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Yr 2 - Cardiology System > Electrical Conductivity of Heart > Flashcards

Electrical Conductivity of Heart Flashcards

1
Q

What is an action potential (excitation signal) created by in the heart?

A

The sinoatrial (SA) node

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2
Q

What is the SA node?

A

A specialised clump of myocardial conducting cells located in the superior and posterior walls of the right atrium

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3
Q

What is the pacemaker of the heart?

A

The SA node

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4
Q

How is the impulse then spread to the AV node and myocardial contractile cells?

A

Via internodal pathways

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5
Q

What are the internodal pathways?

A

3 bands (anterior, middle, posterior) that lead directly from SA node to AV node

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6
Q

How do the cells of the AV node then transmit the action potential?

A

Transmit AP more slowly and delays impulse

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7
Q

As impulse spreads across both atria, what happens?

A

Atria contract –> atrial systole Causes blood to move from atria to ventricles

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8
Q

What is purpose of delay caused by AV node?

A

Ensures atria have enough time to fully eject blood into ventricles before ventricular systole

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9
Q

After the AV node, where does the impulse then pass?

A

Into the atrioventricular bundle (bundle of His). The impulse spreads down to the ventricles along the bundle of His to the apex of the heart.

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10
Q

What is the bundle of His?

A

A continuation of the specialised tissue of the AV node and serves to transmit the electrical impulse from the AV node to the Purkinje fibres of the ventricles

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11
Q

At the apex of the heart, what does the bundle of His divide into?

A

The right bundle branch (RBB) and left bundle branch (LBB)

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12
Q

What is purpose of split into RBB and LBB?

A

Supplies left and right ventricles

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13
Q

What does RBB do?

A

Conducts the impulse to the Purkinje fibres of the right ventricle

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14
Q

What does the LBB do?

A

Conduct impulse to the Purkinje fibres of the left ventricle

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15
Q

What/where are Purkinje fibres?

A

Additional myocardial conductive fibres that spread impulse from AV to the myocardial contractile cells in the ventricles. Network of specialised cells that are abundant with glycogen and have extensive gap junctions.

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16
Q

What is purpose of Purkinje fibres?

A

This rapid conduction allows coordinated ventricular contraction (ventricular systole) and blood is moved from the right and left ventricles to the pulmonary artery and aorta respectively

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17
Q

What are the non-pacemaker action potential cells?

A

Atrial myocytes, ventricular myocytes, Purkinje cells

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18
Q

What are the phases of the AP in non-pacemaker cells?

A
  1. Phase 4 2. Phase 0 3. Phase 1 4. Phase 2 5. Phase 3 6. Phase 4
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19
Q

What is initial phase 4 in non-pacemaker?

A

Resting membrane potential –> stable around -90 mV

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20
Q

Why is the resting membrane potential very negative in phase 4 in non-pacemaker?

A

Potassium channels are open (K+ conductance and K+ currents are high) K+ ions leaving cell and making membrane potential more -ve inside At same time fast Na+ channels and L-type slow Ca2+ channels are closed

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21
Q

How does phase 4 progress to phase 0 in non-pacemaker?

A

Wave of depolarisation goes into contractile cell and membrane potential becomes more positive

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22
Q

What is rapid depolarisation in phase 0 due to in non-pacemaker?

A

Voltage-gated fast Na+ channels open so Na+ enters cell –> membrane potential becomes more positive K+ channels close –> less K+ leaves cell Moves membrane potential away from equilibrium potential for potassium (which is negative) and towards equilibrium potential for sodium (which is positive)

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23
Q

What are the cells rapidly depolarised to in phase 0 in non-pacemaker?

A

A threshold voltage of about -70 mV

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24
Q

What is phase 1 in non-pacemaker?

A

Initial repolarisation

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25
Q

How does phase 0 progress to phase 1 in non-pacemaker?

A

Na+ channels close and membrane starts to repolarise as K+ leaves through opening of special transient outward K+ channel

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26
Q

Is phase 1 long or short in non-pacemaker?

A

Very brief Short-lived, hyper polarising outward K+ current

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27
Q

Briefly describe Na, K and Ca in phases of AP in non-pacemaker cells?

A

4 –> Resting potential 0 –> Increase in permeability to Na 1 –> Decrease in permeability to Na 2 –> Decrease in permeability to K (fast K+ channels close) and increase in permeability to Ca 3 –> Increase in permeability to K (slow K+ channels open) and decrease in permeability to Ca 4 –> Resting potential

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28
Q

What is phase 2 in non-pacemaker?

A

Plateau phase

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29
Q

How does phase 1 progress to phase 2?

