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Cardiovascular Biology 311 > Lecture 7a; Electrical function of the heart > Flashcards

Lecture 7a; Electrical function of the heart Flashcards

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1
Q

What are the three electrical properties of a myocyte?

A
  • Excitability - AP’s
  • Conductivity - Cell-cell spread of electrical activity
  • Automacity- Intrinsic pacemaker activity.

(Co-ordinated electrical activation and thus contraction rely on these properties being appropriately expressed)

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2
Q

Do cells express the same levels of the electrical properties?

A

No, depending on their position and function they express varying levels of properties

i.e slow (pacemaker) vs fast (perkinje) depolarising cells.

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3
Q

What can abnormal cell function result in with regards to electrical activation?

A

Abnormailites in cell function or groups of cells can lead to abnormal electrical activation and hence poor mechnical performance, which can result in cardiac arrest and death.

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4
Q

What is the electrical property ; conductivity?

A

It is the spread of electrical activity from cell to cell by their intercalated discs which contain nexus junctions.

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5
Q

Give a overview of electrical activity spread through the ventricular wall;

A

Activation spreads through the syncytium from the endocardial surface to the epicardial surface because of the rapidly activated purkinje fibre network covering the endocardial surface.

Note, laminar structure means that is is not a continuous syncytium. So must go between layers. but rapidly within them

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6
Q

How does laminar structure influence the spread of electrical activity?

A

Laminar essentially form a radial pattern they do not interfere with endo-epi pattern of spread during normal sinus beats

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7
Q

How does the laminar structure influence spread of electrical activity from ectopic beats?

A

The discontinuous nature of myocardial laminar may influence the activation from ectopic beats and be the basis of some cardiac arrhythmias.

Ectopic beats want to spread perpendicular to myocyte orientation. (vertically)

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8
Q

What does excitability mean in terms of myocytes?

A
  • Has a resting membrane potential

- Capable of repeatedly repolarising.

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9
Q

When creates the resting membrane potential?

A
  • During diastole, K channels are open while other selective ion membrane channels are closed.
  • K FLOWS OUT because of the transmembrane CONCENTRATION gradient created by Na/K ATPase
  • However K also LEAKS back IN because of the ELECTRICAL gradient
  • Equilibrium occurs at potential given by the nerst equation (Ek- expected to be -90mV)

(K out b/c chemical potential gradient = k in b/c electrical potential gradient)

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10
Q

Are the resting membrane potential of myocytes normally -90mV?

A

No, the membranes are no completely impermeable to other ions such as Na and therefore these ions exert some force and the potential is pulled away from Ek(-90mV)

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11
Q

Do cells exhibit the same action potential?

A

No different cell types exhibit different action potentials

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12
Q

What are the types of cells based on their action potentials?

A

Cells with rapid response

Cells with slow response

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13
Q

Describe the depolarisation of AVN and SAN cells?

A

Cells of the AVN and SAN depolarise in phase 0 at a very slow rate 1-15 V s and this is associated with a very slow propagation of electrical activation.

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14
Q

What other properties do cells of the AV and SA node exhibit?

A

SA and AV node cells have unstable membrane potentials during diastole and hence exhibit pacemaker activity

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15
Q

Refer to 205 notes

A

now

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16
Q

Describe the upstrokes of phase 0 in working myocytes and perkinje fibres;

A

Working myocytes: Fast upstrokes in phase 0, 100-200 V s.

Perkinje Fibres; Very fast upstrokes in phase 0, 500-700 V s.

Both are associated with rapid transmission of electrical activation.

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17
Q

What are some examples of cells with rapid response?

A

Atria, ventricles, fast parts of the conduction system.

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18
Q

What is the resting membrane potential and and threshold potential of rapid response cells?

A

Resting potential; -90mV

Threshold potential; -70mV

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19
Q

Write some short notes on slow response cells;

A

Phase 0: Slow upstroke, Slow inward Ca no fast Na current.

RMP; ~-55mV

Velocity propogation= is low

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20
Q

What is the current view on the characteristics of Na channels?

A

Two gates model.

  • Inactivation gate
  • Activation gate
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21
Q

Describe the two gate Na channel function;

A

There is a change in configuration with different kinetics and voltage dependance.

  • RMPl Activation gates are closed while inactivation gates are open.

At threshold potential (-70mV), there is a conformational change of the gates.

