Week 11 - Arrhythmia and Anti-arrhythmic Drugs

Question 1

What is arrhythmia

Answer 1

Is irregular heart rate, rhythm, sequence of conduction or origin of conduction
- one or more of the above are happening at the same time

Symptoms:
- Fast or slow heartbeats
- Chest pain
- Sweating
- Shortness of breaths

Question 2

List the types of dysrhythmias

Answer 2

Classification
- Normal HR = 60-100bpm
- Bradyarrhytmia = <60bpm
- Tachyarrhytmia = >100bpm
- Tachycardia = 150-250
- Flutter = 250-350
- atrial flutter has re-enterant circuit
- Fibrillation >350
- atrial fibrillation caused by multifocal

Question 3

Explain the mechanism for Tachyarrhythmia (>100bpm)

Answer 3

1. Supraventricular Tachyarrhythmia
   - arrhythmia starts from point above ventricle
   Can Be:
   - Sinus tachycardia = SAN firing too fast
   - Focal or Multifocal tachycardia = ectopic focis
2. Ventricular Tachyarrhythmia
   - arrhythmia starts from point in ventricle
   Can Be:
   - Monomorphic (1 ectopic foci) or Polymorphic
   - Polymorphic can be normal or prolonged QT interval
   - prolonged = TDP (torsade de pointes)

Question 4

Explain the mechanism for Bradyarrhythmia (<60bpm)

Answer 4

1. Sinus bradyarrhythmia
   = SAN firing too slow
2. Abnormal AV conduction (heart block)
   - 1st degree = minor delay conduction
   - 2nd degree = longer delay
   - 3rd degree = complete heart block
   - no conduction, no signal between atria + ventricles
3. Sick sinus syndrome

Question 5

Explain the mechanism for Arrhythmia

Answer 5

Arrhythmia is caused by disorders of impulse formation or conduction

1. Automaticity
   - SAN generates own AP without stimulation (SAN cells depolarise)
   - ↓ automaticity = slows conduction from SAN + AVN = ↓ HR = bradyarrythmia
   - ↑ automaticity = ↑ HR and contractility as sympathetic nervous system is activated = tacharrythmia
2. Triggered Conduction
   Due to abnormal leakage of +ive ions into cell, can trigger premature AP
   - Early after depolarisation (EAD)
   - polymorphic V tach with long QT interval (TDP)
   - Delay after depolarisation (DAD)
   - V tach normal QT interval, multifocal / focal atrial tach
3. Re-entrant Circuit
   - Wolf-parkinson white syndrome
   - When signal travels through accessory pathway from ventricles back to atria = atria contracts before SAN fires again
   - signal does NOT end in ventricles
   - abnormal loop of electrical activity

Question 6

What is The Vaughan Williams drug classification system

Answer 6

Groups anti-arrhythmics based on their MoA

Question 7

How do Class 1 drugs: Na+ channel blockers work

Answer 7

Block opening of Na+ channels = slows down rate of depolarisation + ↓ conduction

Class 1a:
Prolonged AP + prolonged refractory period
- blocks fast Na+ channels = slows depolarisation
- blocks some K+ channels = prolong repolarisation / refractory period
- treat ventricular tachycardia + atrial fibrillation
- e.g. Quinidine (↓ secretion of digoxin)
- SIDE EFFECTS: blurred vision, headache

Class 1b
- Blocks Na+ channel = shorten depolarisation, shortened refractory period + short duration of AP

Question 8

How do Class 2 drugs: beta-blockers work

Question 9

How do Class 3 drugs: K+ channel blockers work

Question 10

How do Class 4 drugs: Ca2+ channel blockers work

Question 11

How do Class 5 drugs: Digoxin, Adenosine and Magnesium work

Question 12

What are the problems with The Vaughan Williams system

Answer 12

• Many drugs have multiple sites of action = can fall into many classes
• Many useful drugs are not included
• There are more modern classifications systems
• Site of action may differ in healthy tissue vs disease state
• Individual dysrrhytmias may be treated with drugs from more than one class