Lecture 9: Cardiac Hypertrophy & Arrhythmia Flashcards

1
Q

What is arrhythmia?

A

Abnormalities of electrical rhythm, either benign or malignant

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2
Q

What are the symptoms of arrhythmia?

A

Palpitations, reduced CO

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3
Q

What causes arrhythmia?

A

Altered AP generation or conductance

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4
Q

What happens if normal nodal automaticity is altered?

A

Unstable rhythm, emergence of alternative pacemaker

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5
Q

How does sympathetic activity influence pacemakers?

A

Increase HR by increase If and Ca channels and decreasing K channels

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6
Q

How does parasympathetic activity influence pacemaker cells?

A

Decrease HR by decreasing If and Ca channels and increasing K channels

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7
Q

How can a nodal abnormality happen?

A

Sympathetic effect on a latent pacemaker causing it to take over.

Parasympathetic effect on SA node causing latent pacemaker to take over.

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8
Q

What causes trigger of activity in the ventricle?

A

Altered calcium homeostasis, unstable RMP, oscillation

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9
Q

What is early after depolarisation (EAD) and why does it occur?

A

Depolarisation occurring during AP depolarisation due to long AP duration (QT syndrome).

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10
Q

What are the mutations that lead to QT syndrome?

A

Na channel mutation (SCN5A)

K channel mutation (HERG, KCNQ1)

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11
Q

What happens when there is a mutation in the Na channel?

A

Channel fails to stay inactivated - inward current occurs late in plateau to extend duration

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12
Q

What happens when there is a mutation in the K channel?

A

Decreased depolarising K efflux and plateau termination delayed

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13
Q

What is delayed after depolarisation (DAD) and why does it occur?

A

Depolarisation just after repolarisation due to increased reliance on Na/Ca exchanger for relaxation

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14
Q

What are the effects of hypertrophy on the cell exchanging?

A

More active Na/Ca exchanger, less Ca coming in and out of SR each cycle, more extracellular calcium cycling

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15
Q

What is a conduction block?

A

Inexcusable area in conduction system which may be temporary or permanent and permits latent pacemakers to escape

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16
Q

What is a re-entry circuit?

A

Unidirectional conduction block that produces tachyarrhythmia

17
Q

What are the features of normal conduction block and re-entry?

A

Branch point alone is not a problem, signals from X through alpha and beta extinguish each other

18
Q

What are the features of forward block at branch point conduction block and re-entry?

A

A total branch block alone is not a problem, signals from X through alpha can’t traverse beta route from distal position at y

19
Q

What are the features of normal retrograde conduction velocity conduction block and re-entry?

A

If beta route forward (orthograde) is block but beta reverse route (retrograde) is not, it is only okay if the beta signal is fast and reaches alpha signal when it is in refractory

20
Q

What are the features of slowed retrograde conduction velocity conduction block and re-entry?

A

If beta route reverse (retrograde) is slowed and reaches alpha route after refractory period finishes then a re-entry circuit is set up

21
Q

What dod you need to produce a conduction re-entry arrhythmia?

A

Need a branch point and a partial blockage in one of the branches involving slowed conduction in one direction

22
Q

From the re-entry circuit where does the arrhythmic activity spread?

A

Throughout the electrical syncytium of the myocardial tissue

23
Q

How do hypertrophy and arrhythmia relate?

A
  • Growth means fibrosis
  • Cardiac pump function impairment due to sympathetic activation
  • Bigger muscle mass means more oxygen demand, ischemic regions and emerging pacemakers
  • More external cell calcium cycling, Na/Ca exchanger, DADs