Cardiovascular manifestations of tricyclic antidepressant overdose

Langou, Rene A.; Dyke, Craig Van; Tahan, Steven R.; Cohen, Lawrence S.

doi:10.1016/0002-8703(80)90657-2

Cited by 101 publications

(17 citation statements)

References 28 publications

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“…Intravenous fluids, lidocaine, and respiratory support were all found to be helpful in stabilizing blood pressure and the cardiopulmonary status of TCA-poisoned patients in retrospective level 4 case series (44,225).…”

Section: Intravenous Fluidsmentioning

confidence: 99%

Tricyclic antidepressant poisoning: an evidence-based consensus guideline for out-of-hospital management

Woolf

Erdman

Nelson

et al. 2007

Clinical Toxicology

130

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American Association of Poison Control Centers, Washington, District of Columbia, USAA review of U.S. poison center data for 2004 showed over 12,000 exposures to tricyclic antidepressants (TCAs). A guideline that determines the conditions for emergency department referral and prehospital care could potentially optimize patient outcome, avoid unnecessary emergency department visits, reduce healthcare costs, and reduce life disruption for patients and caregivers. An evidencebased expert consensus process was used to create the guideline. Relevant articles were abstracted by a trained physician researcher. The first draft of the guideline was created by the lead author. The entire panel discussed and refined the guideline before distribution to secondary reviewers for comment. The panel then made changes based on the secondary review comments. The objective of this guideline is to assist poison center personnel in the appropriate prehospital triage and management of patients with suspected ingestions of TCAs by 1) describing the manner in which an ingestion of a TCA might be managed, 2) identifying the key decision elements in managing cases of TCA ingestion, 3) providing clear and practical recommendations that reflect the current state of knowledge, and 4) identifying needs for research. This guideline applies to ingestion of TCAs alone. Co-ingestion of additional substances could require different referral and management recommendations depending on their combined toxicities. This guideline is based on the assessment of current scientific and clinical information. The panel recognizes that specific patient care decisions may be at variance with this guideline and are the prerogative of the patient and the health professionals providing care, considering all the circumstances involved. This guideline does not substitute for clinical judgment. Recommendations are in chronological order of likely clinical use. The grade of recommendation is in parentheses. 1) Patients with suspected self-harm or who are the victims of malicious administration of a TCA should be referred to an emergency department immediately (Grade D). 2) Patients with acute TCA ingestions who are less than 6 years of age and other patients without evidence of self-harm should have further evaluation including standard history taking and determination of the presence of co-ingestants (especially other psychopharmaceutical agents) and underlying exacerbating conditions, such as convulsions or cardiac arrhythmias. Ingestion of a TCA in combination with other drugs might warrant referral to an emergency department. The ingestion of a TCA by a patient with significant underlying cardiovascular or neurological disease should cause referral to an emergency department at a lower dose than for other individuals. Because of the potential severity of TCA poisoning, transportation by EMS, with close monitoring of clinical status and vital signs en route, should be considered (Grade D). 3) Patients who are symptomatic (e.g., weak, drowsy, dizzy, tremulous, pal...

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Section: Intravenous Fluidsmentioning

confidence: 99%

Tricyclic antidepressant poisoning: an evidence-based consensus guideline for out-of-hospital management

Woolf

Erdman

Nelson

et al. 2007

Clinical Toxicology

130

View full text Add to dashboard Cite

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“…Кроме того, повышенный выход пирувата в коронарный проток косвенно свиде тельствует о повреждении митохондрий кардиомиоци тов под влиянием амитриптилина [10]. Перфузия изолированных сердец различными до зами амитриптилина вызывает не только нарушения энергетического обмена миокарда, но и увеличивает вы ход ферментов (АсАТ, ЛДГ, КФК МВ) в коронарный проток (табл.…”

