2.1.1 Normal Cardiac Electrophysiology Flashcards

1
Q

What is an important cellular feature in the conduction of cardiac action potentials?

A

Gap junctions

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2
Q
A

D. Increased rate of phase 4 depolarization in SA node cells

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3
Q

What effect does sympathetic stimulation have on the calcium window?

A

Larger calcium window (shifts the activation curve towards more negative potentials, which mean they open sooner during depolarization)

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4
Q

What four characteristics does the magnitude of the L-type calcium channel current in the SA and AV nodes determine?

A
  1. Threshold potential
  2. Amplitude of the AP
  3. Rate of rise of the AP
  4. Conduction Velocity (CV)

Note: These are the same characteristics affected by the magnitude of sodium channel current in nervous tissue.

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5
Q

Increasing If will have what effects on MDP and phase 4?

A

Maximum diastolic potential (MDP) will be more positive

Phase 4 more steep (reaching threshold sooner)

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6
Q

Phase 0 depolarization of atrial myocytes is seen as what on the ECG?

A

P wave

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7
Q

Describe the sequence of calcium channel gate configurations as it progresses through a ventricular action potential.

A
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8
Q

What effect does NE have on delayed rectifier K+ current?

A

Increases K+ current by causing the delayed rectifier K+ channel activation gates to open sooner

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9
Q

Increasing SYM firing to the heart will increase ICaL and conduction velocity in the AV node. How will this show up on an ECG?

A

Decreased P-R interval

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10
Q

During what phase of the action potential does the activation gate of the funny sodium channel open?

A

Repolarization

(This is how the funny sodium channel got its name b/c all other voltage-gated channels open during depolarization)

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11
Q

How is a CaL channel opened?

A

Phosphorylation

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12
Q

What effect does norepinephrine have on activation curve of funny sodium channels?

A

It shifts the curve to be more postiive causing the funny sodium channels to open sooner during repolarization

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13
Q
A

B. Potassium current through delayed rectifier potassium channels contributes to the magnitude of the maximum diastolic potential

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14
Q

What are two ways to possibly introduce a reentrant loop into a ventricle?

A

Slow CV (conduction velocity)

Decreased duration of ARP

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15
Q

What does MDP stand for? What is it’s significance?

A

Maximum diastolic potential, most negative potential in the SA node (normally about ~50mV)

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16
Q
A

B. decreased duration of the ventricular AP

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17
Q

What structures of the heart have a calcium-dependent action potential? Describe the shape of this AP.

A

SA node and AV node

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18
Q
A

D. Increased sodium current

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19
Q

Compare and contrast the AV and SA node:

Type of action potential, ionic currents, RMP, firing rate, slope of phase 4

A

Same

Ca-dependent action potential

Same ionic currents at play

No stable resting potential

Different

AV has lower intrinsic firing rate

Phase 4 in the AV node is less steep than SA node

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20
Q

What is happening at the following ECG locations:

P wave

PR interval

QRS complex

ST segment

T wave

QT interval

A

P wave: atrial depolarization

PR interval: P wave plus PR segment (AV node)

QRS complex: ventricular depolarization

ST segment: corresponds to phase 2 of ventricular action potential

T wave: ventricular repolarization

QT interval: QRS complex + ST segment + T wave

21
Q

What are the effects of NE (sympathetic) on ionic currents in the SA and AV nodes?

A

Increased If

Increased ICaL

Increased IK

22
Q

As membrane potential becomes more negative, what happens to the number of open funny sodium channels?

A

The number of open funny sodium channels increases

23
Q

What are the effects on HR and duration of the ventricular AP of sympathetic firing?

A

Increased HR

Decreased duration of the ventricular AP

24
Q

What is true about IK and If at maxium diastolic potential?

A

IK = If

25
Q

Describe the RMP of the SA node?

A

Doesn’t exist. Funny sodium channels and repolarizing potassium channels are always competing against one another.

26
Q
A
27
Q

What are the effects of ACh (parasympathetic) on ionic currents in the SA and AV nodes?

