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BMS 242 - CVS respiratory > Electrical activity of the heart > Flashcards

Electrical activity of the heart Flashcards

1
Q

What forms electrical synapses?

What does this allow?How?

A

Desmosomes (cell-cell connections)

Allowing:

  • FAST spread of electrical activity from one cell to the next
  • Coordinated contraction of the atria and the ventricles

As there are NO GAPS between the cells

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2
Q

Describe the pathway of electrical conduction through the heart

A

1) Initiation at the SINO-ATRIAL NODE
2) Conduction to the atria and atrioventricular node
3) Passes through the ATRIOVENTRICULAR RING
4) Passage through the bundle of His in the AV ring
5) Purkinje system distribution at the apex of the heart to the ventricular muscle cells

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3
Q

What is the main pacemaker of the heart?

A

The SINO-ATRIAL node

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4
Q

When can the AV node become the dominant pacemaker of the heart?

A

When there is a problem with the SA node

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5
Q

What is the atrioventricular ring of the heart?

A

The STRUCTURAL part

Where MYOCYTES are attached to

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6
Q

Where is the SA node found?

A

In the POSTERIOR aspect of the heart

At the junction between the superior vena cava and right atrium

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7
Q

Where does the electrical activity from the SA node travel to?

A

To the:
- RIGHT and LEFT atrium (left atrial through the Brachmann’s bundle)

  • Atrioventricular node (via the atrial myocytes)
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8
Q

What is the speed of conduction of the atrial myocardium?

A

1.00m/s

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9
Q

How does the electrical conduction travel from the sinoatrial node to the left atrium?

What does the passage of this electrical activity through here cause?

A

Brachmann’s bundle - the INTERATRIAL tract from the right atrium to left atrium

Causes contraction of both of the atria

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10
Q

Where is the atrioventricular node found?

A

In the posterior part of the heart

RIGHT side interatrial septum

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11
Q

What is the septum?

A

Fibrous structure which spilts the right and left sides of the heart

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12
Q

What is the conductance speed from the AN to the N?

A

0.005m/s (slower than the atrial myocardium)

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13
Q

What is the AV delay?

What is is required for?

A

Delay of impulses from the AV node

Required to:

  • Allow the atrial contraction to finish
  • Maximise expulsion of blood from the atria –> ventricles
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14
Q

What is AV refractiveness?

What is it required for?

A

A delay before electrical activity can pass through the AV node again

Required to:
- Prevent excess ventricular contraction

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15
Q

What is AV refractiveness?

What is it required for?

A

A delay before electrical activity can pass through the AV node again

Required to:
- Prevent excess ventricular contraction

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16
Q

When does the AV refractiveness increase?

Why?

A

At HIGH heart rate

To give more time for the atria to contract and expel blood into the ventricles

As a higher heart rate required higher blood flow in order to provide more oxygen

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17
Q

What is the contraction speed through the bundle of his?

Purkinje fibres?

Ventricular muscle?

What are the different conduction velocities important for?

A

1m/s

4m/s

1m/s

Different velocities are important for the normal timing of the contraction of the different parts of the heart

Maximise the spread of the electrical signal and the contraction of the heart/pumping of blood

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18
Q

Where do the Bundle of His and the Purknje fibres lie in the heart?

A

In the septum

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19
Q

How does the heart contract?

Why?

A

In a twisting/spiraling manner

To evoke a torsion and expel blood into the vessels

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20
Q

Why does spiral muscle contraction occur?

A

Due to the timing and way the ventricular muscles contract

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21
Q

What are the 2 types of cardiac action potentials?

Why are they different to?

A

1) Nodal
2) Contractile (myocyte)

Different to the action potentials seen in nerves

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22
Q

Which parts of the heart have ‘nodal’ cardiac action potentials?

A
  • SA node

- AV node

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23
Q

Which parts of the heart have ‘contractile’ cardiac action potentials?

A
  • Atrial muscle
  • Purkinje fibres
  • Ventricular muscle
24
Q

What do the action potentials from the nodes do?

A

INITIATE contraction of the heart

25
Q

What is the difference between ‘nodal’ and ‘contractile’ action potentials in the heart?

A

Nodal APs are AUTORHYTHMIC:
- Can fire APs without receiving any other signals

Contractile APs are NON-AUTORHYHMIC:
- Need signals from the pacemaker cells to produce an action potential

26
Q

What can modify the nodal AP signals?

A

Inputs from the sympathetic/parasympathetic nervous system

27
Q

What is the shape of the nodal AP?

