Membrane Stabilising Activity: A Major Cause of Fatal Poisoning

Henry, John A.; Cassidy, S.L.

doi:10.1016/s0140-6736(86)91558-8

Cited by 89 publications

(24 citation statements)

References 26 publications

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“…20 This mechanism was substantiated by Kerns and associates, 21 who perfused isolated rat hearts with either propranolol or atenolol. Both agents had negative chronotropic effects and rendered the hearts refractory to pacing, but atenolol also reduced myocardial contractility.…”

Section: Pharmacokinetics Of β β-Blockersmentioning

confidence: 89%

Successful treatment of severe atenolol overdose with calcium chloride

O’Grady

Anderson²,

Pringle³

2001

CJEM

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Atenolol, a selective β 1 -adrenergic antagonist, is commonly used to treat hypertension, ischemic heart disease and cardiac dysrhythmias. Few cases of severe atenolol intoxication have been described, and only one of these reports discussed the use of calcium chloride as a treatment. We present a case of atenolol overdose associated with shock and first-degree heart block, in which administration of calcium chloride led to dramatic improvement after failure of conventional treatment. In addition, we discuss the pharmacokinetics, toxicology and management of β-blocker overdose, focusing on the possible role of calcium chloride. RÉSUMÉ L'aténolol, un inhibiteur des récepteurs β 1 -adrénergiques, est utilisé couramment pour traiter l'hypertension, l'insuffisance coronarienne et les dysrythmies cardiaques. La littérature fait état de peu de cas d'intoxication à l'aténolol et un seul de ces rapports discutait du recours au chlorure de calcium comme forme de traitement. Nous présentons un cas d'intoxication à l'aténolol accompagnée d'un état de choc et d'un bloc cardiaque du premier degré pour lequel l'administration de chlorure de calcium eut des résultats remarquables après l'échec du traitement conventionnel. De plus, nous présentons la pharmacocinétique, la toxicologie et la prise en charge de l'intoxication aux β-bloquants, notre propos étant axé sur le rôle possible du chlorure de calcium.

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Section: Pharmacokinetics Of β β-Blockersmentioning

confidence: 89%

Successful treatment of severe atenolol overdose with calcium chloride

O’Grady

Anderson²,

Pringle³

2001

CJEM

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“…Other authors have also reported that sodium-channel blockers devoid of anticholinergic or adrenergic effects (e.g., propafenone) tend to cause bradycardia and conduction blocks. ciated with a much higher death rate than most other poisonings, 15,17 and the Class Ic antidysrhythmics are particularly toxic. Koppel and colleagues published a series of 120 cases of poisoning with Class Ic agents, including 34 patients with propafenone toxicity.…”

Section: Sodium-channel Blocker Toxicitymentioning

confidence: 99%

Bicarbonate therapy for unstable propafenone-induced wide complex tachycardia

Brubacher

2004

CJEM

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A previously healthy 73-year-old woman presented to hospital with acute atrial fibrillation. After intravenous procainamide failed to restore sinus rhythm, she was treated with 300 mg of oral propafenone and discharged with a prescription for propafenone and propranolol. Six hours later she took 150 mg of propafenone as prescribed. Within 1 hour she became dyspneic and collapsed. On arrival in hospital she was unconscious, with a wide complex tachycardia and no obtainable blood pressure. After defibrillation and lidocaine, she converted to a wide complex sinus rhythm, but remained profoundly hypotensive despite intravenous epinephrine and dopamine. Hypertonic sodium bicarbonate (HCO 3 ) was administered and, shortly thereafter, her blood pressure increased, her QRS duration normalized and her clinical status improved dramatically. In this case of severe refractory propafenone-related cardiac toxicity, intravenous HCO 3 led to a profound clinical improvement. Emergency physicians should be familiar with the syndrome of sodium-channel blocker poisoning and recognize the potentially important role of bicarbonate in its treatment. RÉSUMÉUne femme âgée de 73 ans auparavant en bonne santé s'est rendue à l'hôpital pour une fibrillation auriculaire aiguë. La procaïnamide intraveineuse n'ayant pas réussi à rétablir le rythme sinusal, la patiente reçut 300 mg de propafénone per os et fut renvoyée chez elle avec une ordonnance pour de la propafénone et du propranolol. Six heures plus tard, elle prit 150 mg de propafénone tel que prescrit. Dans l'heure qui suivit, elle devint dyspnéique et s'effondra. À son arrivée à l'hôpital, elle était inconsciente, en tachycardie à complexe large et il était impossible de prendre sa tension artérielle. Après la défibrillation et l'administration de lidocaïne, la tachycardie se changea en rythme sinusal à complexe large. Par contre, la patiente demeura profondément hypotendue malgré l'administration intraveineuse d'épinéphrine et de dopamine. On lui administra du bicarbonate de sodium hypertonique (HCO 3 ) et, peu de temps après, sa tension artérielle augmenta, la durée du complexe QRS redevint normale et son statut clinique s'améliora énormé-ment. Dans ce cas de toxicité cardiaque réfractaire grave liée à la propafénone, l'HCO 3 intraveineux conduisit à une amélioration clinique remarquable. Les médecins d'urgence devraient se familiariser avec le syndrome de l'empoisonnement par un bloqueur des canaux sodiques et reconnaître le rôle potentiellement important du bicarbonate dans le cadre de son traitement.

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“…Rarely, ventricular flutter and/or fibrillation can be observed. [5,6] Thus, in this case malign arrhytmias were determined first as an accelerating idioventricular rhythm then as pulseless VT. It has been previously reported that intoxication with Group 1C antiarrhytmic agents has a higher mortality compared to many other types of intoxication.…”

Section: Discussionmentioning

confidence: 99%

Malign Arrhytmia Development Due To Propafenone Over Dose: A Case Report

et al. 2012

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ÖZET SUMMARYPropafenone is a group 1C antiarrhytmic agent. It is an agent used in patients with symptomatic supraventricular tachycardia requiring treatment, such as atrioventricular node tachycardia, Wolff-Parkinson-White Syndrome and paroxysmal atrial fibrillation. It is also used in life-threatining symptomatic ventricular tachycardia requiring treatment and with excessive intake it has serious side effects on cardiovascular, gastrointestinal, nervous, haematological and dermatological systems. In this report, we present a case of propafenone intake with suicidal purpose and we aim to share our experience with malign arrhytmia development and arrhytmia management. A 22-year-old female patient presented to our emergency department with complaints of general situation distortion and feeling sick after ingesting 20 pills (6 g) of her friend's Propafenone HCl 300 mg for suicidal purpose one hour previously. In the electrocardiography (ECG), regular rhythm, wide QRS and the absence of P-wave was observed. Pulseless ventricular tachycardia developed and defibrillation with 360 joule was performed followed by cardiopulmonary resuscitation. NaHCO 3 administration of 1 mEq/kg every 4 hours was initiated. After the therapy, QRS duration shortened. The patient became conscious with spontaneous ventilation. Early diagnosis and appropriate resuscitative interventions can be vital in propafenone intoxication. NaHCO 3 administration in the presence of hypotension and ECG abnormalities are vital.

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Membrane Stabilising Activity: A Major Cause of Fatal Poisoning

Cited by 89 publications

References 26 publications

Successful treatment of severe atenolol overdose with calcium chloride

Successful treatment of severe atenolol overdose with calcium chloride

Bicarbonate therapy for unstable propafenone-induced wide complex tachycardia

Malign Arrhytmia Development Due To Propafenone Over Dose: A Case Report

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