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CV I > RMP and AP > Flashcards

RMP and AP Flashcards

1
Q

What 3 properties give us consistency of the heart

A

automaticity, conduction system, functional syncytium

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2
Q

What structures are apart of conductions system

A

SA note, inter-atrial pathway, AV node, common AV bundle, R and L bundle fibers and the purkinje fibers

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3
Q

What cells are usually in charge of driving heart rate

A

SA nodes because reach threshold first

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4
Q

What would you expect to see if SA node fails

A

bradycardia

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5
Q

How does SA spread to AV node? left atrium?

A

AV node- internodal pathway

left atrium- brachmanns bundle or known as anterior interarterial myocardial band

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6
Q

3 functional regions of AV node

A

AN
N- nodal
NH

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7
Q

What paths slow conduction

A

AN and N

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8
Q

how does AN slow conduction

A

longer path

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9
Q

how does N region slow conduction

A

slower velocity

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10
Q

Why is there a delay between atria and ventricles

A

so we have time for filling of the heart during diastole

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11
Q

What is decremental conduction

A

effect dies out over time

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12
Q

Which node is common to have conduction blocks

A

AV

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13
Q

Once AV nodes fail what fibers take over

A

purkinje. 20-40 bpm

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14
Q

What do patients with Wolff-Parkinson-White Syndrome have

A

alternate path around AV node(bundle of kent). conducts directly atria to ventricle and is faster. but the ventricle depolarization is slower

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15
Q

Where does the right and left bundle branches go

A

R- down right IV septum

L- splits anterior and posterior

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16
Q

How are purkinje fibers arranged

A

linear like sarcomeres.

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17
Q

Which part of conduction system has fastest conduction velocity and how?

A

purkinje because they have a huge diameter

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18
Q

in which direction are purkinje fibers activated

A

endocardium- epicardium

apex- base

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19
Q

In ventricular m how are APs conducted

A

cell to cell

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20
Q

Which cells repolarize after depolarization

A

base- apex

epicardium- endocardium

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21
Q

What events are significant for ventricular depolarization

A

early contraction of IV septum(anchor)
early contraction of papillary m (prevent backflowto atria)
depolarization apex to base

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22
Q

Where is the slowest conduction velocity in the heart? and why?

A

AV and SA nodes

small diameter

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23
Q

how many nuceli are in cardiac m

A

mononucleated

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24
Q

Where is Ca stored in Cardiac m

A

ECF and SR

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25
Q

what is faster. rate of contraction of skel m or cardiac

A

skel m. cardiac is 1.5x slower

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26
Q

What are markers of myocardial injury

A

Troponin T and I markers and CK-MB

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27
Q

What accounts for the electrical syncitium of the heart

A

all cardiac m cells contract in syncrony

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28
Q

What allows for cell to cell communication

A

intercalated disks

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29
Q

If cell to cell communication is not working properly what do you see on the EKG

A

widened QRS complex

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30
Q

What is the all or none of the heart

A

either all cardiac cells contract or none

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31
Q

how do we alter contractility of cardiac m

A

increase Ca. sympathetic input

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32
Q

Why do we need Ca from ECF

A

to trigger release of Ca from SR

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33
Q

What do we need for relaxation of cardiac cells

A

Sarcolemmal 3Na/1Ca antiporter
and Sarcolemmal Ca pump using ATP
SERCA

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34
Q

Can cardiac m increase force of contraction through tetanus

A

no

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35
Q

Why can cardiac m not go under tetanus

A

AP is long (plateau)

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36
Q

How do we have a long AP in cardiac cells

A

VG L type Ca channels

and delayed K channel

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37
Q

Do pacemaker cells have RMP

A

no- maximum diastolic potential

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38
Q

What do we have instead of RMP in pacemakers

A

slow depolarizaiton phase

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39
Q

What is the RMP of fast conducting cells

A

-80 - -90

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40
Q

Ion distribution for RMP

A

Na and Ca high extracell

K high intracell

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41
Q

What is the RMP permeable to

A

K

42
Q

effect of hyperkalemia

A

increase depolarization

43
Q

Are AP constant thorughout all areas of cardiac cell conduction

A

no, initiation time shape and duration of APS changes depending on what cells.

44
Q

2 main types of cardiac AP

A

fast response fibers and slow response fibers

45
Q

Which RMP is more negative, fast or slow response AP

A

fast is more negative.

