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SMP - Cardiopulmonary Exam 1 > Lectures 9 & 10 - Cardiac Electrophysiology > Flashcards

Lectures 9 & 10 - Cardiac Electrophysiology Flashcards

1
Q

Number of sudden cardiac arrests in the US each year?

A

250,000

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2
Q

What are the 3 requirements for effective ventricular pumping?

A
  1. Contraction of atria/ventricles is controlled by an AP and to ensure that they do not contract simultaneously there must be a substantial delay in the AP going to the ventricles
  2. When the AP spreads across the ventricles it results in almost synchronous contraction (syncytium) via gap junctions to allow for forceful ejection of blood from the heart
  3. There cannot be tetanus like in skeletal muscle because the heart cannot stay contracted for a long time or else it will not properly fill - instead it must contract quickly and forcefully thanks to long absolute refractory periods
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3
Q

How long is the AP generated by the SA node? How does this compare to the AP in skeletal muscle and nerves?

A

0.2 seconds

Much longer (100 fold)

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4
Q

Is the AV node closer to the tricuspid or mitral valve on the IV septum?

A

Tricuspid valve

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5
Q

What causes the AP delay at the AV node?

A

Increased resistance within the cells

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6
Q

Describe the pathway of the heart conduction system.

A

Impulse signaling begins at SA node => impulses spread in a wave along cardiac muscle fibers of atria, signaling atria to contract => some impulses travel along the internodal pathway => AV node => impulse delay for fraction of a second => impulses pass through the AV bundle => impulses divide into R and L bundle branches => halfway through septum they become the subendocardial branches of Purkinje fibers => subendocardial branches approach heart apex and arc superiorly to ventricular walls => ventricular myocardial contraction begins at apex in endocardium and then epicardium

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7
Q

Are cardiac cells myelinated?

A

NOPE

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8
Q

What allows the cardiac cells to have a high conduction velocity?

A

They are large

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9
Q

What is the AV separation made of? Role?

A

Fibrous rings of dense connective tissue => act as an electrical insulator

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10
Q

Describe the APs in the different elements of the heart’s conduction pathway.

A

SA/AV nodes AP is much different from that of the rest of the working cells:

  1. Unstable diastolic potential because slow rising vs the working cells have a very fast depolarization
  2. AP does not have a plateau vs working cells have a plateau and then a slow repolarization
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11
Q

What are the 6 components of the heart conduction system?

A
  1. Sinoatrial node (SA)
  2. Internode fibers
  3. AV node
  4. Atrioventricular bundle
  5. R and L bundle branches
  6. Subendocardial branches of Pujinke fibers
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12
Q

What are “working” cardiac cells?

A

Those that contract myocytes:

  1. Atrial muscle cells
  2. Ventricular muscle cells
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13
Q

Describe the 5 phases of the ventricular AP.

A
  1. Phase 0 = Fast depolarization: controlled by the VG Na+ channels opening when threshold is reached
  2. Phase 1 =
    - Small repolarization due to transient K+ channels
    - Inactivation of VG Na+ channels
  3. Phase 2 = Plateau/Systole:
    - Opening of L and T type VG Ca++ channels allowing influx
    - Opening of delayed rectifier K+ channels with low permeability
    - T-type VG Ca++ channels quickly inactivate
  4. Phase 3 = Repolarization:
    - L-type VG Ca++ channels slowly inactivate (major contribution)
    - Delayed rectifier K+ channels are still open
    - Opening of weak conductance inward-rectifying K+ channels (late and minor contribution)
  5. Phase 4 = Diastolic/resting state: cell hyperpolarizes and this phase is mediated by STRONG current inward-rectifying K+ channels which close when the membrane starts depolarizing again
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14
Q

Describe the kinetics of the ventricular VG Na+ channels.

A

Open and inactive quickly

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15
Q

Which ions are essential for all of the blood to be pumped out of the ventricles?

A

Ca++

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16
Q

What 3 ion channels contribute to the plateau in the ventricular AP?

A
  1. Strong L-type VG Ca++ channels
  2. Absence of inward-rectifying K+ channels open
  3. Weak repolarizing K+ current aka weak delayed rectifier current
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17
Q

What are delay rectifier VG K+ channels? Do cardiac muscle cells have them?

A

VG K+ channels used in skeletal muscle which cause the undershoot because take a while to close

They do! BUT, their conductance is lower than in skeletal muscle

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18
Q

Describe the RMP of cardiac ventricular cells. What is it due to?

