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2. Cardiovascular System > 2. Electrical Activity of the Heart > Flashcards

2. Electrical Activity of the Heart Flashcards

1
Q

What is the sarcolemma?

A

Membrane which surrounds the heart cells which is invaginated

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2
Q

What is the sarcoplasmic retriculum?

A

Big calcium store which is needed to trigger excitation

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3
Q

What type of junctions are found between cardiac cells and what do they allow?

A

Gap junctions; allow electrical connection and passage of signalling molecules from one cell to the next (depolarisation and APs pass from cell to cell)

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4
Q

What ensures a physical connection between adjacent cardiac cells?

A

desmosomes

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5
Q

What is the structure involving desmosomes and gap junctions called?

A

Intercalated discs

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6
Q

What is the difference between AP in skeletal and cardiac muscles?

A

AP in cardiac muscles is much longer and larger

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7
Q

What is needed in cardiac cells to create longer APs?

A

Bigger influx of Ca from outside into the cell

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8
Q

What contraction is created from ca entry into the cardiac cell?

A

sub-maximal contraction

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9
Q

Is there tetanus in cardiac muscle?

A

No tetanus; no prolonger contraction of muscle by prolonged repeated stimuli (tetanus exists in skeletal muscle)

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10
Q

What is the refractory period like in cardiac muscle cells?

A

Long refractory period; cardiac muscle has to relax before it can contract again

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11
Q

What are contractions in cardiac cells like?

A

they are GRADED contractions (whereas skeletal muscle ones are all or none)

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12
Q

What is the force generated by cardiac muscle proportional to?

A

Proportional to number of cross bridges that are active which is determined by how much Ca is bound to troponin

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13
Q

What is the contraction of cardiac muscle dependent on? (2)

A
  1. cytosolic Ca concentration

2. sarcomere length at the beginning of contraction (initial length of muscle fibre)

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14
Q

What is the main difference in action potentials between skeletal and cardiac cells?

A

In cardiac cells;
- rapid depolarization occurs because of Na entry
-steep repolarization occurs because of K leaving
BUT! In cardiac cells the main difference is that there is the lengthening of the AP due to Ca entry

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15
Q

Cardiac muscle cells act as one functioning cell- what is this called?

A

functional syncytium

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16
Q

How are cardiac cells electrically connected?

A

via gap junctions

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17
Q

How are cardiac cells physically connected?

A

via desmosomes

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18
Q

What is the AP of a cardiac muscle in terms of msec compared to skeletal muscle?

A

Cardiac muscle AP= 250msec (much longer AP)

Skeletal muscle AP= 2msec

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19
Q

What is the refractory period of cardiac muscle?

A

Long so cannot exhibit tetanic contraction

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20
Q

What regulates contraction force on a molecular level?

A

Ca entry from outside cell (can be used to vary strength of contraction)

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21
Q

What do pacemaker cells have that other cardiac cells don’t in terms of potentials?

A

they have an unstable resting membrane potential

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22
Q

Why is prevention of having tetanus important in cardiac cells? Why is it NOT needed?

A

Because cardiac muscles must relax between contractions so ventricles can fill with blood

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23
Q

What is tetanus?

A

Sustained contraction (when a series of APs occur in rapid successions)

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24
Q

Why can’t tetanus never occur in cardiac cells?

A

Because longer AP means refractory period and contraction end almost simultaneously (by the time the second AP takes place, the myocardial cell has almost completely relaxed)

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25
Q

Can summation occur in cardiac cells?

A

NO

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26
Q

What is the RMP of non-pacemaker cells? What are they described as?

A

RMP= -90mVP

Very stable cells

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27
Q

What is the RMP in pacemaker cells? What are they described as?

A

RMP= -60mVP

Unstable

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28
Q

Why is the potential for pacemaker cells called “pacemaker potential” rather than RMP?

A

Because it never rests at a constant value

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29
Q

What is the main difference between depolarisation between non-pacemaker and pacemaker cells?

A

In pacemaker cells depolarisation is due to additional Ca channels opening while in non-pacemaker cells this is due to Na channels opening

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30
Q

What creates an RMP in normal non-pacemaker cells?

A

leaky K channels

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31
Q

Describe the 4 steps in non-pacemaker APs by referring to its basic electrophysiology.

A
  1. Resting Membrane Potential
  2. Initial depolarisation
  3. Plateau
  4. Repolarisation
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32
Q

What occurs in step 1; resting membrane potential?

A

High resting PK+ (leaky K channels)

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33
Q

What occurs in step 2; initial depolarisation?

A
  • increase in PNa (influx into the cell)
34
Q

What occurs in step 3; plateau?

A

-increase in PCa (L type; long type)
- decrease in PK
(flattened AP)

35
Q

What occurs in step 4; repolarisation?

A
  • decrease in PCa
  • increase in PK
    (reverse of Plateau)
36
Q

What step in electropysiology is specific to cardiac cells?

A

Plateau stage (which keeps Ca channels open for longer to keep the AP going)

37
Q

What is the AP in PACEMAKER cells due to?

A

Increase in PCa (l type); rather than PNa increase like in non-pacemaker cells

38
Q

If pacemaker cells don’t have an RMP, what do they have instead?

A

Pacemaker potential (or pre-potential)

39
Q

What 3 features are specific to pacemaker APs?

A
  1. gradual decrease in PK
  2. early increase in PNa (Pf)
  3. late increase in PCa (T-type)
40
Q

What do pacemaker create?

