myocardial infarction Flashcards

1
Q

what are arrhythmias clinically described in terms of

A
  • Rate ie bradycardia / tachycardia

- Site of origin ie supraventricular / ventricular

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2
Q

what does automaticity of the heart mean

A

Automaticity is defined as the ability of heart cells to spontaneously depolarize and generate an action potential

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3
Q

what is override suppression

A

SA node pacemaking is normally highest and dominant over the other ‘latent pacemakers’ such as the AV node and Purkinje fibres

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4
Q

what causes loss of override suppression

A
  • May occur if the SA node firing frequency is pathologically low or if conduction impulse from the SA node is impaired
  • May occur if a latent pacemaker fires at an intrinsic rate faster than the SA node rate. A latent pacemaker initiates an ecoptic bear or series of these beats creating an ectopic rhythm
  • Can occur in response to tissue damage
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5
Q

what are afterdepolarizations

A

A normal action potential may trigger abnormal oscillations in membrane potential called afterdepolarizations that occur during or after repolarisation.

AD’s of amplitude sufficient to reach threshold causes premature action potentials and beats

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6
Q

when do early afterdepolarisations occur

A

Occur during the inciting action potential within:

  • Phase 2 - AD mediated by Ca2+ channels
  • Phase 3 - AD mediated by Na+ channels

Most likely to occur when heart rate is slow

Often occur in Purkinje fibres

Associated with prolongation of the action potential and drugs (eg sotalol) prolonging the QT interval

When sustained it can lead yo life threatening arrhythmia ‘ tornadoes de pointes’

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7
Q

what is torsades de pointes

A

Torsades de Pointes is a type of polymorphic ventricular tachycardia characterized by a gradual change in amplitude and twisting of the QRS complexes around an isoelectric line on the electrocardiogram.

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8
Q

what are delayed after depolarisation

A

Occur after complete depolarisation

Are caused by large increases in [Ca2+]I

Most likely to occur when heart rate is fast

Increased and decreased in incidence by prolongation and shortening of the duration of the action potential by drugs, respectively

May be triggered by drugs that increase Ca2+ influx (catecholamines) or release from the SR (digoxin)

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9
Q

what does excessive [Ca2+]I result in

A

Excessive [Ca2+]I results in

  • Oscillatory release of Ca2+ from the sarcoplasmic reticulum
  • a transient inward current (Iti, involving Na+ influx) that occurs in phase 4
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10
Q

what are types of defects in impulse conduction

A

Re-entry
Conduction block
Accessory tracts

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11
Q

what is the re-entry defect in impulse conduction

A

Self sustaining electrical circuit stimulates an area of myocardium repeatedly/rapidly. The reentrant circuit requires:

  • Unidirectional block (anterograde conduction prohibited and retrograde conduction allowed)
  • Slowed retrograde conduction allowed
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12
Q

what is the conduction block (through the AV node) defect in impulse conduction

A

May be partial (incomplete) or complete

  • Partial block = slowed conduction: tissue conducts all impulses but more slowly than usual ie first degree AV block
  • Intermittent block = tissue conducts some impulses, but not others eg second degree AV block occurring as two types
    1. Mobitz type 1 - PR interval gradually increases from cycle to cycle until AV node fails completely and ventricular beat is missed
    2. Mobitz type 2 - PR interval is constant but every nth ventricular depolarisation is missed
  • Complete block = no impulses are conducted through the affected are eg Third degree AV block
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