A

Flattening due to: - Decrease in K+ permeability - Increase in Ca2+ permeability (slow) Voltage gated L-type calcium

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30
Q

Why is there a plateau phase in AP in non-pacemaker?

A

Repolarisation is delayed. Prolongs AP duration. Distinguishes cardiac action potentials from much shorter APs found in nerves and skeletal muscle

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31
Q

What is phase 3 in AP in non-pacemaker?

A

Rapid repolarisation

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32
Q

How does phase 2 progress to phase 3 in AP in non-pacemaker?

A

Calcium channels close Activation of K+ channels (K+ exits rapidly which repolarises cell back to resting potential)

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33
Q

What is depolarisation?

A

Cell undergoes a shift in electric charge distribution, resulting in less negative charge inside the cell

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34
Q

What is repolarisation?

A

Change in membrane potential that returns it to a negative value just after the depolarisation phase of an action potential which has changed the membrane potential to a positive value

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35
Q

Where are cardiac pacemaker cells mostly found?

A

In the SA node

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36
Q

Why are pacemaker cells called auto rhythmic?

A

They beat naturally

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37
Q

What is pacemaker activity?

A

The intrinsic, spontaneous time dependent depolarisation of a cell membrane that leads to an action potential

38
Q

What is any cardiac cell with pacemaker ability able to initiate?

A

A heartbeat

39
Q

What is the hierarchy of pacemakers?

A

The Primary Pacemaker is defined as the tissue with the highest ‘firing’ frequency, in other words the fastest pacemaker sets heart rate and overrides all slower pacemaker tissues.

40
Q

What is order of pacemakers and their frequencies?

A
  1. SA node –> 100 beats/min 2. AV node –> 40 beats/min 3. Purkinje fibres –> 20 beats/min
41
Q

Why are pacemaker cells able to generate APs spontaneously without input from nervous system?

A

Have unstable membrane potential

42
Q

In pacemaker cells, what does membrane potential tend to start as?

A

-60 mV

43
Q

In pacemaker cells, what is the pacemaker potential?

A

Occurs at the end of one action potential and just before the start of the next. It is the slow depolarisation of the pacemaker cells (e.g. cells of the SA node) towards threshold. This is the ‘funny current’.

44
Q

In pacemaker cells, when does cell depolarise?

A

When AP reaches threshold of -40 mV –> triggers an action potential

45
Q

In pacemaker cells, what happens at -40 mV?

A

Voltage-gated calcium channels open causing influx of Ca2+ –> faster rate of depolarisation to reach a positive membrane potential

46
Q

What is the upstroke of AP in pace maker cells?

A

Fast rate of depolarisation to reach a positive membrane potential

47
Q

At the peak of AP in pace maker cells, what occurs (regarding Ca channels and K channels)

A

Ca2+ channels inactive and K+ channels open –> efflux of K+ ions out of cell

48
Q

What does the efflux of K+ ions out of cell in pacemaker cells cause?

A

Membrane to repolarise –> downstroke of AP

49
Q

How does the membrane potential differ between contractile myocardium and auto rhythmic myocardium?

A

Contractile –> Stable at -90 mV Autorhythmic –> Unstable pacemaker potential (usually starts at -60 mV)

50
Q

What events lead to threshold potential in contractile myocardium and auto rhythmic myocardium?

A

Contractile –> Depolarisation enters via gap junctions Autorhythmic –> Net Na+ entry, reinforced by Ca2+ entry

51
Q

Difference in rising phase of AP in contractile myocardium and auto rhythmic myocardium?

A

Contractile –> Na+ entry Autorhythmic –> Ca2+ entry

52
Q

Difference in repolarisation phase of contractile myocardium and auto rhythmic myocardium?

A

Contractile –> Extended plateau caused by Ca2+ entry, rapid phase caused by K+ efflux Autorhythmic –> Rapid caused by K+ efflux

53
Q

Difference in hyperpolarisation of contractile myocardium and auto rhythmic myocardium?

A

Contractile –> None, resting potential is -90 mV (equilibrium for K+) Autorhythmic –> Normally none, when depolarisation hits -60 mV, the If channels open again. Each can hyper polarise the cell

54
Q

Difference in duration of AP of contractile myocardium and auto rhythmic myocardium?

A

Contractile –> extended: 200+ msec Autorhythmic –> variable: generally 150+ msec

55
Q

Difference in refractory period of contractile myocardium and auto rhythmic myocardium?

A

Contractile –> Long because resetting of Na+ channel gates delayed until end of AP Autorhythmic –> Not significant in normal function

56
Q

Why is there no plateau stage in pacemaker cell AP?

A

Opening of Ca2+ channels is not sustained

57
Q

What drugs can affect cardiac potential?

