CPT13 - Arrhythmia Drugs

Question 1

4 broad types of arrhythmias

Automatic Rhythms x2
Triggered Rhythms x2
Conduciton Block
Re-entry

Answer 1

1. ) Automatic Rhythms - abnormal impulse generation
   - enhanced normal automaticity (↑AP from SAN)
   - ectopic focus (AP doesn’t arise from the SAN)
2. ) Triggered Rhythms - abnormal impulse generation
   - early after-depolarisation (due to longer QT interval)
   - delayed after-depolarisation (due to ↑[Ca2+]in)
3. ) Conduction Block - due to abnormal conduction
   - 1st degree, 2nd degree, 3rd degree
4. ) Re-entry - due to abnormal conduction
   - circus movement: e.g. WPW syndrome
   - reflection

Question 2

5 features of class Ib anti-arrythmic drugs

Drug Names x2
Mechanism 
Effect on ECG x1
Usage
Side Effect x3

Answer 2

1. ) Drug Names - lidocaine and mexiletine
   - lidocaine is IV only, whilst mexiletine is given orally
2. ) Mechanism - blocks voltage-gated Na+ channels
   - only blocks damaged depolarised tissue
   - blocks during repolarisation, ↓EADs and DADs
   - fast binding means it dissociates in time for the next AP which is not an issue for normal cardiac tissue
3. ) Effect on ECG
   - ↑QRS interval (slows ventricular depolarisation)
   - effects only seen in patients w/ ischaemic hearts
4. ) Usage
   - ventricular tachycardia after an MI/ischaemia
5. ) Side Effects
   - dizziness, drowsiness, abdominal upset

Question 3

5 features of class Ic anti-arrhythmic drugs

Drug Names x2
Mechanism x2
Effect on ECG x3
Usage x3
Side Effect x2

Answer 3

1. ) Drug Names - flecainide and propafenone
   - can be given oral or IV
2. ) Mechanism - slow binding VG-Na channel blocker
   - slows ventricular depolarisation in both normal tissue and damaged tissues (because it’s slow binding)
   - lengthens AP duration and refractory period
3. ) Effect on ECG
   - ↑QRS interval (slows ventricular depolarisation)
   - ↑QT interval (longer refractory period)
   - ↑PR interval (sign of toxicity)
4. ) Usage - tachycardias w/out myocardial damage
   - atrial fibrillation and atrial flutter
   - premature ventricular contractions (extra-heartbeats)
   - Wolff-Parkinson-White (best drug)
5. ) Side-Effects
   - proarrythmia and sudden death esp w/ chronic use
   - CNS and GI effects

Question 4

5 features of class II anti-arrythmic drugs (beta-blockers)

Drug Names x3
Mechanism x2
Effect on ECG x1
Usage x4
Side Effects x2

Answer 4

1. ) Drug Names - bisoprolol , propranolol, metoprolol
   - bisoprolol is oral only, rest are oral or IV
   - propranolol is non-cardioselective
2. ) Mechanism - blocks ß-1 adrenoceptors
   - slows plateau phase in myocardium to ↓HR
   - reduced myocardial force of contraction (↓Ca2+)
3. ) Effect on ECG
   - ↑PR interval (longer APD and refractory period in AVN)
4. ) Usage - greatest safety/tolerability but worst efficacy
   - always given after an MI (MI ↑sympathetic activity)
   - sinus tachycardia (including VTs)
   - atrial fibrillation or atrial flutter
   - re-entrant arrythmias at the AV node (AVNRT)
5. ) Side Effects
   - bronchospasm: esp w/ propranolol
   - hypotension: severe ↓HR

Question 5

5 features of sotalol (class III anti-arrythmic)

Formulation
Mechanism x2
ECG Effects x1
Usage
Side Effects x2

Answer 5

1.) Administration - oral

2. ) Mechanism - blocks voltage-gated K+ channels
   - slows repolarisation –> ↑refractory period and ↑APD
   - acts on both SAN/AVN and the ventricular tissue
3. ) ECG Effects
   - ↑QT interval (longer refractory period and AP duration)
4. ) Usage - wide spectrum
   - can be used for both SVTs and VTs
5. ) Side Effects
   - proarrhythmic: due to prolonged QT interval
   - fatigue and insomina

Question 6

5 features of amiodarone (class III anti-arrythmic)

Formulation
Mechanism x2
ECG Effects x3
Usage
Side Effects x6

Answer 6

1. ) Administration - oral or IV
   - very long half-life of about 3 months
2. ) Mechanism - blocks voltage-gated K+ channels
   - slows repolarisation –> ↑refractory period and ↑APD
   - also has similar effects to class Ia, II, and IV drugs
3. ) ECG Effects
   - ↑QT interval (longer refractory period and AP duration)
   - ↑PR interval (slowed conduction at AVN, like class II)
   - ↑QRS interval (due to extra class II and IV effects)
4. ) Usage - basically everything
   - when other drugs are contraindicated or ineffective
   - has the greatest efficacy but worst safety/tolerability
5. ) Side Effects
   - proarrhythmic: due to prolonged QT interval
   - hyper/hypothyroidism: contains iodine
   - liver damage and lung damage
   - corneal deposits, optic neuritis, photosensitivity
   - can increase effects of digoxin and warfarin