A

Autorhythmicity

41
Q

Early increase in PNa (pf) is due to Na channels being open from which stage?

A

These channels are open from previous repolarisation from a previous AP not due to depolarisation

42
Q

What are 2 common drugs used that affect forces of contraction?

A
  1. Ca channel blockers

2. Cardiac glycosides

43
Q

How do Ca channels blockers affect force of contraction

A

decrease force of contraction; less Ca released, less bridges formed and weaker contraction

44
Q

How do cardiac glycosides affect force of contraction?

A

increase force of contraction; more bridges formed and stronger contraction

45
Q

How does temperature affect heart rate?

A

Increases heart rate ~10 beats/ min/centigrade

46
Q

How does hyperkalemia (high plasma K) affect heart rate?

A

causes fibrillation and heart block: decreases equilibirum potential and cell is depolarised, APs are uncoordinated

47
Q

How do hypokalemia (low plasma K) affect heart rate?

A

causes fibrillation and heart block (same as hypokalemia)

48
Q

How does hypercalcemia (high plasma Ca) affect heart rate?

A

Increases heart rate and force of contraction

49
Q

How does hypocalcaemia (low plasma Ca) affect heart rate?

A

decreases heart rate and force of contraction

50
Q

What are modulators which affects electrical activity of the heart? (7)

A
  1. sympathetic and parasympathetic nervous systems
  2. drugs (Ca channel blockers and cardiac glycosides)
  3. temperature
  4. hyperkalemia
  5. hypokalemia
  6. hypercalcemia
  7. hypocalcemia
51
Q

Where are fastest pacemaker cells found?

A

At sinoatrial node (controls heart rate); pacemaker ~0.5m/sec
- generates cardiac impulse

52
Q

What is annulus fibrosus?

A
  • Insulator between atria and ventricles, it’s a right fibrous ring surrounding the heart
  • strongest part of fibrous cardiac skeleton
53
Q

Is annulus fibrosus conducting?

A

it’s NON-CONDUCTING

54
Q

What is the atrioventricular node (AV node)?

A
  • slows down impulses and regulates them
  • found inferior to SA node
  • secondary pacemaker and allows atria to work
  • delays APs to ventricle
  • relays and intensifies cardiac impulse
55
Q

What is the AV node regarded as?

A
  • the “delay box”

- ~0.05m/sec

56
Q

Where are Bundle of His found?

A

fibres around ventricles for equal ventricular contraction

57
Q

What does Bundle of His divide into?

A

divides into Purkinje fibres

58
Q

What do Purkinje fibres do?

A
  • rapid conduction system
  • ~5m/sec
  • makes sure depolarisation occurs at the same time
59
Q

Where is SA node located?

A

superior lateral wall opening of superior vena cava

60
Q

Where is the AV node located?

A

posterior septal wall of right atrium

61
Q

Is SA or AV node shorter?

A

SA node is longer and AV node is shorter

62
Q

To what does SA node transmit impulse to?

A

directly to two atria

63
Q

To what does AV node transmit impulse to?

A

to two ventricles through AV bundle (influenced by SA node)

64
Q

Can an AP in a single myocyte evoke a very small extracellular (transmembrane) electrical potential?

A

Yes

65
Q

How can large extracellular electrical waves be created?

A

Lots of small extracellular electrical potentials evoked by many cells depolarising and repolarising at the same time can summate to create these

66
Q

What can be used to record large extracellular waves?

A

They can be recorded at the periphery as the electrocardiogram

67
Q

What does P wave correspond to?

A

atrial depolarisation (systole)

68
Q

What does QRS complex correspond to?

A

ventricular depolarisation (systole)

69
Q

What does T wave correspond to?

A

ventricular repolarisation (depolarisation)

70
Q

What does pre-potential in pacemakers involve?

A
  • decrease in K
  • increase in Na (NaF)
  • increase in Ca (T type) permeability
71
Q

What does AP in pacemakers involve?

A
  • increase in Ca (l type) permability
72
Q

What is 1st degree heart block?

A

Heart’s electrical signals/ conduction are slowed down as they move from atria to ventricles

73
Q

How does 1st degree heart block look like on an ECG?

A

longer and flatter waves between P and R in an ECG

74
Q

What is 2nd degree heart block?

A
  • Electrical signals/ conduction are slowed down between atria and ventricles to a large degree and some signals don’t reach ventricles
  • less contraction of ventricle
75
Q

How does 2nd degree heart block look like on an ECG?

A

On an ECG, the pattern of QRS complex wave doesn’t follow each P wave as it normally would

76
Q

What is 3rd degree heart block?

A

None of the electrical signals reach the ventricles

- is also called complete heart block or complete AV block

77
Q

How does 3rd degree heart block look like on an ECG?

A

P wave occurs at a faster rate and isn’t coordinated with QRS waves (normal pattern is disrupted)

78
Q

What are some examples of arrhythmias?

A
  1. atrial fibrillation
  2. atrial flutter
  3. ventricular fibrillation
79
Q

What is atrial fibrillation?

A

fast and irregular contraction of the atria

80
Q

What is atrial flutter?

A
  • similar to atrial fibrillation
  • main difference is that electrical signals are spread through the atria in a fast and regular pattern (rather than irregular like in fibrillations)
81
Q

What is ventricular fibrillation?

A

disorganised electrical signals make ventricles quiver and send irregular signals

2. Cardiovascular System (42 decks)

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