Lesson 17: Topic 13 - Cardiac Action Potential Flashcards

1
Q

is there pacemaker potential in cardiac cells?

A

no, just the SA node

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2
Q

what is cardiac cells doing?

A

receiving the signal from the SA node, from the pacemaker cells to initiate contraction

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3
Q

is action potential in the cardiac cells autorhytmic?

A

no, its non-autorhythmic because the action potentials is autorhythmic in the SA node

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4
Q

what is the primary purpose of cardiac muscle?

A

to contract

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5
Q

what is the purpose of action potential propogation?

A

regulate contraction of the heart
- referred to excitation-contraction coupling

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6
Q

when does an action potential generate?

A

when the cell membrane of the cardiac muscle cell depolarizes

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7
Q

what is the resting membrane potential in a cardiac muscle cell?

A

-90mV

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8
Q

the -90mV resting membrane potential in cardiac muscle cells is predominantly regulated by?

A

the fact that resting membrane potential is very permeable to potassium

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9
Q

what regulates high potassium and low sodium on the INSIDE of the cell and low potassium and high sodium on the OUTSIDE of the cell?

A

the ATPase pump (sodium-potassium pumps)

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10
Q

in a cell, is there a leak of potassium outside of the cell?

A

yes

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11
Q

membrane potential is recorded where?

A

on the inside of the cell

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12
Q

what is important for maintaining the resting membrane potential in cardiac muscle cells?

A

potassium
- the leaking of potassium out of the cell makes the membrane potential negative because positive potassium ions are leaving the cell

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13
Q

true or false: generally at a resting state, there is a higher permeability of that membrane to potassium compared to sodium

A

true

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14
Q

what initiates the process of membrane potential starting to rise?

A

sodium influx into the cardiac muscle cells

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15
Q

where does the sodium influx into the cardiac muscle cell come from?

A

extracellular fluid
- comes into cardiac muscles cells because the gap junctions are moving them in which increases the membrane permeability to sodium

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16
Q

how is positive feedback happening in a cardiac cell action potential?

A

the sodium influx into the cell causes more sodium to go into the cell

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17
Q

after depolarizing a membrane, what is the next step?

A

we activate the voltage gated calcium channels

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18
Q

what happens in the plateau phase of cardiac action potentials?

A

permeability of the membrane still stays low for potassium but calcium is going to start increasing its influx into the cell

19
Q

what is the voltage-gated calcium channel detecting?

A

the voltage change initiated by sodium on the cell membrane

20
Q

does the L-type calcium channel stay open for a long time?

21
Q

the influx of calcium is how fast while the channel stays open for a long time?

A

while the channel stays open for a long time, the influx of that calcium is slow than what happens with sodium. so the sodium has a really rapid rise in the resting membrane potential and it dips a little bit slowly because of the influx of the positive calcium ion is not as fast as it was with sodium

22
Q

what is responsible for the the non-rapid drop after an action potential peak in the cardiac action potentials?

A

there is a balance between what is happening with the calcium ions that are going inside the cell and also with potassium ions that are going outside the cell
- maintains the plateau phase

23
Q

what does influx mean?

A

going into the cell

24
Q

what does efflux mean?

A

going out of the cell

25
Q

what initiates membrane repolarization in cardiac action potentials?

A
  • calcium influx has done its job and its going to close the L-type calcium channels and now the permeability to potassium is going to increase
26
Q

in cardiac action potentials, if we have more potassium coming out the cell, what happens to the resting membrane potential?

A

make it more negative because positive ions are leaving the cell. potassium is leaving the cell quickly to restore the resting membrane potential back down to -90mV

27
Q

about how long does it take to start and end a cardiac action potential?

28
Q

about how long is atrial muscle cell action potentials compared to ventricular cardiac muscle cells?

A

the action potential duration is a little bit shorter, around maybe 150 msec as opposed to ventricular which is 250 msec

29
Q

what is the purpose of the cardiac action potential?

A

serves the purpose of initiating contraction in the cardiac muscle cells

30
Q

how does the cardiac action potentials cause a contraction in cardiac muscle cells? (excitation-contraction coupling)

A

several processes:
1. membrane depolarization. from this, the action potential travels down t-tubules (transverse-tubules) and in there is the L-type calcium channels which is the initial part of membrane depolarization.
2. there is an entry of calcium into the cell through L-type calcium channels from the t-tubules and that is going to get into the cytoplasm of the muscle cells
3. when it gets into the cytoplasm, calcium is going to bind to a ryanodine receptor (RyR) (Calcium dependent calcium channels)
4. increased release of calcium from the sarcoplasmic reticulum (Ca2+ induced Ca2+ release) and ** Ca2+ is pumped back to SR via SR Ca2+ ATPase (SERCA)
5. calcium binds to tropomyosin to cause unbinding and then cross bridges form for contraction
6. **

31
Q

where are the ryanodine receptors?

A

on the sarcoplasmic reticulum

32
Q

what is the main ion channel that is going to regulate the control of calcium?

A

ryanodine receptors
- predominatly the role of the sarcoplasmic reticulum is to store calcium

33
Q

what is the predominant role of the sarcoplasmic reticulum?

A

store calcium

34
Q

what does the ryanodine receptor in the sarcoplasmic reticulum regulate?

A

the exit of the calcium from the sarcoplasmic reticulum into the cytoplasm

35
Q

the whole process of calcium exiting the sarcoplasmic reticulum into the cytoplasm is initiated by?

A

calcium entry into the cell via the L-type calcium channel

36
Q

what is a refractory period?

A

you cannot have another action potential happening within this time period
- 250 msec in ventricular cardiac action potential
- 150 msec in arterial action potential

37
Q

why can we not have another action potential in the refractory period?

A
  1. you cannot repolarize a membrane within a shorter period of time. in needs the whole 250 msec time to repolarize the membrane of the cardiac muscle cell
  2. the duration is required to have all the processes to occur
    - max force and contraction is already happening so we cannot do more.
38
Q

what is the theoretical made HR based on the 250ms refractory period?

A

240BPM
- this is because there is four potential action potentials in one second of time and there is 60 seconds in a minute so 4 x 60 = 240 BPM

39
Q

is it possible to have a higher heart rate than 240BPM?

A

no, we have physiological processes that cannot simply go faster than that

40
Q

relaxation of the excitation-contraction coupling in cardiac muscle is initiated by?

A

calcium recycling through the SERCA pump into the SR (this is bc calcium leaves the SR via SERCA to bind to tropomyosin)

41
Q

summary of excitation-contraction coupling:

A
  • action potential in cardiac contractile cell
  • travels down t-tubules
  • entry of small amount of calcium from ECF —> release of large amount of Ca2+ from SR
  • increase cytosolic Ca2+
  • troponin-tropomyosin complex in thin filaments pulled aside
  • cross-bridge cycling between thick and thin filaments
  • thin filaments slide inward between thick filaments
  • contraction
42
Q

what is the primary purpose of the plateau phase of the cardiac action potential?

A

to cause calcium induced calcium release

43
Q

What is the threshold potential for cardiac action potentials?