Cardiac Arrhythmias

Question 1

What are the phases in SA node pacemaker AP?

Answer 1

Phase 0: depolarisation, Ca+ in

Phase 3: repolarisation, K+ out

Phase 4: spontaneous depolarisation, Na+ in, Ca2+ in

Question 2

How do PS nerves slow the rate of SA node firing?

Answer 2

GPCR decrease cAMP leading to opening of K+ channels

K+ efflux
– Slows Na+ and Ca2+ fluxes
– Slowed phase 4 repolarisation
– longer to reach threshold
potential (SA node) and slows rate of conduction (AV node)

Question 3

How do Sympathetic nerves increase the rate of SA node firing?

Answer 3

GPCR increase cAMP leading to opening of Ca2+ channels

Ca2+ entry
– increased slope of phase 4 depolarisation (SA & AV nodes)
– increased rate of firing (SA node) and more rapid conduction (AV node)
• Can trigger dysrhythmias

Question 4

What are the phases of the ventricular AP?

Answer 4

Phase 0: depolarisation, Na+ in

Phase 1: rapid repolarisation, K+ out

Phase 2: plateau, Ca2+ in, K+ out

Phase 3: repolarisation, K+ out

Phase 4: stable membrane potential

Question 5

What are the mechanisms that can cause dysrhythmias?

Answer 5

1. Altered impulse formation
2. Altered impulse conduction
3. Triggered activity

Question 6

How do class 1 anti-arrhythmics work and what are their side effects?

Answer 6

Na+ channel blockers

Class 1a (quinidine): moderate Na+ block, prolong repolarisation, Increase ERP

Class 1b (lignocaine): mild Na+ block, shorten repolarisation, Decrease ERP

dose dependent side effects: 
4 Lip and tongue numbness
5 Light headedness
7 Visual disturbance
8 Muscular twitching
10 Convulsions
15 Coma
20 Respiratory arrest
25 Cardiovascular depression 

Class 1c (flecainide): marked Na+ block, same repolarisation, No effect on ERP

Question 7

How do class 2 anti-arrhythmics work and what are their side effects?

Answer 7

β-adrenoceptor antagonists
• Inhibit sympathetic influence on cardiac
electrical activity
– Prevent β1-adrenoceptor effects on SA & AV nodes
– Decrease sinus rate, conduction velocity & aberrant pacemaker activity

• Membrane stabilising effects in Purkinje fibres
– Similar to Class 1 antiarrhythmics

• Adverse effects
– Bradycardia, reduced exercise capacity,
hypotension, AV conduction block
– Bronchoconstriction, hypoglycaemia

Question 8

How do class 3 anti-arrhythmics work and what are their side effects?

Answer 8

K+ channel inhibitors

prolong cardiac AP
– Slowing of Phase 3 repolarization
– decrease incidence of re-entry
– increase risk of triggered events

Amiodarone
• also blocks Na+, Ca+ and β-adrenoceptors
• reversible photosensitisation, skin discolouration and hypothyroidism
• Pulmonary fibrosis with long term use

Question 9

How do class 4 anti-arrhythmics work and what are their side effects?

Answer 9

• Cardioselective Ca2+ channel blockers (Verapamil)
– Act preferentially on SA & AV nodal tissue

• Slows conduction velocity and increase
refractoriness

• Side effects: Facial flushing, peripheral oedema, dizziness,
bradycardia, headache, nausea