Physiology Flashcards

1
Q

What are the factors which affect venous pressure?

A
  • Gravity
  • Muscle Pump
  • Respiratory pump
  • Venomotor tone
  • Systemic filling pressure
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2
Q

How does gravity affect venous pressure?

A

When lying, pressure gradients are created between the hand and the heart and the feet and the heart. These gradients roughly equate to 10-20 mmHg.

When standing, the venous pressure in the head drops another 20-30 mmHG, whereas the venous pressure in the feet increases by abouyt 70-80mmHg

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3
Q

Why does EDV reduce when someone intially stands up?

A

Blood pools in the venous system in the legs

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4
Q

How does the skeletal muscle pump influence venous pressure?

A
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5
Q

What structure in veins prevents backflow of blood?

A

Backflow valves

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6
Q

How does the respiratory pump increase venous pressure, and thus move blood into the thorax?

A

As the chest expands, the diaphragm moves downwards. As a result of this, the thoracic cavity develops subatmospheric pressure. This low pressure decreases pressure in the IVC as it passes through the thorax, which helps draw more blood into the the IVC from the abdomen.

Compression of the abdominal veins also occurs due to a reduction in abdominal cavity volume

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7
Q

How does venomotor tone influence venous pressure?

A

Veins have some smooth muscle, which, when contracted, increases venous pressure, resulting in increased venous return to the heart.

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8
Q

What is systemic filling pressure, and how does it influence venous pressure?

A

This is the pressure created by the ventricles. This pressure is transferred thought the vacular tree and into the venous system

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9
Q

What is systolic pressure?

A

The pressure exerted on the walls of the arteries during systolic phase of the cardiac cycle.

The average is 120 mmHg

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10
Q

What is diastolic pressure?

A

The pressure exerted on the walls of the arteries during the diastolic phase of the cardiac cycle

The average is 80 mmHg

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11
Q

What is pulse pressure?

A

The pressure difference between the systolic and diastolic pressure. It represents the pressure increase from diastolic to systolic

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12
Q

How do you calculate mean arterial pressure?

A

Diastolic Pressure + 1/3(Pulse Pressure)

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13
Q

What is velocity in blood vessels related to?

A

Total cross sectional area

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14
Q

What happens to flow velocity in a vessel as total cross sectional area increases?

A

Flow velocity decreases

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15
Q

What happens to flow velocity in a vessel as total cross sectional area decreases?

A

Flow velocity increases

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16
Q

What is the difference between left ventricular diastolic pressure and aortic diastolic pressure, and why is there a difference?

A

LV diastolic pressure is closer to 0, whereas the elastic nature of the aorta maintiains around 80 mmHg and acts as a presure reservoir

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17
Q

What pressure is systemic filling pressure?

A

Approximately 5 mmHg

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18
Q

What happens to the pressure as you get further away from the heart towards the capillary beds?

A

It decreases

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19
Q

What are characteristics of elastic arteries?

A
  • Wide lumen
  • Elastic walls
  • Damps down pressure variations - absorbs energy during ejection, recoils durting relaxation
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20
Q

What is an example of an elastic artery?

A

Aorta

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21
Q

What are the characteristics of muscular arteries?

A
  • Wide lumen
  • Non-elastic walls
  • Low resistance conduit which allow distribution of blood
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22
Q

What are examples of muscular arteries?

A

Coronary, radial, femoral arteries

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23
Q

What are the characteristics of resistance vessels?

A
  • Narrow lumen
  • Thick contactile wall
  • Control resistance and therefore flow - allow redirection of flow
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24
Q

What are examples of resistance vessels?

A

Arterioles

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25
Q

What are characterisitics of exchange vessels?

A
  • Narrow lumen
  • Thin wall
  • Very big surface area to volume ratio - allow for exchange of materials
26
Q

What are the characteristics of capacitance vessels?

A
  • Wide vessels
  • Distensible walls
  • Low resistance conduit/reservoir
  • Allows fractional distribution of blood between the veins and the rest of the circulation
27
Q

What direction does blood flow in terms of pressure?

A

From high pressure to low pressure

28
Q

How do you calculate flow in a tube/vessel?

A

Darcy’s law

Flow = deltaP/Resistance

29
Q

How is flow of blood related to the resistance of the vessel it is contained within?

A

Flow = 1/R

It is inversely related

30
Q

What factors contribute to overall vascular resistance?

A
  • Radius of the vessel
  • Length of the vessel
  • Viscosity of the fluid
31
Q

What is Poiseuilles law?

A

R = 8Ln/πr4

Where L is length, n is viscosity of fluid, and r is the diameter of the vessel

32
Q

What happens to vessel resistance with an increase in vessel length?

A

Increased resistance

33
Q

What happens to vessel resistance with decreasing vessel length?

A

Decreased resistance

34
Q

What difference will increased viscosity have on vascular resistance?

A

Increased resistance

35
Q

What will decreased radius of a vessel do to vascular resistance?