Section: результаты и обсуждениеunclassified

Mechanisms of the Cardiotoxic Action of Amitriptyline

Чекмарев¹,

Долгих²

2011

rmt

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Первые случаи острого отравления психотропны ми препаратами отмечены в 50 х годах прошлого столе тия [1]. В последние годы увеличивается число отравле ний новыми препаратами с психотропным эффектом: амитриптилином, азалептином, финлепсином. В насто ящее время такие нозологические формы занимают од но из ведущих мест в общей структуре отравлений «ле карственной этиологии», составляя, по данным Всемирной организации здравоохранения, от 10 до 15% [2]. Токсичность амитриптилина, как и всех трицикли ческих антидепрессантов, обусловлена, в первую оче редь, их высокой способностью связываться с белками крови (до 96%), а также длительным периодом полувы ведения из организма, который для амитриптилина со ставляет, по данным литературы, от 31 до 46 часов [2].Цель настоящего исследования -изучить механизмы токсического действия амитриптилина на миокард. Материал и методыИсследования проведены на модели изолированного изово люмически сокращающегося сердца белых беспородных крыс по методу E. L. Fallen et al. (1967) [3]. Было проведено две серии экс периментов. В одной серии (I группа) в раствор Кребса Хензе лайта был добавлен амитриптилин в дозе 250 нг/мл, исходя из то го, что средняя терапевтическая концентрация амитриптилина в крови при назначении терапевтических доз составляет 250 нг/мл [5]. В другой -концентрация амитриптилина в растворе, прохо дившем через коронарное русло, составила 1250 нг/мл (II груп па). Таким образом, проведение подобных экспериментов позво лило оценить непосредственное влияние амитриптилина на сократимость и метаболизм изолированного сердца.Эксперименты выполнены на 30 белых беспородных крысах самцах массой 210-250 г, наркотизированных тиопенталом натрия (25 мг/кг внутрибрюшинно). Через 15 минут после наркотизации животного выполняли срединную торакотомию, сердце быстро из влекали и погружали с целью кардиоплегии в охлажденный до 2-4°С раствор Кребса Хензелайта. Предсердия частично удаляли, а сердце фиксировали, надев аорту на канюлю перфузионной уста Objective: to study the mechanisms of toxic action of amitriptyline on the myocardium. Material and methods. Investigations were conducted using the hearts from 30 outbred albino rats, which had been isolated and perfused according to the proce dure described by Fallen et al. There were two series of experiments: 1) amitriptyline was added in a dose of 250 ng/ml to Krebs Henseleit solution (Group 1); 2) the agent was added at another concentration (1250 ng/ml) to the solution passing through the coronary bed (Group 2). The animals were anesthetized with thiopental sodium (25 mg/kg) peritoneally. Results. Amitriptyline depresses myocardial contractility, which is particularly obvious with high rate pacing. This manifests itself as reduced contractile velocity and force power parameters and elevated left ventricular diastolic pressure. Amitriptyline lowers the efficacy of glucose and increases the release of enzymes into the coronary duct. Conclusion. Hypoergosis, membrane destruction, and cardiomyocyte ion pump failure have been shown to underlie nega...

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“…Few cases have been reported with prolongation of AV and interventricular conduction strikingly similar to the effects of tricyclic antidepressant (TCA) overdose, explained previously. The arrhythmogenic effects of this drug are additive if there is prior exogenous administration of levodopa, dopamine and/or isoproterenol [70, 71]. …”

Section: Selected Substances and Conditions With Identified And/or Pomentioning

confidence: 99%

Proarrhythmia with Non-Antiarrhythmics

Albrecht

2004

Cardiology

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In 1987, at the American College of Cardiology national meeting, a group of physicians from Europe and the United States agreed to use the term ‘arrhythmogenesis’ to refer to an aggravation or provocation of arrhythmias resulting from any cause and specifically to use the word ‘proarrhythmia’ when such arrhythmogenesis is from drug therapy. Proarrhythmia is thus, defined as the potential of cardiac and non-cardiac drugs to induce or exacerbate arrhythmias. It is a relatively common finding in the hospitalized and outpatient settings. It was recognized since the early 1980’s, but still was considered an extremely unusual event. In many instances, unfortunately the first manifestation of proarrhythmia is death. We have identified multiple conditions and non-cardiac medications that have been reported in association with this entity. Basic concepts of ion-channels of the heart are provided in this review, to help understanding the rational of the pathophysiology, which remains of paramount importance, as it gives insight to the diagnosis, that is mostly based on electrocardiographic findings. The careful detection of the presence of comordid diseases, makes it possible to prevent, recognize, avoid mistreatment and treat the condition. We present an overview of the cardiac cellular electrophysiology, mechanisms of cardiac arrhythmias and explain the substrates and targets of the pro-arrhythmic actions of non-cardiac drugs.

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Cardiovascular manifestations of tricyclic antidepressant overdose

Cited by 101 publications

References 28 publications

Tricyclic antidepressant poisoning: an evidence-based consensus guideline for out-of-hospital management

Tricyclic antidepressant poisoning: an evidence-based consensus guideline for out-of-hospital management

Mechanisms of the Cardiotoxic Action of Amitriptyline

Proarrhythmia with Non-Antiarrhythmics

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