Cyanide Poisoning and Cardiac Disorders: 161 Cases

Fortin, Jean-Luc; Desmettre, T.; Manzon, C.; Judic-Peureux, Virginie; Peugeot-Mortier, Caroline; Giocanti, Jean-Pascal; Hachelaf, M.; Grangeon, Marie; Hostalek, Ulrike; Crouzet, Julien; Capellier, Gilles

doi:10.1016/j.jemermed.2009.09.028

Cited by 60 publications

(50 citation statements)

References 8 publications

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“…Our findings are similar to a previous retrospective study of human cyanide toxicity cases by Fortin et al [4]. who also documented cardiac dysfunction including rhythm, repolarization, and conduction disorders.…”

Section: Discussionsupporting

confidence: 93%

“…Reduced ion pump activity can prolong repolarization and impair conduction, producing cardiac dysfunction similar to diffuse ischemia from other causes. This mechanism may account for the ECG changes we observed during the experiment [4]. As in our study, Aberra [8] reported PR prolongation in an in vitro isolated rat heart model with acidosis, resulting in similar finding as our study.…”

Section: Discussionsupporting

confidence: 90%

“…A priori, we divided ECG abnormalities into three categories: rhythm, repolarization, and conduction [4]. Rhythm disorders included sinus tachycardia, dysrhythmias, and supraventricular tachycardia.…”

Section: Methodsmentioning

confidence: 99%

“…Fortin et al [4] described asystole and supraventricular tachycardia (SVT) as the most common cardiac disorders in a retrospective study of critically ill patients with suspected cyanide toxicity. However, the authors did not determine if the dysrhythmias occurred before hypotension or arrest, and they did not report other, specific electrocardiographic interval measurements.…”

mentioning

confidence: 99%

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Acute Electrocardiographic ST Segment Elevation May Predict Hypotension in a Swine Model of Severe Cyanide Toxicity

et al. 2012

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Cyanide causes severe cardiac toxicity resulting in tachycardia, hypotension, and cardiac arrest; however, the clinical diagnosis can be difficult to make. A clinical finding that may precede or predict cyanide-induced hypotension may be a trigger to provide treatment earlier and improve outcomes in cyanide toxicity. Our primary objective was to determine if there is a clinically significant change in ST segment deviation measured on ECG during intravenous cyanide infusion that may predict cyanide-induced hypotension. As part of a larger study comparing antidotes for cyanide-induced shock, 30 swine were anesthetized and monitored and then intoxicated with a continuous cyanide infusion until severe hypotension (50 % of baseline mean arterial pressure) occurred. ECGs were obtained at baseline, every 5 min during infusion, and at the development of hypotension. Repeated measures of analysis of variance were used to determine significance. The mean weight for the 30 swine at baseline was 48 kg (range 45-52), pulse rate 86 beats/min (range 55-121), and systolic blood pressure 109 mmHg (range 90-121). The mean time to hypotension was 31 min (range 16-39). The mean amount of cyanide infused was 5 mg/kg (range 2.5-6.3 mg/kg). All animals (30/30) had ECG changes in repolarization or depolarization during cyanide infusion. Significant rhythm, repolarization, and conduction changes from baseline were observed prior to severe hypotension (p<0.05). Normal sinus rhythm and sinus tachycardia were the most common rhythms preceding hypotension. We observed ST segment elevation in leads V3, V4, III, and aVF and ST segment depression in leads aVL and aVR. The most pronounced ST segment elevation was observed in leads V3 and V4. We also detected significant changes with increased pulse rate, prolonged PR interval, and shortened QTc interval. Other significant changes were increased T axis and reduced QRS axis. We detected ST segment deviations occurring just before the onset of cyanide-induced hypotension in our swine model. Leads V3 and V4 had the most pronounced with ST elevation, but we also detected electrocardiographic ST elevation inferiorly. Shortening of the QTc and lengthening of the PR interval were also detected before hypotension.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 90%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Acute Electrocardiographic ST Segment Elevation May Predict Hypotension in a Swine Model of Severe Cyanide Toxicity

et al. 2012

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“…& Cardiovascular: The initial tachycardia, likely the result of a catecholamine surge, progresses to bradycardia with subsequent hypotension [25][26][27][28]. EKG may show STsegment changes, as well as a variety of arrhythmias [29]. Ultimately, respiratory and cardiac arrest ensues [4,14,[24][25][26][27].…”

Section: What Are Typical Clinical Findings In Cyanide Toxicity Aftermentioning

confidence: 99%

Case Files of the University of Massachusetts Toxicology Fellowship: Does This Smoke Inhalation Victim Require Treatment with Cyanide Antidote?

Hamad¹,

Babu

Bebarta

2016

J. Med. Toxicol.

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Cyanide toxicity is common after significant smoke inhalation. Two cases are presented that provide framework for the discussion of epidemiology, pathogenesis, presenting signs and symptoms, and treatment options of inhalational cyanide poisoning. An evidence-based algorithm is proposed that utilizes point-of-care testing to help physicians identify patients who benefit most from antidotal therapy.

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Smoke inhalation

Hall¹,

Borron²

2015

Toxicology of Cyanides and Cyanogens

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Cyanide Poisoning and Cardiac Disorders: 161 Cases

Cited by 60 publications

References 8 publications

Acute Electrocardiographic ST Segment Elevation May Predict Hypotension in a Swine Model of Severe Cyanide Toxicity

Acute Electrocardiographic ST Segment Elevation May Predict Hypotension in a Swine Model of Severe Cyanide Toxicity

Case Files of the University of Massachusetts Toxicology Fellowship: Does This Smoke Inhalation Victim Require Treatment with Cyanide Antidote?

Smoke inhalation

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