A

Similar to normal AP:

  • Slow increase
  • Reach a peak
  • Slow decrease
28
Q

What is the shape of a contractile AP?

A
  • Very SHARP increase
  • Very TINY but SHARP decrease to a flat line
  • Flat line for a little
  • Gradual decrease
29
Q

What is the resting membrane potential of pacemaker cells?

A

Not constant

30
Q

When do pacemaker cells depolarise?

A

-60mV

depolarise slowly

31
Q

What properties do the pacemaker cells show?

A

Automaticity

Rhythmicity

32
Q

What can happen if the nodes are not functioning?

A

The Purkinje fibres can sometimes act as pacemakers

Switch from contractile to nodal properties

33
Q

What is the dominant node?

A

The node that fires the APs more frequently

Should be the SA node

34
Q

Describe the pacemaker pre-potential

A

Slow influx of Na+ - causes slow increase in membrane potential

35
Q

What is the pacemaker pre-potential mediated by?

A

Low K+ efflux

High Na+ (cation) influx

36
Q

What is the pacemaker pre-potential regulated by?

A
  • Innervation
  • Temperature
  • Other pacemakers (in disease conditions)
37
Q

What is the If current?

A

‘Funny current’:

- Inward current through a hyper-polarization induced CATION selective channel

38
Q

When is the If current inhibited?

A

During REPOLARISATION

39
Q

When is the If current activated?

A

At the END of REPOLARISATION

40
Q

What is the threshold of the pacemaker action potential?

What happens at this threshold?

A

-40mV to -50mV

At the threshold - fast Ca2+ influx to mediate DEPOLARISATION

41
Q

What causes the repolarisation of the membrane?

A

K+ EFFLUX

42
Q

How are pacemaker cells controlled?

How is this done?

A

By fibres regulating the PREPOTENTIAL:
1) VAGAL fibres (ACh)

  • PARAsympathetic NS
    2) SYMPATHETIC fibres (NAdr)

Achieved by:
- Regulating the If current using cAMP
AND/OR
- Calcium clock oscillations

43
Q

How do the vagal fibres regulate the prepotential of the pacemaker cells?

What effect does it have on the heart rate?

A
  • Ach released
  • HYPERPOLARISATION of the membrane (more -ve)

1) LONGER the prepotential slope
- SLOWER the heart rate

2) DECREASED prepotential slope (more -ve)
- Increase time to reach AP

44
Q

How do the sympatheic fibres regulate the prepotential of the pacemaker cells?

What effect does it have on the heart rate?

A

INCREASE the prepotential slope

INCREASE the firing rate (reach AP faster)

INCREASE heart rate

45
Q

How do vagal/sympathetic fibres regulate the If current?

A

Regulate cAMP:
- Ach (from vagal fibres) INHIBITS cAMP by DECREASING the activation of M2

  • NAdr (from sympathetic fibres) ACTIVATES cAMP by INCREASING the activation of B1 and B2
46
Q

What are calcium clock oscillations?

A

Rhythmic alterations of SR Ca2+ release

47
Q

Describe the AP of cardiac muscle

A

1) CONSTANT resting membrane potential (unlike pacemaker cells)
2) MASSIVE INFLUX of Na+ into the cell

  • Huge, sharp increase in membrane potential
  • FAST activation of voltage gated Na+ channels

3) LONG PLATEAU phase
- Elongation of depolarisation
4) FAST DEPOLARISATION and OVERSHOOT

  • K+ channels open
  • Rapid outflow
48
Q

What causes the elongation of depolarisation in the AP of cardiac muscle?

A

Entry of Ca2+ through SLOW calcium channels

49
Q

What is the consequence of the elongation of depolarisation in the AP of cardiac muscle?

A

Unable to undergo SUMMATION

Refractory period

50
Q

What is the difference between the ‘absolute’ and ‘relative’ refractory periods in the AP of cardiac muscle?

A

Absolute:
- CANNOT fire anymore AP

Relative:

  • POSSIBLE to fire AP but must have a very large AP for this to occur
  • RARE in the heart
51
Q

Which channels are involved in the AP of cardiac myocytes?

A

Nav 1.5

Cav 1.2

HCN4

K+

52
Q

What is the NAV 1.5 channel?

A

Na+ voltage gated channel in cardiac myoctyes

53
Q

What inhibits the NAV 1.5 channel?

A

TTX and local anaesthetics

54
Q

What is the Cav 1.2 channel?

A

Ca2+ VG channel

55
Q

What is the HCN4 channels?

A

If channel (pacemaker current)

BMS 242 - CVS respiratory (15 decks)

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