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

Physiology: Origin and Conduction of Cardiac Impulses Flashcards

(47 cards)

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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

Study These Flashcards
A 
Sympathetic:
Increases rate (+ve chronotropic effect)

Parasympathetic:
Decreases rate (-ve chronotropic effect)
20
Q

Which nerve supplies the parasympathetic supply to the heart?

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A

Vagus nerve

It supplies the SA and AV node

21
Q

Why does vagal tone dominate under resting conditions?

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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

23
Q

Define bradycardia and tachycardia

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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

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A

vagal stimulation increases AV nodal delay

25
What is the neurotransmitter in the parasympathetic supply of the heart?
Acetylcholine acting through muscarinic M2 receptors
26
Describe the effect of vagal stimulation on pacemaker potentials
- Stimulation causes a hyperpolarization - Takes longer to reach threshold - Slope of Pacemaker Potential DECREASES - Frequency of action potentials decrease
27
Define a +ve and -ve chronotropic effect
+ve chronotropic effect: HR increases -ve chronotropic effect: HR decreases
28
Define a +ve and -ve inotropic effect
+ve inotropic effect: Increased strength of muscular contraction -ve inotropic effect: Decreased strength of muscular contraction
29
What areas of the heart are innervated by sympathetic nerves?
- SA node - AV node - Myocardium
30
Describe the effect of sympathetic stimulation on the heart
- +ve chronotropic effect - Decreased AV delay - +ve inotropic effect
31
What is the neurotransmitter of the sympathetic stimulation of the heart?
Noradrenaline Acting through β1 adrenoceptors
32
Describe the effect of sympathetic stimulation on pacemaker potentials
- Slope of pacemaker potential increases - Threshold reached faster - Frequency of action potentials increases
33
Which cells exhibit a fast response action potential?
- Atrial and ventricular myocytes | - Purkinje fibres
34
Which cells exhibit a slow response action potential?
- SA node | - AV node
35
Why are fast and slow response action potentials named as they are?
They refer to the speed of depolarisation e.g. atrial and ventricular myocytes depolarise faster hence they exhibit the fast response
36
What are the main directions of ion flow, and there effect on polarisation of: - Na+ - K+ - Ca2+
Na+: - Inwards, depolarising K+: - Outwards, re-polarising Ca2+: - Inwards, depolarising
37
Describe phase 4 of the fast response action potential
- 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
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+?
As although K+ outwards flow is dominant there is a small depolarising 'leak' influx of Na+
39
Describe phase 0 of the fast response action potential
- Rapid depolarisation (upstroke) - Threshold achieved via an action potential from a neighbouring cell through gap 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
Describe the the action of the voltage-activated Na+ channels in phase 0 of the fast response
- Activated after the threshold potential is met (~-65mV) - Threshold achieved via an action potential from a neighbouring cell through gap junctions - Facilitate the inward flux of Na+ - Rapidly inactivate during the depolarisation to a non-conducting state
41
Describe phase 1 of the fast response action potential
- 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
Describe phase 2 of the fast response action potential
- 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
Describe voltage-activated Ca2+ channels (L-type channels) and their role in phase 2 of the fast response action potential
- 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
Describe phase 3 of the fast response action potential
- 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
Describe the differences between the fast response action potential in atrial and ventricular myocytes
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
Describe how the slow response differs from the fast response action potential
- 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
Describe the funny current
- 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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