In the acute setting, pharmacologic cardioversion (e.g., ibutilide, dofetilide) is less commonly used than electrical cardioversion. Procainamide, flecainide, or amiodarone can be used instead if Wolff-Parkinson-White syndrome is suspected. If this happens, the patient will require immediate defibrillation. ĪV nodal blocking agents, particularly calcium channel blockers and digoxin, should be avoided in patients with Wolff-Parkinson-White syndrome and AF because, by blocking the AV node, AF impulses may be transmitted exclusively down the accessory pathway, which can result in ventricular fibrillation.Caution should be exercised in those who are not receiving anticoagulation because amiodarone can promote cardioversion, thereby posing a thromboembolic risk. 5.Īmiodarone has a class IIa recommendation from the ACC/AHA/ESC for use as a rate-controlling agent for patients who are intolerant of or unresponsive to other agents, such as patients with heart failure who may otherwise not tolerate diltiazem or metoprolol. Toxicity is manifested by GI and visual complaints, atrial tachyarrhythmias, heart block, and ventricular tachycardia. A third dose may be needed after 6 to 8 hr the daily dose varies from 0.125 to 0.25 mg (decrease dosage in patients with renal insufficiency and elderly patients) depending on the heart rate and signs or symptoms of digoxin toxicity. When used, give 0.5 mg IV loading dose (slow) and then 0.25 mg IV 6 hr later. It may be a useful adjunct to a beta-blocker in the hypotensive or heart failure patient, which is not infrequent. 4.ĭigoxin is not a potent AV nodal blocking agent and has a potential for toxicity and therefore cannot be relied on for acute control of the ventricular response, but it may be used in conjunction with beta-blockers and calcium channel blockers. ![]() High doses of beta-blockers can have negative inotropic effects in heart failure and should be used with caution. 3.Įsmolol and metoprolol are beta-blockers available in IV preparations that can be used. Main concern is hypotension and heart failure with this medication, and it should not be used in patients with CHF. After the ventricular rate is slowed, the patient can be changed to oral verapamil 80 to 120 mg q6 to 8h. Verapamil 2.5 to 5 mg IV initially, then 5 to 10 mg IV 10 min later if the rate is still not slowed to <100 beats/min. High doses of calcium channel blockers can exacerbate heart failure and thus should be used with caution in patients presenting with symptoms of heart failure or depressed ejection fraction. After the ventricular rate is slowed, the patient can be changed to oral diltiazem 60 to 90 mg q4 to 6h. Onset of action after IV administration is usually within 3 min, with peak effect most often occurring within 10 min. May then follow with IV infusion 10 mg/hr (range, 5 to 15 mg/hr) to achieve a resting heart rate of <100 beats/min. Treatment options for rate control include the following: 1.ĭiltiazem 0.25 mg/kg (maximum of 25 mg) given intravenously (IV) over 2 min followed by a second dose of 0.35 mg/kg (maximum of 25 mg) 15 min later if the rate is not slowed to <100 beats/min. ACC/AHA recommendations for pharmacologic rate control of atrial fibrillation are summarized in Table 3. If the patient is hemodynamically stable, a rate-control strategy is typically pursued initially. It can be stopped after 1 mo as long as AF has not recurred if the patient is deemed low risk of stroke using the congestive heart failure, hypertension, age, diabetes, stroke/TIA, and vascular disease (CHA2DS2-VASc) scoring system ( Table 1). Anticoagulant therapy should be continued for at least 1 mo after cardioversion to minimize the incidence of adverse thromboembolic events. Alternatively, patients can be safely anticoagulated for approximately 1 mo and then undergo cardioversion without transesophageal echocardiogram. However, if transesophageal echocardiography reveals no atrial thrombus, cardioversion may be performed safely after therapeutic anticoagulation has been achieved. The likelihood of cardioversion-related clinical thromboembolism is low in patients with AF lasting 2 days have a 5% to 7% risk for clinical thromboembolism if cardioversion is not preceded by several weeks of anticoagulation therapy. ![]() The ACC/AHA recommendations for cardioversion of atrial fibrillation are summarized in Table 2. If the patient is hemodynamically unstable (hypotension, congestive heart failure, or angina), perform synchronized cardioversion after immediate conscious sedation with a rapid short-acting sedative (e.g., midazolam).
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |