Electrical Events of the Cardiac Cycle Flashcards

1
Q

Sino-Atrial Node

A

Spontaneously firing cells of the heart; located at the right atrial wall near the opening of the SVC

Natural Pacemaker

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2
Q

Atrio-ventricular cells

A

Sponteneously firing cells located at the base of the right atrium near the septum, just above the AV junction

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3
Q

How does an Action Potential travel along the heart

A

An impulse begins in the Sinoatrial Node; this sends a wave of excitation across both atria simultaneously

That impulse then travels to the Atrioventricular Node

This action potential then travels through the bundle of His and separates along the septum; traveling down where it reaches the purkinje fibres then the myocardial cells that make up the ventricles

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4
Q

Spontaneous Discharge Rates of the heart nodes

A

SA Nodes: 70-80 Action Potentials/min

AV Nodes: 40-60 Action Potentials/min

Purkinje Fibres: 20-40 Action Potentials/min

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5
Q

What happens to the cells of the pacemaker when action potential reaches membrane resting potential (-60mv)

A

The voltage changes properties of ion channels in cells

Na+ channels open
Ca2+ channels open
K+ channels close

This causes charge to increase as Na+ and Ca2+ are at higher concentrations outside than inside the cell, leading to depolarisation

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6
Q

What happens when the voltage of pacemaker cells reach threshold potential

A

More Ca2+ channels open and the voltage increases even more to about 0mv as a result of the concentration gradient

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7
Q

What happens to the cells of the pacemaker when action potential reaches 0mv

A

Some Na+ and Ca2+ channels begin to close, but more importantly, K+ channels open, causing an efflux that decreases the voltage leading to repolarisation

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8
Q

Roughly how long does an impulse take to go through the SA node

A

Approximately one impulse per second
(look at x-axis)

**60 bpm

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9
Q

Describe the rates of impulses that travel during a cardiac impulse

A

Impulse travels rapidly from the SA node through the atria, then significantly slows down at the AV node by a factor of 20 to cause a delay

After this it rapidly goes through the bundle of his and purkinje fibres where it spreads rapidly through ventricular muscle cells

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10
Q

Properties that allow waves of excitation to travel rapidly between myocardial cells

A

Gap junctions (nexi) that provide low resistance pathways, allowing cardiac muscles to function as a syncitium (single unit)

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11
Q

What is the role of the AV delay during cardiac contraction

A

This allows atrial excitation and contraction to be complete before ventricular contraction, enabling efficient emptying of blood from atria to ventricles

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12
Q

How is ventricular excitation kept synchronous

A

The rapid spread of impulse down the septum (Bundle of His) and through purkinje fibres

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13
Q

What is the resting potential of a pacemaker cell versus a ventricular cell

A

Pacemaker: -60mV
Ventricular: -90mV

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14
Q

How does an action potential of a ventricular contractile cell begin

A

Unlike pacemaker cells, they are not spontaneous at resting potential (-90mV) until extrinsic factors come into play

When a wave of excitation arrives at the cell, Na+ channels open, causing significant Na+ influx

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15
Q

What happens to a ventricular cell’s action potential after becoming positive and peaking

A

K+ channels open and some K+ ions leave the cell

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16
Q

What creates the plateau phase of ventricular cells during contraction/when K+ ions begin efflux

A

Ca2+ ion channels open and create a plateau as Ca2+ influx counteracts the K+ efflux

17
Q

What causes the ending of the plateau phase of ventricular contraction

A

K+ efflux eventually increases as more channels open, leading to rapid depolarisation back to resting potential

18
Q

Excitation-contraction coupling (Systole)

A

Influx of Ca2+ moves into myocardial contractile cells during action potential; triggering release of further Ca2+ from sarcoplasmic reticulum

Free Ca2+ activates contraction of myocardial fibres (SYSTOLE)

Amount of Ca2+ determines force of contraction

19
Q

Excitation-contraction coupling (Diastole)

A

Once Ca2+ reaches a certain level

there is an uptake of Ca2+ by the sarcoplasmic reticulum
AND
An extrusion of Ca2+ by Na+/Ca2+ exchange
AND
Outward Ca2+ pump

This lowers free Ca2+ allowing relaxation
(Diastole)

20
Q

Role of plateau phase of ventricular contractile cells

A

Cardiac contractile cells have a long refractory period unlike skeletal muscle; this allows the cell to beat then relax as opposed to simply staying contracted as additional stimuli in SkM can cause fused contraction/tetanus

Plateau phase is what provides that long refractory period, preventing tetanus

21
Q

Describe the direction at which cardiac impulse travels

A

From endocardium to epicardium (in to out)

From apex to base

22
Q

Sympathetic Neuronal Modulation of Heart Rate

A

Noradrenaline activates the β1 adrenoceptors in SA node which open ion channels, leading to an increase in the funny current and Ca2+ induced impulse

Increases heart rate (Yellow is sympathetic)

23
Q

Funny Current

A

Mixed sodium–potassium current that causes depolarisation of the heart alongside the calcium induced impulse

24
Q

Parasympathetic Neuronal Modulation of Heart Rate

A

Parasympathetic nerves release ACh which activate M2 muscarinic receptors in SA node

ACh causes hyperpolarisation of cardiac cells by increasing K+ permeability, making them further away from threshold potential

Additionally, ACh decreases the amount of sodium in the funny current, as well as decreasing Ca2+ moving into the pacemaker cells

Decreases heart rate (green is parasympathetic)