Week 1: mechanisms of arrhythmias

Question 1

Outline the two main classifications of arrhythmia

Outline the two main mechanisms of the development of arrythmia

Answer 1

• Main arrhythmias –> tachycardia and bradycardia
• due to altered impulse formation or altered impulse conduction

Question 2

What mechansism can lead to a tachycardia?

Answer 2

• Altered impulse formation:
  
  • Enhanced automaticity
  • Triggered activity
  • Re-entry (undirectional block)
  • Ventricular (broad complex)
  • Supraventricular (SVT) (narrow complex)
• Acronym - Tachy REVS*
• triggered activity, re-entry, enhanced automaticity, ventricular broad complex, supraventricular narrow complex*

Question 3

What mechanisms can lead to a bradycardia?

Answer 3

• Again altered impulse formation or altered impulse conduction
• ​Impulse formation:
  
  • ​Reduced automaticity
• Impulse conduction
  
  • ​Conduction block
    
    • ​sinoatrial node dysfunction
    • atrioventricular conduction disturbance

Question 4

What is enhanced automaticity?

What is it a property of and which regions of the heart does this property normally reside?

What occurs if other cells within the heart exhibit this property?

How does it relate to the cardiac action potential?

Answer 4

• Enhanced cardiac automaticity = accelerated generation of action potential by either normal pacemaker tissue (enhanced normal automaticity) or by abnormal tissue within the myocardium (abnormal automaticity)
• It is a property of spontaneous depolarisation - the ability of cardiac cells to generate sponatenous action potentials
• This is a property normally only within the SAN/AVN and conducting tissues of the heart
• Under certain conditions other myocardial cells can exhibit this property, potentially leading to spontaneous depolarisation at sites other than the SAN, and giving rise to ectopic beats and tachycardias.
• Relates to the cardiac action potential as these factors may either reduce the threshold for a cardiac action potential (around -40mV) or increase the slope of phase 4 depolarisation

Question 5

What factors may enhance the automaticity of the heart?

Answer 5

• Catecholamine excess
• Ischaemia
• Abnormal pH
• electrolyte abnormalities

Question 6

What is triggered activity?

Answer 6

• Triggered activity = impulse initiation caused by after-depolarisations
• After depolarisations are triggered only in the presence of a previous action potential, when they reach threshold a new AP is generated
• This new AP may then become the source of a new triggered response, resulting in self-sustaining triggered activity.

Question 7

What two types of afterdepolarisations can lead to triggered activity?

Answer 7

• Delayed afterdepolarisation –> occurs after full repolarisation
  
  • tends to be rapid rate
  • usually under conditions with increased intracellular calcium e..g cardiac glycosides or catecholamines
  • also in hypertrophy and HF
  • post MI
• Early afterdepolarisation –> occurs early interrupting or retarding repolarisation during phase 2/3 of cardiac action potential
  
  • Typically in cardiac tissue exposed to injury (hypoxia, altered electrolytes, pharmacologic agents, hypertrophy and HF)
  • prolongation of repolarisation usually underlying mechanism
  • usually by reduction of repolarising k+ currents, increase in Ca2+ or Na+ currents
    *

Question 8

How does the electrical activity of the heart move during a normal cardiac action potnetial?

What is re-entry in cardiac arrhythmia and how does it occur?

What conditions involve re-entry?

Answer 8

• During the normal cardiac action potential, electrical activity is conducted in uniform spread of depolarisation in a constant direction
• re-entry occurs when the depolarisation wave is able to form a self propagating looped circuit
• this underlies many tachycardais, including atrial flutter, re-entrant tachycardias (AV nodal re-entrant tachyC and Atrioventricular re-entrant tachyC) and some ventricular tachycardias.

Mechanism of re-entry:

• At least 2 pathways or the presence of a barrier along the conduction pathway.
• There needs to be unidirectional block in one of the pathways.
• Conduction must be slow enough (and/ or the refractory period short enough) to prevent the depolarisation wave encountering refractory tissue within the circuit.

Question 9

Describe the conditions within the image below - how does this relate to re-entry pathophysiology?

Answer 9

• In 1 –> the impulse passes down both limbs of the potential tachycardia circuit –> normal conduction
• In 2 –> the impulse is blocked in one pathway (damaged tissue/ hypoxia etc therefore still in the refractory phase). Impulse proceeds slowsly down pathway B returning along pathway A until it collides with the refractory tissue.
• In 3 –> the impulse travels so slowly along pathway B that it can return along the pathway a and complete the re-entry circuit, producing a circus movement tachycardia.

Question 10

What is the mechanism underlying atrioventricular re-entrant (reciprocating) tachycardia? (AVRT)

Answer 10

• In AVRT there is a circuit set up that involves the AVN and an accessory pathway.
• at rest, rapid conduction through the accessory pathway may give delta waves - slurring of the QRS complex.