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Aims: Sinus tachycardia potentially leads to a deterioration of cardiac function in critically ill infants. The ultrashort-acting beta-blocker landiolol hydrochloride is a new pharmacological option for a selective heart rate (HR) control in patients with sinus tachycardia and heart failure., Methods and Results: This study was a monocentric retrospective medical chart review study at the University Children's Hospital Bonn (Germany) from 01 January 2018 until 30 June 2020. This study included a cohort of 62 term and preterm infants with a diagnosis of ventricular dysfunction and/or pulmonary hypertension (PH), in combination with preexisting tachycardia and treatment with landiolol hydrochloride. Infants were allocated to subgroups according to weeks of gestational age (GA): born at <35 weeks of GA (Group A) and born at >35 weeks of GA (Group B). Tachycardia was defined depending on GA (<35 weeks of GA: >170 b.p.m.; ≥ 35 weeks of GA: >150 b.p.m.). The primary endpoint was defined as percentage of patients achieving HR normalization during the first 24 h of landiolol treatment. Twenty-nine infants were allocated to Group A and 33 infants to Group B. The overall median GA of the infants was 35.3 (23.3/41.3), with 53% female infants. The primary endpoint was achieved in 57 patients (91.9%). The median time to reach target HR was 1.8 (0.3-24) h. The median starting dose of landiolol was 8.8 (3.9-25.3) μk/kg/min, with a median dosing during the first 24 h of landiolol treatment of 9.9 (2.8-35.4) μk/kg/min. The median landiolol dose while achieving the target HR was 10 (2.4-44.4) μk/kg/min. The right ventricular dysfunction improved significantly in both groups 24 h after onset of landiolol infusion (P = 0.001 in Group A and P = 0.045 in Group B). The left ventricular and biventricular dysfunction improved significantly 24 h after onset of landiolol infusion in infants of Group B (P = 0.004 and P = 0.006, respectively). The severity of PH improved significantly after 24 h in infants of Group A (P < 0.001). During landiolol treatment, no severe drug-related adverse event was noted., Conclusions: The use of landiolol hydrochloride for HR control of non-arrhythmic tachycardia in critically ill infants is well tolerated. Reduction of HR can be guided quickly and landiolol treatment is associated with an improvement of ventricular dysfunction and PH., (© 2022 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Background: We describe a case of symptomatic bradycardia resulting from ivabradine toxicity by measurement of ivabradine levels, of which there are limited reports in the literature., Case Presentation: A 43-year-old White female presented with several days of near syncope and dizziness accompanied by a drop in her heart rate to 50 beats per minute. She was taking ivabradine for inappropriate sinus tachycardia. After excluding several other causes of bradycardia, we made the diagnosis of ivabradine toxicity by measurement of serum ivabradine levels, an approach that is currently not clinically available., Conclusions: Measurement of serum ivabradine levels and knowledge of the pharmacokinetic properties of the drug can be utilized to confirm the diagnosis of ivabradine toxicity., (© 2022. The Author(s).)

A 22-year-old woman was referred with exertional dyspnoea and chest tightness 3 weeks following a diagnosis of COVID-19. Evaluation revealed a resting sinus tachycardia and criteria for postural orthostatic tachycardia syndrome were met. After non-pharmacological interventions failed to yield symptomatic improvement, ivabradine was commenced. This intervention was followed by a substantial improvement in the patient's exercise tolerance and energy levels and an objective reduction in supine and standing heart rate., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

