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Physiology 1020 > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

3 components of cardiovascular system

A

heart, vessels and blood

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2
Q

functions of Cardiovascular System

A

-distributes blood
-exchanges gases, nutrients, waste and hormones
-heat regulation
-hemostasis
-modulating inflammatory response

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3
Q

pulmonary circuit

A

to lungs
-gas exchange

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4
Q

systemic circuit

A

blood to all other organs and tissues

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5
Q

superior and inferior vena cava

A

largest vein

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6
Q

apex of heart

A

bottom of heart
contractions spread from here then upwards

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7
Q

aortic valve

A

prevents blood going back in left ventricle
sends blood into systemic circulation

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8
Q

aorta

A

largest artery
blood enters systemic circulation

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9
Q

left atrioventricular AV valve

A

stops back flow from left ventricle to left atrium
-tricuspid valve

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10
Q

left ventricular myocardium

A

thicker than right side

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11
Q

interventricular septum

A

wall separating left and right side

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12
Q

pulmonary valve

A

sends blood into pulmonary circulation

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13
Q

cusps

A

pockets that fill with blood causing them to expand and close

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14
Q

lub dub

A

lub-AV valves closing
dub-aortic and pulmonary valves closing

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15
Q

heart murmurs

A

valves don’t close properly (valve regurgitation)
whoosing sound may be heard

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16
Q

heart arrhythmias

A

irregular heart contractions

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17
Q

cardiomyocytes

A

cardiac muscle cells
-contractile and nodal

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18
Q

contractile cells

A

pumps blood through heart
-communicate between 2 cells using gap junctions
-ions from gap junction go to other cells then causes depolarization

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19
Q

nodal/conducting cells

A

spread electrical activity/AP through heart
self-excitable >make own AP
minimal actin and myosin
don’t contract

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20
Q

sim between skeletal myofibers and cardiomyocytes

A

striated
Ca to contract
mitochondria
need ap

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21
Q

diff between skeletal myofibers and cardiomyocytes

A

Ca>SM-SR, CM- SR and extracellular fluid
mitochondria> more in CM than SM
need ap- SM-motor neuron CM use nodal cells
CM-branched
-single nucleated
-electrically connected through gap junctions

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22
Q

intercalated discs

A

helps connect cardiomyocytes
locked together by desmosomes (protein)
where gap junctions are found

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23
Q

gap junctions

A

allows Na, Ca and other small molecules together to allow communication
-on intercalated discs

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24
Q

nodal/conducting cells examples

A

AV nodes
SA nodes
Atrio-ventricular bundle
subendocardial branches

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25
Q

Ca-induced Ca-released

A

Ca comes in cell from extracellular fluid across plasma membrane through ion channels down concentrated gradient
-this helps release Ca from SR

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26
Q

HR in men and women

A

men- 80 beats/min
women- 70 beats/min

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27
Q

SA node

A

sinoatrial node
in upper right atrium
pacemaker determines heart rate
receives input from PSNS and SNS

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28
Q

intrinsic rate

A

100 AP/min
1 AP every 0.6s

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29
Q

remember depol vs repol

A

D- cell more positive and Na in
R- cell returns RMP, K out

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30
Q

nodal cells AP

A

no stable RMP
reaches threshold by Na and Ca moving in
keep K in-no leaking

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31
Q

SA nodal AP

A

slower AP release >don’t want to fast HR

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32
Q

Steps pace maker potential

A

1) positive charge/graded potential is created by Na and Ca entering cell using their own ion channels (Ca and Na in, K out)
2)Depol- caused by opening Ca channels at threshold
-Ca moves down concentration gradient
3)repol- K leaves cell through K channels
more negative

no hyperpolarization

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33
Q

what happens when SA node fails

A

AV node acts as pacemaker b/c it is the 2nd fastest AP creation

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34
Q

bradycardia

A

too low HR
dizzy, faint

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35
Q

max HR

A

220-age

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36
Q

HR lower than 100 bpm

A

-PSNS
ACh communicates with heart by binding to receptors on SA node cells/ muscarinic R
-slow HR decreases slop of pacemaker potential, >slower hit of AP
-when ACh binds to muscarinic R, decrease Ca and Na permeability (slower coming in), increase K permeability

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37
Q

HR increasing

A

-SNS
adrenergic receptors bind with (nor)epinphrine
threshold hit fast to get quicker AP
increase Na and Ca coming in SA node

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38
Q

heart transplant

A

nerves of ANS don’t reconnect
-this causing higher resting heart and closer to intrinsic rate of SA node

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39
Q

ECG

A

electrocardiogram
-looks at electrical activity in heart
-using electrodes, APs moving through heart can be detected on surface of skin
-body fluid conducts electricity