A

Increased vascular resistance

36
Q

If you were to assume length and viscosity in a vessel system remained constant, what equation would remain to calculate flow?

A

Flow = deltaP/r4

37
Q

What is the outermost layer of the vessel wall?

A

Tunica adventitia

38
Q

What is the middle layer of a vessel wall known as?

A

Tunica media

39
Q

What is the innermost layer of a vessel wall known as?

A

Tunica intima

40
Q

What are the 3 layers of vessels?

A
  • Tunica intima
  • Tunica media
  • Tunica Adventitia
41
Q

What is the tunica intima composed of?

A

Simple squamous epithelium + Basement mebrane + Connective tissue

42
Q

What is the tunica media composed of?

A

Smooth muscle tissue + Elastic fibres

43
Q

What is the tunica adventitia composed of?

A

Fibrous connective tissue

44
Q

What type of vessel is the following?

A

Artery

45
Q

What do capillaries lack in terms of structure compared to arteries and arterioles?

A

Tunica media and adventitia

46
Q

What are the 3 types of capillaries?

A
  • Continuous
  • Fenestrated
  • Discontinuous
47
Q

What is active hyperaemia?

A

A process that occurs in response to increased metabolism in an area - when metabolism increases, levels of O2 decrease, and levels of CO2 increase, as do levels of metabolites.

Endothelium Derived Relaxing factor (paracrine hormone) is released by endothelial cells sensing increased metabolite concentration -> increase in blood flow to the area -> brings more oxygen to meet metabolic demand and transporting more CO2 and metabolites away

48
Q

What is pressure autoregulation?

A

If mean arterial pressure (MAP) decreases (e.g. with blood loss), this results in a decrease in flow. This causes metabolites to accumulate, which is thought to trigger the release of EDRF. This causes the arterioles to dilate and flow to restore to normal.

This is an adaptation to ensure that a tissue maintains its blood supply despite changes in MAP.

49
Q

What is the difference between pressure autoregulation and active hyperaemia?

A

Active hyperaemia results from increased metabolism in the area, whereas pressure autoregulation occurs in response to decreased MAP in the area which results in metabolites accumulating. The outcome of both processes is the same, but the triggers are different

50
Q

What is reactive hyperaemia?

A

This is in response to a period of low perfusion, resulting in local hypoxia and metabolite accumulation in the interstitium. This results in the synthesis of nitric oxide, which is a potent vasodilator.

When flow resumes to the area, the combination of NO, CO2 and other paracrine molecules results in significant vasodilatation. The resultant increase in flow washes away metabolites.

51
Q

What is the basis of the injury response?

A

If skin is damaged, a region of redness appears. C-fibres send action potentials to the spinal cord, which transmit to the brain as a pain signal. The action potential also travels down other sensory channels and reaches the end of the sensory fibre, where it releases substance P (a peptide).

Substance P causes mast cells to release histamine, which is a potent vasodilator (which increases the flow to the area), and also increases permeability in the area.

52
Q

What are extrinsic factors which control arteriolar tone?

A
  • Neural factors - sympathetic/parasympathetic control
  • Hormonal factors - adrenaline, angiotensin, vasopressin etc.
53
Q

How does the sympathetic nervous system control arteriolar tone?

A

Act on arteriolar α1 receptors in the smooth muscles in the tunica media by releasing noradrenaline, which cause arteriolar constriction, increasing resistance and reducing flow. This increase in resistance contributes to total peripheral resistance.

54
Q

How does the parasympathetic nervous system control arteriolar tone?

A

Has no effect normally

55
Q

How does noradrenaline/adrenaline influence arteriolar tone?

A

Binds to α1 receptors can causes arteriolar constriction

In some organs it binds to ß2 receptors, which are involved in causing arteriolar dilatation. The purpose of thise is to control blood flow to vital organs in the fight or flight response e.g. heart, lungs, skeletal muscle

56
Q

How does angiotensin II control arteriolar tone?

A

Causes arteriolar constriction when released in response to low blood volume by the kidneys.

57
Q

How does ADH influence arteriolar tone?

A

This is released in response to low blood volume, and also causes arteriolar constriction (increases TPR, decreases flow)

58
Q

How do atrail natriuretic peptide and brain natriuretic peptide influence arteriolar tone?

A

These are released in response to high blood volume. These cause arteriolar dilation (decreases TPR, increases flow)

59
Q

What are intrinsic factors which regulate arteriolar tone?

A
  • Active hyperaemia
  • Pressure autoregulation
  • Reactive hyperaemia
  • Injury Response
60
Q

How would you calculate mean arterial pressure?

A

MAP = CO x TPR

or

MAP = Diastolic Pressure + 1/3 Pulse Pressure

61
Q

What receptors are resonsible for venoconstriction?

A

Alpha-1 receptors

62
Q

What is a “white clot”?

A

Arterial thrombi superimposed on atherosclerotic lesions are rich in platelets.

Important to remember for treatment - these are treated using antiplatelet therapies such as aspirin and clopidogrel