A

Very negative = -90mV

Close to the equilibrium potential of K+ because ratio of K+ leak channels to Na+ lead channels is 10,000:1 (instead of 100:1 in skeletal muscle cells)

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19
Q

Difference between delay rectifier VG K+ channels and inward rectifier K+ channels?

A
  1. Delay rectifier VG K+ channels: open during depolarization and true VG channel
  2. Inward rectifier K+ channels: open at hyperpolarized RMP and not true VG channel
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20
Q

Do inward rectifier K+ channels cause repolarization of ventricular cells?

A

NOPE, not mainly

The delayed rectifier VG K+ channels are the major responsible channels

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21
Q

What is the role of the Na/Ca exchanger during the ventricular AP? How does it work? When does it turn off?

A

It pumps 3 Na+ for 1 Ca++ in => +1 effect in the direction of the Na+ ions

2 separate actions that both poorly oppose the ion movements during cardiac AP:

  1. Phase 0: when Na+ rushes in through the cell the exchanger works to pump Na+ out of the cell (positive Na+ current)
  2. Phase 2: as the Na+ channels inactivate and the VG Ca++ channels open the exchanger switches direction and actively pumps out Ca++ (negative Na+ current)

Exchanger’s activity is decreased when L-type Ca++ channels inactivated during diastole, but it does not completely stop as it help to keep the internal Ca low

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22
Q

In which cardiac cells are the T-type VG Ca++ channels more prominent?

A

SA and AV node cells

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23
Q

In which cardiac cells are the inward rectifier K+ channels not found?

A

SA and AV node cells, although they have GIRKS which respond to ACh

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24
Q

Negative current: inward or outward?

A

Inward

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25
Q

Positive current: inward or outward?

A

Outward

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26
Q

What are 3 less important ion channels in cardiac cells?

A
  1. ICl: constant Cl- leakage current that helps repolarize the cell
  2. Ipump: Na/K pump that is always active and is important to restore the steady state
  3. IK(ACh): another type of inward rectifier K+ channel that is strongly activated by ACh during end of phase 3 and phase 4
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27
Q

How does the vagus nerve slow down the heart?

A

ACh release on inward rectifier K+ channels at the SA node slows down the heart rate

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28
Q

What is the one cardiac cell K+pump that is only active during pathological conditions? Explain.

A

IK(ATP): these channels are usually inhibited/blocked by the ATP inside the cardiac cells. However, during myocardial infarction ATP levels inside the cell drop, so these channels will open which causes a large outflow of K+ ions, depleting the intracellular [K+] => RMP depolarization

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29
Q

Describe the electrochemical gradients governing in phase of the ventricular AP.

A
  1. Phase 0 = Na+ electrical AND chemical gradient cause ions to rush IN the cells
  2. Phase 1 = K+ electrical AND chemical gradient cause ions to rush OUT of the cells
  3. Phase 2 = Plateau/Systole:
    - Ca++ chemical gradient overrides electrical gradient and rushes IN the cells
    - K+ electrical AND chemical gradient cause ions to rush OUT of the cells
  4. Phase 3 = Repolarization:
    - K+ chemical gradient overrides electrical gradient and rushes OUT of the cells
  5. Phase 4 = Diastolic/resting state:
    - K+ chemical gradient stronger than electrical gradient => electrochemical equilibrium (Ek) => NO NET CURRENT but K+ flowing both in and out
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30
Q

Which are stronger in all phases of the ventricular AP: electrical or chemical gradients?

A

Chemical

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31
Q

What causes Ca+ release by the SR in cardiac cells? What is this called?

A

Ca++ on ryanodine channels => Ca-induced Ca release

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32
Q

How does the AP of a Purkinje fiber differ from the AP of a ventricular cell?

A

Similar, but the rise in intracellular Ca++ and the produced tension is minimal

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33
Q

How does cardiac muscle cell contraction occur?

A

Just like in skeletal muscle with Ca++ activating myosin and actin with the same cross-bridge cycling

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34
Q

How is Ca++ pumped out of cardiac muscle cells after contraction?

A
  1. Taken up by SR by ATP-dependent pump: Ca-ATPase pump

2. Pumped out of the cell through Na/Ca exchanger

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35
Q

What determines the amount of time during which the ventricles push blood through the body during systole aka for how long the cells are contracted?

A

Duration of ventricular AP

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36
Q

Is there a delay in contraction of cardiac cells following AP like in skeletal muscle cells? Why or why not? What does this mean?

