12/1/2014 Medical Physiology Cardiac Electrophysiology I Eric Olson Flashcards

1
Q

Where are the SA and AV nodes located?

A

The right atrium

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2
Q

Conducting cells are found in what areas of the heart?

A
SA node
atrial internodal tracts
AV node
bundle of His
Purkinje "system"
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3
Q

T/F: Conducting cells can generate APs spontaneously.

A

True

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4
Q

Conducting cells are specialized muscle cells that do not significantly contribute to the generation of force in the heart. How then does the heart contract?

A

Contractile cells.

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5
Q

The AP that began at the SA node spreads to the _____ via the atrial internodal tracts.

A

right and left atria and the AV node

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6
Q

What is the important effect of the AV node having a slow conduction velocity?

A

This ensures that the ventricles have sufficient time to fill with blood before they are activated and contracted.

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7
Q

Where is the bundle of His?

A

Near the AV node, almost in the middle of the atria and ventricles.

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8
Q

Once a AP reaches the bundle of His from the AV node, where does it propagate?

A

common bundle of His –> right and left bundle branches –> smaller bundles in Purkinje system that surround the ventricles –> ventricles.

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9
Q

Conduction velocity is not the same in all myocardial tissue. It is slowest in the __1__ and fastest in the __2__.

A
  1. AV node

2. Purkinje fibers

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10
Q

T/F: Skeletal and cardiac muscle have similar AP arcs.

A

False. The skeletal muscle AP happens over 0-20 msec, and it monophasic (up, down, nothing fancy). The cardiac AP can be 300-400 msec and is triphasic (up, down an bit, up, arc down). See page 245 in notes.

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11
Q

In Phase 0 of the ventricular AP, the upstroke, there is a transient increase in what ion?

A

Na+

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12
Q

What is dV/dt?

A

Rate of rise of membrane potential in the upstroke of the ventricular AP.

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13
Q

Phase 1 in the ventricular AP is known as:

A

initial repolarization

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14
Q

The plateau in the ventricular AP curve is what phase?

A

2

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15
Q

Repolarization in ventricular AP curve is what phase?

A

3

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16
Q

Phase 4 in the ventricular AP curve is known as:

A

resting membrane potential or electrical diastole

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17
Q

What ions are going where in Phase 1 of the ventricular AP curve?

A

Na+ gates close, no more Na+ going in;

Outward K+ current cause by large driving force of K+ ions.

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18
Q

What ions are going where in Phase 2 of the ventricular AP curve?

A

Inward Ca2+ current;

Outward K+ current.

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19
Q

What ions are going where in Phase 3 of the ventricular AP curve?

A

Decrease in inward Ca2+ current;
Increase in outward K+ current, followed by a decrease in outward K+ as membrane potential approaches K+ equilibrium potential.

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20
Q

What is the resting membrane potential of cardiac muscle?

A

-85 mV

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21
Q

What ions are going where in Phase 4 of the ventricular AP curve?

A

Na and Ca2+ in, K+ out, all in net equilibrium as cell is repolarized.

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22
Q

The effective refractory period in myocardial muscle is?

A

Right after the absolute refractory period. Still very unlikely to generate an AP.

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23
Q

T/F: All parts of the heart, ie SA node, common bundle, Purkinje fibers etc. have a characteristic AP curve.

A

True. They are all a bit different. See page 247 in notes.

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24
Q

The duration of the AP in cardiac muscle determines the duration of what?

A

The refractory period. 1:1 ratio

25
Q

The AV node and what other tissue can become pacemakers in a pinch, and develop unstable resting membrane potentials to help the heart pump.

A

Purkinje fibers

26
Q

What is the only part of the heart whose upstroke is not characterized by an inward Na+ current?

A

SA node, has inward Ca2+ current instead.

27
Q

What tissue has the shortest myocardial AP, and what has the longest?

A

SA node and atrium both have 150 ms AP duration;

Purkinje fibers have 300 ms AP duration. (Ventricles have 250 ms duration).

28
Q

What is considered a normal heartbeat, corresponding with the normal range of SA node pacemaker firing?

A

60-100 bpm

29
Q

What is a typical AP of the SA node like?

A

Phase 4 at about -65mV (repolarized) rising, Phase 0 upstroke to 0 mV, Phase 3 falling steeply but no arc, back to Phase 4, from

30
Q

V-dep and L-type channels are most known for their involvement in what?

A

SA node calcium channels, open to start upstroke –> massive Ca2+ influx.

31
Q

What causes pacemaker activity in SA node?