46
Q

What is the threshold potential in slow and fast AP

A

slow is -40

fast is -70

47
Q

Which type of cardiac AP has faster upstroke

A

fast

48
Q

Rank conduction veolocities of slow response, fast response in ventricles and fast response in purkinje

A

purkinje fastest
then fast response ventricle
slow response are the slowest

49
Q

which fibers respond to greater AP firing rate

A

fast response fibers because recover fast from refractory period

50
Q

What are the 4 main ion currents in cardiac AP

A

NA, Ca, K, and funny current

51
Q

What phase is Ca responsible for in slow response fibers

A

slow depolarization- AV SA nodes

52
Q

What phase is Ca responsible for in fast response fibers

A

plateau phase

53
Q

What phase is the funny current responsible for in slow response AP

A

“pacemaker current” partialy helps the slow depolarization phase

54
Q

What type of ion current is the funny current

A

Na

55
Q

If the upstroke of a cardiac AP is solely due to Ca influx what type fiber is it

A

slow response AP

56
Q

What two ions contribute to the rapid spike at the begining of a fast response cardiac AP

A

Na and Ca

57
Q

Which type cardiac AP has a transient K current

A

fast response

58
Q

What ions are still moving during the plateau phase in fast cardiac AP

A

K and Ca and tiny bit of Na

59
Q

what ions are moving during the electrical diastolic phase of slow response cardiac AP

A

K Ca and the funny current

60
Q

what ion impacts the conduction velocity

A

Na

61
Q

what are the types of Ca channels in cardiac myocytes

A

L type Ca and T type Ca

62
Q

When does Ca activate and inactivate in fast response AP

A

activate at more positive and inactivate slower than Na

63
Q

What are the two K channels that contribute to respolarization

A

rapid and slow

64
Q

describe K movement in SA and AV node

A

decreases efflux to promote depolarization

65
Q

What would be the effect of a K channel blocker on AP in fast response

A

lose that little dip of repolarization after upstroke. Also prolonged AP

66
Q

What AP is shorter, atrial AP or ventricl

A

AP because faster K efflux to repolarize

67
Q

What are the 4 dependent currents in Purkinje fibers

A

Na Ca K and funny

68
Q

What are the 2 factors that affect conduction velocity

A

AP amplitude

Rate or slope of the depolarization

69
Q

When is there the greatest number of inactivation gates on Na channels

A

right after depolarization

70
Q

How does hyperkalemia slow conduction velocity

A

decreases amplitude and slope depolarization because many of Na channels will be inactivated.

71
Q

When do we see hyperkalemic states in cardio clinically

A

Ischemia- affects ATPase so ion [ ] not normal

Infarcted cells- cells release intracell K

72
Q

When is the effective refractory period

A

after initiation of fast AP, locked Na gates

73
Q

When is the relative refractory period

A

not fully excitable. before repolarization is complete

74
Q

What does AP look like when happens during relative refractory

A

depends when it takes place/ if right before reached depolarization- looks normal.
if right when refractory begins, small amplitude

75
Q

What is the purpose of refractory periods

A

avoid tetanus and gives time for adequate filling (diastole)

also can limit ectopic beats

76
Q

What is an Ectopic foci

A

AP that do not follow normal conduction pathway

77
Q

What does an EKG look like with ventricular ectopic foci? why?

A

wide QRS because takes longer for cells to communicate cell - cell

78
Q

What are proarrhytmias

A

increased inward currents or decreased outward currents for repolarization

79
Q

What do afterdepolarizations result in clinically

A

tachycardia

80
Q

What will an early afterdepolarization look like

A

lower slope, lower amplitude, so slow conduction detrimental. Long QT syndrome– Torsades de pointes

81
Q

What can cause a delayed afterdepolarization

A

elevated Ca

82
Q

What is reentry of cardio

A

abnormal impulse that takes on own path. own pacemaker rhythm

83
Q

What is a global rentry pathway

A

own curcuit

84
Q

what is needed for reentry to occur

A

partial depolarization, unidirectional block, effective refractory period is shorter than necessary time (so new one during relative refractory)

85
Q

Where does global reentry happen

A

between atria and ventricle

86
Q

what can result clinically from global reentry

A

supraventricular tachycardia

87
Q

where does local reentry occur

A

within atria. or within ventricles

88
Q

What can result clinically from local reentry

A

atrial or ventricular tachycardia

89
Q

What can cause reentry

A

autonomic input. sympathetic decreases ERP, vagal increases ERP

90
Q

3 main factors promotin reentry

A

lengthened conduction pathway
decreased conduction velocity
reduced refractory period

91
Q

What can cause lengthened conduction pathway

A

dilated heart chamber

92
Q

What can cause decreased conduction velocity

A

hyperkalmeia, ischemia, purkinje system block

93
Q

what drugs reduce refractory period

A

Epinephrine

94
Q

What is the purpose of an external automated defibrillator EAD

A

alternating current promoting a reset by putting all cells into refractoriness at once- stopping fibrillation

95
Q

How do we change HR in slow response

A

how quickly threshold reached, starting point RMP, or changing threshold itself

96
Q

When is the inward funny current increased

A

the more negative membrane gets. hyperpolarization

97
Q

What is moving through funny channel

A

Na influx, non specific

98
Q

What results if decrease ECF Ca

A

small upstroke and amplitude of fast

99
Q

Will hyperkalemia increase or decrease HR

A

decrease because changes driving form for K and slowing dow repolarization

100
Q

Tetrodotoxin block

A

transitions from fast response to slow response fibers

CV I (7 decks)

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