ATRIAL FIBRILLATION – most common arrythmia
TREATMENT:
- LIFE-THREATENING: electrical cardioversion (rhythm control) – do NOT delay this to
administer anticoagulants (as they take too long to work in emergencies)
- NON-LIFE THREATENING: can be split into TWO:
o A.fib duration < 48 hours – can initiate ANY anti-arrhythmic – NOT digoxin if
for Paroxysmal A.fib (i.e. episodic A.fib < 1 week)
o A.fib duration > 48 hours – should initiate RATE-controlling anti-arrhythmic
RATE VS RHYTHM CONTROL:
- Rate control (preferred choice) – simply reduces HR back to healthy range – presents
lower risk of pro-arrythmia (generating new arrythmias) as they do not try to
terminate the pre-existing arrythmia
- Rhythm control (AKA cardioversion) – tries to terminate the abnormal rhythm whilst
maintaining normal sinus rhythm – often reserved for emergencies or where rate
control has failed
1st LINE - RATE-CONTROLLING ANTI-ARRHYTHMICS:
- β-blockers (cardioselective – so NOT Sotalol)
- Non-DHP CCBs (off-label use of Diltiazem)
- Digoxin
MOA: slow down the rate of AP conduction via the AVN – reduces transfer of fast, irregular
APs from atria to ventricles (bringing down the BPM) – each drug-class does this differently:
- β-blockers: block β1 receptors at AVN
- Non-DHP CCBs: block L-type Ca2+ channels
- Digoxin: stimulates PSNS activity at AVN
RATE CONTROL GUIDANCE (in chronic, non-life threatening A.fib):
- 1st Line – Monotherapy
- 2nd Line – Combination therapy (2 rate-controlling drugs)
- 3rd Line – Switch to Rhythm control (see below)
Do NOT give any CCB if pt has HEART FAILURE (except Amlodipine) – if they have both A.fib
& HF, seek specialist advice usually initiate rhythm control
2nd LINE - RHYTHM-CONTROLLING ANTI-ARRHYTHMICS:
- Class I drugs (e.g. Flecainide)
- Class III drugs (e.g. Sotalol, Amiodarone, Dronedarone)
MOA: slow down conduction of irregular APs in atria to help restore normal sinus rhythm –
each drug class does this differently:
- Class I drugs: Block Na+ influx via channels less depolarisation
- Class III drugs: block K+ efflux via channels extended repolarisation (i.e. extended
refractory period
TREATMENT:
- LIFE-THREATENING: electrical cardioversion (rhythm control) – do NOT delay this to
administer anticoagulants (as they take too long to work in emergencies)
- NON-LIFE THREATENING: can be split into TWO:
o A.fib duration < 48 hours – can initiate ANY anti-arrhythmic – NOT digoxin if
for Paroxysmal A.fib (i.e. episodic A.fib < 1 week)
o A.fib duration > 48 hours – should initiate RATE-controlling anti-arrhythmic
RATE VS RHYTHM CONTROL:
- Rate control (preferred choice) – simply reduces HR back to healthy range – presents
lower risk of pro-arrythmia (generating new arrythmias) as they do not try to
terminate the pre-existing arrythmia
- Rhythm control (AKA cardioversion) – tries to terminate the abnormal rhythm whilst
maintaining normal sinus rhythm – often reserved for emergencies or where rate
control has failed
1st LINE - RATE-CONTROLLING ANTI-ARRHYTHMICS:
- β-blockers (cardioselective – so NOT Sotalol)
- Non-DHP CCBs (off-label use of Diltiazem)
- Digoxin
MOA: slow down the rate of AP conduction via the AVN – reduces transfer of fast, irregular
APs from atria to ventricles (bringing down the BPM) – each drug-class does this differently:
- β-blockers: block β1 receptors at AVN
- Non-DHP CCBs: block L-type Ca2+ channels
- Digoxin: stimulates PSNS activity at AVN
RATE CONTROL GUIDANCE (in chronic, non-life threatening A.fib):
- 1st Line – Monotherapy
- 2nd Line – Combination therapy (2 rate-controlling drugs)
- 3rd Line – Switch to Rhythm control (see below)
Do NOT give any CCB if pt has HEART FAILURE (except Amlodipine) – if they have both A.fib
& HF, seek specialist advice usually initiate rhythm control
2nd LINE - RHYTHM-CONTROLLING ANTI-ARRHYTHMICS:
- Class I drugs (e.g. Flecainide)
- Class III drugs (e.g. Sotalol, Amiodarone, Dronedarone)
MOA: slow down conduction of irregular APs in atria to help restore normal sinus rhythm –
each drug class does this differently:
- Class I drugs: Block Na+ influx via channels less depolarisation
- Class III drugs: block K+ efflux via channels extended repolarisation (i.e. extended
refractory period
