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IB physiology > Mammalian Cardiovascular > Flashcards

Mammalian Cardiovascular Flashcards

1
Q

at the most basic level, what is circulation responsible for?

A

delivering vital life substances to body tissues. Including oxygen ,hormones and nutrients and removing waste.

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2
Q

other uses for circulation than delivering and removing substances

A

immune response, regulation of body temperature and pH, homeostatic functions

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3
Q

which ventricles and atrium of the heart are used for systemic circulation?

A

left ventricle, right atrium

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4
Q

which ventricles and atrium of the heart are used for pulmonary circulation?

A

right ventricle - left atrium - left ventricle. (completing double circuit)

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5
Q

features of blood pressures as it passes along systemic circulation

A

decreases, pulsatile (especially in arteries)

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6
Q

Why is flow continuous despite pulsatile pressure in vessels?

A

always a forward pressure gradient

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7
Q

what is Poisseullie’s law used for?

A

how resistance to laminar flow changes along circulation

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8
Q

what is the role of arteries?

A

Distribution vessels (relatively low resistance)

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9
Q

Why do we use Arterial Blood pressure? (ABP)

A

little loss of pressure as blood passes through arteries, pressure is essentially the same in all large arteries

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10
Q

Diameter of an artery

A

30mm

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11
Q

Arteriole diameter

A

10- 300μm

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12
Q

Why is arteriole total resistance much higher than that of arteries or capillaries?

A

arteries - much larger diameter, capillaries - much larger number in parallel series.

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13
Q

Uses of arterioles (due to highest resistance)

A

primary site of control of blood flow in circulation

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14
Q

Capillary diameter

A

5-10μm

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15
Q

Why does Poisseuille’s law break down for capillaries?

A

diameter is similar to a red blood cell (-7μm ), allowing for bolus flow.

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16
Q

what is Bolus flow?

A

erythrocytes travel singularly, separated by segments of plasma. Reduces resistance to flow of blood through capillaries (Fahreus-Linndquist effect)

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17
Q

what is the function of capillaries?

A

site of exchange between circulation and tissues.

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18
Q

why are all cells close to capillaries?

A

exchange of substances is primarily by diffusion (X = t2/2D)

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19
Q

why does exchange slow along capillary?

A

as exchange occurs, between capillaries and interstitial fluid, becomes more similar.

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20
Q

roughly how many capillaries are present per gram of skeletal muscle?

A

500,000

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21
Q

roughly how many capillaries are pursued at rest ?

A

20-25% (empty and collapsed)

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22
Q

Capillary anatomy

A

single layer of endothelial cells connected by inter endothelial junctions, surrounded basement membranes.

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23
Q

where do the structure of capillaries differ

A

in different organs, gives regional differences in permeabilities to different substances. [e.g. in liver allow passage of newly synthesised plasma proteins, in lungs primarily exhange CO2 and O2]

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24
Q

3 types of capillaries

A

Continuos, Fenestrated and Sinusoidal (discontinues)

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25
Q

why are water movements across a capillary important?

A

influence both circulating volume and local interstitial fluid volume

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26
Q

driving forces for water movement across a membrane

A

convective movements (rather than purely diffusive). Hydrostatic pressure difference and effective osmotic pressure difference.

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27
Q

how does capillary pressure (Pc) change along the length of the capillary?

A

decreases, due to resistance and outward movement of water, is somewhat pulsatile.

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28
Q

when can Pif be negative?

A

non-encapsulated organs (WRT atmospheric pressure)

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29
Q

what is interstitial fluid?

A

complex gel of proteoglycans and water within a network of collagen fibres.

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30
Q

what kind of solutes can exert an osmotic force on capillaries and therefore contribute to colloid osmotic pressure?

A

only solutes that can not easily cross capillary wall.

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31
Q

what is the most important plasma proteins (colloid) in effective osmotic pressure?

A

Albumin (globulin and fibrinogen also contribute)

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32
Q

why is it important to regulate blood flow through tissues?

A

ensures adequate local delivery of O2 and metabolite substrates and remove of products.

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33
Q

why is cardiac output usually proportional to Vo2? (Volume of O2 used per minute)

A

blood flow is very well matched to metabolic demand

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34
Q

how is flow regulated by the arteries?

A

by regulating upstream arteriolar resistance (darcys Law)

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35
Q

What are the 3 principle mechanisms for the regulation of arteriolar resistance?

A

Nerves, hormones/vasoactive substances, local tissue metabolism. (balance of these, often opposing influences)

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36
Q

example of arteriolar resistance being a balance of opposing influences

A

local demand for local vasodilitation competes with systemic vasoconstrictory signals regulating ABP (arterial blood pressure)

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37
Q

what does local control of arteriole resistance match compared to central autonomic control?

A

local - local blood flow to local metabolic demand

central - controls total peripheral resistance (TPR) to maintain constant mean ABP

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38
Q

in what forms can local arteriole resistance regulation be?

