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CP Test 1 > B4-099 Overall View of the Heart's Function > Flashcards

B4-099 Overall View of the Heart's Function Flashcards

1
Q

which layer of the heart wall…

ejection of blood from the heart

A

myocardium

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2
Q

which layer of the heart wall…

protection of the heart from mechanical trauma

A

pericardium

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3
Q

which layer of the heart wall…

stabilize the heart within the thoracic cavity

A

pericardium

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4
Q

which layer of the heart wall…

functions as a lubricant to decrease friction

A

pericardium

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5
Q

which layer of the heart wall…

prevent excessive dilation of the heart

A

pericardium

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6
Q

which layer of the heart wall…

provides a smooth surface for blood flow

A

endocardium

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7
Q

which layer of the heart wall…

releases substances that control heart development

A

endocardium

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8
Q

the closure of the AV valves is heard as a

A

lub

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9
Q

S1

A

closure of AV valves

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10
Q

the closure of SL valves is heard as a

A

dub

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11
Q

S2

A

closure of SL valves

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12
Q

the mitral valve has […] cusps

A

2

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13
Q

capacity to respond to an electrical impulse

A

excitability

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14
Q

ability to initiate electrial impulse

A

automatism

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15
Q

capacity to maintain

A

rhymicity

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16
Q

ability to transmit the electrical stimulus to all areas of the heart

A

conductivity

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17
Q

transient lack of the cardiac cells to respond to stimulus

A

refractoriness

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18
Q

capacity of heart muscle to contract

A

contractility

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19
Q

difference in voltage between the intracellular compartment and the external medium

A

resting membrane potential

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20
Q

cardiac cells can trigger a change in membrane potential, which will lead to

A

cardiac contraction

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21
Q
  • depolarization to repolarization
  • all or none response
A

action potential

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22
Q

return to the cell resting potential

A

repolarization

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23
Q

rapid change in resting membrane potential

A

depolarization

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24
Q

how is cardiac action potential different from skeletal muscle?

A
  1. is it self generating
  2. it can be conducted directly from cell to cell
  3. it has relatively long duration
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25
Q

atrial and ventricular cardiomyocytes and purkinje fibers have a […] response

A

fast

action potential

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26
Q

SA and AV nodes have a […] response

A

slow

action potential

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27
Q

phase 4

A

pre action potential

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28
Q

phase 0

A

upstroke of action potential

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29
Q

phase 1

A

transient repolarization

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30
Q

phase 2

A

plateau phase

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31
Q

phase 3

A

repolarizing phase

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32
Q

in the SA and AV nodes, the action potential only has […] phases

A

3

4, 0, 3

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33
Q

in ventricular myocytes, the action potential has […] phases

A

all 5

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34
Q

different in nodal and myocardial ventricular cells

A

depolarizing current

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35
Q

in the SA and AV nodes, the depolarizing current is the

A

calcium current

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36
Q

in ventricular myocytes, the depolarizing current is the

A

sodium current

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37
Q

important for excitation-contraction of the heart

A

calcium current

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38
Q

the repolarizing current in all areas of the heart is the

A

potassium current

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39
Q

sodium channels are […] gated

A

voltage

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40
Q

slow response action potential is […] dependent

A

calcium

SA and AV node

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41
Q

fast response action potential is […] dependent

A

sodium

cardiomyocytes, bundle of His, perkinje fibers

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42
Q

cardiac chronotropism

A
  • automatism
  • the capacity of the heart to produce electical impulses
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43
Q

automatism depends on the

A

SA node

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44
Q

does not have a stable resting potential

A

SA node

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45
Q

name the phase/location:

  • slow depolarization
  • pacemaker potential due to increased Na+ conductance
  • funny sodium current is responsible for heart’s automaticity
A

phase 4
SA node

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46
Q

name the phase/location:

upstroke of action potential due to inward calcium current

A

phase 0
SA node

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47
Q

name the phase/location:

not present in nodal cells

A

phase 1/2

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48
Q

name the phase/location:

