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MEDSCI 142 > Module 3.2 - Cardiovascular Physiology > Flashcards

Module 3.2 - Cardiovascular Physiology Flashcards

1
Q

initiation of heart beat

A

heart has an intrinsic beat (ability to beat on its own)
=> auto-rhythmicity
- can beat outside body

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2
Q

coordination of contraction

A

of myocardial cells of atria/ventricles through specialised conducting tissue

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3
Q

AP of ventricular contractile fibre

A
  • rapid depolarisation as fast as nerve AP due to being Na+ driven
  • contraction whenever there is Ca2+ => length of contraction is determined by width of plateau
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4
Q

electrocardiogram - Pwave

A

atrial depolarisation
=> atrial contraction

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5
Q

electrocardiogram - QRS complex

A
  • onset of ventricular depolarisation
  • atrial repolarisation (but wave is lost within much bigger QRS complex => shape doesn’t represent)
  • spread of activation through ventricles
  • shape of wave due to direction of spread
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6
Q

electrocardiogram - S-T segment

A

when whole ventricle is depolarised (extended plateau of AP)
=> electrical balance
=> no voltage change
elevation/depression if abnormalities in ventricular wall => chest pain

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7
Q

electrocardiogram - Twave

A
  • ventricular repolarisation (not as rapid)
    => relaxation / start of diastole
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8
Q

electrocardiogram - T-P segment

A

when all cardiac myocytes are at RMP

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9
Q

chronotrope

A

something that changes heart beat
- positive chronotrope: increase heart rate

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10
Q

inotrope

A

something that changes in contractility/contraction power
- positive => increase, negative => decrease

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11
Q

regulation of heart rate

A

(autonomic) nervous system regulation of heart rate originates in the cardiovascular centre of medulla oblongata

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12
Q

input to cardiovascular centre

A

from higher brain centres (forebrain) + receptors (proprio, baro, chemo)

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13
Q

output to effectors

A

parasympathetic (vagus) / sympathetic nerves to heart+ vasomotor nerves (sympathetic) to blood vessels for vasoconstriction

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14
Q

sympathetic / parasympathetic balance at rest

A

SA node is dominated by vagal activity at rest (50-70 bpm)

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15
Q

regulation of blood pressure

A

ANS (autonomic nervous system) innervation of heart/baroreceptor complexes that help regulate BP

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16
Q

regulation of BP - nerve direction

A
  • baroreceptors -> cardiovascular centre in medulla
  • cardiovascular centre ->
    1) SA/AV node - parasympathetic
    2) spinal cord
  • cardiac accelerator nerves -> spinal cord (thoracic level) -> sympathetic trunk ganglion -> SA/AV node, ventricular myocardium (sympathetic)
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17
Q

BP hormones

A

circulating hormones
- adrenalin/noradrenalin
- ion concentrations
etc.

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18
Q

proprioceptor input

A

major stimulus that accounts for rapid rise in HR at onset of physical activity

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19
Q

hyperthermia

A

increases HR

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20
Q

sympathetic nervous system increases

A
  • HR
  • SV
  • spontaneous depolarisation of SA/AV nodes
  • contractility of ventricles/atria
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21
Q

parasympathetic nervous system decreases

A
  • HR
  • rate of spontaneous depolarisation of SA/AV nodes
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22
Q

dicrotic wave

A

rebound from aortic valve closing

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23
Q

can you have negative blood pressure

A

yes

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24
Q

cardiac output

A

amount/volume of blood ejected into aorta per minute

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25
Q

cardiac output unit

A

mL/min
L/min

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26
Q

average cardiac output

A

5 L/min
- between 4-7 L/min at rest
- can go up to 5x e.g during exercise
- 40 L/min for athletes

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27
Q

cardiac output equation

A

= HR x SV

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28
Q

cardiac reserve

A

difference between max. cardiac output and cardiac output at rest (rates at which heart pumps blood)
- shows maximum capacity of heart to pump blood

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29
Q

normal heart rate

A

normal = 60-100 bpm
- controlled by SA node (sympathetic/parasympathetic activity)

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30
Q

normal stroke volume

A

50-100 mL per beat

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31
Q

stroke volume equation

A

= end diastolic volume (EDV) - end systolic volume (ESV)

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32
Q

EDV

A

max. volume (most full)
- 120-140 mL

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33
Q

ESV

A

min. volume
- 50-70 mL

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34
Q

frank-starling law of heart

A

in stable system, venous return (diastole) = cardiac output (systole)
- increased return => heart works harder => stretch of myocytes => energy of ventricular contraction => forcefulness of contraction => SV increases
- greater force of contraction can occur if the heart muscle is stretched first

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35
Q

factors determining SV

A

1) preload
2) contractility
3) afterload

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36
Q

preload

A

force that stretches cardiac muscle prior to contraction
- increased diastolic filling => increase EDV => increased SV

