Sandbox/Afib

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

New onset atrial fibrillation: ❑ The presentation can be any of the following: ❑ Paroxysmal and stop spontaneously ❑ Persistent and stop only with cardioversion ❑ Permanent and present for prolonged periods

Stable: ❑ Asymptomatic ❑ Mild to moderate symptoms

Unstable: ❑ Hypotension ❑ Tachycardia ❑ Cold extremities ❑ Peripheral cyanosis ❑ Mottling ❑ Altered mental status ❑ Ongoing ischemia ❑ Decompensated heart failure

Does the patient require heart rate control therapy?

No

Yes

❑ Identify the underlying etiology and treat accordingly ❑ Proceed with cardioversion & anticoagulation strategy as shown below

Does the patient have any evidence of an accessory pathway (pre-exitation syndrome)

Does the patient has any symptoms and signs of pulmonary edema? ❑ Dyspnea ❑ Crackles ❑ Chest X-ray showing pulmonary edema

No

Yes

Yes

No

Does the patient has any evidence of heart failure with reduced EF

❑ IV procainamide or ibutilide ❑ Catheter ablation if the accessory pathway has a short refractory period that allows rapid antegrade conduction

Manage pulmonary edema: ❑ Initiate oxygen therapy ❑ High doze IV diuretics ❑ BP management ❑ SBP 85 - 100 mm Hg (dobutamine or milrinone) ❑ SBP < 85 mm Hg (dopamine and norepinephrine)

Immediate DC cardioversion

Yes

No

After initial pulmonary edema management proceed with DC cardioversion

Heart rate control: ❑ Digoxin ❑ Oral vs intravenous are based upon the clinical urgency

Heart rate control: ❑ Beta blockers or CCB's ❑ Oral vs intravenous are based upon the clinical urgency

Successful

Unsuccessful

Does the patient respond or the arrhythmia terminate (sinus rhythm)?

Identify the underfying cause and treat accordingly

Repeated attempts may be made after adjusting the location of the electrodes or applying pressure over the electrodes, or following administration of an antiarrhythmic medication

Yes

No

Identify the other underlying etiologies and treat accordingly

Oral vs intravenous amiodarone according to the clinical urgency

Proceed with the anticoagulation strategy as shown below

Does the patient respond or the arrhythmia terminate (sinus rhythm)?

Yes

No

❑ Identify the underlying etiology and treat accordingly ❑ Proceed with anticoagulation strategy as shown below

Proceed with the cardioversion strategy as shown below

Cardioversion Strategy

Does the patient with new onset AF has any contraindication for cardioversion : ❑ Asymptomatic elderly patients (>80 years) with multiple comorbidities ❑ Patients with high risk of bleeding

No

Yes

Anticoagulation strategy

❑ <48 hours

❑ >48 hours ❑ Unknown ❑ Prior history of a thromboembolic event ❑ Prior history of TEE evidence of left atrial thrombus ❑ Mitral valve disease or significant cardiomyopathy or heart failure

IV heparin

3 week oral anticoagulation

TEE

Cardioversion

No LA thrombus

LA thrombus

Sinus rhythm

Atrial fibrillation

Heparin

3 week oral anticoagulation

Assess stroke risk to initiate long term anticoagulation

Repeat TEE showing no LA thrombus

Repeat TEE showing LA thrombus

Cardioversion

Initiate rate control

Atrial fibrillation

Sinus rhythm

{{{ A03 }}}

Repeat cardioversion or use AV nodal blocking agents

Assess stroke risk to initiate long term anticoagulation

Sinus rhythm

Atrial fibrillation

Assess stroke risk to initiate long term anticoagulation

Initiate 4 week anticoagulation therapy

Do's & Dont's

• IV amiodarone or digoxin may be considered to slow a rapid ventricular response in patients with ACS and AF associated with severe LV dysfunction and HF.
• Avoid beta blockers to control the ventricular rate in patients with AF and chronic obstructive pulmonary disease.
• Avoid amiodarone, adenosine, digoxin, or calcium channel antagonists (oral or intravenous) in patients with WPW syndrome who have pre-excited AF.
• In AF with HF, it is reasonable to perform AV node ablation with ventricular pacing to control heart rate when pharmacological therapy is insufficient or not tolerated.
• For patients with AF and rapid ventricular response causing or suspected of causing tachycardia induced cardiomyopathy, it is reasonable to achieve rate control by either AV nodal blockade or a rhythm-control strategy.

References

Template:WikiDoc Sources