A

metabolic, myogenic, vasoactive compounds released from endothelium (NO)

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39
Q

in what forms can central arteriole resistance regulation be?

A

neurogenic or endocrine (hormonal)

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40
Q

Why is arteriolar smooth muscle arranged circumferentially?

A

Contraction increases tension in vessels wall and causes vasoconstriction. (relaxation reduces tension, causing vasodilation)
(TENSION)

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41
Q

what allows for tension to arise in vascular smooth muscle?

A

mostly due to Ca2+ concentration but also modulated by activation of myosin light chain kinase (modulated by phosphorylation)

42
Q

why is vascular tone not fully understood?

[note: vascular tone is different from arteriole resistance]

A

multiple regulatory systems with probably some redundancies.

43
Q

what are the two control pathways for vascular tone?

A

regulation of myosin binding site of actin by caldesmon and and regulation of myosin light chain by phosphorylation

44
Q

how can local regulation of blood flow be demonstrated ?

A

using a cuff that is inflated to above arterial pressure for around 10 minutes. When cuff is removed, large increase in blood flow observed.

45
Q

what is functional hyperaemia?

A

significant increased blood flow to area due to change in metabolites (e.g. when observed when removing an inflated cuff from upper arm)

46
Q

what factors promote vasodilation of systemic arterioles?

A

reduced P(O2), increased P(CO2), decreased pH, increased adenosine and increased extracellular K+ (and changes accompanying anaerobic metabolism)

47
Q

why does reduced O2 and increased CO2 cause vasoconsitriction (opposite to in systemic) in pulmonary circulation?

A

changes reflect poor ventilation, not poor perfusion

48
Q

why is it important for key organs such as the brain, heart and kidneys to be able to change diameter of arterioles?

A

To maintain a constant capillary pressure in these organs.

[ note: may be why poor lymphatic drainage of heart and brain}

49
Q

what time of regulation is present in some organs e.g. brain and heart?

A

myogenic auto regulation of arteriolar resistance

50
Q

how does myogenic auto regulation of arteriole resistance affect metabolic auto regulation?

A

similar effect, increased arterial pressure tends to directly cause vasoconstriction by the myogenic mechanism and indirectly by metabolic mechanism. (increased perfusion washes out local metabolites)

51
Q

when can acetylcholine dilate arteries?

A

Only when endothelium is intact (noradrenaline constricts them even when endothelium had been removed)

52
Q

what is the signal from the endothelium to vascular smooth muscle?

A

NO (nitric oxide)

53
Q

what is the role of acetylcholine and bradykinin in the endothelium?

A

stimulate NO production by the action of NO synthase on L-arginine in the endothelium

54
Q

what is the effect of NO on vascular smooth muscle?

A

stimulates guanylyl cyclase, cGMP-dependant protein kinase then phosphorylates MLCK, inhibiting it

55
Q

how does sildenafil (viagra) work?

A

reduce cGMP breakdown

56
Q

other than vasodilator and vasoconstrictor substances, what does the endothelium release?

A

pro-coagulants, anti-coagulants, fibrinolytics, antibacterials and growth factors. [under physiological conditions, net effect is anti-coagulant and vasodilatory]

57
Q

what conditions is endothelial damage associated with?

A

raised vascular resistance, hypertension, atherosclerosis and increased risks cloths.

58
Q

what is atherosclerosis?

A

buildup of fats, cholesterol and other substances in and on your artery walls (plaque), which can restrict blood flow. The plaque can burst, triggering a blood clot.

59
Q

what tissue is relatively unaffected by sympathetic activity? (arteriole resistance)

A

Brain

60
Q

what is the effect of sympathetic activity in exercise on. blood vessels?

A

causes vasoconstriction in some regions and vasodilatation in others. Divert blood from kidneys, gut and skin in favour of heart and skeletal muscles.

61
Q

what are Eicosanoids used for?

A

actions on blood vessels, involved in clotting and inflammatory responses.

62
Q

what are eicosanoids synthesised by?

A

cyclo-oxygenase (same enzyme inhibited by aspirin)

63
Q

what is the function of prostaglandins? (type of eicosanoid)

A

can be vasoconstrictors vasodilators, involved in inflammation and some parturition processes

64
Q

what is an eicosanoid that is a very potent vasoconstrictor produced by platelets (also cause platelet aggregation)

A

thromboxane A2 (important part of clotting response)

65
Q

what eicosanoid blocks actions of thromboxane A2?

A

prostacyclin produced by endothelium

66
Q

what is the result of endothelium damage on thromboxane A2 and prostacyclin balance?

A

favours thromboxane A2, reduced blood flow and clotting.

67
Q

what is the rationale behind using aspirin to prevent myocardial infarction (in terms of thromboxane A2 and prostacyclin)

A

irreversibly blocks cox-1 (required for both substances), endothelium has nuclei, can synthesise more prostacyclin, production of thromboxane A2 can’t as produced by platelets.