  • repolarizing phase
  • caused by increased K+ conductance
  • leads to outward K+ current
A

phase 3
SA node

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49
Q
  • most negative potential in SA node
  • normally about 50mV
A

MDP

maximum diastolic potential

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50
Q

if the SA node is no longer function, cardiac excitation will be driven by

A

AV node

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51
Q

the action potential of AV node is similar to SA node, but the slope of phase […] is less steep

A

4

52
Q

determines the conduction velocity of the action potential moving through the AV node

A

magnitude of calcium current

53
Q

responsible for sodium entrance and phase 0 depolarization

A

funny sodium channels

54
Q

activated during phase 0 to cause depolarization

A

L-type calcium channels

55
Q

repolarization during phase 3 occurs due to

A

K+ channels

56
Q

name the phase/location:

  • stable resting potential
  • inward rectifier potassium channels
A

phase 4
myocardial cells

57
Q

name the phase/location:

upstroke due to voltage gated sodium current

A

phase 0
myocardial cells

58
Q

name the phase/location:

  • transient repolarization due to K+ moving out of cells
  • decrease in Na+ conductance
A

phase 1
myocardial cells

59
Q

name the phase/location:

  • plateau phase due to balance between Ca+ and K+ currents
  • delayed rectifier K+ channels
A

phase 2
myocardial cells

60
Q

name the phase/location:

repolarization phase due to K+ outward current driven by delayed rectifier potassium cells

A

phase 3
myocardial cells

61
Q
  • responsible for phase 0 depolarization
  • very transient current
A

voltage gated sodium channels

62
Q
  • activated during phase 0
  • little change in membrane potential in phase 2
  • Ca+ inactivation gates close near end of phase 2
A

L-type Ca+ channels

63
Q

repolarization during phase 3 occurs due to

A

K+ channels

64
Q

normal sinus rhythm

A

60-100 bpm

65
Q

what channel contributes to diastolic depolarization in SA and AV nodes?

A

funny sodium channel

66
Q

what channel is active during phase 0 of action potential?

A

voltage gated sodium channel

67
Q

what channels are open during phase 2 of action potential?

A
  • L-type calcium channel
  • K+ delayed rectifier channel
68
Q

what channel maintains high K+ permeability during phase 4 of action potential?

A

K+ inward rectifier channel

69
Q

what channel contributes to phase 1 of action potential?

A

K+ transient outward channel

70
Q

the funny sodium channel opens with

A

repolarization

71
Q

Na+ channels open in response to

A

depolarization

72
Q

voltage gated sodium channels have 3 main conformational states

A
  1. closed
  2. open
  3. inactivated
73
Q

Na+ channels have two separate gates

A
  1. activation gate
  2. inactivation gate
74
Q

at resting membrane potential, the voltage gated sodium channel is

A

closed

75
Q

[…] opens the activation gate of the voltage gates sodium channel

A

depolarization

76
Q

at full depolarization, the [….] gate of the voltage gated sodium channel closes

A

inactivation

77
Q

the activation gate opens [fast or slow]

A

fast

78
Q

the inactivation gate opens [fast or slow]

A

slow

79
Q

in hyperkalemia, the resting membrane potential is more positive than normal.
This causes

A
  • decreased voltage gated sodium current
  • decreased excitability of heart cells
80
Q

the magnitude of the voltage gated sodium current in the cardiac myocytes will determine

A
  1. threshold potential
  2. amplitude of action potential
  3. rate of rise of action potential
  4. conduction velocity
81
Q

the L type Ca+ channel has activation and inactivation curves that overlap called

A

calcium window

82
Q

the magnitude of L-type calcium current in the SA and AV nodes will determine

A
  1. threshold potential
  2. amplitude of action potential
  3. rate of rise of action potential
  4. conduction velocity
83
Q

conduction velocity in the AV node will determine the

A

duration of PR segment on ECG

84
Q

K+ delayed rectifier cells open upon

A

depolarization

very slow to allow depolarization to finish

85
Q

lowest conduction velocity

A

AV node

86
Q

cardiac muscle cells are rectangular shaped cells connected by

A

intercalated discs

87
Q
  • protein lined tunnels
  • allow direct transmission of the depolarizing current from cell-to-cell so they contract in unison
A

gap junctions

88
Q

because of the way gap junctions function, cardiac muscle cells are said to be

A

electrically coupled

89
Q

period in which the cardiac cells is unable to intiate anothe action potential

A

refractory period

90
Q

refractory period allows for

A

complete emptying of the heart

91
Q

heart muscle contraction is reffered to as

A

inotropism

92
Q

process by which the electrical activation of the cardiac myocytes leads to the activation of contraction

