Severe flecainide overdose

Brimacombe, J.; Talbutt, P

doi:10.5694/j.1326-5377.1991.tb142307.x

Cited by 9 publications

(6 citation statements)

References 7 publications

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“…A repeat electrocardiogram revealed sinus rhythm at 62 beats per minute with resolution of LBBB ( Figure 2). T wave inversions in leads V1-V4 after cardioversion were seen due to T wave memory after resolution of Several previous studies have reported hemodynamic compromise in the setting of flecainide toxicity [1][2][3][4]. To our knowledge, this is the first case to document the negative inotropic effects of flecainide toxicity echocardiographically.…”

Section: Introductionmentioning

confidence: 55%

Negative Inotropy from Flecainide Toxicity

Ellis¹,

Thosani²,

Zimetbaum³

2015

agr

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Flecainide is a potent sodium channel inhibitor that slows phase 0 of the cardiac action potential. Rapid heart rates cause greater drug binding to the sodium channel, a phenomenon termed use dependence. High concentrations of bound drug result in adverse effects due to the physiological effects of sodium channel blockade, including conduction velocity slowing and negative ionotropy. The negative inotropic effect of flecainide toxicity, which can cause or exacerbate heart failure, is an underappreciated phenomenon. We report a case of flecainide toxicity where the negative inotropic effects of flecainide were demonstrated echocardiographically. Given the frequency with which flecainide is utilized, it is important for all healthcare providers to recognize this potentially life-threatening consequence of flecainide toxicity.

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Section: Introductionmentioning

confidence: 55%

Negative Inotropy from Flecainide Toxicity

Ellis¹,

Thosani²,

Zimetbaum³

2015

agr

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“…Compared with other acute drug intoxications, overdoses with class 1c antiarrhythmics are associated with a relatively high mortality of the order of 22.5% 1 . The serum level of 3.6 mg/L is high when compared with other reports, and levels of this order have frequently been associated with cardiac arrest or death 2–7 …”

Section: Discussionmentioning

confidence: 97%

“…The adverse effects are an extension of its therapeutic effect of sodium channel blockade, causing slowed conduction, negative inotropy and rhythm disturbances, including bradyarrhythmias with variable atrioventricular block, ventricular tachycardia, ventricular fibrillation, asystole and pulseless electrical activity 8 . Case reports have described rapid cardiovascular collapse occurring within 30 min of ingestion and with levels much lower than this example 3,4 . Flecainide is largely eliminated unchanged by the kidneys and is metabolized to some degree by the hepatic cytochrome P450 2D6.…”

Section: Discussionmentioning

confidence: 99%

“…1 The serum level of 3.6 mg/L is high when compared with other reports, and levels of this order have frequently been associated with cardiac arrest or death. [2][3][4][5][6][7] Flecainide is a sodium channel blocking antiarrhythmic agent in the Vaughn-Williams 1c class, used to treat life-threatening supraventricular and ventricular arrhythmias. It has a very high oral bioavailability and rapid absorption with a large volume of distribution (8-9 L/kg) due to extensive tissue binding.…”

Section: Discussionmentioning

confidence: 99%

“…8 Case reports have described rapid cardiovascular collapse occurring within 30 min of ingestion and with levels much lower than this example. 3,4 Flecainide is largely eliminated unchanged by the kidneys and is metabolized to some degree by the hepatic cytochrome P450 2D6. It has a long elimination half-life (7-24 h), which renders treatment of severe overdoses difficult.…”

Section: Discussionmentioning

confidence: 99%

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Managing cardiovascular collapse in severe flecainide overdose without recourse to extracorporeal therapy

Devin

Garrett

Anstey

2007

Emerg Medicine Australasia

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Flecainide overdose can rapidly result in profound cardiovascular collapse, and is associated with a relatively high mortality. A case is described where a woman with major toxicity and high serum levels was managed without recourse to invasive modalities such as cardiopulmonary bypass or extracorporeal therapies. Hypertonic sodium bicarbonate is recognized as effective therapy for hypotension and arrhythmias. More recent case reports have concentrated on the use of cardiopulmonary bypass. In this report and other reports describing successful resuscitation, the total dose of sodium bicarbonate is conspicuously higher than in reports describing extracorporeal interventions. Sodium bicarbonate should be given early in the resuscitation, and re-administered as frequently as required, targeting an alkaline pH and improved cardiac output, while accepting hypernatraemia. This case demonstrates the maxim that the correct dose of hypertonic sodium bicarbonate is 'enough'. Cardiopulmonary bypass support can be considered as a salvage therapy.

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Toxikologische Notfälle

Zilker

2007

Notfall Rettungsmed

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Severe flecainide overdose

Cited by 9 publications

References 7 publications

Negative Inotropy from Flecainide Toxicity

Negative Inotropy from Flecainide Toxicity

Managing cardiovascular collapse in severe flecainide overdose without recourse to extracorporeal therapy

Toxikologische Notfälle

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