68
Q

why is it important to regulate cardiac output?

A

ensure adequate perfusion of tissues. Critical in determining arterial blood pressure (ABP)

69
Q

how much control does the heart have on CO?

A

very little

70
Q

what experiment was carried out by Guyton et al investigating how the heart effects CO.

A

replaced right atria of dogs with high-output pumps.

71
Q

Guyton et al CO experiment observations

cardiac output

A

reducing pumping capacity of heart below normal reduced cardiac output. BUT - increasing pumping capacity did not increase cardiac output.

72
Q

Guyton et al CO experiment conclusions

A

1) heart is required to MAINTAIN CO but 2) heart does not normally limit CO

73
Q

in veins, what does the pressure have to be (Pv) WRT atmospheric for them to collapse?

A

1-2 mmHg below atmospheric.

74
Q

what is the explanation for increasing pumping capacity of the heart not increasing cardiac output?

A

heart can not increase arteriovenous pressure gradient beyond a point where Pv becomes negative and would cause evens collapse, limiting venous return and cardiac output.

75
Q

how can directly measure right atrial pressure?

A

insert catheter via jugular vein

76
Q

what does a healthy heart do for venous pressure? (measured inserting a catheter via jugular vein)

A

reduces central venous pressure to almost zero, even at rest

77
Q

conclusions for increasing heart rate and cardiac output.

A

changing heart rare by electrical pacing does not greatly change cardiac output as CO is limited by venous return.

78
Q

what needs to be done in order to allow for the heart to have a greater cardiac output?

A

creation of arterio-venous fistula to provide pathway for blood to return to heart. (allows sufficient venous return)

79
Q

what is the main determinant of cardiac output?

A

Mean systemic filling pressure.

80
Q

what use happen in order to increase Pa? (CO)

A 
reduce Pv (but be careful not too much to prevent collapse) 
- solution: raise mean pressure of whole system
81
Q

why is mean systemic filling pressure the main determinant of CO?

A

determines maximum FLOW rate (Darcy’s) for a given resistance

82
Q

what does mean systemic filling pressure represent? (MSFP)

A

pressure that would eventually exist everywhere in system if the heart stopped (mean pressure in the system)

83
Q

how can you increase MSFP?

A

extra filling (e.g blood transfusion or drinking an isotonic solution) or constricting volume e.g. VENOCONSTRICTION

84
Q

what is the approximate normal blood volume in an adult mammal?

A

70-80 ml/kg (5l for a 70kg person)

85
Q

what is meant by ‘unstressed volume’ of circulation?

A

volume of blood that just fills the circulation without stretching vessels wall (~80% of total in adult mammals)

86
Q

what is meant by ‘stressed volume’ in circulation?

A

final 20% of total, Mean pressure will rise. (mean pressure usually around 7-10 mmHg)

87
Q

which form of vessels are more compliant from veins and arteries?

A

veins ! when heart pumps a volume of blood from veins to arteries, pressure in arteries will rise more than pressure in veins will fall.

88
Q

function of arteriovenous pressure gradient

A

drives blood flow from the arteries to the veins.

89
Q

what is implied by the maximum arteriovenous pressure gradient being set by the mean filling pressure?

A
  • heart can’t change mean pressure

- mean pressure determines maximum cardiac output.

90
Q

what is MSFP determined by?

A

volume of blood and the mean tension in blood vessel walls.

91
Q

how can you double CO?

A

increasing blood volume by 20%, doubling stress volume and therefore doubling MSFP and CO

92
Q

why does arteriolar constriction increase TPR but does not influence MSFP?

A

less than 1% of blood contained within arterioles (compared to about 60% in small venues and veins)

93
Q

why does venoconstriction not significantly influence TPR?

A

primarily determined by resistance of arterioles

94
Q

where is CO directly measured in the body?

A

IT’S NOT ! It’s regulated to maintain ABP. (heart responds to changes through intrinsic and extrinsic mechanisms)

95
Q

Intrinsic mechanism for increasing CO when MSFP increases

A

Frank-Starling mechanism (starlings “law of the heart”)

96
Q

what is the principle value controlled by the cardiovascular system?

A

[mean] arterial blood pressure (ABP)

97
Q

what are the determinants of ABP?

A

Cardiac output (CO) and total peripheral resistance (TPR)

98
Q

how does exercise affect TRP?

A

greatly reduces it

99
Q

why is it important for ABP to be kept constant?

A

blood flow to individual tissues can be regulated just by controlling local arteriolar resistance.

100
Q

how does blood loss affect circulation

A

reduces mean systemic filling pressure (MSFP) and therefore CO.

101
Q

what is systolic blood pressure usual value? [make sure you can annotate pressure diagram)]

A

120 mmHg (peak)

102
Q

what is a usual value for diastolic blood pressure?

A

80mmHg (blood flows away from aorta)

IB physiology (4 decks)

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