11.28 A Flashcards

1
Q

Describe the pathway of electrical conductance through the heart.

A
  • SA node through the atria to the AV node along the internodal pathways
  • AV node to Bundle of His
  • through the left and right bundle branches
  • to the purkinje fibers
  • through the ventricular muscle
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2
Q

If the SA node is damaged, what takes over pacemaking in the heart?

A

usually the AV node

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3
Q

How does conductance along the internodal pathways compare to conductance through the atria?

A

the conduction velocity in the internodal pathway is faster than in atrial muscle, so the AP will reach the AV node before the entire atrial wall has depolarized

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4
Q

Describe the conduction velocity through the AV node.

A

it is much slower than in other areas of the heart

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5
Q

Which action potentials in the heart are calcium dependent?

A

those in the SA and AV nodes

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6
Q

Which action potentials in the heart are sodium dependent?

A

atrial and ventricular myocytes, purkinje fibers, and bundle of his

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7
Q

The P wave of an EKG represents what electrical activity in the heart?

A

atrial depolarization

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8
Q

The ST segment of an EKG represents what event?

A

phase 2 of ventricular action potentials

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9
Q

How does the resting potential of SA node cells differ from that of cardiomyocytes?

A

it is more positive, closer to -50 mV, and it isn’t stable

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10
Q

What molecules give SA it’s unstable resting potential?

A

funny sodium channels

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11
Q

What is phase 0 of an SA node action potential?

A

the upstroke, dependent on calcium current

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12
Q

What is phase 3 of an SA node action potential?

A

the repolarization phase where potassium current outweighs calcium current

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13
Q

What is phase 4 of an SA node action potential?

A

the upstroke of the action potential due to calcium channels

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14
Q

SA node depolarization is dependent on ___ current while SA node repolarization is dependent on ____ currents.

A

calcium; potassium

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15
Q

What is MDP?

A
  • maximum diastolic potential
  • the most negative potential in the SA node
  • equivalent to the resting potential of the SA node
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16
Q

The slope of SA node phase 4 and the value of MDP are dependent on what?

A

the balance between the funny sodium current and hte potassium current

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17
Q

What is the major difference between the action potential in the SA node and AV node?

A
  • the slope of phase IV in the AV node isn’t as steep

- thus the intrinsic firing rate is slower

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18
Q

The intrinsic firing rate is slower in which pacemaker node of the heart?

A

the AV node

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19
Q

How is the funny sodium channel gated?

A

it has a single gate, the activation gate, which opens during repolarization

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20
Q

When do the activation gates of funny sodium channels open during an SA or AV action potential?

A

during repolarization

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21
Q

How are voltage-gated L-type calcium channels gated?

A

a slow opening and closing inactivation gate and a fast opening and closing activation gate

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22
Q

What is the calcium window?

A

the overlap of the calcium inactivation gate opening and the activation gate closing or vice versa

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23
Q

L-type calcium channels in the nodes are equivalent to ____ channels in the myocytes, except that…

A

voltage gated sodium channels except for the existence of the calcium window for the L-type channels

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24
Q

Describe the phases of the ventricular action potential.

A
  • phase 0: upstroke
  • phase 2: stable plateau
  • phase 3: repolarization
  • phase 4: stable resting potential
25
Q

The phase 2 plateau of the ventricular action potential is due to a balance of what currents?

A

potassium and calcium

26
Q

What role do sodium channels play in the ventricular action potential?

A

they create a transient positive current during the upstroke just long enough to open calcium channels

27
Q

What role do calcium channels play in the ventricular action potential?

A

they sustain depolarization after they are opened by the sodium current and oppose the repolarizing potassium current

28
Q

There are many potassium currents that function in the ventricular action potential, but the most important is which?

A

the repolarizing current of phase 3 that is mediated by potassium rectifying channels

29
Q

Via what mechanism does the autonomic nervous system regulate heart rate?

A

G-protein coupled regulation of ionic currents via NE and ACh

30
Q

Sympathetic innervation of the SA node is mediated by what NT?

A

norepinephrine

31
Q

Parasympathetic innervation of the SA node is mediated by what NT?

A

acetylcholamine

32
Q

NE released in the SA node by sympathetic innervations acts on what receptor?

A

beta-1

33
Q

Increased sympathetic firing to the heart will increase heart rate primarily modulating what current?

