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Medical Physiology > Exam #2: Electrophysiology of the Heart > Flashcards

Exam #2: Electrophysiology of the Heart Flashcards

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USMLE® Step 1 flashcards
1
Q

What are intercalated discs? What is their function?

A
  • Intercalated discs are interdigitations of sarcolemma between cardiac myocytes
  • Contain gap junctions that increase the speed of signal transduction between myocytes
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2
Q

What are pacemaker cells?

A

Intrinsic rhythm generators in the heart, including nodal cells of:

  • SA node
  • AV node
  • Purkinje fibers
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3
Q

How does the resting membrane potential differ from the equilibrium potential?

A

Resting membrane potential is the summation of the equilibrium potentials for each ion

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4
Q

Describe the intracellular vs. extracellular concentration of Na+, K+. Ca++, & Cl-.

A

Na+= high ECF
K+= high ICF
Ca++=v. high ECF
Cl-= high ECF

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5
Q

Describe the electrical driving forces on the basis of charge. How does this compare to the chemical driving force?

A

Electrical driving force:

  • Cations want to move in (attracted by the negative resting membrane potential)
  • Anions want to remain out of the cell (repulsed by the negative resting membrane potential)

*Chemical driving force is dependent on the concentration gradient for each particular ion.

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6
Q

What is resistance. Write Ohm’s Law.

A

Resistance is the force that impedes the flow of ions.

I= Vm-Veq/R

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7
Q

What maintains the Na+ & K+ concentration gradients?

A

Na+/K+ ATPase Pump

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8
Q

What ion is the cell most permeable to at rest? What is the effect of this?

A
  • The cell membrane is most permeable to K+ at rest

- Resting membrane potential is closest to the equilibrium potential for K+

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9
Q

Describe the general sequence the cardiac action potential in terms of cellular permeability & ion channels.

A

1) Fast Na+ channels open, leading to Na+ entry & rapid depolarization
2) Slow Ca++ channels open leading to the plateau phase caused by Ca++ influx
3) Change in K+ permeability throughout the action potential leads to K+ efflux & causes repolarization

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10
Q

What is the resting membrane potential in a cardiac myocyte?

A

-90mV

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11
Q

What is phase 0 of the AP in a ventricular myocyte?

A

Depolarization due to opening of Fast Na+ channels

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12
Q

What is phase 1 of the AP in a ventricular myocyte?

A

Early repolarization when Fast Na+ channels inactivate (close) & some K+ channels open

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13
Q

What is phase 2 of the AP in a ventricular myocyte?

A
  • Plateau phase where the membrane potential is approximately 0
  • Due to slow Ca++ channels with Ca++ influx, BALANCED by K+ efflux
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14
Q

What is phase 3 of the AP in a ventricular myocyte?

A

Rapid repolarization as Ca++ channels are closing, & K+ channels open

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15
Q

What is phase 4 of the AP in a ventricular myocyte?

A

Resting membrane potential; only K+ channels are open

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16
Q

What is responsible for the absolute (effective/normal) refractory period in the ventricles? What is its duration?

A
  • 0.25-0.3 sec

- Na+ inactivation gate is closed & Na + pore is closed

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17
Q

What is responsible for the absolute (effective/normal) refractory period in the atria? What is its duration?

A
  • 0.15 sec

- Na+ inactivation gate is closed & Na + pore is closed

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18
Q

What is the relative refractory period? What is responsible for the relative refractory period?

A

More difficult to excite, but no impossible

- Na+ channel inactivation ( Na+ pore is closed but the inactivation gate open)

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19
Q

How does the effective (absolute) refractory period in cardiac muscle compare to skeletal muscle?

A

Longer effective refractory period in cardiac muscle; thus, it cannot tetanize

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20
Q

What happens when another action potential is stimulated during the relative refractory period in the cardiac myocyte?

A

Interruption of normal ion flow that may result in ventricular fibrillation

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21
Q

How does the nodal action potential compare to the ventricular myocyte action potential?

A
  • Missing phases 1 &2 i.e. no rapid influx of Na+ b/c no fast Na+ channels
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22
Q

What happens during phase 3 in nodal cell?

A

Repolarization as K+ channels open

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23
Q

What happens in phase 4 in the nodal cell?

A

Slow leak of Na+, called the “funny current” slowly changes the membrane potential until threshold is reached

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24
Q

What is the effect of NE on pacemaker cells?

A
  • Increases Ca++ permeability

- More positive charge enters the cell & cell reaches threshold faster

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25
Q

What is the effect of ACh on pacemaker cells?

A

Increases permeability of K+

26
Q

What is the function of the SA node?

A

Primary pacemaker

27
Q

What are the principal time-dependent & voltage dependent currents of the SA node?

A

Ica, Ik, & If

28
Q

What is the effect of Beta-adrenergic stimulation on the SA node?

