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Y1 - Cardiovascular > Physiology: Origin and Conduction of Cardiac Impulses > Flashcards

Physiology: Origin and Conduction of Cardiac Impulses Flashcards

1
Q

Define autorythmicity

A

The heart is able to beat in the absence of an external stimuli

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2
Q

Where does excitation of the heart originate?

A

The sinoatrial (SA) node

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3
Q

What types of cells initiate heart excitation in the SA node?

A

Pacemaker cells

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4
Q

Where is the SA node located?

A

The upper right atrium

Close to where the superior vena cava enters

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5
Q

Define what is meant by a heart in sinus rhythm

A

When the heart is controlled by the SA node

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6
Q

Describe the resting membrane potential of cells in the SA node

A

Not stable, it moves towards depolarisation before the action potential

Lowest point is -60mV

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7
Q

Describe the pacemaker potential

A
  • occurs between action potentials
  • Slow depolarisation of membrane potential before the action potential
  • Generated by cells of the SA node
  • Takes the membrane potential to the threshold for an action potential
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8
Q

What occurs after the pacemaker potential takes the membrane potential to a threshold?

A

An action potential is generated

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9
Q

Give the factors that contribute to the pacemaker potential

A
  • Decreased K+ efflux (This slows down the depolarisation)
  • Na+ influx (funny current)
  • Transient Ca2+ influx
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10
Q

Describe the ionic basis for the action potential in slow response exhibiting cells

A

Depolarisation:

  • Activation of L-type Ca2+ channels
  • Resulting in a Ca2+ influx

Repolarisation:

  • Inactivation of L-type Ca2+ channels
  • Activation of K+ channels, resulting in K+ efflux
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11
Q

Describe the route by which cardiac excitation spreads across the heart

A

Produced in the SA node

SA node –> AV node

AV node delays the signal

AV node –> bundle of His

Bundle of His branches into left and right branch

–> Purkinje fibres

–> cell-to-cell conduction within ventricles

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12
Q

How does cell excitation spread through both atria?

A

Gap junctions across the intercalated disc between cells

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13
Q

How does cell excitation spread from the SA node to the AV node?

A
  • Mainly gap junctions across the intercalated disc between cells
  • Some internodal pathways
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14
Q

Describe the AV node

A
  • Located at the base of the right atrium
  • Have a slow conduction velocity (delays signals)
  • Only point of electrical contact between the atria and ventricles
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15
Q

What is the purpose of the AV node delaying the conduction?

A

To allow the atrial systole before ventricular systole

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16
Q

Is the action potential in contractile cardiac myocytes the same as in pacemaker cells?

A

No

Contractile cardiac myocytes’ action potentials have phases 0, 1, 2, 3, 4, and 5

Pacemaker cells’ action potentials have phases 0, 3, and 4

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17
Q

Describe the resting potential of Atrial and Ventricular Myocytes

A

-90mV

Remains constant

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18
Q

Describe the basics of the phases of Ventricular Muscle Action Potential

A

Phase 0:
- Rapid upstroke due to Na+ influx

Phase 1:

  • Closure of Na+ channels
  • Transient K+ efflux

Phase 2:
- Ca2+ influx

Phase 3:

  • Closure of Ca2+ channels
  • K+ efflux

Phase 4:
- Resting membrane potential

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19
Q

Describe the effect of sympathetic and parasympathetic stimulation on heart rate

A 
Sympathetic:
Increases rate (+ve chronotropic effect)
Parasympathetic:
Decreases rate (-ve chronotropic effect)
20
Q

Which nerve supplies the parasympathetic supply to the heart?

A

Vagus nerve

It supplies the SA and AV node

21
Q

Why does vagal tone dominate under resting conditions?

A
  • The intrinsic heart rate is ~100 bpm
  • Vagal tone is required to slow the rate to its normal level at ~70 bpm
  • Thus under resting conditions the vagus nerve exerts a constant influence on the SA node
22
Q

Define a the range of a normal resting heart rate

A

60-100 bpm

23
Q

Define bradycardia and tachycardia

A

Bradycardia - RESTING heart rate < 60 bpm

Tachycardia - RESTING heart rate > 100 bpm

24
Q

Describe the effect of vagal stimulation on the AV nodal delay

A

vagal stimulation increases AV nodal delay

25
Q

What is the neurotransmitter in the parasympathetic supply of the heart?

A

Acetylcholine acting through muscarinic M2 receptors

26
Q

Describe the effect of vagal stimulation on pacemaker potentials

A
  • Stimulation causes a hyperpolarization
  • Takes longer to reach threshold
  • Slope of Pacemaker Potential DECREASES
  • Frequency of action potentials decrease
27
Q

Define a +ve and -ve chronotropic effect

A

+ve chronotropic effect:
HR increases

-ve chronotropic effect:
HR decreases

28
Q

Define a +ve and -ve inotropic effect

A

+ve inotropic effect:
Increased strength of muscular contraction

-ve inotropic effect:
Decreased strength of muscular contraction

29
Q

What areas of the heart are innervated by sympathetic nerves?

