Cardiac Action Potentials Flashcards

1
Q

What is the route of the cardiac conduction system?

A

SA Node –> Atria (which contracts/depolarizes) –> AV node –> Bundle of His –> RBB and LBB –> Purkinje Fibers on each side –> lateral walls of the ventricles

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2
Q

Which layers receives AP first?

A

Endocardium of ventricles receive AP prior to epicardium. Right epicardium before left.

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3
Q

Describe importance of fiber size

A

Large fibers have a faster AP transmission and greater velocity

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4
Q

Conduction velocity from greatest to least? Relevance?

A

purkinje fibers > atrial and ventricular muscle > AV node

Delay in AV allows atria to empty into ventricles before ventricles contract

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5
Q

Difference between ventricle and atrium action potentia?

A

Phase 2 of ventricle has a longer length of time in it’s plateau form and stays more positive than atrium AP.

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6
Q

Why does the Ventricle and Atrium AP have a longer refractory period?

A

To make sure that the cardiac muscle relaxes before responding to a new stimulus

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7
Q

Na+ (m)

  • activates when?
  • action, phase
  • features
A
  • activate when membrane potential reaches threshold
  • Na+(m) channels open
  • phase 0 and 1
  • rapid depolarization then automatically closes to allow partial repolarization
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8
Q

K+ (a)

  • activation
  • action, phase
  • features
A
  • activated when cell depolarizes
  • K+(a) channels open
  • phase 1
  • rapid partial repolarization
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9
Q

Ca2+

  • activation
  • action, phase
  • features
A
  • activated when cell depolarizes
  • Ca2+ channels open
  • phase 2&3
  • opens slowly and remains open for a determined amount if time, when it closes it leads to phase 3
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10
Q

K+ (b)

  • activation
  • action, phase
  • features
A
  • activated when cell depolarizes
  • phase 2/3
  • closes slowly and remains closed for a determined amount of time, then it opens (start of phase 3)
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11
Q

K+ (c)

  • activation
  • action, phase
  • features
A
  • remains open (always active)
  • phase 4
  • leak channel maintains RMP
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12
Q

Na+ (f)

  • activation
  • action, phase
  • features
A
  • activation via SA or AP node repolarization
  • Funny Na+ channels opens
  • phase 4
  • specific to SA and AV node only, causes slow depolarization during resting phase (this is basically how it depolarizes during resting when it reaches threshold and how it can keep up maintaining its own AP)
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13
Q

Describe phase 4 in the SA node

A

In the SA node RMP gradually depolarizes until it reaches threshold, then it “fires” (although slower than other regions. Intrinsic spontaneous depolarization makes the SA node the pacemaker because of its automaticity)
Phase 4 happens due to the opening of voltage-gated Na funny channels

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14
Q

Phase 0 of SA node

A

In SA node - phase 0 occurs due to slow opening of Ca2+ channels and closing of K+(b) channels. Balance between Ca2+ coming in and K+ going out

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15
Q

Phase 3 of SA node

A

due to the closing of Ca2+ channels and opening of K+(b) channels (basically a reversal of phase 0)

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16
Q

Difference between SA node vs. AV node AP potential

A

AV node has a slower depolarization during phase 4

If the AV node takes over, the rate is much slower

17
Q

What is the resting potential in fast tissues and what is it sustained by?

A

Phase 4 is the resting potential and is sustained by high K+ (c) conductance

18
Q

What happens in phase 0? (AV node)

A

rapid upstroke by crossing threshold

VG Na+ (m) channels open

19
Q

What happens in phase 1? (mostly AV node)

A

small repolzarization caused by closing of VG Na+ (m) channels and opening of K+ (a) channels

20
Q

What happens in phase 2 of AV node AP?

A

plateau phase is sustained by slow opening of VG Ca2+ channels and closing of special VG K+(b) channels

this event prolongs contraction

21
Q

What happens in phase 3 of AV node AP?

A

complete repolarization (steep curve down) caused by slow VG Ca2+ channels closing and K+ (b) channels opening

22
Q

AV node damage effect

A

further delays conduction - AV Block

23
Q

Purkinje fiber damage effect

A

disrupts natural conduction and contraction of ventricles - Arrthymias)

24
Q

Refractory period importance

A

Refractory periods is when gates have not fully reset so it prevents a second AP to be generated.
RP is important to help prevent arrhythmias and are longer in cardiac cells than neurons

25
Q

ARP

A

no depolarization

26
Q

RRP

A

AP can be generated but will have an abnormal conduction. Conduction of AP is weaker if stimulated during RRP

27
Q

SNP

A

cells is more excitable than normal (phase 4)

28
Q

Chronotropic effect: positive and negative

A

-changes rate of depolarization of SA node and heart rate
(+) –> faster HR
(-) –> slower HR

29
Q

Dromotropic effect

A

speed of conduction changes

30
Q

Inotropic effect

A

changes strength of muscle contraction

31
Q

Lusitropic effect

A

changes rate of muscle relaxation

32
Q

Parasympathetic stimulus

A

NT: Ach
Receptor: muscarinic (M2 or M3)
To SA node and AV node

33
Q

Negative chronotropic effects

A
  • Parasympathetic autonomic effect on AP
  • slow opening of funny Na channels during phase 4
  • hyperpolarization bu increasing outward K+ current
34
Q

Negative dromotropic effects

A
  • parasympathetic
  • reduced Ca2+ inward current
  • increased outward K+ current
35
Q

Sympathetic stimulus on AP

A

to SA node and AV node and to myocytes
NT: NE
receptor: beta-1 adrenergic receptor

36
Q

positive chronotropic effects

A
  • sympathetic NS effect on AP
  • increase opening of funny Na channels during phase 4
  • increase inward current of Ca
37
Q

positive dromotropic effects

A
  • increased Ca2+ inward current during phase 2

- faster AP seen on graph