A

increasing the funny sodium current in the SA node

34
Q

Sympathetic firing to the heart increases what currents?

A

funny sodium and calcium

35
Q

Parasympathetic firing to the heart decreases what currents?

A

funny sodium and calcium

36
Q

How does increased sympathetic firing increase the funny sodium current?

A

by shifting the activation curve for the channels in a less negative direction

37
Q

How do low and high frequency parasympathetic firing to the heart differ in their effects?

A
  • low decreases funny sodium current so the phase 4 slope decreases
  • high decreases the MAD so the cell has further to go to reach threshold
38
Q

Which autonomic innervation of the SA node is in greater control of heart rate under normal conditions?

A

parasympathetic inhibition

39
Q

What is the intrinsic rate of SA firing?

A

110 bpm but it is typically being inhibited and lowered by parasympathetic innervation

40
Q

What current dictates the width of the QRS complex?

A

the sodium current because it determines the rate of rise of phase 0 and conduction velocity of the action potential through the ventricles and atria

41
Q

A spiked T wave will result from an increase in what current?

A

potassium, since it largely dictates the rate of repolarization

42
Q

How does exercise affect the ventricular action potential?

A
  • increased sympathetic nerve firing
  • increased calcium and potassium currents (no change in sodium) in myocytes
  • increased calcium makes phase II of AP more positive
  • increased potassium makes phase III occur sooner
43
Q

How does NE promote the activation of voltage-dependent calcium channels?

A
  • calcium channels must be phosphorylated to open
  • NE acts on a G protein-coupled receptor (beta receptor)
  • the G protein phosphorylates the calcium receptor
44
Q

How will conditions that reduce the level of ATP within myocytes affect the ventricular action potential?

A
  • calcium channels won’t be phosphorylated
  • the duration of the ventricular action potential will be reduced
  • the QT interval will be reduced
45
Q

Sympathetic stimulation does what to the calcium window?

A

it increases it but shifting the activation gate curve towards more negative potentials

46
Q

Why can sympathetic-mediated calcium window increasing cause problems?

A

if the rate of repolarization is slowed, the inactivation gate may reopen before the activation gate has a chance to close

47
Q

Although increasing the calcium window via sympathetic stimulation has the potential to be problematic why isn’t it?

A
  • the possible problem occurs if the rate of repolarization is slowed
  • sympathetic firing will also increase sodium current, though so repolarization usually speeds up with sympathetic firing
48
Q

Describe how parasympathetic firing decreases cardiac currents.

A
  • release of ACh, which binds to an M2-muscarinic receptor
  • activation of an inhibitory G protein
  • inhibition of a kinase
  • less phosphorylation of ion channels
49
Q

Describe how sympathetic firing increases cardiac currents.

A
  • release of NE, which binds a B1 receptor
  • activation of a stimulatory G protein
  • acativation of a kinase
  • more phosphorylation of ion channels
50
Q

Sympathetic firing will ____ heart rate and ___ duration of the ventricular action potential.

A

increase; decrease

51
Q

How do changes in heart rate correlate to changes in duration of the ventricular action potential?

A

they don’t necessarily, the two are independent

52
Q

Which are more prominent, end-to-end gap connections or side-to-side connections?

A

end-to-end ones

53
Q

Is conduction velocity through myocytes faster in a manner parallel or perpendicular to fiber direction?

A

parallel

54
Q

What is anisotropic conduction?

A

the idea that conduction velocity through myocytes is greater in a direction parallel to fiber direction than perpendicular to it

55
Q

How might ischemia impair conduction of the action potentials through the heart?

A
  • ischemia causes reduced metabolic activity
  • this leads to increased intracellular sodium and other ions
  • these increases will increase gap junction resistance
56
Q

What are some factors that increase gap junction resistance?

A
  • increased intracellular sodium
  • increased intracellular calcium
  • intracellular acidosis
  • decreased intracellular cAMP
57
Q

What is the functional refractory period?

A

the refractory period created by the combination of the absolute and relative refractory periods

58
Q

How are refractory periods in cardiomyocytes so important?

A
  • because they prevent an action potential from continuously cycling and propagating through the muscle
  • refractory periods prevent the initial wave of excitation from re-exciting the ventricle
59
Q

A decrease in conduction velocity will likely cause what problem in the heart?

A

it will negate the refractory period and allow the initial action potential to re-excite the ventricle