Cardiac AP - Slow Response/Timing Cells Flashcards

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1
Q

what maintains phase 4 in slow response cells?

A

funny current (Na/K)

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2
Q

what does funny current do?

A

provokes spontaneous depolarization

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3
Q

what controls heart rate?

A

rate (slope) of spontaneous depolarization

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4
Q

what dominates upstroke in slow response cells?

A

Ca channels

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5
Q

what do muscarinic receptors do to channels?

A

decrease iF (funny channel) to hyperpolarize, and increases iK (leading to decreased cAMP)

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6
Q

what do adrenergic receptors do to channels?

A

increase iF and iCa to depolarize faster and decreases iK to be less polarized (more frequent AP)

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7
Q

is there a phase 1?

A

no

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8
Q

is there a plateau?

A

no

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9
Q

what causes phase 3? repolarization

A

increased gK through iK and iK1 channels

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10
Q

is there iK1 channel during phase 4?

A

no

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11
Q

difference between SA and AV node

A

SA depolarizes more, faster, triggered first, and reaches threshold faster

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12
Q

what if SA node is knocked out?

A

slower AP from AV node, reduced force

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13
Q

what occurs if iF turns on during repolarization?

A

causes spontaneous depolarization

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14
Q

how does gCa increase?

A

responds to spontaneous depolarization from iF (and initiates AP)

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15
Q

action during phase 4

A

iK and iK1 turn off during phase 4, allowing funny current to depolarize

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16
Q

when does funny current turn on?

A

once cell repolarized and causes spontaneous depolarization

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17
Q

what channel repolarizes cells?

A

iK

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18
Q

what is threshold of slow response cell?

A

-40mV

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19
Q

threshold of fast response cell

A

-65mV

20
Q

what is resting potential of slow response cell

A

less negative than myocardial cells

21
Q

which cell is more likely to be blocked ?

A

slow response cells

22
Q

what is conductance speed of slow response?

A

slower than fast

23
Q

what is post-repolarization refractoriness?

A

that the relative refractory period extends into phase 4 resting potential, which decreases conduction velocity of impulses that arrive early

24
Q

how do slow respond cells keep rhythm

A

relative refractory period lasts until phase 4 resting potential and decreases conduction velocity of the impulses that arrive early

25
Q

what occurs if interval between AP is short?

A

next AP amplitude is short, or may be blocked.

26
Q

benefit of post-repolarization refractoriness

A

allows ventricles to fill

27
Q

calcium current in SA node

A

little calcium current, but it is important for membrane potential

28
Q

why is resting potential less than ventricular myocytes?

A
  1. fewer iK1 so there is no efflux of K

2. ratio of gK and gNa is low so cell deviates more from the E of K

29
Q

What influences AP frequency of SA node?

A
  1. slope of phase 4 spontaneous depolarization
  2. maximal negativity during phase 4 (starting more hyperpolarized vs more depolarized)
  3. threshold potential
30
Q

how do you change threshold potential?

A

close some Ca channels to make threshold less negative, therefore need to depolarize more to reach threshold (takes longer)

31
Q

how do you change slope of phase 4?

A

decrease iF

32
Q

how do you change negativity of phase 4?

A

hyperpolarize cell so starts from lower starting point)

33
Q

what is overdrive suppression?

A

when HR is excessively high, Na builds up in the cell, which drives Na/K ATP pump at a higher rate, which makes cell more hyperpolarized. therefore, after period of high HR (once stimulus is turned off) may be period of unusually low rate

34
Q

what do muscarinic receptors do to slow response cells?

A

M2 increases gK (which hyperpolarizes the cell) by decreasing cAMP

35
Q

how does acetylcholine affect M2?

A
  1. regulates K channels (suppresses them)
  2. depresses iF Na current and Ca current (less depolarization)
  3. M2 increases gK by decreasing cAMP
36
Q

effect of muscarinic activation on HR?

A
  1. lowers slope of phase 4
  2. raises threshold by closing ca channels
  3. slows HR!
37
Q

what occurs during hypocalcemia?

A

depresses AP amplitude and rate of spontaneous depolarization

38
Q

how does norepi affect slow response cells?

A
  1. increases Na permeability during phase 4 (increase iF slope)
  2. increases gCa via increasing cAMP (opens Ca channels) (increases amplitude)
39
Q

what do CCB (calcium channel antagonists) do

A

reduce phase 4 and phase 0 slopes in pacemaker cells, reduces plateau in myocytes

40
Q

what finding by EMG most strongly and specifically supports dx of neurogenic myopathy?

A

decreased frequency of muscle depolarization with motor nerve stimulation

41
Q

what would a decrease in gCl do in a muscle cell?

A

spontaneous depolarization, causing spontaneous muscle contractions

42
Q

electrical stimulation has normal amplitude and conduction velocity but AP decreases in amplitude with each stimulus. resting membrane potentials of neurons and myocytes is normal. what’s wrong.

A

myasthenia gravis, something wrong at motor end plate

43
Q

what causes irreversible neural disorders?

A

deficiency in NO synthase NOS, poly-ADP-ribose polymerase PARP, or superoxide dismutase (SOD)

44
Q

delayed inactivation of voltage gated Na channels in skeletal muscle most likely to cause what?

A

spontaneous AP and efflux of K causing hyperkalemia

45
Q

what causes neurogenic myopathy?

A

destruction of alpha motor neurons

46
Q

what would demyelination cause

A

decreased sensory transmission and motor disorders

47
Q

what does hypercalcemia do?

A

inacctivates na channels