A

Interaction between I-Ca (T-type channels), I-K and a special current, deemed I-f (funny current).

32
Q

I-f is also known as:

A

the pacemaker current.

33
Q

Why is I-f “funny?”

A

It activates in response to hyperpolarization, not depolarization. It has both an inward Na+ component and an outward K+ component.

34
Q

The effects of the autonomic (S and PS) nervous system on the heart are called:

A

chronotropic effects - S stimulation –> positive chronotropic effect; PS stimulation –> negative chronotropic effect.
The SA node has neuronal input

35
Q

What part of the SA node AP changes with sympathetic stimulation?

A

Phase 4 rate is increased (meaning Phase 4 is shorter) leading to frequency of APs

36
Q

What part of the SA node AP changes with parasymmpathetic stimulation? As with the opposite of stimulation of the sympathetic nervous system, Phase 4 rate is decreased, but somthing else also happens to create the negative chronotropic effect. What is it?

A

PS activation also hyperpolarized the maximum diastolic potential to decrease the frequency of APs.

37
Q

Describe the vagal brake signaling pathway to reduce the heart rate.

A

Vagal activity (Cn X) –> ACh released at SA node –> ACh binding to and activation of M2 receptors –> Activation of Gi –> decrease in cAMP –> Phase 4 rate is slower

38
Q

In parasympathetic inhibition of the SA node, Phase 4 steepness is reduced by a number of factors. What are they?

A
  1. Reducing inward I-f
  2. Reducing inward I-CaT
  3. Increasing outward I-KACh
    Also, threshold of I-CaL is at a more positive value.
39
Q

Describe the sympathetic stimulation pathway that leads to increased heart rate.

A

Norepi binds to B-1 adrenegic receptors (metabotropic) –> Gs activated –> AC activated –> cAMP increases –> pacemaker rate increases

40
Q

In sympathetic stimulation of the SA node, does Phase 4 get steeper or less steep?

A

Steeper, leading to faster rates of depolarization.

Steeper due to increasing inward I-f and increasing inward I-CaT; threshold of I-CaL at more negative value.

41
Q

Cardiac APs are propagated through gap junctions. In this way, the atria and ventricles are both _____ of cells.

A

Syncytia

42
Q

What proteins make up gap junctions

A

Connexins

43
Q

Like SA node cells, AV node cells have:

A

an instrinsic pacemaker activity

44
Q

T/F: Sympathetic and parasympathetic influence can act on the AV node as well as the SA node.

A

True

45
Q

The intrinsic firing rate of the AV node is:

A

40 bpm

46
Q

The intrinsic firing rate of the Purkinje fibers is:

A

< 20 bpm and irregular

47
Q

What is the source of the pacemaker current in the Purkinje fibers?

A

The funny current

48
Q

What is the order of ventricular muscle activation?

A

Ventricular apex (endo to epicardium) –>via Purkinje fibers –> ventricular base (top) (endo to epicardium) = coordinated contraction

49
Q

What are the refractory periods of the ventricular AP?

A
  1. Absolute (biggest)
  2. Effective (Absolute + a bit longer)
  3. Relative (Overlaps slightly with Effective)
  4. Supranormal period
    See page 265 in notes for graph.
50
Q

When does the supranormal period occur?

A

In ventricular AP, it begins last, at about -70, going to -85 mV. The cell is more excitable than normal during this period.

51
Q

What is the intrinsic firing rate of the Bundle of His?

A

About 40 impulses/min

52
Q

What happens if the intrinsic firing rate of one of the pacemakers should become faster than that of the SA node?

A

The latent pacemaker takes over

53
Q

Parasympathetic effects on the heart always involve what kind of receptor?

A

Muscarinic

54
Q

Alpha-1 and Beta-2 both act on the vasculature during SNS stimulation. What are their effects?

A

Alpha-1 –> Constriction (vascular smooth muscle ie splanchnic)
Beta-2 –> Dilation (skeletal)

55
Q

Name two beta blockers and say what they do:

A

Slow heart rate by blocking Beta-1 receptors in heart, “cardioselective”
Propranolol
Atenolol

56
Q

Name an agent that affects muscarinig ACh receptors and when it would be administered.

A

Atropine, during CPR

Blocks M2 receptors leading to tachycardia

57
Q

A nerve agent which inhibits acetylcholinesterase has what effect on the heart?

A

Bradycardia, ie sarin gas (also causes convulsions and death, think Japanese terrorist attack)

58
Q

Some antidepressants affect heart rate, how?

A

They block the reuptake of norepi, ie Prozac and elavil, leading to increased heart rate