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CV > 11. Basic EKG > Flashcards

11. Basic EKG Flashcards

1
Q

Responsible for the rapid upstroke (phase 0) of AP in non pacemaker cells

A

Na entry through fast Na channesl

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2
Q

Responsible for depolarization of pacemaker cells (PKJ and myocytes) or phase 2

A

Ca entry through Ca channels

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3
Q

Responsible for repolarization leading to resting potential or Phase 4 of nonpacemaker cells

A

K+ EXIT through K+ channel

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4
Q

What maintains the low intracell Ca++ concentration

A

Na/Ca exchanger

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5
Q

What maintains conc gradients for Ca/K/Na

A

Na/KATPase pump

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6
Q

How is Ca removed to external environment and to SR

A

via active Ca transporters.

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7
Q

Channel responsible for rapid depolarizing non-nodal

A

INa+

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8
Q

Channel that depolarizes nodal AP and myocyte contraction

A

ICa+

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9
Q

Channel responsible for repolarizing all myocytes

A

IK+ (activated during repolarization)

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10
Q

Channel that is key for pacemaker current and activated during hyperpolarization

A

If or the funny channel = Na/K channel

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11
Q

What is the basic structure of ion channels

A

glycosylated proteins with repeat transmembrane domains. Each domain has 6 segments

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12
Q

Difference between Na, K, Ca channels

A

K: has 4 seperate domains in tetramer Ca and Na have 4 domains covalently linked as single uint

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13
Q

What part of Na channel serves as inactivation gate?

A

part connecting domains III and IV

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14
Q

What part of Na channel has sequence of + charged aas?

A

S4 segment of each domain==confers channels voltage sensitivity

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15
Q

What forms the selective filter in the Na channel?

A

Segment 5 and 6 of peptide loops allow only Na in

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16
Q

What is the confirmation of the inactive and active gates in the “Resting” state of Na channel

A

The inactivation gate is open but the activation gate is closed thus Na+ ions cannot get back in

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17
Q

How do we open up the activation gate in the ‘resting’ state of the Na channel?

A

Rapid depolarization changes cell membrane voltage– forces the activation gate to open (remember inactivation gate is already open) Na++ can then permeate the cell

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18
Q

How does the Na+ channel close or transition to the “inactive” state

A

Inactivation gate will spontaneously and quickly close via the peptide loop between III and IV then Na+ current ceases.

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19
Q

Channel can’t reopen directly from the inactive state–How do we get back to the “resting” state

A

Cellular repolarization returns channel to resting condition… at high negative membrane voltages, the acitvation gate closes and the inactivation gate reopens

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20
Q

Resting potential of cardiac cell is determined by balance of concentration gradient and electrostatic forces of:

A

Potassium. K+ is the only channel open at rest!

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21
Q

Concentration gradient favors____ movement while electrostatic favors ______ movement

A

outward inward

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22
Q

How do we approximate the resting membrane potential?

A

Nernst for K+ -26.7ln ([K+]in/[K+]out) = -91mV

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23
Q

What is the equilibrium potential for Na Ca K

A

Na: +70 mV Ca: +130 mV K: -90 mV

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24
Q

Label the following as having greater intracellular or extracellular concentrations Na: Ca: K:

A

Na: greater extracellular Ca: greater extracellular K: greater intracellular

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25
Q

Whats going on in Phase 4?

A

This is our resting potential

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26
Q

What stage is depolarization and what is happening

A

Phase 0… have influx of Na+ and get a rapid upstroke

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27
Q

What is resonsible for partial repolarization during phase 1

A

Transient outward K+ current gives partial repolarization

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28
Q

What causes the platue in phase 2?

A

slow Ca++ influx

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29
Q

What’s responsible for the rapid repolarization in phase 3?

A

Rapid efflux of K+

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30
Q

Largest current in the heart

Has classic voltage gated channel with a and b subunits

A

Na+

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31
Q

What subunits in Na+ gated channel can be phosphorylated by cAMP dependent kinase (PKA)

A

subunit a

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32
Q
A
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33
Q

Some Na channels stay activated during platue phase which will:

A

prolounge phase 2

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34
Q

How is depolarization spread through neighboring cells?

A

Major current spreads through GAP junctions

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35
Q

Ca++ current travels mostly through

A

Ltype Ca channels

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36
Q

What contributes to slower pacemaker activities of SA and AV node and slower spread of depolarization btwn neighboring cells causing delay btwn SA and AV nodes?

A

Ca+ Current

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37
Q

In atrial and ventricle cells, channels rapidly _____ and slowly _____

A

active

inactivate

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38
Q

What contributes to the Repolarizing K+ current seeing during phase 3

A

Two currents contribute to Ik

Ikr- : rapid component

Iks- : slow component

Thus Ik slowly activates but doesn’t inactivate

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39
Q

What happens during Early outward K+ current?

