Action Potentials Flashcards

1
Q

How does the Na/K ATPase pump work?

A

pumps 3 Na out & 2 K in creating a more negative membrane potential

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2
Q

Explain how the Na/Ca Exchanger will work under high & low concentrations of intracellular sodium.

A

Low IC Sodium: pumps 1 Ca out & 3 Na in creates a more positive membrane potential; High IC sodium: pumps out 3 Na & 1 Ca in creating a more negative potential

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3
Q

How many phases does a fast response action potential have?

A

Five

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4
Q

Describe what happens during phase 0 of a fast response AP.

A

Fast sodium channels open causing a sodium influx that will depolarize the membrane potential

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5
Q

What happens during phase 1 of a fast response AP?

A

major event is repolarization via transient outward potassium chain; these channels only stay open for a short period of time

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6
Q

What are the principle players of phase 2 for a fast response AP?

A

Major inward ion movement is calcium facilitated by L-type Ca channels; Major outward ion movement is potassium via delayed rectifier K+ channels; this phase is also referred to as the plateau phase b/c these channels open slowly which prolongs the phase

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7
Q

What happens during phase 3 of a fast response AP?

A

Ca channels are closed; Delayed rectifier K channels have reached maximum opening; stimulation of inward rectifying K channels to open

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8
Q

What happens during phase 4 of a fast response AP?

A

only IKs remain open; Na/K & Ca ATPases remove extra Na & Ca from cytoplasm and bring potassium back in

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9
Q

How does hyperkalemia affect the membrane potential?

A

makes it more positive which increases excitability and delays sodium channel recovery leading to cardiac arrest

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10
Q

How does hypokalemia affect membrane potential?

A

makes it more negative; this increase AP duration & delays repolarization thus increasing the risk for arrhythmia

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11
Q

What ion event occurs during a myocyte contraction?

A

influx of Ca from L-type Ca channels will trigger release of Ca from the SR; SERCA will facilitate Ca movement back into the SR after contraction is ended

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12
Q

How many phases does a slow response action potential have?

A

three

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13
Q

What happens during phase 0 of a slow response action potential?

A

AP generated by L-type Ca channels causing depolarization to happen slower

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14
Q

What happens during phase 3 of a slow response action potential?

A

K rectifier channels are open to repolarize the cells

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15
Q

What happens during phase 4 of a slow response action potential?

A

Spontaneous depolarization is initiated by pasmic chain/funny channels; Iks are deactivated & T-type Ca channels are activated to help facilitate spontaneous depolarization

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16
Q

after which phase can another AP be fired for fast response fibers?

A

beginning of phase 4

17
Q

after which phase can another AP be fired for slow response fibers?

A

at the end of phase 4

18
Q

What variable determines the duration of a cardiac AP?

A

ERP; increased ERP is associated w/ increased duration of an AP

19
Q

Skeletal muscle fibers have prolonged contractions due to very short ERP and AP duration; the summation of APs for prolonged contraction is referred to as tentanization; longer cardiac ERP prevents tetanization; why is this a good thing?

A

it is essential for the heart to have a relaxation phase before firing another contraction AP; this gives the blood time to flow into the chambers b/t contractions

20
Q

what ions can be used to activate a pacemaker current?

A

sodium & potassium

21
Q

How do the membrane potentials differ with fast vs. slow response APs and what is the physiological significance of these differences?

A

Fast response APs have a more negative resting membrane potential compared to slow response APs; additionally, slow response APs have a much shorter AP peak; reduced distance b/t resting state & peak will make it easier to fire APs

22
Q

What part of the heart initiated the relay of electrical propagation?

A

Right Atrium at the SA node

23
Q

Via what pathway does electrical propagation from the RA reach the LA?

A

bachman’s bundle

24
Q

describe the differences b/t longitudinal & transverse conduction.

A

pathways of longitudinal conduction have fewer cells w/ more gap junctions and therefore generate a much faster current; transverse conduction pathways have more cells w/ fewer gap junctions, slowing the rate of conduction

25
Q

In which direction relative to the anatomical orientation of the heart, will the atrial currents flow?

A

they will flow downward into the ventricles

26
Q

what is the main conductor that relays atrial electrical conductance to the ventricles?

A

the AV node

27
Q

where is the AV node located?

A

lower interatrial septum b/t tricuspid valve & coronary sinus

28
Q

What pathway relays electrical conductance to the ventricular myocytes?

A

His-Purkinje system; first through the His bundle; then to the purkinje fibers to be handed off to the ventricular myocytes

29
Q

Myocytes in which ventricle and in what layer of the heart will be excited first?

A

endocardium of the left side via the interventricular septum

30
Q

Which direction will the ventricular condance flow?

A

up towards the aorta

31
Q

Why do epicardial myocytes have a shorter AP duration compared to endo & myocardial myocytes and why is this physiologically significant?

A

epicardial myocytes have a higher density of IK channels which will speed up repolarization; if the outer layer is contracted, the rest of the ventricle cannot naturally relax

32
Q

What cardiac fibers have the fastest conduction velocity?

A

His bundle branches & purkinje fibers

33
Q

which cardiac fibers have the slowest conduction velocity?

A

SA & AV nodes

34
Q

which cardiac fibers have the largest cells?

A

purkinje fibers

35
Q

which cardiac fibers have the smallest cells?

A

SA & AV nodal cells

36
Q

How does the vagus nerve slow HR?

A

acetylcholine acts on M2 receptors to activate Gi to activate ligand gated potassium channels to hyperpolarize the cells

37
Q
A