A

NOPE because the series elastic element has less of an effect on cardiac muscle cells and because the cardiac AP is so much longer

AP and contractile response overlap (contractile response often outlasts the AP)

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37
Q

Length of ventricular AP? What is this?

A

350-400 msec = length of systole

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38
Q

Waves of ventricular AP on extracellular recording of a single cardiac cell? What does this resemble?

A
  1. QRS complex = ionic movement during phase 0 => depolarization
  2. Line between S wave and T wave = Phase 1 and 2 with little ion movement
  3. T wave = repolarization during phase 3

=> EKG recording

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39
Q

What does the length of the Q-T interval correspond to?

A

Duration of ventricular AP

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40
Q

Describe the AP of pacemaker cardiomyocytes. What is this called? When is this same mechanism observed in pathology?

A
  1. Cell membrane potential is GRADUALLY depolarized, which GRADUALLY activates and inactivates VG Na+ channels, therefore the influx of Na+ is small
  2. However, during the gradual and slow depolarization the L-type VG Ca++ channels GRADUALLY open, along with various other currents aka the “funny current” which generate the pacemaker potential until threshold
  3. VG Ca++ channels all open => AP
  4. As the L-type VG Ca++ slowly close, the delayed rectifier K+ channels open and cause repolarization and hyperpolarization

Pathology: ischemia in ventricular cells

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41
Q

Do pacemaker cardiomyocytes cells have inward rectifier K+ channels?

A

NOPE

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42
Q

What does the rate of spontaneous discharge of pacemaker cells depend on?

A
  1. Magnitude of diastolic prepotential: the potential at the beginning of diastole after the cell has repolarized
  2. The rate of diastolic depolarization
  3. Level of the threshold potential
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43
Q

Do cardiac muscle cells have a threshold to fire APs?

A

YUP

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44
Q

What does the heart rate depend on?

A

The slope of funny current of pacemaker cells

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45
Q

What ions make up the funny current?

A

Na+, K+, Ca++

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46
Q

What would a fast depolarization of pacemaker cells cause?

A

Tachycardia

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47
Q

What would a slow depolarization of pacemaker cells cause?

A

Bradycardia

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48
Q

Notation for funny current?

A

If

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49
Q

Overall definition of the funny current?

A

Current causing diastolic depolarization of the pacemaker cells which involves multiple ion currents

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50
Q

What other theory has been proposed to explain the rate of depolarization of cardiac pacemaker cells?

A

As the funny current is happening, some Ca++ is entering the cells through L-type and T-type Ca++ channels slowly opening, and some through the funny current. This jump starts the Na/Ca exchanger to bring sodium inside the cell, causing further depolarization.

Therefore, both the funny current and entry of sodium through the exchanger contribute to diastolic depolarization which eventually reaches threshold and causes all of the L-type Ca++ channels to open during the upstroke of the AP

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51
Q

What % of cardiac cells are pacemaker cells?

A

1%

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52
Q

What would happen without the LONG absolute refractory periods of the heart cells?

A

Arrhythmia

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53
Q

Review of skeletal AP?

A
  1. Threshold reached causes Na+ VG channels to open causing depolarization close to sodium’s equilibrium potential
  2. Na+ VG channels inactivate (absolute refractory period)
  3. Delay-rectifier VG K+ channels open and cause repolarization
  4. Undershoot due to delay-rectifier K+ channels (relative refractory period)
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54
Q

Are the APs in all working cardiac muscle cells the same as in the ventricular muscle cells?

A

YUP

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55
Q

Are the myocyte’s inward rectifier K+ channels leaky channels?

A

YUP

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56
Q

When do the myocyte’s inward rectifier K+ channels open? Purpose?

A

When the cell is HYPERpolarized

To make sure the heart fills properly during diastole

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57
Q

When do the myocyte’s inward rectifier K+ channels close?

A

When the cell depolarizes

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58
Q

What phases of the ventricular cell AP correspond to systole? Diastole?

A
  1. Systole = 0, 1, 2, 3

2. Diastole = 4

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59
Q

Notation of inward rectifier K+ channels?

A

IKr or IK1

60
Q

Other name for L-type CA++ channels?

A

Dihydropyridine channels

61
Q

Notation of delayed rectifier K+ channels?

A

IK

62
Q

What 4 ion channels are responsible for the repolarization of muscle ventricular cells?