A

Atrail and ventricle cells – activated by depolarization resulting in rapid inactivation

Part of phase 1

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40
Q

What happens during G protein activated K+ current?

A

Inward K+ current mediated by GIRK K+ channel and is regulated by Ach!!!!

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41
Q

Where are GIRK K channels prominent

A

in SA and AV nodal cells. When activated by Ach… get decrease in pacemaker rate and slows conduction rate through AV node

42
Q

ATP sensitive K+ channels that play a role in electrically regulating contractile behavior

A

K ATP current

43
Q

What’s ‘funny’ about the If current?

A

They are not activated by depolarization but activated by HYPERPOLARIZATION during phase 3

–result is slow activation, and slow inward depolarizing current (doesn’t inactivate)

44
Q

Where are the If current channels found

A

SA, AV, PKJ

45
Q

What does the If channel conduction?

A

Both Na+ and K+ thus it’s nerst potential is about -20mV (between K+ and Na+ potential)

46
Q

Rough idea of ion conductance during Action potential

A

See that K is mostly outward rectifying except at phase 4

Na inward during phase 0

Ca+ is inward:

Ltype during 1 and 2

T type during 1

47
Q

Primary intinsic pacemaker

Has spontaneous depolarization leading to AP generation

A

SA node

48
Q

What makes SA our pacemaker?

A

Other cell types (AV, PKJ) have intrinsic pacemaker, this guy has fastest intrinsic spontaneous depolarization, thus dominant (60-100 bpm)

49
Q

Electrical synapses connecting cardiac myocytes; allows intracellular flow from cell to cell

A

Gap junctions

50
Q

Current spread determined by _____

A

Ohms law

directly proportional to voltage difference between cells and inversely proportional to resistance btwn cells

V= IR

51
Q

Secondary pacemaker and introduces delay between atrial and ventricle contraction

A

AV node

52
Q

Speed of AP upstroke divides cells into slow response ______ and fast respsonce cells____

A

slow = SA, AV, nodal cells

fast = atrial and ventricle myocytes, PKJ

53
Q

What determines cardiac fnx?

A

Electrical excitation!

54
Q

PKJ fibers originate in AV node with Bundle splitting into left and right bundles.

The left further divides into:

A

left anterior fasicle and left posterior fasicle

55
Q

PKJ has what type of conduction

A

very rapid but slow intrinsic pacemaker activity

56
Q

Phase 4 is characterized by gradual, spontaneous depolarization due to pacemaker current:

A

If (funny current)

57
Q

Threshold potential is reached at _____ in pacemaker cells followed by upstroke of AP

A

-40mV

58
Q

Why is the upstroke phase 0 less rapid in pacemaker cells then in nonpacemaker cells?

A

Bc current represents Ca++ influx through slow Ca++ channels

59
Q

Whats the difference between slow nodal and fast nonnodal cardiac AP

A

Slow: SA and AV nodal cells~~ RMP is -40 to -70 mV with AP upstroke of 1-10V/sec; and slow conduction

Fast: atrial/ventricle/PKJ fibs~~ RMP s -80 to -90mV with AP upstroke of >100/500 V/sec faster conduction

60
Q

Why is there a difference in conduction between fast and slow cardiac AP cells?

A

Due to fast Na+ in the atrial/ventricle/PKJ

And the spontaneous slow opening Ca+ channels in the nodal pacemaker cells

61
Q

What causes the spontaneous depolarization in the SA node?

A

Pacemaker Channels I (HCN)

HYPERPOLARIZATIONG activated, cyclic nucleotide gated and cation selective; Ehcn~ 0 mV

62
Q

Ach released from Vagus (PNS) onto SA and AV node has what affect on:

on If

on GIRK

on Ica

A

On If: in SA node and reduces steepness of phase 4

Ach opens GIRK–> thus increase K+ conductance and makes diastolic potential more negative

ACh reduces Ica–> reduces steepness of phase 4 and moves threshold to more positive value

63
Q

What effect does ACh have in the AV node

A

simular to that in the SA; but mostly it will sloooow down conduction velocity. Mainly by decreasing Ica thus threshold is more positive and more difficult for one cell to depolarize neighbors

64
Q

Nepi is released from SNS and acts on beta-adrenergic receptors in SA and AV node: How does it affect:

If

A

Increases If– thus increases steepness of phase 4 (vs Ach which has opp effect)

65
Q

Nepi is released from SNS and acts on beta-adrenergic receptors in SA and AV node: How does it affect:

Ica

A

Ica is increased thus steepens phase 4 and makes threshold more negative (vs ACh which reduces Ica and decreaes steepness and moves threshold +)

66
Q

Nepi is released from SNS and acts on beta-adrenergic receptors in SA and AV node: How does it affect:

A
67
Q

What affect does Nepi have on maximum diastolic pressure

A

NONE! Ach makes diastolic pressure potential more negative and Nepi doesn’t do shit

68
Q

What effect does Nepi have on atrial and ventricular cells?