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40
Q

p wave

A

result of depolarization of atria

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41
Q

QRS wave

A

result of depolarization of ventricles
larger than P wave b/c ventricles have a larger mass

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42
Q

T wave

A

result of repolarization of ventricles

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43
Q

atria repolarization

A

at same time as QRS wave
so small, masked by ventricles depolarization

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44
Q

systole

A

period when cardiomyocytes are contracting

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45
Q

diastole

A

period when cardiomyocytes are relaxing

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46
Q

cardiac cycle

A

isovolumetric ventricular systole
ventricular systole
isovolumetric ventricular diastole
late ventricular diastole
atrial systole

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47
Q

isovolumetric ventricular systole

A

ventricles start contracting, blood isn’t being pumped out of heart

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48
Q

ventricular systole

A

ventricles are contracting
blood moves out of heart and into aorta or pulmonary artery

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49
Q

isovolumetric ventricular diastole

A

ventricles start relaxing and not filled with blood

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50
Q

late ventricular diastole

A

ventricles are relaxing and start filling with blood from atria

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51
Q

atrial systole

A

atria contracting and blood moving in ventricles

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52
Q

blood movement

A

high to low (pressure) blood will flow

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53
Q

isovolumetric ventricular systole graph

A

ECG: QRS> started at atrial contraction
Volume: no change
Valves: closed
Pressure: increase ventricular P
aortic P > vent P

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54
Q

ventricular systole graph

A

ECG: no new
Volume: decrease ventricular volume
Valves: aortic open, AV closed
Pressure: vent P > aortic P

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55
Q

isovolumetric ventricular diastole graph

A

ECG: T wave in phase 2
Volume: no change
Valves: closed
Pressure: lower vent p, higher aortic p

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56
Q

late ventricular diastole graph

A

ECG: no new
Volume: increase ventricular volume
Valves: AV open, aortic closed
Pressure: higher atria P, lower vent P

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57
Q

atrial systole graph

A

ECG: p wave
Volume: increase ventricular volume
Valves: AV open, aortic closed
Pressure: lower vent p, higher atrial p

58
Q

ESV

A

end systolic volume
amount of blood in ventricle at end of systole after ventricle contract
-decrease ESV means more effective heart

59
Q

EDV

A

end diastolic volume
amount of blood in ventricle before ventricular contraction

60
Q

SV

A

stroke volume
amount of blood ejected by ventricle with each heart beat
SV= EDV-ESV
influence cardiac output

61
Q

cardiac output

A

amount of blood the heart pumps each minute
=HRxSR
at rest 5-6L/min
in L

62
Q

how to adjust SV

A

ANS innervation
preload on heart/EDV

63
Q

ventricular muscle

A

some muscarinic and lots of adrenergic receptors

64
Q

Ca’s role in contraction

A

more in cytoplasm, stronger contraction
increase excitation contraction coupling

65
Q

ANS innervation adjusting SV -S

A

SNS: innervates ventricular cardiomyocytes
epinephrine binds to adrenergic receptors
-when activated, increase Ca permeability >increases strength of contraction + increase SV

66
Q

ANS innervation adjusting SV -PS

A

parasympathetic: some innervation of contractile cardiomyocytes
-ACh binds muscarinic receptors
decrease Ca permeability >decreases strength of contraction + decrease SV

67
Q

preload adjusting SV

A

increase EDV= increase preload
-increase stretch of contractile cells of ventricles
-increase force of contraction
-increase amount of blood pumped out heart
increase SV=increase cardiac output

68
Q

preload

A

load on heart prior to contraction
-blood that has filled ventricle=EDV
larger EDV/fuller heart, more stretch

69
Q

Frank Starling’s Law of the heart

A

more EDV= more SV
this protects heart from over filling then bursting

70
Q

types blood vessels

A

arteries, arterioles, capillaries, venules, veins

71
Q

vessels in organs

A

all are supplied by major arteries
-has own smaller arteries, arterioles, cap, venules, smaller veins
-return to heart by superior or inferior vena cava

72
Q

total blood volume + % based on systems

A

4-6L
15% of blood between pulmonary circuit and heart
85% of blood in systemic circuit

73
Q

blood % in systemic circuit

A

A 10%
cap 5%
V 70%

74
Q

lumen

A

area where blood flows through center of vessel

75
Q

general blood vessel structure

A

have 3 tunics except capillaries
> tunic externa, media, interna

76
Q

tunica externa

A

outermost layer
-composed of connective tissue > protection and maintains structure
-has neurons of SNS to communicate with tunica media

77
Q

tunica media

A

middle layer
-has smooth muscle to contract or relax >changes diameter
-elastin>elastin fiber, allows for stretch
-collagen
-different amount of contains for different vessels

78
Q

tunica interna

A

innermost layer
-has endothelial cell> special cells that line blood vessels
-important for vessel function

