PHM421 - ATRIAL FIBRILLATION SUMMARY
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)
Pathophysiology
- 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
Treatment
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
1
B-Blockers
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
Digoxin
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
2
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
Warfarin
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
ASA
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
Parameter
Stroke
INR
Heart Rate
Palpitations
Degree of change
Prevent
2-3
< 100 bpm
Absent
3
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
Parameter
Degree of change
Time frame
Bleeding on warfarin
No significant bleeds During, of therapy
INR
Prevent levels >3
Duration of therapy
Heart Rate
Not < 60 bpm
Duration of CCB therapy
Bronchospasm, depression, fatigue Prevent
Duration of βB therapy
Hypotension
Prevent
Duration of therapy
Monitoring Plan
Parameter
INR
BP/HR/ECG
K, Mg levels
Bleeding
Start
OD days 1-3
Baseline
Frequency
Then q1wk
Qshift, ECG OD
Q2-3d
OD
4
Stop
Then q1month
Whom
MD, phm
MU, nurse
MD, phm
pt