Antiarrhythmic drugs

Question 1

Class 1 antiarrythmic drugs

Answer 1

RHYTHM
MOA = Na+ channel block - binds to inactivated/open Na channels to prevent influx of Na+
ELECTROPHYSIOLOGICAL ACTION = reduce rate of depolarisation of AP + increase ERP + decrease AV conduction
- negative iontropic effect
CLINICAL USE = ventricular fibrillation associated with MI

Question 2

Class 1a

Answer 2

Disopyramide

- lasr resort due to side effects = may cause arrythmias - ventricular fibrillation/ impairs cardiac contractility

Question 3

Class 1b

Answer 3

Lidocaine

• second choice option - cocaine derivative
• class 1B agents rapidly associate/dissociate from Na+ channels = actions are greater when cardicac cell is depolarised and firing rapidly

Question 4

Class 1c

Answer 4

Flecainide 
- supresses phase 0 upstroke in purkinje + myocardical fibres - automaticity is reduced to increase threshold potential 
- class 1c = slowly dissociate from resting Na+ channels - show prominent effects at normal heart rates 
NEGATIVE INOTROPIC AND PROARRYTHMIC EFFECTS - avoided in patients with structural heart disease

Question 5

Class 2

Answer 5

RATE
1st choice
MOA = beta adrenoreceptor antagonism
ELECTROPHYSIOLOGICAL ACTIONS = slowed pacemaker activity + increased AV refractory period
CLINICAL USE = dysrhythmia prevention in MI + paroxysmal atrial fibrillation due to sympathetic activity
NEVER USED WITH CLASS 4
Bisoprolol/Propanolol/Atenolol

Question 6

Class 3

Answer 6

RHYTHM
2nd choice
MOA = K+ channel blocker
ELECTROPHYSIOLOGICAL ACTIONS = increased AP and increased ERP
CLINICAL USE = atrial fibrilliation/ventricular fibrillation
Amiodarone/Sotalol
POTENTIAL TO INDUCE ARRHYTHMIAS

Question 7

Amiodarone

Answer 7

diminish the outward K+ current during repolarisation of cardiac cells - prolong the duration of AP without altering phase 0. Prolong the effective refractory period - increasing refractoriness
Side effects - photosensitivity

Question 8

Soltalol

Answer 8

nonselective B-blocker activity = slow rate and rhythm
maintenace of sinus rhythm in patients with atrial fibrillation/atrial flutter or refractory paroxysmal supraventricular tachycardia
used in patients with left ventricular hypertrophy or atherosclerotic heart disease
low rate of adverse effects
dose extended - drug is renally eliminated
HOSPITAL MONITORED

Question 9

Class 4

Answer 9

RATE
MOA: Ca channel blocker
ELECTROPHYSIOLOGICAL ACTIONS: decreased APD + slowed AV conduction
CLINICAL USE: supraventricular tachycardias + atrial fibrillation
decrease workload on heart - used in combination = not sole drug
Verapamil/Diltiazem
ADVERSE EFFECTS: bradycardia/hypotension/peripheral oedema
- metabolised by CYP3A4 - adjusted in hepatic dysfunction

Question 10

Adenosine

Answer 10

MOA: K+ channel activation
- short duration of action - rapid uptake by erythrocytes/endothelial cells
ELECTROPHYSIOLOGICAL ACTIONS: slowed pacemaker activity + slowed AV conduction
CLINICAL USE : IV for supraventricular tachycardia
ADVERSE EFFECTS: low toxicity - flushing/chest pain/hypotension
IMPENDING DOOM - heart stops for 5-20 secs

Question 11

Digoxin

Answer 11

MOA: inhibits Na/K ATPase pump - shortens refractory period in atrial&ventricular myocardial cells - prolong the effective refractory period - diminish conduction velocity in the AV node
CLINICAL USE: ventricular response rate in atrial fibrillation + flutter - sympathetic stimulation overcomes inhibition
ADVERSE EFFECTS: causes ectopic ventricular beats - result in VT and fibrilation

Question 12

Atrial flutter

Answer 12

P wave: saw tooth
PR interval: none
CAUSES: valvular heart disease/MI/CHF/Pericarditis

Question 13

Atrial flutter treatment

Answer 13

GOAL: control ventricular rate and maintian sinus rhythm
RATE CONTROL: Bisoprolol (less side effects) B blockers
Diltiazem/Verapamil (rapid control) Ca blockers
Digotoxin - contriol inadequate - heart failure
RHYTHM CONTROL: anticoagulation first - conversion to sinus rhythm
- Cardioversion - rapid control
- Catheter ablation - recurrent atrial flutter
STROKE RISK

Question 14

Atrial fibrillation

Answer 14

P wave: wavy&unidentifiable
PR interval: none
CAUSES: Ischemic heart disease/hypertension/valvular heart disease/hyperthyroidism

Question 15

Atrial Fibrillation Treatment

Answer 15

RATE: ventricular rate control
- first line beta blocker/calcium channel blocker
RHYTHM: restoration and maintenance - electrical/pharmacological

Question 16

Acute presentation of atrial fibrilation

Answer 16

new onset/life threatening
PRESENTATION: rapid pulse &hypotension&ongoing chest pain
TREATMENT: cardioversion

Question 17

Paroxysmal atrial fibrillation treatment

Answer 17

Intial treatment: use B blockers to control rate
THEN
Rhythm control drugs: Amiodarone/Sotalol/Flecainide

Question 18

Paroxysmal Supraventricular Tachycardia Treatment

Answer 18

Goal = reduce atrial rate + maintain cardiac output
Rate control - reduce AV conduction
- manouveres ineffective = IV adenosine given
- adenosine contraindicated - non-dihydropyradine CCB with a beta blocker
CARDIOVERSION

Question 19

Torsdae de Pointes treatment

Answer 19

GOAL = shorten QT interval/ clear drugs responsible/reverse brachycardia/prevent ventricular fibrillation
RHYTHM: class 1b - avoid 1a/1c/3 (as lengthen QT interval)
- beta blockers
- IV magnesium sulfate
ELECTRICAL: tempoary pacemaker/chronic = ICD