Wednesday, June 2, 2010

AF

Source:http://emedicine.medscape.com/article/757370-treatment

Treatment
Prehospital Care

* Care of hemodynamically unstable patients is guided by ACLS protocols, including direct current (DC) cardioversion.
* Symptomatic patients may benefit from intravenous (IV) rate-controlling agents, either calcium-channel blockers or beta-adrenergic blockers.

Emergency Department Care

Immediate interventions – ABCs

* Patients placed on cardiac monitor, O2, and ABCs are being assessed, ECG, IV access
* Unstable patients require immediate DC cardioversion.8
o Hypotension
o Decompensated CHF
o Ongoing ischemia or infarction
* These initial interventions occur simultaneously by the team of physicians and nurses taking care of the patient.

Routine care

* In most circumstances, the patient is stable but has an elevated ventricular response and will require rate-controlling medications, with a heart rate goal of under 80. This recommended heart rate target was challenged in the RACE II study that examined HR of 110 versus less than 80. The lenient arm had no difference than the strict control arm per a composite outcome of cardiac death, CHF, stroke, systemic bleeding, and life-threatening arrhythmic events.11
* If there is another clinical condition driving the tachycardia, such as fever, infection, or dehydration, then efforts at temperature control and restoration of normovolemia will aid in controlling the tachycardia.
* Consideration of anticoagulation based upon patient risk factors may also begin in the emergency department.

Cardioversion

Cardioversion can be pharmacologic based or electrical.

Anticoagulation and cardioversion may be indicated. Since there is a risk of thrombus formation and fragmentation, patients in atrial fibrillation for greater than 48 hours should receive therapeutic anticoagulation (INR 2-3 range) for 3 weeks prior to cardioversion. Alternatively, these patients can undergo heparinization, and TEE, and cardioversion if no thrombus is detected. In each case, anticoagulation needs to be continued for an additional 4 weeks.

Electrical cardioversion

* DC cardioversion is the treatment of choice in the unstable patient with atrial fibrillation. Cardioversion is indicated in patients with first time atrial fibrillation or in patients with paroxysmal atrial fibrillation.
* Since atrial fibrillation begets atrial fibrillation, one may delay or prevent permanent atrial fibrillation by decreasing the overall time spent in atrial fibrillation in these early clinical stages.
* There is little utility in cardioverting stable patients with permanent atrial fibrillation, and the goal in this group is rate control.
* Placement of pads or paddle positions include anterior-lateral (ventricular apex and right infraclavicular) and anterior-posterior (sternum and left scapular), with at least one study suggesting increased efficacy with the anterior-posterior method.
* Biphasic waveforms are proved to convert atrial fibrillation at lower energies and higher rates than monophasic waveforms.
* Strategies include dose escalation (70, 120, 150, 170J for biphasic) or (100, 200, 300, 360J for monophasic) versus beginning with single high energy/ highest success rate for single shock delivered.
* Patients who are stable and/or awake and can tolerate sedation should be pretreated, with typical regimens involving midazolam, fentanyl, and propofol.
* Cardioversion of patients with implanted pacemakers and defibrillator devices is safe when appropriate precautions are taken. Keeping the cardioversion pads in an AP orientation ensures that the shocks are not directly over the generator. Alteration in pacer programmed data has been reported, as well as heart block and elevated enzymes if the current gets conducted through a pacer lead.
* Stunning of the atria and stasis can occur after cardioversion, and this can lead to thrombus formation even though the patient is in sinus rhythm. Therefore, patients would undergo anticoagulation for several weeks afterwards.
* Risks of cardioversion
o Risks with sedation
o Risk of thromboembolism (<1%>70 kg) was evaluated. This treatment was successful in terminating AF in 94% of episodes (mean time to symptom resolution of 133 minutes).

Rate control

In most instances, patients presenting to the ED have preexisting atrial fibrillation and a rapid ventricular response. These individuals may already be on beta-blockers or calcium channel blockers, and initial attempts at rate control should be initiated with same class medications given intravenously, trying to avoid mixing classes of nodal blocking agents.

* Extreme care must be taken in patients with preexcitation syndrome and atrial fibrillation. Blocking the AV node in some of these patients may lead to AF impulses exclusively transmitted down the accessory pathway, and this can result in ventricular fibrillation. (If this happens, the patient will require immediate defibrillation.) Alternative therapies for the treatment of arrhythmia in this group include procainamide and amiodarone.
* Intravenous diltiazem or metoprolol are commonly used drugs for AF with RVR.
* Amiodarone has been used in patients with CHF who may otherwise not tolerate diltiazem or metoprolol. Digoxin may also be used, but its peak effect may not be for 6 hours.

Antiarrhythmic drugs

Antiarrhythmic drugs that can terminate atrial fibrillation include procainamide, disopyramide, propafenone, sotalol, flecainide, amiodarone, ibutilide, and dronedarone. The efficacy of antiarrhythmic drugs has been linked to the duration of atrial fibrillation.

