Electrical Activity of the Heart - Quiz 2 Flashcards

1
Q

The oustide of the cell is _______ charged relative to the inside of the cell which is _______ charged.

A

Positively, Negatively

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2
Q

Is concentration of Potassium higher inside or outside the cell

A

Inside

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3
Q

Is sodium concentration higher inside or outside the cell?

A

Outside

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4
Q

What stops potassium from leaking out of cell when concentration K+ is the same inside and outside?

A

Electrostatic force - the negativity inside the cell

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5
Q

What does the Nernst Equation calculate?

A

Equilibrium Potential

Chemical Force = Electrostatic Force
(Of Potassium)

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6
Q

Goldman Equation

A

Membrane Potential when Na, K, and Cl are involved

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7
Q

What ion contributes the most to the resting membrane potential of the cardiac cell?

A

Potassium

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8
Q

What ion makes a small contribution of the resting membrane potential?

A

Sodium

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9
Q

The ion pump that returns ion concentrations back to baseline in resting membrane potential?

A

Na+, K+ ATPase

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10
Q

Sodium/Potassium-ATP Pump

A
  • Steady inward leak of Na+ would depolarize cell
  • Metabolic pump, pumps out Na from cell and pumps in K+
  • Pumps OUT 3 Na+ and Pumps IN 2 K+
  • Electrogenic Pump
  • Partially inhibited by digitalis
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11
Q

What ion moves rapidly into a cell during depolarization?

A

Sodium

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12
Q

How is the baseline electrical charge restored during cell repolarization?

A

Potassium channels open and rapid diffusion of potassium to exterior reestablishes normal resting membrane potential

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13
Q

Where are the Fast-Response Action Potentials located?

A

Atrial Myocardial Fibers

Ventricular Myocardial Fibers

Purkinje Fibers

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14
Q

Where are the Slow-Response Action Potentials?

A

SA & AV Node

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15
Q

Differences between Fast and Slow Cardiac 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
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16
Q

Phases of Fast Response Action Potential

A

Phase 0: Depolarization

Phase 1: Partial Repolarization

Phase 2: Plateau

Phase 3: Repolarization

Phase 4 Resting Membrane Potential

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17
Q

Phase 0 (Fast Response)

A

Depolarization - fast sodium channels open - rapid influx of sodium (+20 mv)

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18
Q

Phase 1 (Fast Response)

A

Initial Repolarization - fast sodium channels close - potassium leaves cell through open potassium channels

19
Q

Phase 2 (Fast Response)

A

Plateau - L-type calcium channels open. Ca+ entering is equal to K+ leaving

20
Q

This entry of this small amount of ion into the cell triggers release of a large amount of calcium into the sarco plasmic reticulum.

A

Calcium through the L-type calcium channels

21
Q

What happens when a large amount of calcium leave the sarcoplasic reticulum

A

Calcium binds with Troponin-C

Myosin binds to actin and contraction of the myocyte

22
Q

Which ion is the major determinant of the Resting Membrane Potential?

A

Potassium

23
Q

Phase 3 (Fast Response)

A

Rapid Repolarization - calcium channels close and potassium channels open.

Potassium exits cell, ending plateau phase and returns cell membrane to resting level.

24
Q

Phase 4 (Fast Response)

A

Restoration of Ionic Concentrations

  • Na+, K+-ATPase
  • Na+-Ca++ Exchanger
  • ATP-driven Ca++ Pump
25
Q

Phases of Slow Response (Pacemaker) Action Potential

A

Phase 4: Cations from adjacent cell

Phase 0: Calcium Influx

Phase 2: very brief plateau phase

Phase 3: Repolarization: Ca+ channels close and Lots of K+ leaves

26
Q

Effective Refractory Period

A

Absolute Refractory Period - impossible for another action potential to triggered

27
Q

Relative Refractory Period

A

Period where an action potential can be triggered if the stimulus is large/strong enough

28
Q

Automaticity

A

Ablity of a focal area of the heart to generate pacemaking stimuli

29
Q

What is the heart’s dominate pacemaker

A

SA Node

30
Q

Where does the depolarization wave flow from the SA node?

A

In all directions

31
Q

Diastolic Depolarization

A
  • Inward Na+ - via funny sodium channels
  • Ca++ Influx
  • K+ Efflux
32
Q

What effects on aspects of diastolic depolarization will cause changes in heart rate

A

Neurotransmitters

Norepi, acetylcholine, succinylcholine, T1-T4 cardiac accelerators

33
Q

Overdrive Supression

A

Sinus node controls beat of heart because its discharge is faster than any other part of the heart.

Automaticity of pacemaker cells become depressed after a high frequency of excitation

  • Due to Na+, K+-ATPase
  • More Na+ is forced out than K+ entering at higher heart rates - hyperpolarize
  • Slow diastolic depolarization needs more time to reach threshold
34
Q

What is a sarcomere?

A

Structural unit of striated muscle tissue between two Z-lines

35
Q

The name of the branching network that cardiac cells are arranged in

A

Intercalated Discs

36
Q

T-Tubules

A

Extensions of cell membrane that penetrate into the center of skeletal and cardiac muscle cells

  • Open to exterior of muscle fiber - can communicate with fluid surrounding muscle fiber
37
Q

Sarcoplasmic Reticulum

A

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

38
Q

What is the process called when large amounts of calcium are released form the Sarcoplasmic Reticulum into the cell?

A

Calcium-Induced Calcium Release (CICR)

39
Q

What ion allows binding between actin and myosin?

A

Calcium

40
Q

Function of Troponin

A

Inhibit Actin and Myosin From Binding

  1. Calcium binds to Troponin C - conformational change
  2. Myosin heads bind to actin leading to cross-bridge movement and shortens sarcomere
  3. Calcium goes back to SR
  4. Calcium is removed from Troponin-C and myosin unbinds from actin
41
Q

Function of ATP in the heart

A

ATP needed for crossbridge movement, muscle shortening (contraction), and muscle relaxation

42
Q

Excitation Contraction Coupling

A

Coupling between myocyte actional potentials and contraction

43
Q

Sliding Filament Model

A

Mechanism of muscle contraction

Myosin (thick) filaments slide past actin (thin) filaments during muscle contraction