A

Class 1 –> Na+ channel blocker Class 4 –> Ca2+ channel blockers Class 3 –> K+ channel blocker Class 2 –> B-blocker

58
Q

What are gap junctions?

A

Specialised connections between cells that depolarising currents pass through

59
Q

Where are gap junctions located?

A

Intercalated disks

60
Q

Why is conducting pathway needed?

A

If electrical signals from atria were conducted straight down, you would get contraction at top of ventricles (squeezing blood to bottom). But want ventricles to contract from bottom.

61
Q

What is an ECG?

A

Electrocardiogram –> placement of surface electrodes on body to record electrical signal of heart

62
Q

How many leads/electrodes are used in ECGs?

A

12 leads, 10 electrodes

63
Q

Describe placement of 6 leads on chest in ECG

A

V1–> 4th intercostal space on right side of sternum V2 –> 4th intercostal space on left of sternum V3–>  In between V2 and V4 V4–>  5th intercostal space mid clavicular V5 –> 5th intercostal space, left axillary line (same horizontal plane as V4) V6–>  5th intercostal space, left mid axillary line (same horizontal plane as V4 and V5)

64
Q

Describe placement of 4 leads on limbs in ECG

A

 Right arm (inner wrist)  Left arm (inner wrist)  Right left (inner ankle)  Left leg (inner ankle)

65
Q

What does electrical activity towards an electrode result in on ECG?

A

Positive deflection

66
Q

What does electrical activity away from electrode result in on ECG?

A

Negative deflection

67
Q

What are the 5 prominent points on the ECG?

A
  1. P wave 2. QRS complex 3. T wave
68
Q

What does the P wave represent?

A

Represents depolarisation of the atria. Atria contract approx. 25ms after start of P wave.

69
Q

What does the QRS complex represent?

A

Represents depolarisation of ventricles

70
Q

Why does depolarisation require of ventricles require much larger signal?

A

Because of the larger size of the ventricular cardiac muscle

71
Q

What does the T wave represent?

A

Repolarisation of the ventricles

72
Q

When does repolarisation of atria occur on ECG? Why is it masked?

A

During QRS complex (same time as depolarisation of ventricles)

73
Q

What are segments on ECGs?

A

The regions between two waves

74
Q

What are intervals on ECGs?

A

Invervals include one segment plus one or more waves

75
Q

What is the PR interval?

A

Conduction through AV node and AV bundle.

Measures duration from beginning of atrial depolarisation (P wave) to initiation of QRS complex

Delay in impulse from SA node to AV node visible in PR interval

76
Q

What is the rate at which the SA node generates impulses influenced by?

A

The autonomic nervous system (sympathetic and parasympathetic)

77
Q

How does the parasympathetic NS affect SA node?

A

Decreases firing rate of the SA node, and thus decreases heart rate

78
Q

How does the sympathetic NS affect SA node?

A

Increases firing rate of the SA node, and thus increases heart rate

79
Q

What is the 1ary/2ary/3ary pacemakers of heart?

A

1ary –> SA node

2ary –> AV node

3ar –> all other electrically active myocytes (Purkinje fibres)

80
Q

When do the ventricles begin to contract on the ECG?

A

As the QRS reahces the peak of the R wave

81
Q

What is the PR segment on the ECG?

A

Begins at end of P wave and ends at beginning of QRS complex

82
Q

What part of the ECG is a delay in impulse from SA node to AV node visible in?

A

PR interval

83
Q

Picture of normal sinus rhythm

A
84
Q

What occurs in atrial fibrillation? Why are ventricles beating normally?

A

Rapid and irregular beating of atria. Not normally life-threatening. Ventricles beating normally due to AV node delay

85
Q

ECG of atrial fibrillation. What shows there is problem with atria?

A

No P waves. QRS looks ok but frequency between them has increased

86
Q

What is atrial flutter?

A

Commonly degenerates to atrial fibrillation. More organised atria

87
Q

What is ventricular fibrillation?

A

Ventricles not pumping blood around body. Heart quivers instead of pumping due to disorganized electrical activity in the ventricles

88
Q

What is ventricular tachycardia?

A

May lead to ventricular fibrillation. Heart pumping fast so no time for diastole to occur and blood not being effectively pumped around body

89
Q

What does first degree heart block manifest on ECG?

A

Prolonged PR interval. Atria contract but slight delay to ventricles (common with ageing)

90
Q

What is 3rd degree AV block?

A

No connection between atria and ventricles so they do what they want

Very unwell or can just have very low heart rate with episodes of collapsing

91
Q

What detected rhythms would you shock?

A

Ventricular fibrillation

Ventricular tachycardia

Yr 2 - Cardiology System (25 decks)

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