2.1.1 Normal Cardiac Electrophysiology Flashcards by Miles Sanderson

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

Gap junctions

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

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What effect does sympathetic stimulation have on the calcium window?

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

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

Threshold potential
Amplitude of the AP
Rate of rise of the AP
Conduction Velocity (CV)

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

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

Maximum diastolic potential (MDP) will be more positive

Phase 4 more steep (reaching threshold sooner)

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

P wave

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

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

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

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

Decreased P-R interval

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

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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How is a CaL channel opened?

Phosphorylation

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

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

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

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

Slow CV (conduction velocity)

Decreased duration of ARP

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

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

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B. decreased duration of the ventricular AP

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

SA node and AV node

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D. Increased sodium current

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Compare and contrast the AV and SA node:

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

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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What is happening at the following ECG locations:

P wave

PR interval

QRS complex

ST segment

T wave

QT interval

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

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

Increased I_f

Increased I_CaL

Increased I_K

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

The number of open funny sodium channels increases

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

Increased HR

Decreased duration of the ventricular AP

What is true about I_K and I_f at maxium diastolic potential?

I_K = I_f

Describe the RMP of the SA node?

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

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

**Decreased I_f** **Decreased I_CaL** Decreased I_K (low to moderate vagal activity) Increased I_KACh (high vagal activity)

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

Phase 4: pacemaker potential where I_f (funny sodium current) is \> I_K Phase 0: Upstroke of action potential due to I_CaL Phase 3: Repolarizing phase where I_k is \> depolarizing currents

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

Activation gate closed, inactivation gate open

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

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

What causes the calcium window?

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

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

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

What contracts during the P wave?

Atrial muscle

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

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

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

When do the FRP, ARP, RRP occur?

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

SA node

What is occuring at the following phases of ventricular action potential: Phase 4 Phase 0 Phase 2 Phase 3

Phase 4: Stable resting potential (inward rectifier potassium channels) Phase 0: Upstroke due to I_Na Phase 2: Plateau phase due to balance b/t I_CaL and I_K Phase 3: Repolarization phase due to I_K (delayed rectifier potassium channels)

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

ß-Adrenergic

How does sympathetic innervation affect atrial and ventricular myocyte AP?

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

What are some factors that can increase junction resistance?

Increased intracellular sodium increased intracellular calcium intracellular acidosis ischemia and hypoxia decreased intracellular cyclic-AMP

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

ATP

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

What normally acts as the pacemaker of the heart?

SA node

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

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

Activation gate: Open and closes rapidly Inactivation gate: Opens and closes slowly

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

Magnitude of I_Na

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

AV node: ~0.05 m/sec (slowest conduction w/in heart) Bundle of His: ~2 m/sec

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.