A

ionotropic effect: Increase Ica–> increased Ca+ influx–> CICR from SR–> increases senstivity of Ca release channel (Ry-re) and enhances SR pumping to stimulate SERCA to store more Ca+

69
Q

Overall affects of how PNS ACh release alters heart rate of nodal depolarization

A
  1. Decreaes RATE of depolarization: decrease in If
  2. Decreaes maximium diastolic pressure: increase in Ik
  3. Increase in threshold potential: decrease in Ica

***ALL three cause more time to reach threshold

70
Q

When is cell unexcitable to simulation

A

ARP: absolute refractory

71
Q

Refractory period is brief time before ARP (when localized depolarization wont propagate). At RP what can happen

A

stimulation produces a weak AP that propagates, but slower then usual

72
Q

When can a weaker then normal stimulus can trigger AP

A

At supranormal period

73
Q

Impuluse conduction: the speed of depolarization depends on:

A

resting potential

Normal RP gives rapid rise to phase 0

less negative RP results in slower rise of phase 0 and lower maximum amplitude of AP

74
Q

Affect of temperature on heart

A

increases SA node firing via slope of phase 4

see 10 beats/min with 1 degree elevation

75
Q

What effect does Hyperkalemia have on heart

A

increase K+ increaes resting potential: see fast inward current that reduces rate of rise and amplitude of AP… slooooows conduction

Reduces P wave amplitude

widens P-R inderval

decreaes force of cnx

76
Q

How does hyperkalemia accelerate repolarization

A

shortens duration of AP

shortens Q-T inveral

see tall T wave peaks

77
Q

What happens in severe hyperkalemia

A

Disapperance of P wave, AV nodal block and V-fib and sudden death

78
Q

What affect does HYPOkalemia have on

RMP:

AP:

T wave

PR and QT intervals:

A

RMP is decreased

slowing of repolaization and prolongation of AP

T Wave is flattened

P-R and QT intervals are prolongued

79
Q

What happens in severe HYPOkalemia

A

cause AV block and ventricular fibrilation

80
Q

What effect does HYPOcalcemia have on the myocardial action during AP?

A

shortens ventricular AP duration via shortening phase 2 of AP–> thus shortens ST segment == shorter Q-T interval

81
Q

What effect does HYPERcalcemia have on the myocardial action during AP?

A

Prolongues phase 2 of AP and prolongues ST segment thus QT interval

82
Q

Imbalance of what two electrolytes can have serious effects on the heart?

A

K and Ca

83
Q

Mineralcortacoids are key in maintaining:

A

Na and K+.. in ECF: loss of mineralcorticoids can cause lifethreatening abnormalities in electrylyte and fluid balanc

84
Q

As + charge enters heart during depolarization we get a flow of + charge downstream via gap junctions: this produces….

A

discharge of extracellular + charged ions associated with cell membrane and flow of + extracell charge upstream

85
Q

Intracellular and extracellular current must be:

A

equal and opposite

86
Q

How is ECG generated?

A

Extracellular currents produce instantaneous electrical vectors that the ECG measures together throughout the heart

87
Q

P wave is:

A

atrial depolarization

88
Q

QRS complex is

A

ventricular depolarization

89
Q

T wave is

A

ventricular repolarization

90
Q

PR is:

A

AV node conduction

91
Q

QT interval is

A

ventricular depolarization and repolarization

92
Q

Phase 0

A

Na+ influx fast Na+ channel or Ca++ influx in pacemaker cells triggered by depolarization

93
Q

Phase 1

A

Transient repolarization K+ efflux

94
Q

Phase 2

A

Ca++ influx and K+ efflux, plateau d/t small net current flow

95
Q

Phase 3

A

Repolarization mediated by K+effux, decline Ca++ influx. Domiant repolarizating current is Ikr; rapidly activiating repolarization current carried by hERG-KCNE2 gene product (can be targeted by lots of drugs causing AP duration prolongation)

Iks or slow acting repolarizing current aslo contributes to phase 3

96
Q

Phase 4

A

Restoration ionic balance between Na/KATPase exchanger and Ca++ATPase

nonpacemaker cells return to RP

slow phase 4 depolarirzation in pacemaker cells

Funny current If deporarlizing current SA node, influx Na+ and K+

97
Q

Function of K+ channel blockers

A

Increase AP duration and ERF or phase 3

98
Q

Effect of Ca++ channel blockers

A

L-type Ca, slows rate in SA and AV nodes

99
Q

Na channel blockers

A

reduce phase 0 and slope of depolarization

100
Q

Action of Beta Blockers

A

prevent Ca entry into cell

Decrease: HR, conduction velocity, strength of contraction

–Used to tx lots of CVS conditions: HTN, angina or MI and arrythmias

CV (11 decks)

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