B1 Atrial Fibrillation - Individual.utoronto.ca

Common DRPs
1. Pt not receiving a drug that is required (eg anticoagulation for stroke prophylaxis, supplemental doses of K or Mg)
2. Pt receiving drug that is not indicated (eg patient with chronic atrial fibrillation is receiving an anti-arrhythmic)
3. Pt not receiving the most appropriate drug (eg digoxin for rate control in an active patient)
4. Pt at risk of developing adverse drug reactions (eg pro-arrhythmias)
5. Pt at risk of developing a drug interaction (eg pharmacokinetic interaction between amiodarone and digoxin or
warfarin; pharmacodynamic interaction between beta-blockers, calcium channel blockers and amiodarone)
- supraventricular tachyarrhythmia characterized by uncoordinated atrial activation with consequent deterioration of
atrial mechanical function.
- caused by 1) abnormal impulse formation or 2) abnormal impulse conduction
- characterized by extremely rapid (300-600 bmp) and disorganized atrial activation. AV node filters this, resulting in a
fast, irregular ventricular rate of 100-120 bpm
- ventricular rate: atrial rate is 1:3; if know the ventricular rate (i.e. heart rate) then know the approximate atrial rate
- may be due to an ectopic beat that doesn’t let AV node work properly; end up with “irregularly irregular” pulse
- “atrial kick” contributes 20% of the cardiac output
- during afib, cardiac output ↓s, not enough blood gets to the body = SOB, weakness, etc.
Urgency (medical perspective): very urgent, although not usually life threatening right now. Can lead to
complications such as MI, stroke, ischemia, thrombus formation.
Signs and Symptoms
- shortness of breath, weakness, dizziness, lightheadedness, reduced exercise tolerance, palpitations , asymptomatic –
paroxysmal afib, ↑ HR, ↑ or ↓ BP, crackles on auscultation, ECG – irregular, CXR: pulmonaryy edema
Differential Diagnosis
Supraventricular Arrhythmias : originate above the Bundle of His, normal QRS, i.e. sinus bradycardia, atrial flutter
Ventricular Arrhythmias: originate below the Bundle of His, PVC (?), VT, VF
Risk Factors: male, ↑ age - doubles by every decade of life, electrolyte abnormalities – hypoMg, hypoK, CAD,
congenital heart defects, damage to heart: MI, ischemia, COPD, high catecholamine states - alcohol withdrawal,
excessive physical exertion, thryrotoxicosis, valvular disorders, sepsis, hypertension, diabetes, cardio-thoracic surgery
Diagnosis: irregular ECG (may not have an identifiable P wave), direct auscultation, CXR shows pulmonary edema
Due to drug?
- Digoxin - high doses can cause fibrillation (more commonly ventricular; artrial very rare), β1 agonists: epinephrine,
β2 agonist – cause vasodilation and reflex tachycardia, Caffeine – incr. sympathetic tone, Theophylline,
Amphetamines, Excess alcohol (holiday heart syndrome), Thyroxine - dose too high, drugs that prolong QT interval =
↑ risk of ventricular fibrillation, erythromycin, co-triamoxazole, TCAs
Management Strategies: Control ventricular response rate – VRR, Restore and maintain normal sinus rhythm –
Cardioversion, ↓ risk of stroke
1. Controlling Ventricular Response Rate – most common way of controlling AF
Which drugs? Digoxin, Beta Blockers, Calcium channel blockers : only use verapamil or diltiazem because these are
the only CCBs that control AV nodal response rate so they work by slowing conduction in SA, AV nodes
Which Patients?
- symptomatic
- at least 50% of patients will spontaneously convert so maintain VRR &  symptoms while waiting
- some antiarrhythmics have anticholinergic properties (i.e. Ia) so it would speed up conduction thru AV node
- before starting an anti-arrythmic (to cardiovert) that has anticholinergic properties, you have to get control of the VRR
- all antiarrhythmics decrease the atrial rate = the AV node filters less beats = ventricular response rate may go up
Efficacy: slows SA, AV node conduction, not well tolerated in pts w/ actue HF
Onset: Fast iv-min, po-hrs
Convenience: OD-QID
Side Effects: ↓ HR , hypoTN, dyspnea, fatigue, ↓ exercise tolerance, heart block, mask ssx hypoglycemia,
bronchospasm in asthmatics, depression (less w/ aten, nad)
DIs: digoxin, CCB, amiodarone, ↓ βB dose by 25-50%
Calcium Channel Blockers – Verapamil, Diltiazem
Efficacy: directly suppresses AV node conduc’n, work in tissue, no vagomimetic activity, not well tolerated in pts w/
actue HF
Onset: fast
Convenience: iv or po TID
Side Effects: hypoTN,  HR, heart block, constipation, flushing, caution in pts w/ CHF
DIs: βB, digoxin, amiodarone
2. Cardioversion
Goal: convert to normal sinus rhythm – HR = 80-100 bpm
Which Drugs?
- Antiarrhythmics that work on atrial tissue and, therefore, must work on Na channels
- Class Ia – procainamide, quinidine
- Class Ic – flecainide, propafenone,
- Not Class Ib b/c they don’t work on atrial tissue
- Class III : sotolal (beta blocker but it has antiarrhythmic prop), amiodorone (least pro-arrhythmic drug on market),
ibutilide (works in 10 minutes; only in hospital, not long term)
Which Patients?
