Abstract

BackgroundCalcium antagonist overdose can cause severe deterioration of hemodynamics unresponsible to treatment with beta adrenergic inotropes. The aim of the study was to evaluate in an experimental model the effects of levosimendan during severe calcium antagonist intoxication.MethodsTwelve landrace-pigs were intoxicated with intravenous verapamil at escalating infusion rates. The infusion containing 2.5 mg/ml verapamil was used aiming to a reduction of cardiac output by 40% from the baseline value. Intoxicated pigs were randomized into two groups: control (saline) and levosimendan (intravenous bolus). Inotropic effect was measured as a change in a maximum of the positive slope of the left ventricular pressure (LV dP/dt). The survival and hemodynamics of the animals were followed for 120 min after the targeted reduction of cardiac output.ResultsIn the control group, five out of six pigs died during the experiment. In the levosimendan group, one pig died before completion of the experiment (p = 0.04). In the levosimendan group a change in LV dP/dt was positive in four out of six pigs compared to one out of six pigs in the control group (p = ns).ConclusionsIn this experimental model, the use of levosimendan was associated with improved survival.

Highlights

  • Calcium antagonist overdose can cause severe deterioration of hemodynamics unresponsible to treatment with beta adrenergic inotropes

  • The animals were ventilated with a volume-controlled mode (Servo 900, Siemens, Elema AB, Solna Sweden) with 5 cmH2O of positive end-expiratory pressure (PEEP)

  • Baseline data on hemodynamics and the laboratory values of calcium and lactate are presented in Tables 1 and 2

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Summary

Introduction

Calcium antagonist overdose can cause severe deterioration of hemodynamics unresponsible to treatment with beta adrenergic inotropes. The aim of the study was to evaluate in an experimental model the effects of levosimendan during severe calcium antagonist intoxication. In the year 2004 more than 10000 toxic exposures to calcium channels blockers were reported in the United States. Of those exposures, 3.3% were associated with severe bradycardia, hypotension and acute negative inotropy. There were 62 (0.6%) deaths due to calcium channel blocker overdoses. The majority of the exposures occurred accidentally (79%), but a significant (18%) part was suicide attempts. A small amount of overdoses was in children or due to iatrogenic treatments [1]. The number of toxic incidents is increasing [2,3]

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