A
  1. Weak delayed rectifier VG K+ channels
  2. Inactivation of VG Na+ channels
  3. Inactivation of VG Ca++ channels
  4. Gradual opening of inward rectifier K+ channels
63
Q

In which cardiac cells are the K(ACh) channels more prominent?

A

SA and AV node

64
Q

What happens to ionic currents during a stroke?

A

[K+] extracellular increases, causing depolarization

65
Q

What triggers excitation contraction coupling in cardiac cells? Explain the 4 steps

A
  1. L-type VG Ca++ channels MAINLY (and other pathways) let Ca++ flow in the cells
  2. Depolarization stimulates release in intracellular Ca stores from subsarcolemma and SR
  3. Contraction via cross-bridges
  4. Calcium is reuptook intracellularly and also pumped out of the cell
66
Q

What does the lack of delay between the cardiac AP and the contractile response mean for summation?

A

NO temporal summation is possible in cardiac muscle

67
Q

How does the length of the cardiac AP compare to the absolute refractory period in cardiac cells?

A

SAME amount of time

68
Q

What fraction of the cardiac cycle does the cardiac AP comprise AT REST?

A

~1/3

69
Q

Heart rate of 60 beats/min: what is the cardiac cycle length? Systole/diastole breakdown AT REST?

A

1000 ms = 350 systole + 650 diastole

70
Q

Describe the ion currents at threshold.

A

VG Na+ channel conductance = K+ inward rectifying channel conductance

71
Q

Threshold of cardiac cells?

A

-75 mV

72
Q

What are the 5 areas of the heart that have pacemaker capability?

A
  1. SA node
  2. AV node
  3. Bundle of His
  4. Bundle branches
  5. Purjinke fibers
73
Q

What special characteristic do cardiac pacemaker cells exhibit?

A

Automaticity

74
Q

Describe the parasympathetic control of the heart.

A

Slows down heart rate by:

  1. Decreasing the rate of diastolic depolarization in SA node cells via vagal innervation and ACh release onto G-protein inward rectifier K+ (GIRK) channels => hyperpolarization of the cells => will take longer for the pacemaker potential (aka funny current) to generate an AP
  2. Decreasing AV node conduction (minor compared to #1)
75
Q

Describe the sympathetic control of the heart (5 effects). Name each effect.

A
  1. CHRONOTROPIC EFFECT: release of NE and EPI on pacemaker cells triggers cAMP mediated phosphorylation of L-type VG Ca++ channels, making them last longer and be more efficient => increased intracellular Ca++ concentrations => faster activation of Na/Ca exchanger => increased rate of diastolic depolarization => increased HR
  2. CHRONOTROPIC EFFECT: Affects funny current of pacemaker cells by increasing Na+ conductance => increased rate of diastolic depolarization => increased HR
  3. DROMOTROPIC EFFECT: Enhances AV node conduction
  4. Enhances automatic/spontaneous activity in pacemaker cells (sometimes ventricular cells, which is pathological)
  5. INOTROPIC EFFECT: Increases contractility of all working cells
76
Q

Other name for heart rate?

A

Sinus rate

77
Q

What can be said of the sympathetic control of the heart?

A

It is very diffuse, not just localized to the SA node

78
Q

How frequently do the Purjinke fibers generate APs compared to the AV node?

A

Half as frequently

79
Q

How frequently does the AV node generate APs compared to the SA node?

A

Half as frequently

80
Q

Through what mechanism does the SA node control the AV node and the Purjinke fibers’ rates of firing?

A

Overdrive suppression

81
Q

What allows overdrive suppression?

A

During the firing by the SA node, the large amount of Na+ in and K+ out stimulates the Na/K pump to work more, and the enhancement of this pump causes it to continue for a little while during overdrive suppression creating a larger outward Na+ current that slightly hyperpolarizes the cells of the other pacemaker cells => this prevents spontaneous depolarizations

82
Q

What happens when overdrive suppression stops?

A

Pacemaker activity of the other “downstream” pacemaker cells starts

83
Q

How is the length of the cardiac AP affected by an increased HR (tachycardia)? What mechanism underlies this effect?

A

It is shortened because when HR increases, the heart spends less time in diastole

This means the heart needs to spend less time in systole, to allow for appropriate ventricular filling

Activity dependent increase of delayed rectifier VG K+ channels underlies this effect

84
Q

What are cardiac cell intercalated disks?

A

Points of connection between cardiac cells containing gap junctions that allow the spread of depolarization and desmosomes

85
Q

Are the atria and ventricles electrically connected?

