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ANS and Cardiac Physiology > Electrophysiology, Excitation, and Contraction Coupling > Flashcards

Electrophysiology, Excitation, and Contraction Coupling Flashcards

1
Q

Sequence of Cardiac Electrical Activation

A

SA Node

Atrium

AV node

Bundle of His

Purkinje Fibers

Ventricles

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2
Q

Which action potentials are similar in the heart, which are unique? SA node, atrium, AV node, Purkinje fibers, ventricle

A

SA node similar to AV node.

Atrium unique

Ventricle similar to purkinje fibers

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3
Q

Where is this AP taken? What are the phases called? Explain the movement of ions during each of the phases.

A

Ventricular AP.

Phase 0: Upstroke, Na+ influx

Phase 1: Notch, Na in, K out

Phase 2: Plateau, Ca in, K out

Phase 3: Repolarization, K out

Phase 4: Resting potential, K out, NCX in

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4
Q

What is the resting potential of a ventricular myosite vs an SA node myosite?

A

-85 mV vs -60 mV

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5
Q

Where is this AP taken? What ion movements are responsible for each phase?

A

From SA node

Phase 0: Ca influx

Phase 2: Ca in and K out

Phase 3: K out

Phase 4: NCX and If

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6
Q

Differences between SA nodal firing and ventricular firing?

A

SA nodal firing occurs spontaneously, ventricular firing does not.

Phase 0 is much faster in ventricle!

Phase 1 is absent in SA node

Plateau (phase 2) is subtle and abbreviated in SA node

Phase 3: Same

Phase 4: Voltage increases in SA node and is less negative.

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7
Q

Absolute vs Relative Refractory Period

A

ARF: Impossible to trigger second AP

RRP: Strong stimuli trigger weak APs.

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8
Q

What is negative current in a whole cell clamp experiment?

A

Positive charge flowing inward

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9
Q

V=IR

A

It’s true.

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10
Q

Equilibrium potential of K, Na, Ca

A

K= -89

Na= +70

Ca= +133

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11
Q

Driving force

A

DF= V- Equilibrium potential

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12
Q

What happens if V=Ex, V-Ex>0, V-Ex<0?

A

V=Ex: No ion movement

V-Ex>0: Positive current (cation moves out)

V-Ex<0: Negative current (cation moves in)

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13
Q

What ion does this represent? Why?

A

Sodium, look at reversal potential around +70.

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14
Q

What ion does this represent?

A

L-type calcium current, activates and inactivates more slowly than sodium

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15
Q

Role of L-type Ca current in ventricular myocytes

A

Plateau of action potential, initiate SR calcium release

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16
Q

Role of L-type Ca current in SA and AV nodal myocytes

A

Action potential upstroke (phase 0)

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17
Q

Why do Calcium channel blockers (Type IV antiarrhythmics, antihypertensives) have multiple bad effects?

A

Because Ca channels present in many diverse tissues.

18
Q

Which ion and channel does this represent?

A

Current through KIR Channel (IK1)

19
Q

Purpose of KIR

A

Stabilizes resting potential around ~85mV, also responsible for long plateau when it inactivates

20
Q

What do these represent?

A

Delayed rectifier K currents.

Rapid IKr

Slow IKs

Responsible for repolarizing membrane after plateau

21
Q

Funny Current

A

IF occurs in SA node, channel is open at very negative voltages, but opens at more positive voltages. Caused by mostly sodium (some K) going in. Supplies depolarizing current to drive voltage upward in SA node.

22
Q

Where is KIR located?

A

In ventricle, not in SA node

23
Q

Why is upstroke (phase 0) so much faster in ventricle?

A

Because of INa, which is not present in SA node. There, the upstroke is caused by ICa, which is very slow

24
Q

Which cardiomyosites have delayed rectifier K channels?

A

SA and ventricle

25
Q

How do the concentrations of calcium in the SR and cytosol compare?

A

SR concentration is MUCH higher (10,000x)

26
Q

CICR

A

Calcium Induced Calcium Release. Can’t have release of Ca from SR without calcium. Required for contraction.

27
Q

Steps of EC coupling in cardiac muscle

A

Excitation is coupled to contraction. First, depolarization causes L-type calcium current. Ca binds to ryanodine receptors in the SR membrane, which releases 4x more calcium, which causes contraction by binding to troponin.

28
Q

How is such a large concentration of Ca built up in SR?

A

SERCA, transports Ca in using ATP

29
Q

NCX

A

3 Na in along gradient, 1 Ca out against gradient

30
Q

EC coupling in skeletal muscle

A

NAChR opening causes influx of sodium, which induces action potential in muscle cell, which causes activation of Ltype Ca channels that are bound directly to ryanodine receptors. NO extracellular CA influx necessary.

31
Q

How does Ca influx induce contraction in cardiomyocytes if they are so huge?

A

T tubules (membrane invaginations) extend into cell interior. This way, calcium that surrounds the cell can sit near interior.

32
Q

T Tubules and RyR location

A

RyRs sit close to T tubules so calcium doesn’t have to diffuse too far in order to cause CICR.

33
Q

How does the cardiac myocyte relax after contraction?

A

70% of calcium is pumped back into SR, 20% pumped out via NCX.

34
Q

In steady state conditions, total amount of Ca entering through L type Ca current must equal…

Total amount of Ca released via RyRs must equal…

A

Total amount of Ca exiting via NCX

Total amount resequestered by SERCA

35
Q

How is strength of contraction modulated?

A

By altering the amount of Calcium stored in the SR. Also, the effect is nonlinear.

36
Q

What happens in non-steady state conditions? When does this happen?

A

Total Ca entering different than total amount exiting. This causes more IC calcium, more in SR. Causes bigger contractions. This happens during exercise.

37
Q

Can RyRs randomly and spontaneously release Ca?

A

Yes. Usually these effects are harmless and localized, but it can be bad sometimes!

38
Q

What happens when multiple RyRs open spontaneously?

A

High IC calcium can diffuse to other RyRs causing increased opening. This will increase IC Ca some more, and the NCX will have to work harder. This can create a depolarizing current due to the fact that more sodium in brought into the cell, causing inappropriate action potentials.

39
Q

DAD

A

Delayed after depolarization. One is okay usually, but more can initiate aberrent action potential.

40
Q

Cellular correlates of heart failure

A

Weaker contractions, slower relaxation. Caused by downregulation of SERCA. So, less Ca is pumped into the SR, less released, smaller contractions. Also, disrupted T-tubule structure, which causes increased distance to ryanodine receptors.

41
Q

Digitalis

A

Na-K pump inhibitor. Used in heart failure. Inhibition causes increased IC Na, so NCX is less effective. More intracellular Ca, which is pumped into SR. This causes stronger contractions upon release. But can lead to arrhythmias.

42
Q

Positive Inotropy

A

Stronger contractions

ANS and Cardiac Physiology (10 decks)

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