A

cardiac excitation contraction coupling (ECC)

93
Q

increases inotropy and stroke volume

A

calcium

94
Q

Frank-Starling’s Law

A

the energy of contraction is proportional to the initial length of the cardiac muscle fiber

95
Q

stroke volume increases when

A

preload is increased

96
Q

as preload increases, sarcomere length

A

increases

allows more cross bridging during systole

97
Q

increased sarcomere length allows

A

more cross bridges to form during systole

98
Q

increasing EDV allow more overlap of

A

thick and thin filaments

more crosslinking

99
Q
  • all cardiac valves are closed with no blood flow
  • pressure in ventricles is low
A

isovolumic relaxation

diastole

100
Q

mitral and tricuspid valves open, pulmonic valves are closed

A

ventricular filling

diastole

101
Q

during ventricular filling, the pressure in the ventricles drops below

A

that of the atria

102
Q
  • all cardiac valves are closed with no blood flow
  • ventricular pressure raises
  • atrial pressure raises
A

isolvolumic contraction

systole

103
Q

aortic and pulmonic valves are open; mitral and tricuspid are closed

A

ejection

systole

104
Q

when the heart rate is high, […] is shortened the most

A

diastole

105
Q

the AV node will not conduct beyond

A

230 bpm

106
Q

Ejection fraction=

A

stroke volume/
EDV

107
Q

normal value for EDV

A

120-140 mL

108
Q

normal value for ESV

A

40-60 mL

109
Q

normal value for SV

A

60-100 mL

110
Q

normal value for ejection fraction

A

0.5-0.7

111
Q

normal value for cardiac output

A

5.0-6.0 L/min

112
Q

normal value for cardiac index

A

2.6-4.2 L/min/m2 of body surface area

113
Q

way to normalize values for cardiac output to differences in body size

A

cardiac index

114
Q

myocardial action potential

  • rapid upstroke and depolarization
  • voltage gated Na+ channels open
A

phase 0

115
Q

myocardial action potential

  • initial repolarization
  • inactivation of voltage gated Na+ channels
  • voltage gated K+ channels begin to open
A

phase 1

116
Q

myocardial action potential

  • Ca+ influx through voltage gated Ca+ channels balances K+ efflux
  • Ca+ influx triggers Ca+ release from sarcoplasmic reticulum and myocyte contraction
A

phase 2

Ca+in =K out causes platwo

117
Q

myocardial action potential

  • rapid repolarization
  • massive. K+ efflux due to opening of delayed rectifier K+ channels
  • closure of voltage gated K+ channels
A

phase 3

118
Q

myocardial action potential

  • resting potential
  • high K+ permeability through K+ channels
A

phase 4

119
Q

myocardial action potential occurs in all cardiac myocytes except

A

SA and AV node

120
Q

pacemaker action potential

  • upstroke
  • opening of L type Ca+ channels
  • results in slow conduction velocity
A

phase 0

121
Q

pacemaker action potential

  • repolariztion
  • inactivation of Ca+ channels
  • increased activation of K+ channels
  • increase K+ efflux
A

phase 3

122
Q

pacemaker action potential

  • slow spontaneous diastolid depolarization due to funny sodium current
A

phase 4

123
Q

neurotransmitters that decrease the rate of diastolic depolarization and HR

A
  • ACh
  • adenosine
124
Q

neurotransmitters that increase depolarization and HR

A

chatecholamines

125
Q

increases the chance that funny sodium channels are open and thus increases HR

A

sympathetic stimulation

CP Test 1 (16 decks)

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