A

NOPE, except at the AV node

86
Q

What 3 main characteristics determine the velocity of the impulse conduction through the heart?

A
  1. Upstroke velocity of the AP
  2. Size of the cells and their internal complexity
  3. Number and complexity of gap junctions between the cells
87
Q

What does the size of cardiac cells and their internal complexity affect conduction velocity?

A
  1. Size: the larger the cell => the lower the internal resistance => the faster the conduction velocity
  2. Myofibril density and large sarcoplasmic reticulum will increase internal resistance and lower the space constant, slowing down the conduction velocity
88
Q

In what cardiac cells are the fastest conduction rates seen? Why?

A

Cells in Bundle of His and Purkinje because they are very large and have very few myofibrils

89
Q

Why do the cells of the AV and SA node have slower conductance?

A

Because they are made of smaller cells

90
Q

Describe the resistance in gap junctions?

A

Lower

91
Q

Can gap junctions close?

A

YUP

92
Q

How can dysfunctional gap junctions worsen myocardial infarctions?

A

During MI, parts of the heart is not receiving blood and therefore those cells lose their ionic gradients and are unable to conduct the electrical signal to other cells.

If the gap junctions surrounding these cells do not close, then the signal will stop at these cells and they will be firing asynchronously or not at all, causing death

93
Q

What % of cardiac cells are worker cells?

A

95%

94
Q

Are cardiac worker cells resistant to fatigue?

A

YUP

95
Q

Are cardiac worker cells structurally similar to skeletal muscle cells?

A

YUP, except that they are very branched and form a syncytium through intercalated disks

96
Q

Describe the electrophysiology taking place during myocardial ischemia.

A
  1. No O2 => no oxidative phosphorylation => excess H+ in mitochondria pumped out in cytoplasm => intracellular pH drop => gap junctions close in an attempt to isolate the defective tissue
  2. Decrease in ATP => Ca-ATPase pump no longer working => increase in intracellular Ca++ => depolarized sarcolemma
  3. ATP-gated K+ channels open => Na/K ATPase pump fails => increase in extracellular [K+] between cardiac cells and at T-tubules => Ek increases (less negative) => RMP depolarization => increased inactivation of Na+ VG channels (and some Ca channels) => slower upstroke of AP and decreased AP amplitude => decrease in conduction velocity and APs may even need to be caused by VG Ca++ channels OR even worse, no AP at all
97
Q

What ion channel opens during excessive stress response? Explain

A

Ins (non-specific cation channel) => pathological response causing automaticity of ventricular cardiac cells risking them to trigger other APs during Phase 4

98
Q

Are conduction specialized cardiac cells also muscle cells?

A

YUP

99
Q

By convention, what is current defined by?

A

Flow of positive ions

100
Q

Conduction velocity of His bundle?

A

2 m/s

101
Q

Conduction velocity of AV fibers?

A

0.05 m/s

102
Q

Conduction velocity of myelinated neurons?

A

50 m/s

103
Q

Does the RMP affect conduction velocity?

A

YESSSS

RMP depolarization => inactivation of Na+ VG channels => slower upstroke of AP => decrease in conduction velocity

104
Q

Does the length of the plateau phase of ventricular APs affect conduction velocity?

A

NOOOOOOOO

105
Q

How do the APs differ in the endocardium and the epicardium? What does this mean?

A
  • Endorcardium: happen first and are longer
  • Epicardium: happen after and are shorter

The depolarization travels from inside the heart to outer layer surface and repolarization travels in the opposite direction

106
Q

What can a boxer getting punched in the heart cause?

A

Closing of gap junctions and arrhythmias, leading to potential fibrillation

107
Q

What is fibrillation? Treatment?

A

Rapid, irregular, and unsynchronized contraction of muscle fibers

Electrical shock to depolarize them all at once and resynchronize the cardiac cells

108
Q

Is the inward rectifier K+ channel a VG channel?

A

NOPE, it’s just voltage sensitive (through complicated mechanisms), but structurally it’s a leakage channel

109
Q

What is an AV block?

A

Impaired conduction between atria and ventricles

110
Q

Could you ablate certain portions of the heart to treat arrhythmias?

A

YUP

111
Q

Do cardiac pacemaker cells have an RMP?

A

NOPE, the diastolic potential is NOT an RMP

112
Q

What ions are flowing during the “funny current”?

