Ventricular tachycardia

Question 1

Reentrant ventricular tachycardia

Answer 1

• myocardium is diseased/damaged
• Scar tissue left to slow conduction
• slow conduction gives time for myocyte repolarisation
• continous circuit forms within ventricle

Question 2

Focal ventricular tachycardia

Answer 2

1. Ventricles have ventricular pacemaker cells within them
2. If pacemaker cells become irritated then ventricular pacemaker cells begin to fire off signals more rapidly
3. Take over from SA node

Question 3

Ventricular fibrillation pathophysiology

Answer 3

1. tissue heterogenity - heart muscle cells get damaged or stressed causing them to gain different properties
2. Different conduction circuits develop causing different areas to contract at different times
3. Ventricular tachycardia can progress to ventricular fibrillation

Question 4

Ventricular fibrillation

Answer 4

• > ventricular fibres start quivering from uncoordinated contraction
• > can lead to death within minutes

Question 5

Treatment for ventricular fibrillation

Answer 5

1. Class 1 - Fast sodium channel blocker
2. Class 2 - Beta blockers
3. Class 3 - K channel blocker
4. Calcium- L type channel blocker

Question 6

Class 1

Answer 6

Fast sodium channel blockers
• sodium channels not present in the node
• delay onset of depolarisation

Question 7

Class 2

Answer 7

Beta blockers
• Blocks sympathetic response by preventing epinephrine and norepinephrine binding
• prevents intracellular calcium loading thus increase in contractility

Question 8

Class 3

Answer 8

K channel blocker - Amiadrone
• Last resort
•Acts on phase 3 of action potential -> prolongs repolarisation and lengthens action potential

Question 9

Class 4

Answer 9

Ca - L type Ca channel blocker ( Adenosine/Degoxine)
• effects phase 0
• reduces firing of nodal and other automatic cells
• reduces conduction velocity
• lengthens depolarisation at AV node