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Cardiology > Electrophysiology > Flashcards

Electrophysiology Flashcards

1
Q

The action potential triggers

A

Contraction

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2
Q

How does the cardiac muscle AP differ from the skeletal muscle AP?

A

Duration of cardiac AP is longer

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3
Q

What generates the resting membrane potential of cardiac myocytes?

A

Relative permeability to charged ions and Ion pumps

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4
Q

Then, different ion concentrations create the

A

Electrical potential difference

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5
Q

A change in the electrochemical gradient for an ion that is permeable can alter the

A

Resting membrane potential

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6
Q

A change in ion conductance can alter the

A

Resting membrane potential

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7
Q

What is the effect on RMP for a cell if there is decreased Extracellular concentration of K+?

A

RMP becomes more negative

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8
Q

When we have loss of Na+/K+ ATPase due to ischemia, what happens to the RMP?

A

Becomes more negative

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9
Q

Characterized as rapid depolarization

A

Cardiac myocyte AP phase 0

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10
Q

In phase 0, action potential depolarizers cell to threshold (from -90 to -60), then we see rapid opening of

A

Voltage-gates Na+ channels

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11
Q

Voltage-mediated activation of fast Na+ channels allows

A

Rapid depolarization

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12
Q

Inactivate quickly during phase 0 so that conductance decreases

A

Voltage-gated Na+ channels

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13
Q

Inactivated channels cause the

A

Refractory period

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14
Q

What determines the rate of rise of the phase 0 upstroke?

A

Inward Na+ current

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15
Q

What is the effect of a pharmacological blockade of Na+ channels on the cardiac myocyte AP?

A

Peak would be lower and amplitude would be lower

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16
Q

How would a pharmacologic blockade of Na+ channels change the ECG?

A

QRS would be prolonged

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17
Q

How would phase 0 change if we had an increase in extracellular K+?

A

Cell slowly depolarizers and RMP becomes more positive

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18
Q

Slow depolarization from excess extracellular K+ causes Na+ channels to go from

A

Closed to inactive, without being activated

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19
Q

What is phase 1 of the cardiac myocyte AP?

A

Brief Repolarization

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20
Q

Characterized by a transient outward current (IKto) and rapid inactivation of FAST Na+ channels

A

Brief repolarization

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21
Q

Cells in the subepicardium are characterized as having a

A

Shorter AP

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22
Q

Phase 2 of the cardiac myocyte AP is?

A

Plateau phase

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23
Q

The major current leading to the plateau phase is the

A

Slow inward Ca2+ through L-type channels

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24
Q

Major Ca2+ channel in cardiac cells

-important pharmacologic targets

A

L-type channels

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25
Q

Counter-balance inward Ca2+ during the plateau phase

A

Outward K+ currents

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26
Q

Permits sufficient calcium entry into the cell to maintain the stores required for contraction

A

Plateau phase

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27
Q

Keeps the fast sodium channels inactivated for a substantial period of time to prevent too frequent APs

A

Plateau phase

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28
Q

Phase 3 of the cardiac myocyte AP is

A

Repolarization

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29
Q

Results in repolarization

A

IKr current

30
Q

The action potential becomes narrower and we get faster repolarization if the

A

IKr current increases

31
Q

What changes would we see in the cardiac myocyte action potential with a drug that blocks IKr?

A

Prolonged repolarization and longer AP

32
Q

What changes would we see in the ECG of a patient taking a drug that blocks IKr?

A

Long QT interval

33
Q

A long QT interval predisposes patients for

A

Arrhythmias

34
Q

Phase 4 of the cardiac myocyte AP is the

A

Stable resting membrane potential

35
Q

Characterized by a stable RMP, a sustained period of depolarization, and a LONG duration (150-250 msec)

A

Cardiac myocyte Non-pacemaker AP

36
Q

Characterized by cells that lack the inward rectifying type of K+ channel (IK1) so RMP is less negative

A

Pacemaker potential

37
Q

Characterized by an unstable RMP, automaticity, and no sustained plateau

A

Pacemaker APs

38
Q

Phase 0 of the cardiac pacemaker potential is

A

Depolarization

39
Q

During phase 0 of pacemaker potentials, we see increase Ca2+ conductance via

A

Voltage-gated L-type Ca2+ channels

40
Q

One major characteristic of pacemaker potentials is that there is NO

A

Fast Na+ current

41
Q

Phase 3 of the cardiac pacemaker potential is

A

Repolarization

42
Q

In a pacemaker potential, depolarization leads to opening of

A

Delayed rectifier K+ channels

43
Q

Phase 3 of the pacemaker potential ends when the cell reaches the

A

Maximum negative diastolic potential

44
Q

Phase 4 of the cardiac pacemaker potential is the

A

Spontaneous depolarization cardiac pacemaker current

45
Q

Which 3 currents contribute to the cardiac pacemaker current (phase 4)?

A

IF (funny current), outward K+ (IK+), and inward Ca2+ (ICa2+)

46
Q

Activated by hyperpolarization (Anything greater than -50 mV)

-The more negative the membrane potential, the more intense this current is

A

Funny current (IF)

47
Q

The “funny” current is regulated by

A

CAMP

48
Q

The IF current moves through channels called

A

HCN channels

49
Q

Is reverse-voltage dependent and has no inactivation state

A

Funny current

50
Q

The HCN channels of the funny current are permeable to

A

Na+ AND K+

51
Q

The K+ ion is more easily conducted across HCN channels, BUT under physiologic conditions, HCN channels carry

A

Inward Na+ current

52
Q

Reverse-voltage dependence makes them unique among ion channels

A

HCN channels

53
Q

Causes increased HCN activity

A

cAMP

54
Q

The opening and closing of HCN channels determines the slope of

A

Phase 4

55
Q

Activated towards the end of phase 4 of pacemaker potential

A

Inward Ca2+ (T-type) channels

56
Q

Accelerates the rate of diastolic depolarization

A

T-type channels

57
Q

Which three factors influence the intrinsic firing rate of the pacemaker cells?

A
  1. ) Slope of phase 4
  2. ) Maximum negative diastolic potential
  3. ) Threshold potential
58
Q

The primary pacemaker is the

A

SA node

59
Q

Has the fastest rate and suppresses the firing of other pacemakers

A

SA node

60
Q

SA node activity is regulated by the

A

Autonomic Nervous System

61
Q

The regulation of heart rate is called

A

Chronotropy

62
Q

Increasing sympathetic ton causes an increase in

A

HR (positive chronotropic effect)

63
Q

Increasing vagal tone causes a

A

Decrease in HR

64
Q

In the heart, norepinephrine binds to

A

B1 adrenergic receptors

65
Q

When norepinephrine binds to B1 adrenergic receptors, we see an increase in

A

cAMP

66
Q

This increase in cAMP has what two main effects?

A
  1. ) Stabilized HCN in open position

2. ) Opens L(and likely T)-type Ca2+ channels

67
Q

When acetylcholine is release, what does it bind to in the heart?

A

Muscarinic receptors (M2)

68
Q

When acetylcholine binds muscarinic receptors (M2), it decreases

A

cAMP and If

69
Q

Acetylcholine binding M2 activates a LIGAND-gated

A

K+ channel

70
Q

Activation of the ACh-gated Ik will

A

Hyperpolarize the cell

Cardiology (27 decks)

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