A

Na+, Ca++, K+

113
Q

How to write out the rate of depolarization of cardiac pacemaker cells?

A

dV/dt

114
Q

Do both the funny current and local calcium concentration modulation equally contribute to the pacemaker potential?

A

YUP

115
Q

Can Purkinje cells contract?

A

NOPE

116
Q

Are cardiac muscles made of red or white fibers? What does this mean?

A

Red: perform oxidative phosphorylation to produce ATP

117
Q

Why is the absolute refractory period of cardiac cells so long?

A

Because the calcium ions coming in keep the cells depolarized aka the Na+ CG channels inactivated

118
Q

How is the AP affected my myocardial ischemia?

A

APs are Smaller, Shorter, and Slower due to main effect on Phase 0 of the AP

THE AP BECOMES INCREDIBLY SMALL to the point that it cannot generate contractility => localized region of non contractility

119
Q

How is K+ permeability affected during myocardial infarction?

A

Increased! IK(ATP)

120
Q

Where are gap junctions sparse in the heart?

A

SA and AV node

121
Q

What is the length of the AP in a ventricular cell dependent on?

A

Action potential duration is dependent on the preceding cycle length, which is dependent on the heart rate

122
Q

What is the diastolic potential of SA and AV node cells?

A

-60 mV

123
Q

What is overdrive suppression preceded by?

A

A period of rapid beating and then a pause before pacemaking activity starts

124
Q

What is observable following acute AV block?

A

Overdrive suppression

125
Q

Does overdrive suppression usually resolve spontaneously?

A

YUP

126
Q

Do cardiac muscle cells use chemical transmission for intercellular communication?

A

NOPE, electrical

127
Q

Is cardiac muscle striated?

A

YUP

128
Q

Diameter range of cardiac cells?

A

2-17 micrometers

129
Q

Is contraction of ventricular muscle cells controlled by sodium influx?

A

YUP

130
Q

Will MI cause increased extracellular Ca++?

A

NOPE - no ATP mediated Ca pump on plasma membrane

131
Q

Why is the absolute refractory period of cardiac cells very long?

A

Because of the LONG AP

132
Q

How does exercise affect the heart’s electrophysiology?

A

Increased HR => AP is shorter => risk of extra systole

133
Q

Where are the terminal filaments of the Purkinje fibers located in the RV and LV?

A
  • RV: start at apex and go up the lateral wall

- LV: start in IV septum and go up the lateral wall

134
Q

Are Purkinje cells conducting or working cells?

A

Conducting

135
Q

Is spatial summation possible in cardiac myocytes?

A

Possible but irrelevant because almost all of their Na+ VG channels open to cause contraction so would not make a difference

136
Q

What 2 parameters are affected by increased rate of depolarization of cells of the SA node?

A
  1. Conduction velocity is increased

2. HR is increased

137
Q

What are we referring to when speaking of “diastolic depolarization”

A

Depolarization of pacemaker cells ONLY

138
Q

What is the difference between upstroke velocity and depolarization rate?

A
  • Upstroke velocity refers to AP of working cells in heart

- Depolarization rate of pacemaker cells

139
Q

Is the AP upstroke in pacemaker cells carried primarily by Na+?

A

NOPE, some sodium in the funny current will help pacemaker cells reach threshold, but the upstroke is due to Ca++ through L-type channels

140
Q

Are the APs at the SA and AV nodes shorter since they do not have a plateau?

A

YES

141
Q

What portion of the SA node AP is the funny current?

A

End of repolarization of previous AP + pacemaker potential portion

142
Q

Do ventricular cells and neurons have a similar influx of Na+ during depolarization?

A

YES

143
Q

Difference between delayed rectifier channels in ventricular and pacemaker cells?

A

More dominant in pacemaker cells

144
Q

Can cardiac cells contract if we remove extracellular calcium and electrically stimulate them?

A

NOPE - need calcium induced calcium release for them to contract

145
Q

Where is the AP the longest in the whole heart conduction system? List all of them. What does this depend on?

A

Length of AP depends on if another AP should be prevented elsewhere:

  1. Longest AP at AV bundle because needs to prevent all cells further in pathway from spontaneously depolarizing
  2. Bundle branches
  3. Purkinje fibers
  4. Ventricular muscle
  5. SA node
  6. Atrial muscle
  7. AV node
146
Q

Diastolic potential of SA and AV node cells?

A

-60 mV

SMP - Cardiopulmonary Exam 1 (28 decks)

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