A
  • Increased conduction velocity

- Increased pacemaker rate

29
Q

What is the cholinergic effect on the SA node?

A
  • Decreased pacemaker rate

- Decreased conduction velocity

30
Q

What is the function of the atrial muscle?

A

Expel blood from the atria

31
Q

What are the principal time-dependent & voltage dependent currents of the atria?

A

Ina, Ica, Ik

32
Q

What is the effect of beta-adrenergic stimulation of the atria?

A

Increased strength of contraction

33
Q

What is the effect of cholinergic stimulation on the atria?

A

Little effect

34
Q

What is the function of the AV node?

A

Secondary pacemaker

35
Q

What are the principal time-dependent & voltage dependent currents of the AV node?

A

Ica, Ik, If

36
Q

What is the effect of beta-adrenergic stimulation of the AV node?

A
  • Increased conduction velocity

- Increased pacemaker rate

37
Q

What is the effect of cholinergic stimulation of the AV node?

A
  • Decreased pacemaker rate

- Decreased conduction velocity

38
Q

What is the function of the Purkinje fibers?

A
  • Rapid conduction of action potential

- Tertiary pacemaker

39
Q

What are the principal time-dependent & voltage dependent currents of the Purkinje fibers?

A

Ina, Ica, Ik, If

40
Q

What is the effect of beta-adrenergic stimulation of the Purkinje fibers?

A

Increased pacemaker rate

41
Q

What is the effect of cholinergic stimulation of the Purkinje fibers?

A

Decreased pacemaker rate

42
Q

What is the function of the ventricular muscle?

A

Expel blood from ventricles

43
Q

What are the principal time-dependent & voltage dependent currents of the ventricular muscle?

A

Ina, Ica, Ik

44
Q

What is the effect of beta-adrenergic stimulation of the ventricular muscle?

A

Increased contractility

45
Q

What is the effect of cholinergic stimulation of the ventricular muscle?

A

Little effect

46
Q

Describe the sequence of depolarization in the heart.

A

1) SA node
2) Atria
3) AV node
4) Septum
5) Apex
6) Ventricular free walls

47
Q

What is the velocity of signal conduction through the purkinje fibers?

A

4 m/s

48
Q

What is the velocity of signal conduction through the cardiac myocytes?

A
  1. 3-0.5 m/sec

* Roughly a 1/10 of the purkinje fibers

49
Q

What is the SA node?

A

Normal impulse generator of the heart (70-80 bpm)

50
Q

How does impulse from the SA node reach the left atria?

A

Internodal tracts

51
Q

How does the resting membrane potential of the SA node compare to the cardiac myocytes?

A

Less negative (-60mV vs. -90mV)

52
Q

What is the function of the AV node?

A

Delay of impulse

- Allows for atrial contents to fill the ventricle

53
Q

How does the AV node slow conduction?

A

Expression of fewer gap junctions

54
Q

What are the branches of the left bundle branch?

A

1) Septal fascicle
2) Left posterior fascicle
3) Left anterior fascicle

55
Q

What is the function of the purkinje fibers?

A

Very rapid transmission of the electrical impulse that allows for the synchronous contraction of ventricular myocytes

56
Q

Outline the steps of excitation-contraction coupling in the heart.

A

1) Action potential spreads down T-tubule & there is an inward Ca++ movement through L-Type Ca++ channels (Dihydropyridine receptors)
2) Ca++ induced Ca++: Ryanodine receptor on SR activated to release MORE Ca++
3) Increased ICF Ca++ binds Troponin C & displaces tropomyosin from myosin-binding sites on actin
4) Cross-bridging occurs

Relaxation occurs when Ca++ is reaccumulated in the SR via Ca++ ATPase (SERCA) & out of the cell via the Ca++/Na+ exchanger

57
Q

How do the concentration & electrical gradients differ for Cl-?

A

Cl- concentration is high on the outside of the cell; however, resting membrane potential of the cell is negative. Thus,

  • Concentration gradient favors entry into the cell
  • Electrical gradient favors efflux from the cell
58
Q

What are the effects of increased extracellular potassium (hyperkalemia)?

A

1) Slows HR
2) Dilates heart
3) Can block conduction through AV-bundle

59
Q

What is the effect of hypercalcemia on the heart?

A

Increases cardiac contraction (positive ionotrope)

60
Q

What is the effect of hypocalcemia on the heart?

A

Decreased cardiac contraction (negative ionotrope)

61
Q

What are the effects of K+ channel blockers on the heart?

A

1) Increased AP duration & absolute refractory period

2) Prolongation of QT interval on ECG

62
Q

What are the effects of Ca++ channel blockers on the heart?

A

Slows the rate of conduction at the SA & AV nodes by delaying Ca++ entry

E.g. verapamil

Medical Physiology (74 decks)

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