Lecture 6 - Cardiac Rhythm Flashcards

1
Q

What are the two types of arrhythmias?

A
  1. Impulse formation.

2. Impulse conduction.

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2
Q

Briefly describe impulse conduction?

A

This is typically due to a re-entrant circuit, LBBB/RBBB or partial/complete AV block. It can be divided into two types:

  1. Global - atria to ventricles and back.
  2. Local - circle in dead tissue.
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3
Q

What is required for a re-entrant circuit to appear?

A
  1. Unidirectional block.
  2. Length of refractory period.
  3. Critical timing.
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4
Q

What is a unidirectional block?

A

This is where a signal cannot go down through dead tissue, however the other signal on the other side of the block can come up through it. Basically the block is only in one direction.

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5
Q

Describe what normally happens with signals?

A

If a signal travels down pathway 1 and 2 they will propagate normally. If there was a pathway 3 that connected 1 and 2, the two action potentials would meet and cancel one another.

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6
Q

What happens if there is a unidirectional block?

A

If there was a unidirectional block in pathway 2, an action potential would propagate down pathway 1 but not pathway 2. The action potential propagated would then travel back up pathway 2. If by the time the action potential comes through to pathway 1 and the refractory period is over then re-entry occurs as another AP can occur.

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7
Q

What happens in small local re-entry?

A

There is a unidirectional block, and parts of the ventricles contract out of sync with the rest of it. Even if the SA node sends signals down, it can’t get into the re-entry circuit.

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8
Q

What happens in global re-entry?

A

There is an accessory pathway from the ventricles to the atria e.g. WPWS (‘bundle of kent’). The cycle of re-entry keeps occurring and can result in a supraventricular tachycardia.

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9
Q

Can you still get a re-entry circuit with just a unidirectional block alone?

A

Normally the AP will go around the tissue (like described before) and when it reaches pathway 1, it will stop because the muscle is still in the relative refractory period. This means re-entry won’t occur. For re-entry to occur:
Wavelength = ERP x CV.

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10
Q

What happens if conduction velocity has slowed down combined with a unidirectional block?

A

If conduction velocity of the AP has slowed down, it indicates that the signal must not be coming from SA node or AV node it could be due to an ectopic beat. When the CV has slowed down (decreased) then by the time the signal comes around the block, the relative refractory period is over (ERP) so a re-entry occurs as the signal/AP keeps looping.

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11
Q

What happens if relative refractory period time has decreased combined with a unidirectional block?

A

ERP only decreases when the plateau of the AP (due to calcium influx) has decreased. Basically something is causing the cell to push out calcium ions quickly. This means that when the AP comes around to pathway 1, the cell is not in ERP so the AP continues and keeps looping.

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12
Q

What happens with ischaemic tissue?

A

The tissue is dead so it forms a block in the heart.

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13
Q

Briefly describe impulse formation?

A

There is a problem with how the signal is formed e.g. ectopic beats, EADs, DADs.

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14
Q

What are early-after-depolarisations (EADs)?

A

This is when there is another AP created too quickly.

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15
Q

Describe EADs?

A

These are caused by prolonged APs which allow the ICa2+ (L) to reactivate - essentially allowing calcium into the cell. This channel is time dependent - so after certain amount of time being closed it will open again. Basically the calcium channels open again still in plateau causing the plateau to be going for longer thus creating a prolonged AP.

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16
Q

What causes a prolonged AP?

A
  1. Drugs e.g. amiodarone.
  2. Decrease in serum potassium - hypokalaemia.
  3. Ion channel mutations - IKs (LQT1), IKr (LQT2), INa (LQT3).
17
Q

How does hypokalaemia cause a prolonged AP?

A

Potassium normally causes the plateau to end, if there is not enough potassium in the blood then the plateau is longer and AP is longer as well.

18
Q

What are delayed-after-depolarisations (DADs)?

A

This is when there is dead tissue and caclium is released in diastole (when relaxed).

19
Q

Describe what happens in DADs?

A

There is an influx of calcium around the T wave (diastole - relaxing) so depolarisation occurs but it is delayed. This can lead to arrhytmias.

20
Q

What happens to conduction in myocardial infarcts?

A

The conduction has slowed down in the MI. This is because in dead tissue there are low ATP levels, which means there is a decrease in the activity of Na+/K+/ATPase channel. The gradient in this channel cannot be maintained so sodium remains in the cells, thus the cells are at a constant state of depolarisation. In order to get an AP to occur, it will take longer. By decreasing conduction velocity you are decreasing the wavelength and increasing the chances of a arrhythmia occurring.

21
Q

What happens to AP duration in myocardial infacts?

A

There is a reduced AP, this is due to the Na+/K+/ATPase channel not doing its job therefore there is more K+outside the cell (ECF). There is an increase in activity of IKr (K+ rectifier cells), therefore the AP duration has decreased. This decreases the relative refractory period so it increases the chance of arrhythmia occurring.

22
Q

What happens to cardiac rhythm in heart failure?

A
  1. Atrial dilation.
  2. Increase in atrial pressure.
  3. Atrial fibrosis.
  4. Na+/Ca2+ exchanger changes.