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Many patients with an implanted cardioverter defibrillator (ICD) also receive antiarrhythmic drug therapy. Although an expanding number of patients are receiving ICD therapy, many will not have received previous antiarrhythmic treatment. For patients with an ICD, infrequent arrhythmias and a low probability of inappropriate device discharges, no antiarrhythmic therapy is required. However, for those patients who require an antiarrhythmic drug, amiodarone is a reasonable first choice because of safety in patients with poor LV function. It may be particularly useful for patients with high density ventricular arrhythmias. However, the interactions between ICDs and antiarrhythmic therapy requires close monitoring in order that patient benefit can be optimised, and this review focuses on those interactions.
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An implantable cardioverter defibrillator (ICD) may be effective in reducing the risk of sudden cardiac death. The high cost of ICD treatment, however, compared with alternatives raises the question of whether this new technology is an efficient use of scarce health care resources.
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Early prophylactic amiodarone not only significantly reduces SVT but also reduces SVT-related hospital and ICU stay. We strongly recommend prophylactic early use of amiodarone in COPD patients.
We present the case of a 20-year-old woman with a history of hypoplastic left heart syndrome, D-transposition of the great arteries, and mitral/pulmonary valve atresia without surgical palliation, who was admitted with persistent atrial flutter/fibrillation and worsening cardiac function from amiodarone-induced thyrotoxicosis. Despite maximal medical therapy, she continued to have uncontrolled thyrotoxicosis and underwent successful emergent thyroidectomy under general anesthesia. With advances in the treatment of congenital heart disease, more patients are surviving to adulthood and require emergent noncardiac surgery. Therefore, anesthesiologists must understand the principles for managing patients with congenital heart disease and how the patient's physiology may affect the anesthetic plan.
To evaluate the change in mean arterial pressure when utilizing 2 intravenous amiodarone formulations.
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Amiodarone is an extremely effective antiarrhythmic drug that is known to cause many adverse effects such as pulmonary, thyroid, and liver toxicities. Of these, pulmonary toxicity is most serious. Pulmonary toxicity can present as interstitial pneumonitis, organizing pneumonia, pulmonary nodules and masses, and very rarely pleural effusions. We present a case of a 73-year-old male who presented with progressive exertional dyspnea, nonproductive cough, generalized fatigue, and weakness. He was found to have multiorgan toxicity secondary to long-term treatment with high doses of amiodarone. This case illustrates that amiodarone may cause toxicity involving multiple organs simultaneously in patients receiving long-term therapy and represents the first reported case of amiodarone-induced loculated pleural effusion without associated lung parenchymal involvement.
Here we describe a wide complex tachycardia after bupropion overdose that was responsive to sodium bicarbonate. This rhythm was likely secondary to bupropion-induced sodium channel blockade and corrected QT interval (QTc) prolongation. It is critical for the emergency medicine physician to recognize that a wide complex rhythm in a patient with bupropion overdose may be secondary to sodium channel toxicity and prolonged QTc as this rhythm may be responsive to sodium bicarbonate. Identifying this rhythm as purely ventricular tachycardia can lead to the administration of medications such as amiodarone that may further prolong QTc and contribute to sodium channel blockade, exacerbating bupropion-induced cardiotoxicity.
Amiodarone via iodine excess can determine thyroid dysfunction.
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Amiodarone causes changes in thyroid function tests in about 15-20% of patients, inducing either hypothyroidism or thyrotoxicosis. The iodine load and the destructive thyroiditis caused by amiodarone produce thyrotoxicosis. We report a case of amiodarone-induced thyrotoxicosis diagnosed when investigating the reason for worsening of cardiac function. Prognosis and treatment of cardiac disorder were determined by thyrotoxicosis. The management needed a closed monitoring of thyroid function. Treatment was based on high doses of propylthiouracil and dexamethasone, but they couldn t control cardiac condition and surgery was warranted. When amiodarone-induced thyrotoxicosis is refractory to medical treatment, we believe surgery should be considered earlier.
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Prospective randomized study aimed at evaluating efficacy of early direct current cardioversion (DCCV) following successful PBMV in patients with long-standing AF. Group 1 (n=20) had patients of rheumatic MS with AF who underwent successful PBMV. Group 2 (n=15) patients were DC cardioverted and administered oral Amiodarone for 6 weeks. Primary endpoint was maintenance of SR after 6 months. Secondary endpoints were functional capacity, number of embolic episodes, adverse drug effects, and all-cause mortality.
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One hundred one patients (48 men, mean age 64 +/- 9 years) with atrial fibrillation lasting >3 weeks participated in the study. Thirty-four patients received amiodarone (300 mg intravenously over 1 h, followed by 20 mg/kg over the next 24 h plus 600 mg orally, in three doses, for 1 week, then 400 mg/day orally, for three weeks), 32 received propafenone (2 mg/kg intravenously over 15 min, followed by 10 mg/kg over 24 h and then 450 mg/day orally, for one month) and the remaining 35 served as control subjects. All patients received digoxin and anticoagulant treatment as indicated (International Normalized Ratio 2 to 3).
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To assess the impact on the incidence of PPIVC by implementing a catheter management protocol and to determine risk factors for PPIVC development in hospitalized patients.
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Our algorithm based on VKORC1, CYP2C9 and CYP4F2 polymorphisms can help to predict the warfarin maintenance dose in Chinese Han Population.