Electrical Activity Flashcards

1
Q

Define depolarisation

A

Cell becomes less polarised. The inside of cell is less negative than normal

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2
Q

How do pacemaker cells / autorhythmic cells generate action potentials spontaneously?

A

Because it has an unstable resting membrane potential.

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3
Q

Which two ion channels are responsible for the unstable resting membrane potential of authorhythmic cells? Describe the movement of ions.

A

Funny channels = slow entry of Na into cell (causes depolarisation)
T type calcium channels = transient calcium influx

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4
Q

Which ion is higher in concentration outside the cell compared to inside? Calcium, potassium or sodium?

A

Sodium and calcium. K is more concentrated inside

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5
Q

When do the funny channels close?

A

Half way through the pacemaker potential. Once closed, T-type calcium channels open, which allows for further depolarisation until the threshold is reached.

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6
Q

Which ion and ion channel is responsible for the rapid depolarisation of autorhythmic cells?

A

L-type calcium channels open, allowing for large influx of calcium.

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7
Q

Which ion and ion channel are responsible for the repolarisation of autorhythmic cells?

A

At peak of depolarisation, voltage gated K channels open, allowing for large K efflux

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8
Q

Which ion channel maintains the stable resting membrane potential of contractile cells?

A

A leaky K channel. Slow K efflux

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9
Q

Once the flow of current arrives via gap junctions, what causes the depolarisation of contractile cells?

A

Voltage gated Na channels = rapid Na influx

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10
Q

Explain the two ion channels contributing to the plateau of the contractile cell’s action potential

A

Transient K channels open, allowIng quick but brief K efflux. Causes slight repolarisation, then channel closes
L-type Ca channels open, allowimg slow Ca influx, which prolongs the peak of thr action potential

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11
Q

What causes the repolarisation of contractile cells?

A

L-type calcium channels close, causing voltage gated K channels to open. Fast K efflux repolarises cell

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12
Q

Primary, secondary and tertiary pacemaker of heart?

A

SA node
AV node
Purkinje fibres

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13
Q

What happens when damage to AV node causes purkinje fibres to become primary pacemaker?

A

Complete heart block.
Caused by no electrical signal tranduction between atria and ventricles
Purkinje fibre AP rate is also far too slow

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14
Q

Define an ectopic focus

A

When purkinje fibres become faster than SA node. Causes premature heart beats and PVC

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15
Q

Define PVC

A

Premature ventricular contraction

= less blood ejected

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16
Q

Causes of ectopic focus?

A

Alcohol, nicotine, stress, caffiene, anxiety, etc

17
Q

What is the major connection between atria and ventricles?

18
Q

Why is there a delay of transduction at the AV node?

A

To allow the atria to finish contracting before the ventricles start

19
Q

Why is the refractory period of a cardiomyocyte longer than regular muscle cells?

A

To ensure each contraction is followed by enough time to ensure the chambers refill before the next contraction. Prevents tetanus contractions

20
Q

Where does the electrical signal travel after SA node and AV node?

A

Bundle of his, then apex of ventricle

21
Q

After the electrical signal reaches the ventricle apex, where does it go?

A

To the purkinje fibres, then to the rest of the ventricle

22
Q

P wave of ECG =?

A

Atrial depolarisation + contraction

23
Q

QRS complex =?

A

Venctricular depolarisation + contraction + simultaneous repolarisation of atria

24
Q

T wave =?

A

Ventricular relaxation + repolarisation

25
What would ventricle fibrillation look like on ECG?
Rapid, disorganised and irregular signals
26
Describe atrial flutters
Increased rate of atrial contractions. Doesnt allow for ventricles to fill properly. Ventricles will not contract with every atrial contraction (e.g. 3:1)
27
Describe complete heart block
AV node impairment, resulting in ventricles not being stimulated. The atria will contract normally, but the ventricles will generate their own pulses that are much slower than atria pulses / contractions.
28
Complete heart block appearance on ecg?
Normal P wave (due to normal atrial contractions) Slow QRS and T waves (slow, but still regular) Extra lines may appear which represent atrial repolarisation (normally masked by QRS complex, but they are no longer simultaneous)
29
PSNS effect on ions and HR?
Opens K channels, causing hyperpolarisation, meaning takes longer to reach threshold. = slower HR
30
SNS effect on HR and ions?
Increases closure of K channels, meaning threshold is reached sooner. Increases HR
31
PSNS vs SNS transmitter?
``` Acetylcholine = PSNS Adrenaline = SNS ```