  • Activation gates open allowing Na to flow in, allowing more activation gates to open.
  • the voltage dependance of inactivation gates is opposite (voltage closes them) that of activation gates so there is 1-2 miliseconds before these close. This is the window for Na to enter the cell.
    i. e There are two voltage gates
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22
Q

In Na channels what creates the time window for Na to enter?

A

Voltage dependance and time dependance of the activation and inactivation gates provide a narrow time window for Na entry.

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23
Q

Describe the characteristics of iK1 channels.

A
  • iK1 channels are open at RMP and are the major contributor to maintaining RMP.
  • These channels exhibit inward (anomalous) rectification (permeability reduced with depolarisation) (inward rectifier)
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24
Q

Describe the characteristics of iK channels;

A

iK channels also display inward rectification and are activated near the end of phase 0 (slight repolarisation), but opening of the channels carrying this current is delayed until the end of phase 2

These channels are called the delayed rectifiers (recently described as rapid and sow phases)

The time course for delayed rectification is affected by external factors such as catecholamines.

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25
Q

What generates the absolute refractory period?

A

Na channels display time-dependance and voltage dependance.

Their inactivation gates remained closed throughout phase 2 and half of three phase, this forms the ARP.

Once membrane potential drops below threshold potential, the inactivation gates and activation gates reset.

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26
Q

What is the relative refractory period?

A

This is a time period in the second half of phase 3 and is created by the population of Na channel properties (i.e not all are uniform) and so all reset at different membrane potentials

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27
Q

Describe the refractoriness of perkinje fibres;

A

pirkinje fibres have long refractory periods and hence block many premature excitations of the atria which are conducted through the av junction.

This protection is epescially pronounced at slow heart rates because PF AP duration and hence refractory period varies inversely with heart rates.

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28
Q

How is refractoriness different in the av node cells?

A

The av node’s refractory period does not change over the normal range of heart rates and actually increases at very rapid rates. Therefore when the atria are excited at hgih rates it is the av node which protect the ventricles from the high rate.

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29
Q

What cells are found to have automacity?

A

Normally found in:

Slow response cells;

  • SA node
  • Some cells around the AVN

Fast response cells;
- His-pirkinje network.

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30
Q

What creates automacity?

A

Decrease outward current iK1 and inward current (Ca)

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31
Q

Which outward currents are decreased in cells with automacity?

A
  • Delayed rectifier iK

- Inward rectifier iK1

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32
Q

What inward currents are increased in cells with automacity?

A

Inwards currents increased;

  • iF (inward funny current), mainly inwards Na, activated at negative potentials
  • iCa (slow inwards Ca channels), small contribution which continues into diastole. May contribute to early diastolic repolarisation.
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33
Q

What mechanisms can alter the intrinsic rate of pacemaker discharge?

A

1) Alter the rate of depolarisation (slope)
2) Alter threshold potential
3) Alter maximum diastolic potential.

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34
Q

How do catecholamines alter HR and how?

A

Catecholamines A & NA increase the magnitude of all the pacemaker currents, and also accelerate opening and closure of the iK channel. Overall effect is to increase the rate of diastolic depolarisation.

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35
Q

How does AcH effect HR?

A

Main effect of Ach is to increase membrane K permeability (iK,Ach). Resulting in hyperpolarisation and slower rate diastolic depolarisation.

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36
Q

Why do arrthymias occur?

A

Problems with the conduction system

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37
Q

Describe the cardiac activation sequence;

A 
SA node
atrial myocardium + internodal tracts
AV node
bundle of his
bundle branches
purkinje network
ventricular myocardium
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38
Q

What influences arrthymia properties?

A

Speed of propogation determines the arrthymia properties.

39
Q

What determines the rate of propogation of electrical activity?

A

The spatial and temporal properties of these currents determines the rate of propogation of electrical activity

40
Q

What is the unique storage property of myocyte cell membranes?

A

The cardiac cell membrane can seperate and store charge, and hence exhibits the electrical property of capacitance.

41
Q

What generates membrane resistance?

A

Ionic current flows through ion channels in the cell membrane both at rest and and during excitation and the net permeability of these channels may be represented as membrane resistance.

42
Q

Describe the electrical resistance of the myocardium

A

The electrical resistance of intracellular and extracellular spaces will determine the axial currents which flow in these compartments.

43
Q

What is the electrical properties of the myocyte defined by?

A 
Cm = Membrane capacitance
Rm= membrane resistance
Ri= internal resistance
Ro= external resistance

Ro is much less than Ri or Rm

44
Q

What at a cellular level causes myocyte capacitance?

