PHM421



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

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

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 |Degree of change |Time frame |

|Stroke |Prevent |During, a/f therapy |

|INR |2-3 |Within 3-5 days |

|Heart Rate |< 100 bpm |Within 24-48 hrs |

|Palpitations |Absent |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 |Start |Frequency |Stop |Whom |

|INR |OD days 1-3 |Then q1wk |Then q1month |MD, phm |

|BP/HR/ECG | |Qshift, ECG OD | |MU, nurse |

|K, Mg levels |Baseline |Q2-3d | |MD, phm |

|Bleeding | |OD | |pt |

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