pressure, e.g. Heart failure (aortic stenosis, stiffening of the ventricle)
  3. Reduced diastolic arterial pressure, e.g. hypotension, aortic regurgitation
43
Q

When is coronary blood flow restricted?

A

During systole: pressure is greater in he ventricles than in the aorta so there is no coronary perfusion

44
Q

What is an example of cutaneous circulation?

A

A skin ulcer due to impaired microvascular flow

45
Q

What are four special properties of cutaneous circulation?

A
  1. Defence against the environment
  2. Lewis triple response to trauma (increased blood flow)
  3. Temperature regulation
  4. Skin temperature is dependent
46
Q

How is temperature regulated in curtaneous circulation?

A
  • Blood flow delivers heat from body core
  • Radiation (proportional to skin temperature)
  • Conduction to skin: convection from skin (skin temperature)
  • Sweating (latent heat of evaporation)
  • The skin is an organ
  • Skin temperature can range from 0C to 40C briefly without damage (poikilothermic rather than homeothermic)
47
Q

What does skin temperature depend on?

A
  • Skin blood flow

- Ambient temperature

48
Q

What are three special structural features of cutaneous circulation?

A
  1. Arterio-venous anastosomoses
  2. Sympathetic vasoconstrictor fibres
  3. Sudomotor vasodilator fibres
49
Q

Describe arterio-venous anastosomes (AVAs)

A

They are direct connections of arterioles and venules, which expose blood to regions of high surface areas.
- Convection, conduction, radiation, evaporation

50
Q

Role of sympathetic vasoconstrictor fibres in cutaneous circulation

A

They release noradrenaline acting on a1 receptors

51
Q

Role of sudomotor vasodilator fibres in cutaneous circulation

A
  • Acetylcholine acting on endothelium to produce nitric oxide
  • Driven by temperature regulation nerves in the hypothalamus
52
Q

How does the cutaneous circulation help heat loss?

A

Increasing ambient temperature causes vaso- and venodilation

53
Q

How does the cutaneous circulation help to conserve heat?

A
  • Decreasing ambient temperature causes vaso and venoconstriction
  • Severe cold causes ‘paradoxical cold vasodilation’
  • Core temperature receptors in hypothalamus control sympathetic activity to skin and hence skin blood flow
54
Q

What are the effects of cold-induced vasodilation?

A

CONSERVES HEAT:

  • Sympathetic nerves react to local cold by releasing noradrenaline
  • Noradrenaline binds to a2 receptors on vascular smooth muscle in the skin
  • a2 receptors bind noradrenaline at lower temperatures than a1 receptors
55
Q

What are the effects of paradoxical cold vasodilation?

A

PROTECTS AGAINST SKIN DAMAGE:

  • Caused by paralysis of sympathetic transmission
  • Long-term exposure leads to oscillations of contract/relax
56
Q

What is the effect of increased curtaneous perfusion with increased core temperature, e.g. exercise

A

Increased core temperature results in the stimulation of warmth receptors in the anterior hypothalamus

57
Q

What does the stimulation of warmth receptors in the anterior hypothalamus cause?

A

SWEATING: Increased sympathetic activity to sweat glands mediated by acetylcholine
VASODILATION: Increased sympathetic sudomotor activity such that acetylcholine acts on the endothelium to produce NO which dilates arterioles in the extremities

58
Q

Explain ADH-stimulated vasoconstriction of skin blood vessels

A
  • Blood is directed to more important organs/tissues during loss of BP following haemorrhage, sepsis, acute cardiac failure
  • Mediated by sympathetic vasoconstrictor fibres, adrenaline, vasopressin, argotensin II. Responsible for pale cold skin of patient in shock
  • During haemorrhage warming up the body too quickly may reduce cutaneous vasoconstriction and be potentially dangerous, blood flow to the skin is not vital
    in organs/tissues
59
Q

Examples of functional specialisations of the cutaneous circulation

A
  • Emotional communication, e.g. blushing

- Response to skin injury, such as The Lewis triple response

60
Q

What is the Lewis triple response of skin to trauma?

A
  1. Local redness: site of trauma
  2. Local swelling: inflammatory oedema (wheal)
  3. Spreading flare: Vasodilation spreading out from the site of trauma
61
Q

What is the role of the C-fibre axon reflex?

A

It mediates the flare to trauma

62
Q

How are invading pathogens dealt with in the Lewis triple response?

A

Increased delivery of immune cells and antibodies to the site of damage

63
Q

Response to trauma

A

Trauma -> C-fibre (nocieptive afferent) -> main axon -> Dorsal root ganglion

OR

Trauma -> C fibre -> Axon collateral -> Substance P -> Histamine (FLARE) -> Mast cell degranulation -> Dilation

64
Q

Problems that can occur as a result of prolonged obstruction of flow by compression

A

Severe tissue necrosis

- Bed sores, on heels, buttocks, weight bearing areas

65
Q

How can bed sores be avoided?

A
  • Shifting position/turning causing
  • Reactive hyperaemia (on removal of compression)
  • High skin tolerance to Ischaemia
66
Q

Problems that can occur as a result of postural hypotension / oedema due to gravity

A
  • Often standing for long periods of time in hot weather will decrease central venous pressure (hypotension) and increased capillary permeability (oedema)
  • Feeling fain and rings of fingers can be tighter as a result
67
Q

What are the effects of increasing curtaneous perfusion with increased core temperature?

A

SWEATING: Increased sympathetic activity to sweat glands mediated by acetylcholine
VASODILATION: Increase sympathetic sudomotor activity such that acetylcholine act on endothelium to produce NO which dilates

Cardiovascular system (16 decks)

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