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Cardiovascular > Components of Cardiovascular System > Flashcards

Components of Cardiovascular System Flashcards

1
Q

Components of CVS

A 
Heart
Arteries
Veins
Arterioles
Capillaries
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2
Q

Arteries

A

Passageway of blood from heart to tissue

pressure must be maintained

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3
Q

Arterioles

A

Major resistance Vessels

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4
Q

Capillaries

A

Site of exchange of gas, nutrients and water between blood and tissue

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5
Q

Veins

A

contain most blood volume at rest- capacitance vessels

blood from tissue to heart

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6
Q

Regulation of SVR

A

Vascular smooth muscles

  • contraction increases SVR and MAP
  • controlled by intrinsic and extrinsic mechanisms
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7
Q

Relationship between blood flow and resistance

A

R is directly proportional to blood viscosity and blood vessel length and inversely proportional to the radius of blood vessel^4

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8
Q

Which nerve fibres control vsm? Which nt is involved?

A

sympathetic nerve fibre

noradrenaline acting on alpha receptors

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9
Q

Vasomotor tone

A

vascular smooth muscle is partially constricted at rest

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10
Q

What causes vasomotor tone?

A

tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline
* increasing sympathetic discharge increases vasomotor tone-> vasoconstriction

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11
Q

Hormones involved in control of VSM

A

Mainly adrenaline

also angiotensin II, andiuretic hormone (vasopressin)

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12
Q

What effect does adrenaline acting on alpha receptors have?

A

Vasoconstriction

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13
Q

What effect does adrenaline acting on beta-2 receptors have?

A

Vasodilation

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14
Q

Where are alpha receptors predominantly found?

A

skin, gut, kidney arterioles

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15
Q

Where are beta-2 receptors predominantly found?

A

cardiac and skeletal muscle arterioles

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16
Q

Effect of angiotensin II on VSM

A

vasoconstriction

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17
Q

Effect of vasopressin on VSM

A

vasoconstriction

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18
Q

Intrinsic control of VSM

A

matches blood flow of different tissue to their metabolic needs
can override extrinsic mechanisms
includes chemical and physical factors

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19
Q

Local metabolites

A

these chemical changes influence contraction of arteriolar smooth muscle

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20
Q

Factors causing vasodilation and metabolic hyperaemia

A
  • Decreased local PO2
  • Increased local PCO2
  • Increase local [H+]/ decreased pH
  • Increased ec [K+]
  • Increased ECF osmolality
  • ATP release of adenosine
21
Q

Influence of local humoral agents

A

contraction of arterial and arteriolar smooth muscle

22
Q

When are local humoral agents released?

A

Response to injury or inflammation

23
Q

Humoral agents which cause vasodilation

A

Histamine
Bradykinin
NO (constantly released by endothelial cells in arteries and arterioles)

24
Q

Production of NO

A

constantly produced from L-argenine in vascular endothelium through action of Nitric Oxide Synthase

25
Q

Is NO a vasodilator or constrictor

A

Potent vasodilator

Has life of only a few seconds

26
Q

Flow dependent NO formation

A

Stress, due to increased flow, on vascular endothelium causes vascular endothelial cells to release calcium. This activates NOS

27
Q

Receptor stimulated NO formation

A

Chemical stimulation allows vasoactive substances to act

28
Q

Activation of formation of cGMP

A

NO diffuses from vascular endothelium to surrounding smooth muscle cells, activating formation of cGMP

29
Q

Role of cGMP

A

second messenger for signalling smooth muscle relaxation

30
Q

Humoral agents which cause vasoconstriction

A

Serotonin
Thromboxane A2
Leukotrienes
Endothelin

31
Q

Endothelin

A

potent vasoconstrictor released from endothelial cells

32
Q

Characteristics of endothelial produced vasodilators

A

anti-thrombotic
anti-inflammatory
anti-oxidants

33
Q

Characteristics of endothelial produced vasoconstrictors

A

pro-thrombotic
pro-inflammatory
pro-oxidants

34
Q

Effect of temp of VSM

A

cold- vasoconstriction; warm- vasodilation

35
Q

Myogenic response to stress

A

MAP rises= automatic constriction of resistance vessels

Important in tissue like brain and kidneys

36
Q

Sheer stress in terms intrinsic control of vascular smooth muscle

A

Dilation of arterioles causes stress in arteries upstream, making them dilate also
- increases blood flow to metabolically active tissue

37
Q

Autoregulation of Cerebral blood flow

A

Myogenic response keeps cerebral blood flow constant over wide range of MAPs

38
Q

Sympathetic nervous system role

A

primarily role of the control of arteriolar radius and SVR (the brain is an exception)

39
Q

Factors which cause an increase in venous return

A

Increase in venomotor tone
increase in blood volume
increase in respiratory pump
increase in skeletal muscle pump

40
Q

Impact of increased venous return on stroke volume

A

causes increase on arterial pressure-> increased EDV-> increased SV

41
Q

Increased Venomotor Tone

A

Increased venous return, SV and MAP

42
Q

What happens to intrathoracic and intraabdominal pressure during inspiration? What impact does this have on venous return?

A

ITP decreases
IAP increases
increases pressure gradient for venous return and creates suction effect, moving blood from veins to heart

43
Q

Effect of increasing rate and depth of breathing on venous return?

A

Increases venous return

44
Q

Impact of increased muscle activity on venous return

A

increases venous return to heart

large veins limbs lie between skeletal muscles

45
Q

Acute CVS responses to exercise

A

increase in sympathetic nerve activity
->increase in HR, SV and hence CO, causing increased SBP
->reduced flow to kidneys and gut
metabolic hyperaemia overcomes vasomotor drive in skeletal and cardiac muscle
-> vasodilation in proportion to metabolic activity
-> decreased SVR and DBP (PP increases)

46
Q

Effect of sympathetic stimulation on heart

A

increases HR by increasing firing rate of SAN and decreasing AVN delay
Increases force of contraction

47
Q

Effect of noradrenaline on pacemaker cells

A

increase in slope of pacemaker potential, causing pacemaker potential to reach threshold quicker and frequency of action potential to increase (+ve chronotropic effect)

48
Q

Effect of sympathetic stimulation on ventricular contraction

A

Peak ventricular pressure rises, causing contractility of heart at given EDV to rise
FS curve shifts to left

49
Q

Chronic CVS responses to exercise

A

reduced sympathetic tone and noradrenaline levels
increased parasympathetic tone to heart
cardiac remodelling
Reduced plasma renin levels
Improved endothelial function (increase in vasodilators; decrease in vasoconstrictors)
Decrease in arterial stiffening

Cardiovascular (14 decks)

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