A

Capacitance is created by lipid storing charge.

45
Q

What does the time taken to reach threshold potential influence?

A

The time taken to reach threshold potential sets the rate at which the action potential spreads and is affected by;

  • cellular electrical characteristics
  • magnitude of the current injected
46
Q

What factors determine the conduction velocity?

A
  • Local current intensity
  • Length constant
  • Time constant
  • Fibre diameter
47
Q

Describe local current intensity.

A

It is the intensity of the local circuit current and hence the rate of rise and the magnitude of the AP and the tissue characteristics.

48
Q

What factors in local current intensity determine the AP?

A
  • Cell type
  • RMP
  • Membrane capacitance
  • Temperature
49
Q

What would decrease local current intensity?

A

A low rate of which membrane potential is brought to threshold.

50
Q

Describe how local circuit current intensity influences conduction velocity when there is a low rate of which membrane potential is brought to threshold;

A

A low rate of which membrane potential is brought to threshold results in;

Delayed AP, resulting in reduced time winow between Na activation gates opening and inactivation gates closing.

Thus less Na enters the cell, generating less local current for further propagation.

51
Q

What does the inward current injected during activation (Na channel) depend on?

A

The density and status of membrane Na channels.

52
Q

Under what circumstances does maximum dV/dt decrease?

A

max dV/dt decreases with;

  • Increased membrane capacitance
  • cooling
  • Partial depolarization (voltage inactivation of Na channels)
53
Q

Describe how the length constant influences conduction velocity;

A

When a current is injected the surrounding cells depolarise to threshold potential. The influence of this current injection decreases with distance (length constance) and depends on the ratio of Rm to longitudinal resistance (Ro + Ri)

Thus AP velocity depends on how far its associated current reaches and hence the electrical properties of the tissue

54
Q

What is the time constant and how does it influence conduction velocity?

A

The time taken for the membrane voltage to reach steady state, is determined by the electrical properties of the myocytes and is expressed as time constant (tm)

Tm = Rm Cm

55
Q

How does the time constant change for conduction velocity?

A

If Rm or Cm increase, then time to reach a new voltage (threshold) is also increased and propagation will be slowed.

56
Q

How does fibre diameter influence conduction velocity?

A
  • Longitudinal resistance to current flow is inversely proportional to fibre cross sectional area.
  • Rate of propagation also depends on fibre radius

Q = Squere root of fibre radius

57
Q

Based on the conduction factors previously evaluated, explain why different parts of the heart conduct at different speeds.

A

SAN and AVN cells have small diameter and few gap junctions (Ri is high) (no Na channels)

Perkinje fibres have large diameter, many gap junctions so Ri is low, plus high density of Na channels

58
Q

What normally ensures co-ordinatation of cardiac excitation?

A

1) Entrainment and supression of lower pacemakers
2) Coordinated excitation via specialised conduction system
3) Existence of prolonged refractory period in the myocardium

Failure of any one of these can result in arrthymias

59
Q

How can arrthymias present?

A

Single or short run of abnormal beats through the ongoing normal rhythm

60
Q

What can mechanisms of arrhythmia be divided into?

A

1) Disorders of impulse formation

2) Disorders of impulse conduction

61
Q

What are the types of disorders of impulse formation?

A
  • Abnormal automacity
  • Triggered activity (afterdepolarisation)
    - EAD
    - DAD
62
Q

What are the types of disorders of impulse conduction?

A
  • Conduction Block
  • Re-rentry
  • Fibrillation
  • Defibrillation
63
Q

How does abnormal automacity contribute to disorders of impulse formation and thus arrhythmia?

A

Either;
- Enhanced automacity in intrinsic pacemaker cells
or
- Automatic properties in non-pacemaker cells

Abnormal automacity occurs because of the three mechanisms which normally ensure pacemaker activity.

64
Q

What causes a cell to more likely have abnormal automacity?

A

Cells with partially depolarised resting membrane potentials.

i.e injured atrial or ventricular cells.

65
Q

What is afterrepolarisation/triggered activity?

A
  • Under some circumstances the resting membrane potential in working myocytes may be unstable during diastole due to fluctuations in transmembrane ion flux.
  • If these resting membrane potentials reach threshold, depolarisation can be triggered generating an ectopic beat
66
Q

What are the types of afterdepolarisations?