79
Q

arteries

A

blood away from heart
distribution vessel
larger diameter 25%
alot of elastin to stretch during vent. diastole
-pulsatile pressure
take BP here

80
Q

pulsatile pressure

A

high pressure during systole and pow pressure during diastole

81
Q

arterioles

A

thick walls>50%
-resistance vessels> higher muscle than elastin
-large drop in pressure
smooth muscle innervated by SNS
regulates blood flow

82
Q

capillaries

A

-smallest blood vessels
-also called endothelial cells
-only single layer of endothelial
-super thin
-exchanges vessels
-hormones go capillaries to bind receptors on target cells
low BP

83
Q

venules

A

low blood pressure

84
Q

veins

A

-blood back to heart
capacitance vessels
-large diameter, thin walls
-low P
-uses valves in lumen
-some smooth muscle + elastin for stretch and increase diameter

85
Q

valves in veins

A

prevent back flow
-have cusps that fill with blood

86
Q

venous return

A

-amount of blood returned to heart
-ANS can innervate veins
-SNS cause small contraction, decrease diameter and more blood goes back to heart
-increase venous return, EDV, SV, cardiac output

87
Q

increase venous return by moving

A

skeletal muscle pump
-contraction of smooth muscle squeezes on veins > decrease diameter to forced to heart

88
Q

varicose veins

A

-enlarged, twisted veins
-common in legs and feet
-occur from malfunctioning vein valves causing blood to pool + veins to swell, increasing P

89
Q

why does blood flow need to be regulated

A

to increase blood flow to active tissues
maintain blood supply to vital organs
maintain BP
to increase or decrease heat loss

90
Q

resistance affect on blood flow

A

decreases flow

91
Q

what affects blood resistance

A

-lumen radius (^r, smaller resistance)
-viscosity (^, ^resist)
-length of blood vessels (lined with endothelial cells increase friction> ^resist)

92
Q

blood pressure equation

A

pressure gradient x radius to the power of 4

93
Q

resistance in arterioles

A

has greatest resistance by 50
capillary- 35
venules 15

94
Q

where do you take blood pressure

A

taken from brachial artery

95
Q

vasoconstriction

A

increase pressure before where there is vasoconstriction ie. artery
decrease pressure afterwards ie. capillary

96
Q

luminal membrane

A

membrane that is closest to capillary lumen

97
Q

basolateral membrane

A

membrane that is closest to interstitial fluid

98
Q

transcellular transport

A

substance enters and then exits endothelial cell

99
Q

paracellular transport

A

-substance can move between 2 endothelial cells lining capillaries through intercellular clefts
called bulk flow
fluid and anything that dissolved in it that are small enough fit through intercellular cleft

100
Q

intercellular clefts

A

have proteins called tight junctions between them
-vary in size and leakiness of cleft
-small slits
-found at borders of where 2 endothelial cells meet

101
Q

continuous capillaries

A

most abundant> in muscles, brain lungs, heart
-varies in permeable
-intercellular clefts
ex. brain almost no permeability through intercellular clefts

102
Q

fenestrated capillaries

A

found in kidneys and intestines
-intercellular clefts
-more bulk flow than continuous capillaries

103
Q

sinusoidal capillaries

A

found in liver and spleen

104
Q

filtration during bulk flow

A

fluid and other substances moves out capillaries using bulkflow
-happens in capillaries, site of exchange

105
Q

edema

A

excessive filtration causing swelling

106
Q

filtration forces

A

because capillaries have blood under pressure, molecules in blood will experience filtration through intercellular clefts

107
Q

starling forces

A

promotes or prevent filtration
-hydrostatic forces causing fluid to move
-promotes reabsorption, increase return of fluid back into capillaries

108
Q

Capillaries hydrostatic forces

A

high BP at start and forces force fluid out by filtration
at end of capillaries, BP lowers and has some reabsorption

109
Q

lymphatic system

A

returns excess interstitial fluid back in circulation
-blood is filtered by bulk flow
-interstitial fluid moves back into lymphatic capillaries to go through lymphatic system then blood is put in circulation to heart
-doesn’t work leads to edema

110
Q

3 major regulatory systems for controlling flow

A

local regulation, humoral regulation, neural regulation

111
Q

local regulation

A

-mechanism involves changes in conditions of tissues
-intrinsic mechanism
-most tissues
-also called autoregulatory mechanism b/c tissues autoregulates flow
temp, gases pressure

112
Q

types of local regulation

A

myogenic theory and metabolic theory

113
Q

extrinsic mechanism

A

signal to change blood flow comes from outside the tissue

114
Q

intrinsic mechanism

A

stimulus to change blood flow comes from within the tissues that need it

115
Q

myogenic theory

A

-muscle stretch
-increase BP leads to increase blood flow
this stretches arterial wall
reflexive contraction of smooth muscle (decrease radius, vasoconstriction)
decrease blood flow and BP in capillaries to protect the capillaries