A
  • SA node
  • AV node
  • Myocardium
30
Q

Describe the effect of sympathetic stimulation on the heart

A
  • +ve chronotropic effect
  • Decreased AV delay
  • +ve inotropic effect
31
Q

What is the neurotransmitter of the sympathetic stimulation of the heart?

A

Noradrenaline

Acting through β1 adrenoceptors

32
Q

Describe the effect of sympathetic stimulation on pacemaker potentials

A
  • Slope of pacemaker potential increases
  • Threshold reached faster
  • Frequency of action potentials increases
33
Q

Which cells exhibit a fast response action potential?

A
  • Atrial and ventricular myocytes

- Purkinje fibres

34
Q

Which cells exhibit a slow response action potential?

A
  • SA node

- AV node

35
Q

Why are fast and slow response action potentials named as they are?

A

They refer to the speed of depolarisation

e.g. atrial and ventricular myocytes depolarise faster hence they exhibit the fast response

36
Q

What are the main directions of ion flow, and there effect on polarisation of:

  • Na+
  • K+
  • Ca2+
A

Na+:
- Inwards, depolarising

K+:
- Outwards, re-polarising

Ca2+:
- Inwards, depolarising

37
Q

Describe phase 4 of the fast response action potential

A
  • Resting potential
  • During diastole
  • Constant at -90mV
  • Outward flux of K+ is dominant
  • K+ outflow due via inward rectifier K+ channels
  • Ion concentrations are maintained by Na+/K+-ATPasw
38
Q

Why is the membrane potential of a fast response action potential exhibiting cell at phase 4 not the same as the equilibrium potential for K+?

A

As although K+ outwards flow is dominant there is a small depolarising ‘leak’ influx of Na+

39
Q

Describe phase 0 of the fast response action potential

A
  • Rapid depolarisation (upstroke)
  • Threshold achieved via an action potential from a neighbouring cell throughgap junctions
  • At threshold: rapid activation of voltage-activated Na+ channels
  • Inward flux of Na+ is dominant
  • The voltage-activated Na+ channels rapidly inactivate during the depolarisation to a non-conducting state
40
Q

Describe the the action of the voltage-activated Na+ channels in phase 0 of the fast response

A
  • Activated after the threshold potential is met (~-65mV)
  • Threshold achieved via an action potential from a neighbouring cell throughgap junctions
  • Facilitate the inward flux of Na+
  • Rapidly inactivate during the depolarisation to a non-conducting state
41
Q

Describe phase 1 of the fast response action potential

A
  • Small re-polarisation before phase 2
  • Voltage-activated Na+ channels from phase 0 inactivate
  • Transient outward K+ current, mediated by voltage activated K+ channels

Summary:
Na+ influx stops, transient outflow of K+, so re-polarisation

42
Q

Describe phase 2 of the fast response action potential

A
  • Plateau phase
  • Ca2+ influx (depolarising) balances with an outward flux
    of K+
  • Inward flux of Ca2+ is via voltage-activated Ca2+ channels (L-type channels)
  • The phase ends when the voltage-activated Ca2+ channels inactivate, and K+ outflow dominates
43
Q

Describe voltage-activated Ca2+ channels (L-type channels) and their role in phase 2 of the fast response action potential

A
  • Activate during the upstroke (phase 0) at ~-30mV
  • Activate slowly
  • Allow inward flux of Ca2+
  • Then inactivate very slowly
  • Their slow inactivation produces a long lasting Ca2+ current, which allows for the crucial to cardiac muscle contraction
44
Q

Describe phase 3 of the fast response action potential

A
  • Re-polarisation
  • Starts as voltage-activated Ca2+ channels inactivate, and K+ outflow dominates
  • Ikr initially contributes to re-polarisation, the Iks does more slowly
  • Ik1 contributes to re-polarisation and assumes dominance in phase 4 again
45
Q

Describe the differences between the fast response action potential in atrial and ventricular myocytes

A

Atrial myocytes have an additional ultra-rapid delayed outward rectifier K+ current

This allows phase 3 to begin faster

Thus the plateau phase is less evident (shorter)

46
Q

Describe how the slow response differs from the fast response action potential

A
  • Phase 4 is not constant
  • The maximum polarisation is -90mV in the fast response, but -70mV in the slow response
  • Upstroke (phase 0) is less steep
  • Upstroke is due to the opening of L-type Ca2+ channels (rather than voltage-activated Na+ channels)
  • No phase 2, but a more gradual phase 3
  • Phase 3 due to opening of delayed rectifier K+ channels
47
Q

Describe the funny current

A
  • At the end of phase 3 HCN channels activate in response to hyperpolarization
  • HCN channels conduct Na+ ions inwards, causing depolarisation
  • This contributes to the pacemaker potential

Y1 - Cardiovascular (19 decks)

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