A

Decreased If

Decreased ICaL

Decreased IK (low to moderate vagal activity)

Increased IKACh (high vagal activity)

28
Q

Describe what happens during phase 4, phase 0, and phase 3 of the SA node action potential.

A

Phase 4: pacemaker potential where If (funny sodium current) is > IK

Phase 0: Upstroke of action potential due to ICaL

Phase 3: Repolarizing phase where Ik is > depolarizing currents

29
Q

What is the status of the two gates of a voltage-gated L-type calcium channel at rest?

A

Activation gate closed, inactivation gate open

30
Q

What structures of the heart use a sodium-dependent action potential? Describe the shape of this type of AP.

A

Atrial myocytes, Bundle of His, Purkinje Fibers, Ventricular myocytes

31
Q

What causes the calcium window?

A

The calcium window is due to the overlap of the curves (probability of an open gate)

32
Q

What happens near the end of phase 2 of the ventricular AP that allows the ventricular myocyte to progress into phase 3 (repolarization)?

A

The Ca++ inactivation gates will close. This allows for repolarization due to IK

33
Q

What contracts during the P wave?

A

Atrial muscle

34
Q

Describe how different regions of the heart become excited and the pathway of excitation through the heart.

A
35
Q

Describe the sequence of excitation in the heart including nodes, muscle, and fibers that conduct the action potential.

A
  1. SA node
  2. atrial muscle
  3. AV node
  4. common bundle
  5. bundle branches
  6. Purkinje fibers
  7. ventricular muscle
36
Q

When do the FRP, ARP, RRP occur?

A
37
Q

Sympathetic and parasympathetic control of HR is due the modulation of ionic currents in what part of the heart?

A

SA node

38
Q

What is occuring at the following phases of ventricular action potential:

Phase 4

Phase 0

Phase 2

Phase 3

A

Phase 4: Stable resting potential (inward rectifier potassium channels)

Phase 0: Upstroke due to INa

Phase 2: Plateau phase due to balance b/t ICaL and IK

Phase 3: Repolarization phase due to IK (delayed rectifier potassium channels)

39
Q

Exercise leads to the stimulation of what receptor results in changes of HR?

A

ß-Adrenergic

40
Q

How does sympathetic innervation affect atrial and ventricular myocyte AP?

A

NE, from sympathetic nerves, has no effect on INa but it does increase ICaL and IK. Duration of the ventricular AP is mainly determined by phase 2 and phase 3. If IK is increased, AP duration is decreased as the rate of repolarization is increased (spiked T wave)

41
Q

What are some factors that can increase junction resistance?

A

Increased intracellular sodium

increased intracellular calcium

intracellular acidosis

ischemia and hypoxia

decreased intracellular cyclic-AMP

42
Q

Reduced levels of what within myocytes will impair calcium channel current during the AP?

A

ATP

43
Q

Describe the effects on HR of blocking sympathetic and parasympathetic innervation of the SA node.

A
44
Q

What normally acts as the pacemaker of the heart?

A

SA node

45
Q

Decribe the temporal relationship of the major ionic currents responsible for generating phase 4 depolarization, phase 0 depolarization, and phase 3 repolarization.

A
46
Q

The voltage-gated L-type calcium channel has two gates. What are they and their rates of open and closure?

A

Activation gate: Open and closes rapidly

Inactivation gate: Opens and closes slowly

47
Q

The rate of rise of phase 0 and conduction velocity of the AP through the ventricles and atria are dependent upon what?

A

Magnitude of INa

48
Q

What is the conduction velocity of electrical impulses in the in the AV node? Bundle of His?

A

AV node: ~0.05 m/sec (slowest conduction w/in heart)

Bundle of His: ~2 m/sec

49
Q

Describe the net effects of beta receptors on cardiac currents [Calcium L-type, Potassium delayed rectifier, Sodium funny (SA)] and the pathway through which it causes those effects.

Do the same for M2-muscarinic receptor.

A