116
Q

metabolic theory

A

metabolic needs
-increase co2, H, adenosine, temp, decrease o2 during metabolically active tissue
this then increases blood flow by increase radius and vasodilation

117
Q

vasodilator metabolites

A

co2, H, adenosine

118
Q

humoral regulation

A

-mechanism involves substance that are travelling in blood through BV
-substances change radius of BV, usually by binding to receptors
-usually hormones
-extrinsic mechanism

119
Q

epinephrine causing regulation

A

-released by adrenal gland when SNS is activated
-binds to adrenergic receptors on smooth muscle cells of BV
-alpha and beta found in same BV

-binds to alpha adrenergic receptor causing vasoconstriction, decrease BF, increase BP
-binds to beta adrenergic receptors causing vasodilation, decrease BP

120
Q

angiotensin II causing regulation

A

hormone that binds to receptors on smooth muscle cells of BV causing vasoconstriction, increase BP
-stimulus for release is low BP

121
Q

antidiuretic hormone

A

-released by posterior pituitary gland
-promotes water reabsorption in blood
-binds to receptors on smooth muscle cells of BV causing vasoconstriction and increase BP
-stimulus for release is low BP

122
Q

histamine

A

chemical released by inflammatory cells like allergic reactions
-not hormone
-binds to receptor on BV causing vasodilation, increase blood flow, decreases BP

123
Q

atrial natriuretic peptide

A

-hormone produced by atria
-response to increase BP
-binds to receptors on smooth muscle cells on BV causing vasodilation, decrease BP

124
Q

neural regulation

A

neurons from SNS innervate smooth muscle cells found in tunica media of many BV
-neurons release norepinephrine that binds to adrenergic receptors to cause vasoconstriction
-extrinsic

125
Q

what nervous system innervates blood vessels

A

SNS

126
Q

blood pressure

A

force exerted by blood on the walls of blood vessels

127
Q

systolic pressure

A

higher value
pressure in arteries when heart contracts

128
Q

diastolic pressure

A

lower value
pressure when heart is a rest

129
Q

MAP stands for

A

mean arterial pressure

130
Q

MAP

A

average BP in arteries during one cardiac cycle
heart is in diastole longer than systole
changes when change in activity of heart/pressure, radius, CO, TPR, HR, SV
-maintains adequate blood flow and sufficient amounts of oxygen and nutrients

131
Q

MAP equation

A

MAP =CO x TPR
or
=DP + 1/3 (SP -DP)

132
Q

PSNS affect on BP

A

decreases HR, SV (small amount) decrease BP
indirectly as it doesn’t innervate BV
- using PSNS, use less SNS causes vasodilation b/c no constriction

133
Q

baroreceptor reflex

A

-keeps MAP in normal range
-negative feedback for BP

134
Q

hypertension

A

high BP
can damage BV leading to heart disease and stroke

135
Q

hypotension

A

low BP
-low blood flow to organs causing dizziness, faintng adn shock

136
Q

baroreceptors

A

mechanoreceptor >sense stretch
found in carotid sinus (neck) and aortic arch

137
Q

steps of baroreceptor reflex SNS

A

-baroreceptors stretch and detect change in BP
-sends sensory info to cardiovascular center in medulla oblongata
-then info heart and blood vessels
-the SNS info is sent out to SA node to change heart’s pace by increasing slope of pacemaker potential and change ventricular myocytes
-increase SV by increase contractility
increase HR (SA node), TPR
then increase MAP

138
Q

steps of baroreceptor reflex PSNS

A

-baroreceptors stretch and detect change in BP
-sends sensory info to cardiovascular center in medulla oblongata
-then info goes to SA not to blood vessel
-decrease HR, SV (contractility), SNS activation (decrease TPR)
therefore decrease MAP

139
Q

conducting system: AP conduction

A

1)SA node
2) atrial cardiomyocytes
3)signals go to AV node
4)atrioventricular bundle
5)bundle branches
6)subendocardial branches-
7)ventricular cardiomyocytes

140
Q

more indepth AP conduction

A

1)SA node
2) atrial cardiomyocytes >these will contract, moving blood into ventricles
3)signals go to AV node
-AV node connects APs between atria and ventricles
-pause >AP slows b/c atria need to finish contracting before ventricles get excited and contract
4)AP goes to ventricles>atrioventricular bundle
5) atrioventricular bundle split into bundle branches (L+R) spreading AP to l/r vent
6)subendocardial branches- spread AP from bottom to top of vent
-fast AP
7)then ventricular cardiomyocytes will contract from from bottom to top

Physiology 1020 (3 decks)

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