- patients with AF < 48h b/c the shorter the duration of fibrillation, the better the chances of cardioversion
- patients who are hemodynamically unstable - use the paddles to electrically cardiovert
- patients who remain symptomatic despite normalizing VRR – done to restore “atrial kick”
- spontaneous conversion – most will occur in 24h
- not everybody converts even when using antiarrythmics
- refractory AF: the longer the are in AF the harder it is to convert, heart failure – atrium is continuously stressed, so
predisposed to AF
- if not going to convert, control VRR (see #1)
Why are we getting away from giving anti-arrhythmics long-term?
- risk with using antiarrythmiac b/c they are all pro-arrhythmic - predisposes pt to haing future arrythmias
- ↑ mortality via pro-arrythmics
Efficacy: see adv/disadv chart below, good for pts with heart failure (ionotropic), CHF, vagomimetic – decr. efficacy
with pts with high sympathetic tone
Onset: slow
Convenience: Loading dose – ½ dose stat; ¼ dose in 4-6 hr, last ¼ dose in 4-6 more hrs - then OD
Side effects: bradycardia, N/V, visual disturbances, pro-arrhythmic, ↓ HR, heart block
DI: βB, CCB, amiodarone, propafenone, quinidine: ↓ digoxin dose by 25-50%
Class 1 Antiarrhythmics - Na Channel Blocker
1a – Qunidine, Procainamide
Efficacy: slow AV node conduction
Convenience: Q6H-Q8H
Side effects: GI, aggravation of underlying HF, torsades de pointes, Quin – thrombocytopenia, hepatitis, Proc –
agranulocytosis, systemic lupus erythematosus
DI: ↓ digoxin dose by 50%
1c – Flecainide, Propafenone
Efficacy: slow AV node conduction
Convenience: Q8H-Q12H
Side Effects: pro-arrhythmic, Flec- blurred vision, tremor, CHF, Prop - constipation, HA, metallic taste
DI: Prop – active metabolites accum. in rapid metabolizers
Class III Antiarrhytmics – K channel blockers
Sotalol, Amiodarone, Bretylium, Dofetilide, Ibutilide
Efficacy: slow AV node conduction, also affect refactoriness , sotalol is a βBer w/ anti-arrythmic properties
Convenience: Q12H
Side Effects: Sota – torsades, hypoTN, bradycardia, wheezing, Amio – pulmonary toxicity, CNS effects,
hyper/hypoTN, photosens, hepatic tox, corneal deposits, Dofe – HA, torsades
DI: Digoxin, diltiazem, verapamil: may cause AV block, bradycardia
3. Decrease Stroke
Which drugs? Warfarin and ASA
Which patients?
- high risk of stroke, chronic AF, paroxysomal AF – long term anticoagulation, AF>48h
- pts you plan to cardiovert
start therapy 3 weeks b/f; continue for 4 weeks after cardioversion
continue a/f cardioversion is done b/c although the heart’s electrical function is normal, the mechanical
function may take time to return to normal
- do not use in patients who have an electrolyte imbalance
Efficacy: good in pts w/ mod–high risk of stroke, i.e. age >65-75, underlying CAD, CHF, HTN, DM, target INR = 2-3
Onset: 3-5 days to reach ther INR
Convenience: po
Side Effects: ↑d risk of bleeding in pts w/ uncontrolled HTN, ↑ age, the ↑er your age, the ↑er the risk of
complications from warfarin use but the ↑er the benefits
DIs: NSAIDs, ASA, amiodarone, all can ↑ INR
Efficacy: - good in pts w/ low risk of stroke (< 65yo, no underlying cardiovascular disease)
Convenience: 325mg OD
Side Effects: GI bleeding, dyspepsia
Treating Specific Patients
Hemodyanmically Unstable AF : electrical cardioconversion
Recent onset AF
- control VRR b/c 50-67% of patients will spontaneously convert
- if onset < 48hrs – cardiovert chemically
- if onset > 48hrs – do anticoagulation therapy for 3 wks, then cardiovert chemically
Chronic AF : VRR and anticoagulation
Once converted : symptomatic long term antiarrythmic therapy to maintain sinus rhythm, anticoagulants
Care Plan
Clinical Outcomes : reduce symptoms, prevent complication (i.e. stroke)
Pharmacotherapeutic Outcomes : Patient should receive the right drug at the right dose, strength, frequency and
duration without any intolerable side effects or interactions.
Pharmacotherapeutic Endpoints
Heart Rate
Degree of change
< 100 bpm
Time frame
During, a/f therapy
Within 3-5 days
Within 24-48 hrs
Within 24-48 hrs
Therapeutic Endpoints
Positive endpoints: same as Pharmacotherapeutic Endpoints above
Negative endpoints: S&Sx of drugs chosen
Degree of change
Time frame
Bleeding on warfarin
No significant bleeds During, of therapy
Prevent levels >3
Duration of therapy
Heart Rate
Not < 60 bpm
Duration of CCB therapy
Bronchospasm, depression, fatigue Prevent
Duration of βB therapy
Duration of therapy
Monitoring Plan
K, Mg levels
OD days 1-3
Then q1wk
Qshift, ECG OD
Then q1month
MD, phm
MU, nurse
MD, phm