A

EAD - Early Afterdepolarisation

DAD- Delayed afterdepolarisation

67
Q

When does EAD occur?

A

These occur during phase 2 and 3 of the AP when heart rate is slow and hence action potentials are prolonged.

68
Q

What is thought to the cause of EAD?

A

EAD during phase 2 ( Ca plateau) is thought to be due to reactivation of Ica, the inward current generating renewed depolarisation

(Ica channels finish refraction early and above threshold so re-open)

69
Q

When do DAD occur?

A

These occur soon after repolarisation in situations where cells have become overloaded with Ca such as high heart rates.

70
Q

What causes DAD to occur?

A
  • Increased SR Ca leads to cycles of spontaneous Ca release and oscillatory changes in intracellular Ca concentration.
  • This leads to oscillations of the NCX current and thus oscillations in the RMP which may reach threshold and trigger an AP.
71
Q

In disorders of impulse conduction what is conduction block?

A

Failure of propagation for example though the AV node.

72
Q

What are the basic requirements for a re-entrant arrhythmia?

A

1) An anatomical circuit
2) Unidirectional conduction block
3) Slowed retrograde conduction

(conditions which are often found in diseased hearts)

73
Q

Describe how the reentrant arrhythmia wors

A

Conductions through the myocardium. Unidireciton conduction block is reached. The propagating action potential goes another route. In doing so it reaches the tissue that was blocked off and proceeds in a slow conduction through the unidirection conduction block (as in this direction of propogation there is no block)

Thus when it reaches the origianl tissue pre-block, if it has repolarized the re-entry can occur and this sets up a sustained local sight of cyclic activation, resulting in tachycardic arrhythmia.

74
Q

What is decremental conduction?

A

The progressive reduction in impulse amplitude as an AP propagates.

75
Q

Where can decremental conduction be observed?

A

In areas characterized by slow Ca currents

  • AV node
  • Normal myocytes damaged by ischemia (have inactivated Na channels)
76
Q

If ischemic damage is severe enough what can occur?

A

The AP generated will not be of sufficient amplitude to fully excite the tissue ahead and ‘block’ will occur.

77
Q

What may decremental conduction factors lead to?

A

These factors may lead to a bi-directional conduction block.

78
Q

What causes a unidirectional conduction block?

A

If the damage to tissue is asymmetric, the depression in conduction will be asymmetric also. Thus decremental conduction can lead to a unidirectional conduction block in one direction and slowed conduction in the other

79
Q

What happens if re-entrant circuit is very small?

A

The re-entrant circuit may be very small (few cells) in which case the activation will spread out in a rotating centrifugal pattern or rotor.

80
Q

Whats an example of a large re-entrant circuit?

A

Wollf parkinson white syndrome

81
Q

What is the functional circuit “lead circle concept” in disorders of impulse conduction?

A

Re-entry may occur around an area of functional block. The centre of the circuit is invaded my multiple wavelets converging on causing block in the center.

Refer to page 65

82
Q

What is fibrillation?

A

Total disorganisation of excitation sequence.

83
Q

Does ECG show a pattern to fibrillation?

A

No

84
Q

What does fibrillation lead to?

A

The disorganised contraction of the heart and thus no coordinated pump activity.

85
Q

What can fibrillation be divided into?

A

Atrial Fibrillation

Ventricular fibrillation

86
Q

Who is atrial fibrillation common in?

A

Older people

87
Q

What does atrial fibrillation lead to?

A

There is no co-ordinated contraction of the atriums therefore no ventricular top up.

Leads to reduced exercise tolerance and can cause stroke.

88
Q

What is ventricular fibrillation also known as?

A

Cardiac arrest

89
Q

What happens in ventricular fibrillation?

A

no co-ordinated contraction of the ventricles, no CO thus no oxygen supply to the brain or any organs, death ensues

Unless CPR is done till defibrillation restores normal rhythm.

90
Q

When does ventricular fibrillation normally occur?

A

Normally occurs in ischemic hearts (MI), or the result of electric shock, or may result from the degeneration of another abnoraml rhythm such as ventricular tachycardia.

91
Q

What is defibrillation?

A

Return of heart to normal rhythm.

92
Q

How does defibrillation work?

A

A large electric shock is applied across the heart and depolarises all cells at once allowing normally pacemaker activity to take over.

93
Q

What contributes to defib effectiveness?

A

The disconuities in myocardium resulting form the laminar organisation.

Cardiovascular Biology 311 (18 decks)

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