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Atrial fibrillation with a rapid ventricular rate often adds to the impaired haemodynamic status of patients with depressed left ventricular function.1 Intravenous amiodarone has been shown to be effective in slowing the heart rate during atrial fibrillation.2 For continuous infusion of the drug a central venous access is recommended.3 We tested the hypothesis that amiodarone, given as a single bolus through a peripheral vein access, is effective and does not cause phlebitis.
Forty patients with documented heart disease and atrial fibrillation (ventricular heart rate ⩾ 135 beat/min) were included in the study. Mean (SD) age of the patients was 72 (12) years, 22 were men, and the mean ejection fraction was 38 (12)%. Cardiogenic shock was present in eight patients, 12 had pulmonary oedema, and 20 had exacerbated congestive heart failure. Mean systolic blood pressure was 111 (28) mm Hg. The onset of the tachyarrhythmia could be documented in 18 patients within 24 hours (15 (13) hours) before amiodarone treatment; in the remaining 22 patients the duration was unknown. Depending on clinical presentation and duration of the arrhythmia, patients were pretreated with digoxin, verapamil, or β blockers. All the patients were admitted to the coronary care unit and monitored during amiodarone treatment and for the following 24 hours.
Undiluted amiodarone was administered through a peripheral vein access within one minute, followed by a flush of 10 ml saline solution. All patients received 450 mg regardless of their weight. Heart rate was monitored continuously, and blood pressure and clinical status were documented every 10 minutes. During this time no other drugs with potential effects on heart rate were administered.
All values are expressed as mean (SD). Intraindividual changes of haemodynamics are compared with the paired Student'st test. Probability values of p ⩽ 0.05 were considered significant.
Normal sinus rhythm occurred in 13 patients within 30 minutes, and another eight patients converted during the following 24 hours. Heart rate reduction was smaller in the group with persistent arrhythmia as compared to the group who was in sinus rhythm after 30 minutes (fig 1). In both groups the reduction in heart rate was significant (p < 0.0005 for each group). After 30 minutes, treatment with conventional drugs was initiated if considered necessary.
In the group of patients who reverted to sinus rhythm there was a moderate increase in systolic blood pressure from 106 (17) mm Hg to 120 (20) mm Hg within 30 minutes after drug administration (p < 0.05). In the group with persistent arrhythmia there was no significant effect. No prolongation of the QTc interval, ventricular tachyarrhythmia, or inadvertent bradycardia could be observed. In two patients a decrease in systolic blood pressure from 115 to 80 mm Hg and from 130 to 100 mm Hg occurred and was reversible without specific treatment.
At the site of venous access no inflammatory reaction was documented until the needle was removed.
Thirty minutes after administration of amiodarone, the ensuing antiarrhythmic treatment was based on the individual clinical course. All patients were followed until discharge from hospital. During this period nine patients died because of pump failure 3.5 (4) days after amiodarone infusion; six of these patients initially presented with cardiogenic shock. One additional patient died from pulmonary embolism.
Intravenous amiodarone reduces the ventricular rate during atrial fibrillation by affecting the atrioventricular node. This was proven clinically in a series involving 38 patients with different atrial tachyarrhythmias in which intravenous amiodarone was used at a mean dose of 242 mg in the first hour followed by a continuous infusion.4 The differences between doses used were remarkably high (60–1000 mg within the first hour). In this study the mean heart rate was reduced from 146 to 109 beat/min within one hour. We achieved a similar reduction in heart rate within 10 minutes with our more aggressive protocol (fig 1). In addition, 13 patients (32%) in our study population converted to normal sinus rhythm within 30 minutes compared to no patients in the series of Clemo and colleagues.4
Clinical use of intravenous amiodarone has been limited by reports of severe decreases in blood pressure. A 26% incidence of this complication has been reported and considered to be one of the most limiting side effects of the drug.5 However, the patients treated had had ventricular tachyarrhythmias, and it is not fully clear whether the blood pressure response was a side effect of the drug or represented the natural course of severely ill patients. The latter appears to be more likely with respect to Clemo's report on 38 patients with atrial tachyarrhythmias, where no significant drop of blood pressure occurred with a similar infusion rate of amiodarone.4
In our study 10 patients died during their hospital stay. In view of the number of severely ill patients, the number of deaths as a result of pump failure may not be unexpected.
The obvious benefits of the dose regimen used were: (1) the rapid reduction of heart rate within minutes after amiodarone application; (2) the absence of contraindications in severely ill patients, even in the settings of low blood pressure and cardiogenic shock; and (3) the ease of application without the necessity of a central venous access. However, further studies involving a great number of patients are needed to demonstrate clearly the clinical benefit of lowering heart rate using intravenous amiodarone.
Our study was not a placebo controlled trial. The degree of heart rate reduction and the relatively high conversion rate to normal sinus rhythm within 30 minutes after drug administration could be attributed in part to the drugs previously administered and the short duration time of atrial fibrillation in some patients.
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