12.3 Physiological mechanism of arrhythmias Flashcards

1
Q

What is the definition of an arrhythmia?

A

An irregular heart rhythm

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2
Q

What is bradycardia & give examples

A
  • Slow HR <60bpm
    • Sinus bradycardias (physiological or Sinus node disease)
    • Atrioventricular (AV) block
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3
Q

What is tachycardia & give examples

A
  • Fast HR >100bpm
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4
Q

What things cause arrhythmia?

A
  • Electrolyte disturbances
  • Ion channel modification or defects
  • Structural/anatomy abnormalities
  • Cell damage

These lead to…

  • Disturbances in impulse generation
  • Disturbances in impulse propagation
  • Or a bit of both!
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5
Q

Risk factors of arrhythmia?

A
  • Cell/structural changes
    • Myocardial infarction
    • Myocarditis
    • Fibrosis
    • Toxins (e.g. alcohol)
    • Chemotherapy
  • Ion channels
    • Long QT syndromes
    • Drugs
  • Environmental factors –> cellular dysfunction
    • Temperature
    • Hypoxia
    • Levels of K+, Ca2+, Mg2+
    • Acidaemia
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6
Q

What are some disorders of impulse formation?

A
  • Disorder in automaticity
  • Triggered activity (EADs & DADs)
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7
Q

What is automaticity & abnormalities of automaticity (show on ECG)?

A
  • The property of a fiber to initiate an impulse spontaneously - without needing prior stimulation

Abnormalities of automaticity

  • Inappropriate discharge rate (ie sinus tachycardia, sinus bradycardia)
  • Ectopicpacemaker takes over and controls atrial or ventricular rhythm
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8
Q

What could decreased automaticity indicate?

A

Sinus node disease

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9
Q

Explain how cardiac automaticity takes place (steps)

A
  • Pacemaker cells have a pacemaker potential (Phase 4) enabling them to self-generate their own action potentials
  • The rate of rise of ion influx at the pacemaker cell sets the intrinsic heart rate
  • The SA node rate is then influenced by the autonomic nervous system
  • A balance of sympathetic and parasympathetic tone sets the resting heart rate = ~60-100 bpm
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10
Q

Draw a pacemaker action potential & explain the graph & phases

A
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11
Q

Draw a cardiac myocyte action potential (non-pacemaker) & explain the phases

A
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12
Q

At what Bpm do different pacemakers function?

A

SA node = ~100bpm

AV node = ~50bpm

Purkinje = ~35bpm

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13
Q

Explain what is meant by triggered activity

A
  • “triggered activity” = after-depolarizations
  • These are depolarising “oscillations” in the resting membrane voltage induced by one or more preceding action potentials
    • Ie an unstable depolarisations (activations) that occur when the heart should be repolarising (resting)
    • These oscillations can trigger (or be triggered by) extra heart beats
    • Can trigger an arrhythmia like Torsades de Pointes or VT
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14
Q

Explain what is meant by EAD (triggered activity) (& how seen AP of cardiac myocyte & ECG and what it can lead to)

A
  • Early after-depolarisations (EAD) arise from an abnormal membrane potential during phase 2 and 3
  • Lots of “Aborted” Action potentials usually due to changes in the ion channels
    • Ie increased opening of Ca channels
    • Increased opening of Na channels
  • EAD: Nothing, Prolong QT, Sustained Arrhythmia (Torsades de Pointes)
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15
Q

Explain what is meant by DADs (triggered activity) (& how seen AP of cardiac myocyte & what it can lead to)

A
  • Late or Delayed After-Depolarisations (DADs) occur after phase 4
    • Due to increased/altered movement of calcium
    • Activate a Na/Ca exchanger triggering an AP
    • DADs occurs at a more negative membrane potential
  • DAD: Nothing, Ectopic beat, Sustained Arrhythmia (Ventricular Tachycardia)
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16
Q

What are some causes of EAD?

A
  • Low serum K
  • Slow HR (Bradycardia)
  • Drug toxicity ie quinidine
17
Q

What are some causes of DAD?

A
  • Increased serum Calcium
  • Increased Adrenaline
  • Drug Toxicity ie Digoxin
  • Myocardial Infarction
  • Can be an SVT
18
Q

What are some disorders of impulse conduction?

A
  • Re-entry
  • Conduction block
19
Q

Explain how a re-entry takes place (disorder of impulse conduction)

A
  1. Two possible routes for electrical impulse to flow down
  2. Fast-pathway’ and ‘slow-pathway
  3. Impulse flows down one pathway, back up the other, and gets caught in a loop.
20
Q

Give some examples of re-entrant rhythm conditions

A
  1. AV nodal Re-Entrant Tachycardia (AVNRT)
  2. AV Re-Entrant Tachycardia (AVRT)
  3. Atrial Flutter
  4. Atrial Fibrillation
  5. Ventricular Tachycardia
21
Q

What is required in order for re-entry to occur (disorder of impulse conduction)?

A

Central area of block

  • e.g. scar tissue, refractory cells

Area/path of variable blocking

  • e.g. dead myocytes, myocytes with different refractory period/ conduction velocity, etc.
22
Q

Explain supraventricular tachycardia & how it will be seen on an ECG

A
  • Supraventricular Tacchycardia (AVNRT or AVRT)
  • Regular tacchycardia between 130-250bpm
  • There is 1 p-wave for each QRS, but they may not be visible
  • QRS duration is usually narrow (normal), as after the AV node the impulse is conducted normally through the ventricles
23
Q

Explain how the accessory pathways take place in a patient with SVT

24
Q

What condition is this?

A

Left sided accessory pathway (SVT)

  • As short PR
  • +ve v1 wave means pathway is on the left
25
What condition is this?
**Wolf Parkinson White** - narrow complex regular tachycardia
26
What condition is this?
SVT (doesnt matter what lead you look at)
27
What condition is this?
**Atrial Fibrillation** - *Irregularly irregular*
28
What condition is this?
29
What are the disorders of **impulse conduction** (*conduction block examples*)?
1. 1st Degree AV Block 2. 2nd Degree AV block 1. Type 1 (*wenkebach*) 2. Type 2 3. 3rd Degree (**Complete**) AV Block
30
What condition is this?
**AV block** - 1st degree
31
What condition is this?
**AV block** - 2nd dgree Type 1 - *Wenchebach*
32
What condition is this?
**AV block** - 2nd degree Type 2
33
What condition is this?
**AV block** - 3rd degree
34
How might **ischaemic heart disease** cause **AV block**?
1. ***Right Coronary Artery (RCA)*** most commonly supplies blood supply to *SA* and *AV node* 2. Blockage to RCA causes *SA* and *AV* *node ischaemia* * *Sinus bradycardia* * *AV Block*
35
What are the **consequences** of arrhythmia?
* Patients may be *_asymptomatic_* **Cardiac output = stroke volume x HR** * *Low HR* will cause direct *drop in CO* * But, *stroke volume* is reliant on *LV filling in diastole* * Tachycardia will limit how much the ventricle can fill, *reducing SV*, *reducing CO* * So both *tachy* and *brady* *cardias* can cause _haemodynamic compromise_
36
What is the haemodynamic compromise of **arrhythmia**?
* Prolonged Arrhythmia can lead to * *Heart Failure* * *Cardiac ischaemia* due to reduced coronary filling * *Hypotension* * Poor renal perfusion -\> *renal failure* * Poor liver perfusion-\> *liver failure* * Poor brain perfusion -\> *syncope, confusion*