Components of Cardiovascular System Flashcards

(49 cards)

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
Is NO a vasodilator or constrictor
Potent vasodilator | Has life of only a few seconds
26
Flow dependent NO formation
Stress, due to increased flow, on vascular endothelium causes vascular endothelial cells to release calcium. This activates NOS
27
Receptor stimulated NO formation
Chemical stimulation allows vasoactive substances to act
28
Activation of formation of cGMP
NO diffuses from vascular endothelium to surrounding smooth muscle cells, activating formation of cGMP
29
Role of cGMP
second messenger for signalling smooth muscle relaxation
30
Humoral agents which cause vasoconstriction
Serotonin Thromboxane A2 Leukotrienes Endothelin
31
Endothelin
potent vasoconstrictor released from endothelial cells
32
Characteristics of endothelial produced vasodilators
anti-thrombotic anti-inflammatory anti-oxidants
33
Characteristics of endothelial produced vasoconstrictors
pro-thrombotic pro-inflammatory pro-oxidants
34
Effect of temp of VSM
cold- vasoconstriction; warm- vasodilation
35
Myogenic response to stress
MAP rises= automatic constriction of resistance vessels | Important in tissue like brain and kidneys
36
Sheer stress in terms intrinsic control of vascular smooth muscle
Dilation of arterioles causes stress in arteries upstream, making them dilate also - increases blood flow to metabolically active tissue
37
Autoregulation of Cerebral blood flow
Myogenic response keeps cerebral blood flow constant over wide range of MAPs
38
Sympathetic nervous system role
primarily role of the control of arteriolar radius and SVR (the brain is an exception)
39
Factors which cause an increase in venous return
Increase in venomotor tone increase in blood volume increase in respiratory pump increase in skeletal muscle pump
40
Impact of increased venous return on stroke volume
causes increase on arterial pressure-> increased EDV-> increased SV
41
Increased Venomotor Tone
Increased venous return, SV and MAP
42
What happens to intrathoracic and intraabdominal pressure during inspiration? What impact does this have on venous return?
ITP decreases IAP increases increases pressure gradient for venous return and creates suction effect, moving blood from veins to heart
43
Effect of increasing rate and depth of breathing on venous return?
Increases venous return
44
Impact of increased muscle activity on venous return
increases venous return to heart | large veins limbs lie between skeletal muscles
45
Acute CVS responses to exercise
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
Effect of sympathetic stimulation on heart
increases HR by increasing firing rate of SAN and decreasing AVN delay Increases force of contraction
47
Effect of noradrenaline on pacemaker cells
increase in slope of pacemaker potential, causing pacemaker potential to reach threshold quicker and frequency of action potential to increase (+ve chronotropic effect)
48
Effect of sympathetic stimulation on ventricular contraction
Peak ventricular pressure rises, causing contractility of heart at given EDV to rise FS curve shifts to left
49
Chronic CVS responses to exercise
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