The American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) Guidelines make the following recommendations regarding pharmacologic conversion of atrial fibrillation (AF):

* Conversion of AF less than or equal to 7 days15
o Agents with proven efficacy include dofetilide, flecainide, ibutilide, propafenone, and to a lesser degree, amiodarone and quinidine.
o Less effective or incompletely studied agents in this scenario include procainamide, digoxin, and sotalol.
* Conversion of AF lasting greater than 7 days
o Agents with proven efficacy include dofetilide, amiodarone, ibutilide, flecainide, propafenone, and quinidine.
o Less effective or incompletely studied agents in this scenario include procainamide, sotalol, and digoxin.
* Conversion of AF lasting greater 90 days - Oral propafenone, amiodarone, and dofetilide have been shown to be effective at converting chronic AF to normal sinus rhythm (NSR).

The US Food and Drug Administration (FDA) mandates inpatient monitoring for dofetilide initiation. Patients who start sotalol usually require inpatient monitoring (for torsade de pointes), although patients with no heart disease, QT interval <450>75 Age 65-74
Mechanical heart valve HTN Female gender
Mitral stenosis CHF CAD
EF <=35% Thyrotoxicosis DM High risk factor Moderate risk factor Low risk Prior CVA/TIA Age >75 Age 65-74
Mechanical heart valve HTN Female gender
Mitral stenosis CHF CAD
EF <=35% Thyrotoxicosis DM Aspirin can be 81 mg or 325 mg Warfarin - INR goal of 2-3 * Risk factors - Aspirin or no therapy * One moderate risk factor - Aspirin or warfarin * More than one moderate risk factor or one high risk factor - Warfarin * Lone AF - Age 60-74 years, aspirin * Age 60-74 years, CAD – Warfarin Disposition A number of studies have looked at whether low-risk patients with new-onset atrial fibrillation can be treated and discharged from an emergency department setting.18 * A study by Michael et al looked at 289 patients seen during an 18-month period in an emergency department setting.8 Sixty-two percent (180) underwent attempted chemical cardioversion with a 50% success rate, and 28% (80) had attempted electrical cardioversion with a 89% success rate. Ninety-three percent of electrical cardioversions were performed by emergency physicians. They concluded that cardioversion and immediate discharge of patients who present to the ED with acute atrial fibrillation appears to be both safe and effective. * Reasons for hospitalization would include but not be limited to the following: o Presence of comorbidities o For workup or treatment of underlying etiology of atrial fibrillation, including evaluation for acute coronary syndrome or myocardial infarction o For elderly patients o For patients with underlying heart disease o Patients at risk of complications from AF therapies Consultations * A cardiologist may become involved emergently if complicating factors are present or if the patient is experiencing ongoing cardiac ischemia or infarction not treatable with DC cardioversion, rate reduction measures, and standard chest pain protocols.19 A patient with acute myocardial infarction (AMI) and new-onset AF who is stable may benefit from simple rate-control measures (eg, intravenous beta-blockers) while being prepared for the catheterization laboratory and intravenous nitrates, heparin, and aspirin are begun. In the patient with an ST elevation MI, the main emphasis, however, is to minimize door to open artery time. * A patient's cardiologist plays a vital role in determining the most appropriate long-term strategy for a patient with atrial fibrillation and provides crucial follow-up care. Medication Pharmacologic agents in atrial fibrillation (AF) fall into 1 of 2 classes: rate-controlling drugs and rhythm restoring/rhythm maintenance drugs (though some overlap exists with some drugs, such as amiodarone, exhibiting both qualities). Rate-controlling drugs In patients without ventricular preexcitation, rate is controlled most effectively with intravenous verapamil, diltiazem, or beta-adrenergic blockers. Beta-blockers are especially effective in the presence of thyrotoxicosis and increased sympathetic tone or in patients with myocardial ischemia/AMI. The non-hydropyridine calcium channel blockers may be chosen in patients lacking any history of heart failure and in patients with reactive airway disease. Anecdotally, intravenous diltiazem has become many emergency medicine physician's first-line rate-controlling drug in patients without a history of heart failure. Digoxin is ineffective in controlling ventricular rate during acute episodes. In patients with acute or chronic heart failure, digoxin or amiodarone should be used. (Amiodarone does not currently have FDA approval for this intervention.) Antiarrhythmic drugs Antiarrhythmic drugs that can terminate atrial fibrillation include procainamide, disopyramide, propafenone, sotalol, flecainide, amiodarone, and ibutilide. The efficacy of antiarrhythmic drugs has been linked to the duration of atrial fibrillation. The American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) Guidelines make the following recommendations regarding pharmacologic conversion of AF: * Conversion of AF less than or equal to 7 days o Agents with proven efficacy include dofetilide, flecainide, ibutilide, propafenone, and to a lesser degree, amiodarone and quinidine. o Less effective or incompletely studied agents in this scenario include procainamide, digoxin, and sotalol. * Conversion of AF lasting greater than 7 days o Agents with proven efficacy include dofetilide, amiodarone, ibutilide, flecainide, propafenone, and quinidine. o Less effective or incompletely studied agents in this scenario include procainamide, sotalol, and digoxin. * Conversion of AF lasting greater 90 days - Oral propafenone, amiodarone, and dofetilide have been shown to be effective at converting chronic AF to normal sinus rhythm (NSR). When considering drug therapy for atrial fibrillation, remember the treatment caveat: "Electrical cardioversion is the preferred modality in the patient whose condition is unstable." Calcium channel blockers These agents are more effective than digoxin when given orally for long-term rate control and should be the initial DOC. They reduce rate of AV nodal conduction and control ventricular response. Formulations administered IV are discussed as they apply to the control of severe symptoms related to a rapid ventricular rate in an emergent situation.

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