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37
Q

factors changing diastolic filling

A
  • ∆venous return
  • ∆blood volume (more blood in system => more blood to heart)
  • ∆filling time (duration of ventricular diastole)
  • ∆respiratory pump (inhaling => negative pressure around lungs and heart shares same space => also affected - decreased diastolic filling)
  • ∆compliance (MI - myocardial infarction damage - becoming stiffer, can’t contract as well due to scarred tissue, attack, disease etc.)
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38
Q

venous return

A

amount of blood returning to heart each min from venous system

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39
Q

contractility

A

performance (forcefulness of contraction) of heart (esp left ventricle) at a given preload/afterload
- aka inotropy
- increased contractility => decreased ESV => increased SV

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40
Q

factors changing contractility

A
  • autonomic nervous system (increased sympathetic => increased contractility)
  • venous return (increased preload => increased contractility)
  • [Ca2+] (all factors affecting contractility act by changing [Ca2+])
  • drugs (inotropes) - target contractility not longetivity as it doesn’t address underlying conditions
  • ion balances
  • circulating levels of various hormones
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41
Q

afterload

A

amount of pressure that the heart needs to exert to eject blood during ventricular contraction (what heart works against)
- increased afterload => increased ESV => decreased SV

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42
Q

factors affecting afterload

A
  • hypertension - high blood pressure
  • valve pathologies
  • aortic plaques - constriction in aorta
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43
Q

ventricular pressure-volume relationship

A

A: mitral valve opens
B: mitral valve closes
C: aortic valve opens
D: aortic valve closes

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44
Q

ventricular pressure-volume relationship - A-B

A

ventricular filling
- first: pressure decreased due to suction effects of relaxing muscle
- later: pressure rises passively as volume increases

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45
Q

ventricular pressure-volume relationship - B-C

A

isovolumetric contraction
- pressure increases steeply
- no change in volume as aortic valve closed

46
Q

ventricular pressure-volume relationship - C-D

A

blood ejection

47
Q

ventricular pressure-volume relationship - D-A

A

isovolumetric relaxation

48
Q

stroke work

A

heart’s pumping action is achieved by mechanical work of myocardium
= area of pressure-volume curve of ventricular contraction (total external work carried out by ventricles during one cardiac cycle)

49
Q

stroke work equation

A

work done = ∆pressure x ∆volume

50
Q

blood volume distribution

A

1) systemic veins and venules (blood reservoirs) - 64%
2) systemic arteries and arterioles - 13%
3) pulmonary veins - 9%
4) heart - 7%
5) systemic capillaries - 7%

51
Q

blood pressure

A

pressure of circulating blood against vessel walls which can vary throughout cardiac cycle

52
Q

mean arterial pressure (MAP) equation

A

cardiac output (CO) x total peripheral resistance (TPR)

53
Q

total peripheral resistance

A

amount of force affecting resistance of blood flow through circulatory system

54
Q

poiseuille’s law

A

describes flow is related to factors such as velocity

55
Q

if CO decreases while MAP constant

A

TPR increases by sympathetic stimulation of smooth muscles => reduce diameter (vasoconstriction) => increase resistance

56
Q

blood hydrostatic pressure (BHP)

A

force exerted by blood confined within vessels
- arterial: ~35 mm Hg
- venous: ~16 mm Hg

57
Q

blood colloid osmotic pressure (BCOP)

A
  • aka oncotic pressure
    form of osmotic pressure induced by proteins in blood
  • ~26 mm Hg
58
Q

decreasing BCOP

A

deficiency/low plasma protein level

59
Q

hemorrhage

A

release of blood from broken blood vessel

60
Q

interstitial fluid hydrostatic pressure (IFHP)

A

mechanical pressure exerted on interstitial fluid by elastic recoil of tissues in any region of body
- ~0 mm Hg

61
Q

interstitial fluid osmotic pressure (IFOP)

A

osmotic force which is the result of differences in water conc. between plasma and interstitial fluid
- ~1 mm Hg

62
Q

capillary exchange

A

exchange/movement of material between blood and interstitial tissue/fluid across capillary wall

63
Q

ways of capillary exchange

A

1) diffusion
2) trancytosis
3) bulk flow/filtration

64
Q

diffusion

A

solute exchange, down conc grad

65
Q

trancytosis

A

vesicles (contents wrapped in membrane) of large, lipid-soluble (insoluble in H2O/blood)
e.g insulin

66
Q

bulk flow/filtration

A
  • passive movement of flow + substances
  • faster than diffusion alone
  • net flow is driven by difference between balance of hydrostatic pressure / osmotic pressure gradients (starling’s law of capillaries)
67
Q

net filtration - favours filtration

A

BHP + IFOP
- arterial: 35 + 1
- venous: 16 + 1

68
Q

net filtration - favours reabsorption

A

BCOP + IFH
- arterial and venous: 26 + 0

69
Q

pressures

A

(BHP + IFOP) - (BCOP + IFHP)
- arterial: +10 mm Hg
- venous: -9 mm Hg

70
Q

negative pressure means

A

favours reabsorption

71
Q

organ without lymph vessels

A

brain - glymphatic system

72
Q

oedema/edema

A

accumulation of fluid outside vessels
- common symptom of many conditions
- most obvious in legs due to gravity

