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Physiology I: Cardiovascular System > Lectures 26 & 27: Cardiac Electrophysiology > Flashcards

Lectures 26 & 27: Cardiac Electrophysiology Flashcards

1
Q

Types of cardiac action potentials

A
  • Fast response

- Slow response

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2
Q

Fast response type cardiac APs

A
  • Contracting fibers
  • Fast conducting tissue (like the Purkinje fibers)
  • NOT nodal cells
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3
Q

Slow response type cardiac APs

A
  • SA node
    AV node
  • Remaining conducting fibers
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4
Q

Phases of the fast response AP

A
  • Phase 0 = upstroke
  • Phase 1
  • Phase 2
  • Phase 3
  • Phase 4
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5
Q

Phase 0/upstroke

A
  • Fast response action potentials are generated in cells that have fast sodium channels
  • Activation gates open quickly
  • Voltage declines rapidly in myocardial cells (even faster in Purkinje fibers)
  • As membrane depolarizes, Na inactivation gates start to close
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6
Q

Absolute refractory period (phase 0)

A
  • Voltage dependence of the inactivation gate
  • If membrane depolarized more positive than -55 mV, the
    cell membranes are inexcitable due to voltage inactivation
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7
Q

Overshoot

A
  • End of phase 0

- Membrane depolarization beyond 0 mV

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8
Q

Also beginning during phase 0

A
  • Activation of slow calcium channels
  • Reduction of potassium conductance below resting levels
  • Effects manifest during phase 2
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9
Q

Phase 1

A
  • Rapid repolarization
  • Activation of transient outward current ito
  • Due to opening of a specific K+ channel (4-aminopyridine blocks this K+ channel)
  • Prominent in Purkinje and certain ventricular epicardial fibers
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10
Q

Phase 2

A
  • Two nearly balanced ion conductances

- Plateau region of the AP

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11
Q

L-type calcium channel activation (phase 2)

A
  • Membrane reaches about -30 to -40 mV (during upstroke/phase 0)
  • Voltage-dependent calcium conductance is activated
  • Slow type channel (activated slowly)
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12
Q

Effects of the reduced potassium conductance are seen (phase 2)

A
  • As membrane depolarizes during phase 0
  • With depolarization NDF causing outward potassium movement increases
  • Causes more K+ ions to leave than Ca2+ to enter
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13
Q

To keep the potential relatively constant for the plateau period (phase 2)

A
  • Potassium conductance must be reduced during the plateau phase
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14
Q

Three channels carrying potassium during the plateau (phase 2)

A
  • ito (not completely inactivated yet from phase 1)
  • iK
  • iK1
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15
Q

Inward Ca2+ ionic current together with the reduced outward K+ conductance during phase 2

A
  • Maintains membrane depolarized around 0 mV for about 200 msec
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16
Q

Towards the end of phase 2

A
  • Slow Ca2+ channel starts to inactivate
  • K+ conductance (iK and iK1) that repolarizes starts to increase
  • Accelerates repolarization process
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17
Q

Phase 3 channel activity

A
  • Slow Ca2+ channel is rapidly inactivating
  • K+ channel conductance increases (enhancing the outward ionic flux of K+)
  • Rapidly repolarizes the fiber (same three potassium channels as in plateau are involved)
  • Occurs when K efflux exceeds calcium influx
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18
Q

Phase 4 is flat in

A
  • Ventricular working fibers

- Atrial working fibers

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19
Q

In Purkinje fibers and in SA and AV node fibers (phase 4)

A
  • Maximal Diastolic Potential
  • The most negative potential achieved at the end of repolarization
  • Followed by diastolic depolarization
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20
Q

Slow response fibers of cardiac APs channel activity

A
  • Slow inward Na+/Ca2+ channels (similar to channels responsible for plateau)
  • Fast response action potential in Purkinje fibers can be converted into slow response type by exposure to TTX
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21
Q

The fast Na+ channels become fully activated when

A
  • Vm reaches and declines beyond a threshold value of about -65 mV
  • Channel activation sets into motion slower processes that will result in the inactivation of the Na+ channels
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22
Q

When the resting potential is artificially held constant at -70 mV

A
  • About 50% of the fast Na+ channels become inactivated
  • In a normal action potential all the fast Na+ channels remain inactivated (voltage inactivation) until the membrane repolarizes to potentials more negative than -55 mV
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23
Q

During the absolute refractory period

A
  • All fast Na+ channels are inactivated

- No matter how great the stimulus applied to a cardiac muscle cell, you cannot elicit another AP

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24
Q

Relative refractory period

A
  • As a cell repolarizes from -55mV to the resting potential, more voltage dependent channels become available
  • Becomes possible to elicit an action potential
  • However, amplitude of the upstroke is initially small, increasing as the cell repolarizes
  • Stimulus intensity required to elicit an action potential progressively declines until it equals the intensity required in a quiescent cell
  • Full repolarization marks the end of this period
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25
Q

Refractory period of atrial muscle

A
  • Much shorter than that of ventricles

- So atria can contract at much faster rate than ventricles

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26
Q

In slow response heart fibers, such as the SA and AV nodes, the absolute refractory period

A
  • Extends well beyond Phase 3
27
Q

The relative refractory period then extends into Phase 4

A
  • Vm is nearly constant

- Slope is slightly rising due to diastolic depolarization

28
Q

Impulses arriving at a slow response fiber early in its relative refractory period

A
  • Conducted much more slowly than those arriving late in the period
  • Thus, the greater tendency for conduction blocks in these fibers
29
Q

The adult heart normally contracts at a rhythmic rate of

A
  • 70 beats per minute
  • Does so in a coordinated manner
  • Coordination is provided in two ways
30
Q

