Arrhythmias Flashcards

1
Q

Describe the initiation and spread of electrical activation

A
  • SAN- intrinsic pacemaker
  • Wave of electricity through myocardium when activated
    Atria–> AVN (delay) –> bundle of His –> down septum –> Purkinje fibres
  • Co-ordinated heart beat
  • SAN in RA near superior vena cava opening
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2
Q

What is sinus rhythm?

A
  • Normal rhythm from SAN- cardiac pacemaker

- 60-100bpm normally

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3
Q

Describe cardiac action potentials

A
  • Occur at cellular level

- Different sections have different action potentials

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4
Q

What is automaticity?

A
  • Depolarise without stimulation
  • AP starts with flat line- threshold potential
  • SAN- unstable resting potential- gradually rises with Na and Ca influx
  • Potential decreases with K efflux (repolarisation)
  • Na spontaneous inward movement- funny channels allow this (gradual rise) until threshold reached
  • Normal AP after this
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5
Q

Describe inherent rates of automaticity

A
  • SAN, AVN and Purkinje fibres
  • SAN- 60-100pm
  • AVN- 40-50pm
  • PF- 35pm
  • SAN pacemaker- fastest rate
  • Once AVN and PF activated by adjacent cell- own automaticity becomes irrelevant
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6
Q

Describe pacemaker modulation

A
  • HR changes due to PNS and SNS effect on pacemaker cells
  • PNS slows- hyperpolarisation, slow depolarisation- automaticity slower- less APs in same time frame
  • SNS- speeds up- reduced depolarisation, steeper slow, more rapid APS in the same time frame
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7
Q

What are the effects of parasympathetic and sympathetic nervous systems on the heart?

A
  • Sympathetic: increases HR, increases conduction through AVN
  • Parasympathetic: decreases HR, decreases conduction through AVN
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8
Q

What are the mechanisms of arrhythmogenesis?

A
  • Automaticity
  • Re-entry
  • After depolarisation (triggered activity)
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9
Q

Describe how automaticity causes arrhythmia

A
  • Normal phenomena (ANS)
  • Modulated by drugs
  • Overactive/underactive/fails
  • Induced wrong time
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10
Q

Give examples of automaticity causing arrhythmia

A
  • Sinus tachycardia: fever, exercise, absence of clear driver, hyperthyroidism
  • Sinus bradycardia: hypothyroidism, SAN diseased, hypothermia, chronotropic incompetence
  • Focal atrial tachycardia: areas not SAN, abnormal atrial section firing after than SAN- pacemaker
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11
Q

What is re-entry?

A
  • Most common
  • Short circuit forms 2 anatomically/ functionally distinct pathways
  • Focus of treatment usually- burning/freezing circuit
  • Small, can form in ventricles, atria, AVN or combo
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12
Q

What are the two pathways that re-entry requires?

A
  • Path 1: slow conduction, short refractory period (need to be able to recover quickly)
  • Path 2- rapid conduction, long refractory period
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13
Q

Describe how pathway mechanism works

A
  • Combination of pathways and formation due to non-electrically active tissue drives re-entry
  • Electrical impulse conducted both pathways simultaneously
  • Fast path activates everything below system and sends upwards signal that collides with slow- collision stops them
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14
Q

Describe re-entry with an ectopic beat- premature

A
  • May travel down slow conduction pathway (Fast still recovering)
  • Refractory period differentiation becomes significant
  • May reach bottom of fast when it recovers- goes up fast
  • Formation of a circuit- slow has recovered, so travels down slow pathway
  • Everything above and below activated
  • Wave re-enters pathway- re-entry
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15
Q

What are the combination factors that lead to re-entry circuits?

A
  • 2 pathways with different conduction velocities and recovery times
  • Around an area which is electrically inert
  • Requires tissue not electrical active to go around
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16
Q

Give examples of re-entry circuits

A
  • Atrial flutter (macro re-entry circuit, around annulus of tricuspid valve)
  • AVN re-entry tachycardia (entire re-entry circuit within AVN)
  • AV re-entry tachycardia (accessory pathway, abnormal pathway between A-V)
  • Atrial tachycardia (single atrial focus
17
Q

What is triggered activity?

A
  • After depolarisation
  • Oscillation of membrane potential (may occur during/ immediately after AP)
  • Threshold reached- triggered AP–> self-sustaining tachycardia
  • Cell vulnerability can lead to this
  • Early dp- plateau phase of AP
  • Delayed dp- from resting pot
18
Q

Describe how triggered activity leads to depolarisation

A
  • At after depolarisation- small depolarisation
  • Triggered action potential
  • Could continue to occur- sustained trigger activity
  • Single tissue fires- repeated APs
  • Subsequent AP- triggered by oscillation
19
Q

Give examples of triggered activity

A
  • Long QT syndrome- rhythm disturbance (Torsade de Pointes)
  • Brugada syndrome (VF, inherited channelopathy)
  • Right ventricular outflow tract VT
  • Catecholanergic polymorphic VT (rare, suggest of Adr cause uncontrolled triggered activity and ventricular dysrhythmia)
20
Q

What are the consequences of arrhythmias?

A
  • Asymptomatic
  • Palpitation- abnormal sensing of heart beat
  • Angina- chest pain
  • Dyspnoea
  • Syncope- unconsciousness
  • Sudden death
  • Thromboembolic events (atrial flutter/ fibrillation)- clotting
21
Q

What is the clinical classification of arrhythmias?

A
  • HR- tachy/bradycardia
  • Irregular/ regular heart rhythms
  • Site of origin (supraventricular- atrium, ventricular- ventricle)
  • ECG distinction