Test 1: Wk2: 4 Cardiac Electrophysiology - Puri Flashcards

1
Q

at rest the cardiac myocyte is only permeable to

A

K+

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2
Q

at rest the cardiac RMP =

A

Nernst potential for K+

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3
Q

potential is reliant upon — concentration inside and outside the cell

A

K+

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4
Q

depol — probability of both open and inactive channels

A

increases

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5
Q

repolarization induces recovery from — to —

A

inactive to closed

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6
Q

the number of cation channels available for the next cycle and there readiness depends on

A

RMP

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7
Q

Outward rectifiers

A

open as the membrane depolarizes, K+ rapidly repolarizes the cell

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8
Q

Inward rectifiers

A

open at rest and allow K+ to leave cell when Vm

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9
Q

what direction does K+ always go in

A

leaves the cell

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10
Q

phase 0

A

rapid upstroke - depol of cardiac muscles

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11
Q

phase 1

A

initial repolarization

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12
Q

phase 2

A

stabilization of membrane potential - plateau phase

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13
Q

refractory period

A

duration of phase 2

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14
Q

phase 3

A

rapid repolarization

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15
Q

phase 4

A

return to resting membrane potential

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16
Q

phase 0 ions

A

Na in

K x

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17
Q

phase 1 ions

A

K out

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18
Q

phase 2 ions

A

Ca in

K out

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19
Q

phase 3 ions

A

Ca x

K out

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20
Q

phase 4 ions

A

K open but no outward movement of K when equilibrium is reached
Na/ATPase restores balance

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21
Q

— drive repolarization and remain open from phase — to —

A

outward rectifiers

1 3

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22
Q

— close as the Vm approaches 0 and the action potential is made possible

A

inward rectifiers

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23
Q

— sodium channels are the main targets of antiarrhythmic drugs

A

SCN5A

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24
Q

Na channels open when mV =

A

-70

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25
Q

Na channels have —

A

time dependent inactivation

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26
Q

reactivation of Na channels requires almost complete — of Vm

A

repolarization

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27
Q

— Ca channels are critical for — cardiac contraction

A

L type

initiating

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28
Q

— open slowly as the membrane depol and remain open until — mV

A

delayed outward rectifiers

-70

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29
Q

— open when mV reaches — and remain open at rest

A

inward rectifiers

-60

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30
Q

absolute refractory period

A

inactivation of fast Na channels

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31
Q

relative refractory period -

the action potential has

A

some Na channels recover to closed state and cane be activated at higher than normal threshold

reduced conduction velocity

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32
Q

Supernormality

the action potential is

A

threshold for activation is lower than resting cardiac myocyte

still slow

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33
Q

the duration of refractoriness depend on the — and — of the repolarizing current via —

