DNURS 827 Week 2 Resting membrane potential / Excitation-Contraction Coupling / Electrical activity of the heart Flashcards

1
Q

Resting Membrane Potential

A
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2
Q

1.) Relative to the outside of a cell, is the inside positive or negative in charge?

A
  • Negative
  • The diffusion carries positive charges to the outside but leaves the nondiffusible negative anions
    on the inside, thus creating electronegativity on the inside
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3
Q

2.) Is potassium higher in concentration inside or outside of a cardiac muscle cell?

A
  • Inside
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4
Q

3.) Is sodium higher in concentration inside or outside of a cell?

A
  • High concentration of sodium ions outside the membrane and a low concentration of sodium ions on the inside.
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5
Q

4.)What prevents potassium from leaking out of a cell until the concentration is the same on the outside and inside of the cell?

A
  • Electrostatic force
  • As K+ leaves cell, negativity increases on the inside of the cell membrane and electrostatically
    attracts K+. This electrostatic force prevents K+ from leaving the cell.
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6
Q

5.) What does the Nernst Equation calculate?

A
  • Equilibrium potential = The membrane voltage that perfectly balances an ion’s tendency to diffuse down its concentration gradient
  • Chemical force = electrostatic force
  • NO net movement of K+= equilibrium
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7
Q

Resting Membrane Potential

A

The Stable electrical potential across the cell membrane caused by ions, predominantly potassium, flowing down the electrochemical gradient that was established by the sodium potassium pump

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8
Q

6.) What ion makes the major contribution to the resting membrane of the cardiac muscle cell?

A
  • Potassium
  • Potassium is the major determinant of the resting membrane potential
  • potassium and sodium ion channels allow leakage of these ions across cell membranes
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9
Q

7.) What ion makes a small contribution to the resting membrane potential?

A

Chloride

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10
Q

8.) What ion pump returns ion concentrations back to baseline?

A
  • Na+, K+- ATPase
  • sodium-potassium pump
  • Metabolic pump which extrudes Na+ from the cells and pumps in K+
  • Pumps in 3 sodium to 2 potassium ratio
  • Na-Ca Pump
  • Electrogenic pump
  • partially inhibited by digitalis
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11
Q

9.) How does the Na+-K+ - ATPase pump contribute to the resting membrane potential?

A
  • the pumping of more sodium ions to the outside than the potassium ions being pumped to the inside causes continual loss of positive charges from the inside of the membrane creating an additional degree of negativity (about -4 mV) on the inside beyond that which can be accounted for by diffusion alone.

Digoxin reduces effectiveness of pump

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12
Q

Action Potential

A

A mechanism by which excitable cells (neurons, myocytes) can rapidly transmit electrical signals along their cell membranes and to adjacent cells

Consists of a stereotypical change in membrane potential that’s caused by a sequence of ion channels opening and closing

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13
Q

1.) What ion moves rapidly into a cell during depolarization?

A

Sodium

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14
Q

2.) What ion exits the cell to restore the baseline electrical charge in a cell during repolarization?

A

Potassium

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15
Q

3.) What restores ion concentrations back to their baseline levels?

A

The decrease in sodium entry to the cell and the simultaneous increase in potassium exit from the cell combine to speed the repolarization process leading to full recovery of the resting membrane
potential.

Sodium Potassium Pump

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16
Q

Electrical Activity of the Heart

A
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17
Q

1.) In what part of the heart are Fast-Response Action Potentials (non-pacemaker action potentials) found?

A
  • Atrial myocardial fibers
  • ventricular myocardial fibers
  • purkinjefibers
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18
Q

2.) In what part of the heart are Slow-Response Action Potentials (pacemaker action potentials) typically found?

A
  • SA and AV node
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19
Q

3.) What are some of the differences between Non-pacemaker and Pacemaker action
potentials?

A
  • Resting membrane potential: slow> fast
  • slope of upstroke: fast> slow
  • Amplitude of action potential: fast >slow
  • Overshoot of action potential: fast>slow

Calcium = depolarization in slow
no phase 1 or 2 in slow

20
Q

4.) What are the 5 phases of the Non-pacemaker (Fast-Response) action potential?

A
  • Phase 0: depolarization- sodium in
  • Phase 1: partial repolarization- Potassium out
  • Phase 2: plateau- calcium in, potassium out- contraction
  • Phase 3: repolarization- potassium out
  • Phase 4: resting membrane potential- diastole
21
Q

5.) Which ions contribute to the various phases?

A
  • Phase 0: sodium in
  • Phase 1: potassium out
  • Phase 2: calcium in, potassium out- calcium ions that enter during this plateau phase active the
    muscle contractile process: CICR
  • Phase 3: potassium out
  • phase 4: sodium-potassium pump, Na+- Ca2+ exchanger, ATP driven Ca++ pump (SERCA)
22
Q

6.) What is another name for Phase 2 in a Non-pacemaker cell?

A

Contraction, plateau

23
Q

7.) Release of a large amount of calcium from the Sarcoplasmic Reticulum is triggered by the entry of which ion?

A

Calcium

24
Q

8.) What is the function of the Sarcoplasmic Reticulum within a cardiac muscle cell?

A

Membrane-bound structure in muscle cells that store and regulate calcium movement

Regulatesintracellular Calcium

25
Q

9.) Which ion is the major determinant of the Resting Membrane Potential in Cardiac cells?

