Lecture 10 Theme B Flashcards

1
Q

What are the types of cardiac arrhythmia?

A

some arrhythmias are benign. Others are malignant.

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2
Q

What are symptoms of arrhythmias?

A

palpitations to critical reduction.

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3
Q

Why does the SA node control the heart’s contraction?

A

SA node pacemaker overdrives the other pacemakers. (fastest creeper to threshold is the one that controls the heartbeat)

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4
Q

How is SA node activity regulated?

A

SA node activity is modulated by the action of sympathetic and parasympathetic hormones.

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5
Q

How do hormones influence heart beat?

A

increase in I-funny, Land T type calcium channels and a decrease in I-K occurs in response to adrenaline and sympathetic hormones.

Opposite happens in response to muscarinic receptor activation by Ach.

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6
Q

How can increased neurotransmitter activity cause arrhythmia?

A

Increase in sympathetic activity causes other muscle cells to suddenly become pacemakers.

Increase in parasympathetic activity causes latent pacemakers to emerge.

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7
Q

How does injury affect pacemaker cells?

A

injured node area cells develop pacemaker function which causes loss of RMP.

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8
Q

What are the 2 types of arrhythmicity?

A

Normal nodal altered automaticity.

Triggered activity in the ventricle (ectopic pacemaker)

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9
Q

What causes the formation of an ectopic pacemaker?

A

Altered calcium ion homeostasis.

Oscillation of RMP

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10
Q

What are the types of oscillation of the RMP?

A

Early afterdepolarisation

Delayed afterdepolarisation

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11
Q

What happens during early afterdepolarization (EAD)?

A

during early afterdepolarization there is a spike in electric potential right before repolarization (opening of potassium channels) occurs. This can continue and could cause long AP duration which causes long QT syndromes.

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12
Q

What goes wrong during EAD?

A

Repolarization typically goes wrong due to faulty potassium channels causing tacchyarryhthmias.

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13
Q

What happens if a sodium channel is mutated?

A

Channel fails to stay inactivated meaning inward current occurs late in the plateau leakage of more positive into the cell causing an extended AP duration.

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14
Q

What does the P wave represent on an ECG?

A

P wave is when action potential is spreading across most of the surfaces into the tissues of the atria to move blood into the ventricle from the atria.

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15
Q

What happens at the QRS complex of the ECG?

A

At the QRS complex the ventricular action potential is spreading through the muscles of the ventricle via the purkinje fibers.

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16
Q

What does the T wave represent?

A

T waves mark repolarization.

17
Q

What is the main fast sodium channel called?

A

SCN5A

18
Q

What potassium channels are typically mutated to cause EAD?

A

KCNQ1

HERG

19
Q

How do mutated potassium channels cause EAD?

A

decrease in repolarization K efflux and plateau termination is delayed. As a result there is a long QT interval.

20
Q

What occurs during delayed afterdepolarization (DAD)?

A

after completed action potential another depolarization occurs soon after.

21
Q

Why are hypertrophied cells more likely to experience arrhythmias (DAD)?

A

hypertrophied cells rely on external calcium due to the weakness in the SERCA2 protein. Extracellular calcium cycling results in higher chance of forming an action potential within the cell

22
Q

How does digitalis increase the RMP?

A

Digitalis increases the amount of sodium in the cell which is exchanged with calcium as the built up sodium flows out. After contraction the built up calcium exits the cell and sodium enters the cell the amount of sodium is higher due to blocked Na/K exchanger and so the RMP is higher.

23
Q

Why is it dangerous to have a higher RMP (as is the case with digitalis)?

A

Delayed afterdepolarization can occur while the fast sodium channels remain dormant, as a result the L-type channels can activate due to hitting the threshold. This causes ectopic beats to form.

24
Q

What are the causes of a conduction block in the heart?

A

A conduction block could occur due to ischemia or fibrosis (hypertrophy could cause fibrosis). These blocks could be temporary or permanent and could cause latent pacemakers to activate.

25
Q

What is a re-entry circuit?

A

A re-entry circuit is a unidirectional conduction block that produces tachyarrhythmia.