73
Q

hypertension =>

A

arterial BHP increases
- vasoconstriction
- increased arterial tone

74
Q

arterial tone

A

degree of constriction relative to maximally dilated state

75
Q

kidney disease =>

A

loss of blood proteins (more in urine) => BCOP decreases => low capillary reabsorption

76
Q

heart failure =>

A

venous BHP increases

77
Q

long-haul travel =>

A

venous volume increases as heart tries to hold volume (more filled up) => SV increases
venous BHP increases

78
Q

how does long-haul travel increase BHP

A
  • gravity
  • leg swelling => venous compression
    => blood pools in venous sytem
    => BHP increased without changing overall blood volume
79
Q

venous volume increases =>

A

capillary permeability increases => IFOP increases

80
Q

nervous control effect on TPR

A

decreased frequency of sympathetic nerve activity => vasodilation in systemic blood vessels => increased radius of vessel lumen => decreased resistance to blood flow => decreased total peripheral resistance

81
Q

effect of blood volume on nerve activity

A

decreased blood volume
=> decreased EDV => decreased SV
and
=> decreased BP => baroreceptors sense => increase sympathetic activity to heart + decreased parasympathetic / vagal
(reflex neural mechanisms that respond to change in arterial pressure)

82
Q

reason for having parallel structure of circulatory structure

A

allows same hydrostatic gradient at each organ

83
Q

relationship between bloodflow and total cross-sectional area in different blood vessel types

A

velocity is inversely proportional to cross-sectional area (of all of that type of blood vessel)

84
Q

to increase blood flow

A

1) increase cardiac output (increase HR and/or SV)
2) redirect existing cardiac output/blood flow to organs that need it (vasoconstriction)

85
Q

what control direction of bloodflow

A

precapillary sphincters

86
Q

coping with haemorrhage - challenge to homeostasis

A
  • vasoconstriction
  • increase HR (need CO to maintain blood)
  • clotting to stop bleeding (+ maintain BP)
  • redirection
  • increase SV by increasing contractility (not much by venous return as blood is being lost
87
Q

baroreceptors

A
  • respond to ‘stretch’ in arterial wall
  • signals connect up to brain via cranial nerves
88
Q

baroreceptors and tonicity

A

tonically active
- can respond to increases/decreases in BP (not on/off)

89
Q

baroreceptor location

A
  • carotid sinus
  • aortic arch
90
Q

carotid sinuses

A

sits above bifurcation of carotid artery (into two other arteries) along with carotid body
- one of smallest organs

91
Q

vascular tone - increased electrical signals from neuron =>

A

norepinephrine release onto receptors increases => vasoconstriction / increased HR => increased BP

92
Q

vascular tone and blood vessel size

A

effect of hormones in response to electrical signals is esp prominent in small arteries/arterioles due to ratio of muscle
- bigger change is required for bigger arteries to cause change

93
Q

total spinal anesthesia

A

block transmission across neurons in spinal cord from a specific point (below level of heart) down

94
Q

muscle activity in veins and BP

A

there is smooth muscle in veins but this has a smaller effect on BP due to low pressure, instead affects venous return

95
Q

what increases BP

A

increased:
- HR
- TPR
- VR (venous return)

96
Q

possible stimuli of change in BP

A
  • haemorrhage
  • drinks (1L of water/energy drink)
  • standing up quickly
  • temperature (hot day => peripheral vasodilation)
97
Q

resistance and radius

A

resistance is inversely proportional to radius^4

98
Q

redundant physiology

A

multiple systems that overlap in different ways to affect same variable

99
Q

slow response to increased blood volume

A

blood volume homeostasis (decreasing) via compensation by kidneys
- need to solve fundamental issue

100
Q

angiotensin II

A

vasoconstrictor peptide
- increased as a result of low BP (not affected by cardiac sympathetic activity)

101
Q

glossopharyngeal nerves

A

from carotid sinus -> cardiovascular centre

102
Q

vascular resistance is

A

1) size of lumen
- inversely proportional to radius^4
2) viscosity
- directly proportional
3) (total) length of blood vessel
- directly proportional

103
Q

alpha receptors

A
  • skeletal muscle
  • smooth muscle (blood vessels - arteries/arterioles)
104
Q

beta receptors

A
  • cardiac muscle (myocardium): ventricular muscles, SA/AV nodes
105
Q

Starling’s Law of the Capillaries

A

the volume of fluid reabsorbed at the venous end of a capillary is nearly equal to the volume of fluid filtered out at the arterial end

106
Q

vagus nerve

A

only affects heart rate
- NOT contractility/inotropy or vasomotor

107
Q

right subclavian vein

A

behind collar bone

108
Q

superior sagittal sinus

A

runs above longitudinal fissure

109
Q

long haul flights

A

decreased skeletal muscle action => decreased venous return (preload => SV => CO) => increased venous volume => increased venous BHP => stretched pores => increased capillary permeability (large solutes exit vessel) => IFOP increases => NFP increased => interstitial fluid increased => oedema (lymphatic can drain)

110
Q

lactic acid

A
  • causes vasodilation => decrease in BP
  • NOT produced when standing still
111
Q

proprioceptive input

A

does NOT affect HR
- only sends info about location/orientation of joints etc.

MEDSCI 142 (8 decks)

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