A

strength and rapidity
K+
outward rectifiers

34
Q

P wave represents

A

atrial deopl

35
Q

QRS complex is produced by

A

the summed up phase 0 ventricular myocytes action potentials

36
Q

QRS complex is wider when

A

velocity is decrease

37
Q

ST segment corresponds to

A

the plateaus of the action potentials

38
Q

ST segment is dependent on balance of

A

incoming Ca and outgoing K

39
Q

T wave is produced by

A

ventricular repol

40
Q

T wave depends on

A

strength of outward K current

41
Q

QT interval is the

A

action potential duration

42
Q

TP segment is phase — of the —

A

phase 4 of fast action potential

43
Q

many antiarrhythmic drugs target

A

fast Na channels

44
Q

lidocaine

A

delay recovery of fast Na channels from inactivation at -65

SCN5A recover at -80

45
Q

quinidine, amiodarone

A

prevent or delay SCN5A opening - slowing upstroke of fast action potential

46
Q

amiodarone

A

interrupt cardiac rythym

prolong the ERP - K+ channel blockers

47
Q

verapamil

A

Ca channel blocker

reduce strength of cardiac contraction -0 shorten ERP

48
Q

action potential in the nodes have no

A

phase 1 or 2

49
Q

Nodes phase 0

A

opening of L Ca channels ➡ Ca mediated inward current

50
Q

Nodes Phase 3

A

Kr and Ks channels open ➡ mediated inward current

51
Q

Nodes resting membrane potential

A

less negative - fewer K open

52
Q

phase 4 autonomic depol

A

funny current

53
Q

what is the natural pacemaker of the heart, why

A

SA node

highest density of HCN channels

54
Q

HCN channel order of density

A

SA > AV > His-Purkinje

55
Q

SNS Control of HR

A

beta adrenergic stimulation increases Gas and increases cAMP and PKA

56
Q

SNS Control of HR

increases HCN activity ➡

A

⬆ slope of phase 4 depol

57
Q

SNS Control of HR

lower threshold for opening of

A

L Ca channels

58
Q

SNS Control of HR

faster opening of L Ca channels ➡

A

⬆ slope of phase 0

59
Q

SNS Control of HR

faster repol vie increased Ik currents ➡

A

⬆ slope of phase 3

60
Q

PNS Control of HR

PNS stimulation activates — and reduces — ➡ ⬇ — phosphorylation ➡ —

A

Gi
cAMP
HCN
slower phase 4 depol

61
Q

PNS Control of HR
↓ — → ↓ — phosphorylation → higher threshold for — channel opening
and —

A

↓ cAMP → ↓ L-type phosphorylation → higher threshold for Ca++ channel opening
and slower phase 0 depolarization

62
Q

PNS Control of HR

Stimulation of — rectifiers — the resting membrane Vm

A

Stimulation of KAch inward rectifiers lowers the resting membrane Vm

63
Q

– tone is the predominant tone regulation resting HR

A

parasympathetic

64
Q

Automatic phase —depolarization of the SA node predominate, and spread to the left atria via the —

A

Automatic phase 4 depolarization of the SA node predominate, and spread to the left atria via the Bachman’s bundle

65
Q

— is the first to depolarize

A

Right atria is the first to depolarize → depolarization
spread from right to left, and downwards towards the
AV node–this is sinus rhythm

66
Q

— nodes depolarizes the bundle of His which divides

into — in the septum

A

AV nodes depolarizes the bundle of His which divides

into left and right branches in the septum

67
Q

depolarization in the septum spreads from — to —

A

depolarization in the septum spreads from left to right

68
Q

— terminate in Purkinje fibers, which

make contacts with myocardial cells

A

Bundle branches terminate in Purkinje fibers, which

make contacts with myocardial cells

69
Q

Depolarization spreads across the — by

myocardial cell-to-cell conduction

A

Depolarization spreads across the ventricles by
myocardial cell-to-cell conduction → spread across
ventricles is more or less uniform

70
Q

— facilitate cell-cell transmission of the cardiac —

A

Gap junctions facilitate cell-cell transmission of the cardiac action potential

71
Q

structure or gap junctions

A

formed by the interaction of the connexons of two neighboring cells

72
Q

Connexon

A

composed of six membrane-spanning proteins (connexins) with a central pore
In cardiomyocytes

73
Q

connexons control

A

control the passage of electrical stimulus

74
Q

The impulse from the — node depolarizes the resting cardiac myocyte

A

The impulse from the SA node depolarizes the resting cardiac myocyte

75
Q

How does the electrical

impulse propagate?

A

see slide

76
Q

current sink

A

Positive charges from the membrane ahead of the
action potential flow into the area of negative charge
represented by the action potential

77
Q

what causes current sink

A

due to the flow of electrons on

either side of the membrane

78
Q

Speed of impulse propagation is termed

A

conduction velocity

79
Q

— have the slowest conduction

velocity in the heart

A

Nodes have the slowest conduction

velocity in the heart

80
Q

Na/Ca exchanger is

A

bidirectional

81
Q

Na/Ca exchanger # Na exchanged for # Ca

A

3 Na for 1 Ca