A

Potassium

26
Q

10.) What are the various phases found in Pacemaker (Slow Response) Action Potentials?

A
  • Phase 4: due to inward sodium current (funny current) (spontaneous depolarization)
  • Phase 0: inward calcium current after threshold is reached (depolarization)
  • Phase 3: repolarization due to outward potassium current (repolarization)
  • The process by which pacemaker cells in the SA node spontaneously depolarize is automaticity
27
Q

11.) Which ions contribute to the various phases in the Pacemaker Action Potential?

A
  • Phase 4: sodium (funny current)
  • Phase 0: inward calcium
  • Phase 3: outward potassium
28
Q

12.) What are the different refractory periods associated with the cardiac action potentials?

A
  • Absolute refractory period/Effective refractory period- no subsequent action potential can occur. Largely due to the inactivated state of the sodium channel. (0, 1, 2, 3, early phase 4)
  • Relative refractory period-
  • Supranormal period- the cell is more excitable than normal - it requires less of an electrical (slow, 0, 2, early 3)
29
Q

13.) What is automaticity?

A
  • The process by which pacemaker cells in the SA node spontaneously depolarize is automaticity
  • Ability of focal area of the heart to generate pacemaking stimuli.
30
Q

14.) What is diastolic depolarization?

A
  • Inward Na+ (via funny sodium channels)
  • Ca2+ influx
  • K+ efflux (opposes effects of other ions
31
Q

15.) What effects on aspects of diastolic depolarization will cause changes in heart rate?

A
  • Vagal stimulation releases ACh at the SA node decreases the slope of phase 4 by inhibiting funny currents thereby causing the pacemaker potential to take longer to reach threshold and slowing HR (negative inotropy)
  • The steeper the slope of phase 4, the faster the threshold potential will be reached, and the faster the HR
  • Neurotransmitters, acetylcholine, succinylcholine, T1-T4 cardiac accelerators

Hypoxia
Bradycardia

32
Q

16.) Which pacemaker region of the heart is typically dominant?

A

SA Node

33
Q

17.) What is Overdrive Suppression?

A
  • Sinus node controls beat of heart bc it discharge is faster than any other part of the heart.
34
Q

Excitation-Contraction Coupling:

A
35
Q

1.) What is a sarcomere?

A
  • defined as the region of the myofilament structure between two Z-lines.
  • Repeating micro-anatomical units- the basic contractile unit of the myocyte
  • Structural unit of striated muscle tissue between two Z-lines

The sarcomere is defined as the region of myofilament structures between two Z-lines. The sarcomere is composed of thick and thin filaments – myosin and actin, respectively. Chemical and physical interactions between the actin and myosin cause the sarcomere length to shorten, and therefore the myocyte to contract during the process of excitation-contraction coupling.

36
Q

2.) Cardiac cells are arranged in a branching network that is known as what?

A

Synctium

37
Q

3.) What are T-tubules in a cardiac muscle cell?

A

a. The T tubules are small and run transverse to the myofibrils. They begin at the cell membrane and penetrate all the way from one side of the muscle fiber to the opposite side. Not shown in the figure is the fact that these tubules branch among themselves and form entire planes of T tubules interlacing among all the separate myofibrils.

b. Also, where the T tubules originate from the cell membrane, they are open to the exterior of the muscle fiber. Therefore, they communicate with the extracellular fluid surrounding the muscle fiber and contain extracellular fluid in their lumens.

c. When an action potential spreads over a muscle fiber membrane, a potential change also spreads along the T tubules to the deep interior of the muscle fiber. The electrical currents surrounding these T tubules then elicit the muscle contraction.

  • internal extensions of the cell membrane that penetrate into the center of cardiac (or skeletal muscle cells)
  • Open to exterior of muscle fiber- can communicate with the extracellular fluid surrounding the muscle fiber
38
Q

4.) What is the Sarcoplasmic Reticulum?

A
  • Membrane-bound structure in muscle cells that store and regulate calcium movement.
39
Q

5.) What is Excitation-Contraction coupling?

A
  • Coupling between myocyte action potentials and contraction
40
Q

6.) What is the trigger for the release of large amounts of calcium from the Sarcoplasmic Reticulum?

A
  • Influx of Ca2+ from the interstitial fluid during the action potential triggers the release of Ca2+
    from the sarcoplasmic reticulum
41
Q

7.) What is this process called whereby large amounts of calcium are released from the Sarcoplasmic Reticulum into the cell?

A
  • Calcium-Induced calcium release (CICR)
42
Q

9.) The presence of what ion allows binding between actin and myosin?

A

Calcium

43
Q

10.) What is the function of Troponin in the binding between actin and myosin?

A
  • Inhibit actin and myosin from binding
  • Calcium binds to troponin c- conformational change
  • myosin heads bind to actin leading to cross-bridge movement and shortening of the sarcomere
  • Calcium goes back into the SR
  • Calcium is removed from troponin-c, and myosin unbinds from actin
44
Q

11.) What is the Sliding Filament Model ?

A
  • Mechanism of muscle contraction
  • myosin (thick) filaments slide past actin (thin) filaments during muscle contraction
45
Q

12.) Is ATP required for cardiac muscle relaxation?

A

Yes