topics / مواضيع

  Sung RJ et al. Mechanisms of spontaneous alternation between reciprocating tachycardia and atrial flutter/fibrillation in the Wolff-Parkinson-White syndrome. Circulation. 1977;56:409. Tijunelis MA et al. Myth: intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-ParkinsonWhite syndrome in the emergency department. CJEM. 2005;7:262–265. Gulamhusein S et al. Acceleration of the ventricular response during atrial fibrillation in the Wolff-ParkinsonWhite syndrome after verapamil. Circulation. 1982;65:348. Falk RH. Proarrhythmia in patients treated for atrial fibrillation or flutter [published correction appears in Ann Intern Med. 1992;117:446]. Ann Intern Med. 1992;117:141. Aliot E et al. Twenty-five years in the making: flecainide is safe and effective for the management of atrial fibrillation. Europace. 2010;13:161–173. Krahn AD et al. A randomized, double-blind, placebo controlled evaluation of the efficacy and safety of 101. 102. 103. 104. 105. 106. 107. 108.

  175 showed significantly lower rates of 1-month survival and 1-month survival with favorable neurologic outcomes in out-of-hospital cardiac arrest patients with shockable rhythm, who received epinephrine before hospital arrival, relative to patients who did not receive epinephrine (p < 0.001). On the basis of these trials, it would be reasonable to use a single dose of vasopressin 40 units as an alternative to either the first or second dose of epinephrine 1 mg in the treatment of VF (or pulseless VT). CASE 15-9, QUESTION 3: One of the physicians delivering ACLS for M.N. wants to initiate corticosteroid therapy. What is the evidence supporting the use of corticosteroid therapy in patients experiencing cardiac arrest? A randomized, double-blind, placebo-controlled, parallel-group trial performed by Mentzelopoulos et al. 176 assessed the impact of using two different strategies for managing in-hospital cardiac arrest patients on: (a) survival to hospital discharge with favorable neu

  140 Liver toxicity can range from an asymptomatic elevation of transaminases (2–4 times normal) to fulminant hepatitis. The mean latent period between the start of amiodarone therapy and evidence of liver injury is 10 months (onset can be as short as 3–4 days), but with rapid IV loading of amiodarone, a Reye’s-like fulminant hepatitis can occur as early as 1 day after starting therapy, most likely caused by the IV vehicle polysorbate-80. The precise mechanism of amiodarone-induced hepatotoxicity has not been fully elucidated. However, higher doses and prolonged drug use appear to place patients at higher risk of experiencing hepatotoxic effects of amiodarone. Thus liver enzymes should be monitored at baseline, 1, 3, 6 months, and semiannually afterward. 140,141 The most common GI complaints are nausea, anorexia, and constipation, which occur in 25% of patients receiving amiodarone. 140 Both hypothyroidism and hyperthyroidism have been reported, although hypothyroidism is more common.