Question 7

6 features of class IV anti-arrhythmic drugs (non-dihydropyridine CCBs)

Drug Names x2
Mechanism x3
ECG Effects x1
Usage
Contraindications x5
Side Effects x2

Answer 7

1. ) Drug Names - verapamil and diltiazem
   - verapamil is oral or IV, diltiazem is oral only
2. ) Mechanism - L-type VG-Ca channel blockers
   - slows plateau phase in myocardium to ↓HR
   - reduced myocardial force of contraction (↓Ca2+)
   - also increases the refractory period in the AVN
3. ) ECG Effects
   - ↑PR interval (longer APD and refractory period in AVN)
4. ) Usage - all supraventricular tachycardia
   - has greatest safety/tolerability but worst efficacy
5. ) Contraindications
   - verapamil + ß-blocker together can cause asystole
   - anything causing a decreased cardiac output
   - atrial fib/flutter caused by accessory pathways
   - AV nodal block (heart block)
   - SA nodal block or sick sinus syndrome
6. ) Side Effects
   - hypotension, some GI problems e.g. constipation

Question 8

5 features of adenosine as an anti-arrhythmic

Formulation
Mechanism x3
Usage x2
Contraindication
Side Effect

Answer 8

1. ) Administration - rapid IV bolus
   - very short half-life (seconds)
2. ) Mechanism - causes hyperpolarisation in SAN/AVN
   - binds to A1 adenosine receptors at SAN/AVN which ↑K+ conductance causing hyperpolarisation
   - hyperpolarisation –> ↓AVN conduction, ↓APD and ↓HR
   - stops the heart temporarily
3. ) Usage
   - re-entrant SVTs (e.g. WPW)
   - diagnosing CHD: slows HR temporarily so compares coronary artery perfusion between fast and slow HRs
4. ) Contraindication
   - usage w/ dipyridamole as it also ↑[adenosine] which can cause bradycardia
5. ) Side Effect
   - patient will feel like they are about to die becausing blocking the AVN causes ventricular asystole

Question 9

4 features of vernakalant as an anti-arrhythmic

Administration
Mechanism x2
Usage
Side Effects x4

Answer 9

1.) Administration - IV bolus over 10 minutes

2. ) Mechanism - slows atrial conduction
   - blocks atrial specific K+ channels
   - the faster the heart rate, the more effective it is
3. ) Usage
   - recent onset atrial fibrillation
4. ) Side Effects
   - hypotension and AV (heart) block
   - sneezing and taste disturbances

Question 10

4 features of ivabradine as an anti-arrhythmic

Administration
Mechanism x2
Usage x2
Side Effects x2

Answer 10

1.) Administration - oral

2. ) Mechanism - slows down SA node
   - blocks funny current (If) in SAN
   - has no effect on blood pressure and contractility
3. ) Usage
   - ↓HR in HF and angina (no effect on contractility)
   - inappropriate sinus tachycardia
4. ) Side Effects
   - flashing lights
   - avoid in pregnancy (teratogenicity unknown)

Question 11

4 features of digoxin (cardiac glycosides) as an anti-arrhythmic

Administration
Mechanism
Usage
Side Effects

Answer 11

1.) Administration - IV

2. ) Mechanism - +inotropy and slows AVN conduction
   - blocks Na pump causing ↑[Na+]in which ↓NCX activity, causing an increase in Ca2+ ions inside the cell
   - also ↑vagal activity –> ↓AVN conduction and ↓HR
3. ) Usage
   - atrial fibrillation and flutter
   - has very little effect upon exertion (↑sympathetic activity reverses the effect of ↑vagal activity)

4.) Side Effects
- GI disturbance, dizziness, confusion, blurry or yellow vision, arrhythmias.
- narrow therapeutic window: stopped during AKI due to increased risk of toxicity
-

Question 12

3 features of atropine as an anti-arrhythmic

Administration
Mechanism
Usage

Answer 12

1.) Administration - IV

2. ) Mechanism - selective anti-muscarinic
   - ↓vagal activity to speed AV conduction and ↑HR
3. ) Usage
   - vagal bradycardia

Question 13

what are 2 non-pharmacological ways to slow supraventricular tachycardias (SVTs)?

Answer 13

1. ) Carotid Sinus Massage - stimulates the vagus nerve
   - helps differentiates SVTs from VTs

2.) Valsalva Maneuver - forceful attempted exhalation against a closed airway

Question 14

what is the problem with treating a patient who has had continous atrial fibrillation for greater than 48 hours?

Answer 14

increased risk of blood clot