Two ways coordination is provided in heart conduction

A
  • Gap junctions allow spread of AP from one fiber to another

- Specialized conducting system facilitates the rapid and coordinated spread of excitation

31
Q

Origin of the heart beat

A
  • SA node
32
Q

Some muscle cells in SA node are autorhythmic

A
  • Capable of spontaneous rhythmical self-excitation
33
Q

SA node

A
  • Found in posterior wall of the right atrium
  • Small strip of specialized muscle
  • Initiates the cardiac beat
  • Nodal cells are also continuous with the atrial fibers but are not contractile
34
Q

Characteristics of SA nodal cells

A
  • Vm more positive (-55mV to –65mV) than surrounding contractile atrial cells
  • Do not have a steep phase 0
  • Do not have phase 1
  • Do not have a flat phase 4
  • High Na+ conductance (gNa) means Na leaks into cells (causes Vm to be constantly in a state of being depolarized toward threshold during phase 4)
35
Q

Diastolic depolarization

A
  • Vm constantly in a state of being depolarized toward threshold during phase 4
  • A slow response action potential is fired
36
Q

Each time the ‘resting’ membrane potential is re-established during phase 3

A
  • It gradually decays (diastolic depolarization) until threshold is reached
  • AP is fired
  • After it is over gK is high and a repolarization occurs (π)
  • As the, K+ conductance deteriorates the high gNa causes another gradual depolarization until threshold is reached
37
Q

With the generation of the rhythmic impulse in the SA node, the impulse spreads to

A
  • Rest of the atrial muscle

- Via the gap junction between atrial fibers themselves

38
Q

Contraction of the atrium results in

A
  • Forcing blood through the AV valves into the ventricles
39
Q

Three tracts that convey cardiac impulses directly from SA to AV node are a mixture of

A
  • Ordinary myocardial cells

- Specialized conducting fibers

40
Q

The cardiac impulse does not travel into the ventricles too rapidly; time is allowed for

A
  • Atria to empty their contents into the ventricles before ventricular contraction begins
41
Q

AV node delay

A
  • The AV node and its associated conductive fibers delay the transmission
42
Q

The node and its special fibers are the only

A
  • Electrical connections of the atrium to the ventricles
43
Q

The impulse reaches the AV node about

A
  • 40 msec after it is initiated

- 110 msec to get out of the node

44
Q

About one-half of AV time lapse occurs in

A
  • Junctional fibers

- Low conduction velocity

45
Q

AV node delay (time lapse)

A
  • One-half occurs in the junctional fibers (low conduction velocity)
  • Second delay in nodal fibers
  • Further delay in transitional fibers and finally into the AV bundle
46
Q

Purkinje fibers run from

A
  • Fibers from AV node through the bundle of His into the ventricles
47
Q

Purkinje fibers size

A
  • Large diameter
  • High conduction velocity
  • Immediate transmission of the cardiac impulse throughout the entire ventricular system
48
Q

Puekinje fibers travel between

A
  • Valves of the heart into the ventricular septum

- Divide into right and left branches

49
Q

Purkinje fiber branches

A
  • Each spreads down to the apex of each ventricle

- Then curves back around the lateral wall

50
Q

Purkinje fiber impulses travel (speed)

A
  • 60 msec from the AV node to all the ventricular fibers

- Thus, ventricle fibers contract at essentially the same time

51
Q

Primary pacemaker

A
  • The SA node
52
Q

Ectopic foci

A
  • Other parts of the heart can exhibit rhythmic contractions

- Although, cardiac impulse normally arises in the SA node (primary pacemaker)

53
Q

Secondary pacemaker

A
  • AV node

- Rate of 40-60 beats/ min

54
Q

Tertiary pacemaker

A
  • Purkinje fibers

- Discharge at 15-40 beats/min

55
Q

Overdrive suppression

A
  • Since the SA node has a greater rate, it controls the beat of the entire heart (via overdrive suppression) and is the normal pacemaker of the heart
56
Q

Rhythmic discharge rate

A
  • Occasionally developed by other parts of the heart as the AV node or Purkinje fibers
  • A pacemaker elsewhere than the SA node is an ectopic pacemaker
  • Leads to an abnormal sequence of contraction
57
Q

Ectopic beat

A
  • An abnormal beat that results from a spurious impulse of the cardiac muscle
  • Occurs during the non-refractory period
58
Q

Autonomic control of heart

A
  • Parasympathetics via Vagus (CN X)

- Stimulation causes acetylcholine release

59
Q

Stimulation of acetylcholine release causes

A
  • Decrease in rate of rhythm of the SA node

- Decreased excitability of AV junctional fibers (slows transmission of cardiac impulses to the ventricles)

60
Q

Ventricular escape

A
  • Very strong vagal stimulation can stop ventricular beating for 4-10 seconds
  • Purkinje fibers will develop a rhythm of their own
  • Cause ventricular contraction at 15-40 beats/min
61
Q

Acetylcholine acts by

A
  • Reducing membrane conductance to Ca2+ and Na+
  • Increasing it to K+
  • This hyperpolarizes the cell membrane
  • Slows down the diastolic depolarization
  • Thus, more Na+/Ca2+ must enter before depolarization is sufficient to reach threshold
62
Q

The level of parasympathetic nerve stimulation will determine

A
  • If the effect is a delay or a blockage of action potential conduction
63
Q

Sympathetic heart stimulation

A
  • Releases norepinephrine
  • Increase rate of SA node discharge
  • Increase excitability of all parts of the heart
  • Increases the force of contraction
  • Increases the conduction velocity from the atria to the ventricles
64
Q

Sympathetics increase Na+/Ca2+ conductance and

A
  • Accelerates the onset of self-excitation

- Increases heart rate

Physiology I: Cardiovascular System (12 decks)

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