Cardiovascular Collapse with Intravenous Amiodarone in Children: A Multi-Center Retrospective Cohort Study.

OBJECTIVE: To determine the incidence of cardiovascular collapse in children receiving intravenous (IV) amiodarone and to identify the population at risk. DESIGN: A multicenter study of patients ≤ 18 years of age who received intravenous amiodarone between January 2005 and December 2015. A retrospective analysis was performed to identify patients who developed cardiovascular collapse (bradycardia and/or hypotension). RESULTS: Of 456 patients who received amiodarone, cardiovascular collapse occurred in 47 patients (10%). Patient risk factors for collapse in a univariate analysis were as follows: age < 3 months (p = 0.04), depressed cardiac function (p < 0.001), blood pressure below 3rd percentile (p < 0.001), high lactate at baseline (p < 0.001). Administration risk factors included bolus administration (p = 0.04), and bolus administration over ≤ 20 min (p = 0.04). In multivariate analysis, age, baseline blood pressure less than 3rd percentile, and rapid bolus delivery were independent risk factors for cardiovascular collapse in the study group. The mortality rate was significantly higher in the collapse group (28% versus 8%). CONCLUSION: We found an association between IV amiodarone administration and the risk of developing cardiovascular collapse in a significant subset of children. Extreme caution and careful hemodynamic monitoring is recommended when using IV amiodarone in this population, especially in young infants, hemodynamically compromised patients, and in patients receiving rapid amiodarone bolus administration.

Delayed cardiac dysrhythmias after fingolimod administration.

A 51-year-old woman with relapsing-remitting multiple sclerosis was initiated on fingolimod. She developed a Mobitz Type I (Wenckebach)second-degree atrioventricular (AV) heart block during the initial 6-hour monitoring. She was transferred to the emergency department for further monitoring, where she went into a junctional tachycardia then went back into a Mobitz Type I AV block. The patient was symptomatic with a heart rate nadir of 38 beats per minute and treated with atropine. Junctional tachycardia has not been previously reported with fingolimod use. Patients may require extended cardiac monitoring after fingolimod administration.

Ventricular arrhythmias and QT-prolongation during therapy with ketanserin: report of a case.

A patient is reported who developed a marked prolongation of QTc and life threatening ventricular arrhythmias during oral Ketanserin therapy. No other factors contributing to the QTc prolongation or to the occurrence of ventricular arrhythmias were found. The relevant literature is reviewed.

Supraventricular tachycardia emergencies: diagnosis and management.

A variety of acute supraventricular tachycardias may be encountered. In many instances the therapies for these rhythm disturbances overlap, but a rational approach to individual disturbances should be based on an understanding of the anatomy and physiology involved in the individual dysrhythmia. Numerous investigative approaches are underway at present, especially with regard to interruption of arrhythmia pathways by electroshock therapy or surgical therapy. In addition, pacing overdrive may be very effective, especially in patients with reentrant arrhythmias.

Iatrogenically induced intractable atrioventricular reentrant tachycardia after verapamil and catheter ablation in a patient with Wolff-Parkinson-White syndrome and idiopathic dilated cardiomyopathy.

In a patient with WPW syndrome and idiopathic dilated cardiomyopathy, intractable atrioventricular reentrant tachycardia (AVRT) was iatrogenically induced. QRS without preexcitation, caused by junctional escape beats after verapamil or unidirectional antegrade block of accessory pathway after catheter ablation, established frequent AVRT attack.