Yohimbine is an indole alkaloid from the leaves and bark of the Pausinystalia johimbe tree that has acquired an enviable reputation in treating erectile dysfunction. This report presents four simultaneous severe poisoning/death cases caused by yohimbine. The test samples comprised the venous blood of four middle-aged men (aged 47-65) who were suspected of poisoning; one of the men died due to ineffective rescue. Ethanol concentration determination and toxicological routine screening were performed using gas chromatography with flame ionization detection (GC-FID) and liquid chromatography-tandem mass spectrometry (LC-MS/MS). A specific LC-MS/MS method was developed to quantify yohimbine, which showed concentrations of 459, 249, and 301ng/mL in three poisoned blood samples and concentrations as high as 5631ng/mL in the deceased. Moreover, the deceased's autopsy ruled out death from trauma and previous illness, and no other common toxic components were detected in his blood. Therefore, yohimbine poisoning appears to be the most likely cause of death. As a type of alkaloid that can be employed in the treatment of clinical diseases and additives for supplements, the danger of yohimbine should be of widespread concern in society., Competing Interests: Declaration of Competing Interest The authors report no declarations of interest., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Background: Methanol is widely used in industry; however, methanol poisoning is not common. In this regard, a number of outbreaks have been recently reported due to inappropriate processing of alcoholic beverages. Shiraz, a city located in the southern part of Iran, faced one of such outbreaks in 2020 during COVID-19 pandemic. There is no sufficient literature on the electrocardiographic findings in methanol toxicity. This study aimed to address this gap in the literature., Method: A total of 356 cases with methanol toxicity referred to Shiraz University of Medical Science Tertiary Hospitals (Faghihi and Namazi) in March and April, 2020. The clinical findings of blindness and impaired level of consciousness, lab data such as arterial blood gas, electrolytes, and creatinine, and the most common findings from ECGs were collected., Results: The most common ECG findings were J point elevation (68.8%), presence of U wave (59.2%), QTc prolongation (53.2% in males and 28.6% in females), and fragmented QRS (33.7%). An outstanding finding in this study was the presence of myocardial infarction in 5.3% of the cases. This finding, to the best of our knowledge, has only been reported in a few case reports. Brugada pattern (8.1%) and Osborn wave (3.7%) were the other interesting findings. In multivariate analysis, when confounding factors were adjusted, myocardial infarction, atrioventricular conduction disturbances, sinus tachycardia, and the prolonged QTC > 500 msecond were four independent factors correlated with methanol toxicity severity measured with arterial blood PH on arterial blood gas measurements, with odds ratios of 12.82, 4.46, 2.32 and 3.15 (P < 0.05 for all), respectively., Conclusion: Electrocardiographic variations during methanol intoxication are remarkable and well-correlated with poisoning severity. Myocardial infarction was an egregious and yet a common concerning finding in this sample, which need to be ruled out in methanol toxicity.

A 13-year-old girl presented to the emergency department with acute onset of chest pain, nausea and tremor. The patient denied drug ingestion, and urine toxicology was negative. ECG demonstrated sinus tachycardia, prolonged QTc (541 ms) and ST depression. Laboratory testing demonstrated metabolic acidosis, hypokalaemia, hypophosphataemia and hyperglycaemia. She was commenced on continuous cardiac monitoring and treated with intravenous fluids and electrolyte replacement. Presenting features and laboratory abnormalities resolved within 48 hours. The National Poisons Information Service and Clinical Biochemistry were integral to her management, advising the clinical team on the likeliest aetiology. Five weeks after discharge, urine toxicology, using mass spectrometry, identified clenbuterol. Clenbuterol is an oral β2-agonist with anabolic and lipolytic effects that is misused as a performance and image enhancing drug. Clinicians must be aware of the increasing availability of these drugs and their potential for causing harm in children and adolescents., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Aripiprazole is an atypical antipsychotic with a long half-life. Overdose can result in protracted somnolence and cardiac disturbances, particularly QT interval prolongation., Methods: This is a single case report of a 14-year-old boy who took an overdose of aripiprazole and developed QRS widening., Case: A 14-year-old boy intentionally ingested 20 tablets of aripiprazole (5 mg). He was brought to the emergency department when his ingestion was discovered. The patient's vital signs were as follows: temperature, 37.7°C; heart rate, 108 beats/min; blood pressure, 138/98 mm Hg; and respirations, 16 breaths/min. Activated charcoal was administered within 90 minutes of ingestion. Initial electrocardiogram (EKG) showed sinus tachycardia, with a QRS of 138 ms and QT interval of 444 ms. QRS duration was 90 ms on an EKG performed 3 months earlier. A bolus of sodium bicarbonate was administered, and the patient was transferred to the pediatric intensive care unit. Repeat EKG demonstrated a QRS of 156 ms, and a sodium bicarbonate infusion was initiated. The patient continued to have QRS prolongation for the next 8 days, reaching a peak of 172 ms 3 days postingestion. Despite aggressive treatment with sodium bicarbonate, there was persistent QRS prolongation; however, the patient did not have any dysrhythmias and remained hemodynamically stable. The patient was discharged 9 days postingestion when the QRS duration normalized to 82 ms. Genetic testing revealed that the patient was a CYP2D6 poor metabolizer., Conclusions: This case suggests that aripiprazole toxicity may possibly be associated with QRS prolongation without associated dysrhythmias or cardiovascular compromise. In addition, toxicity may be prolonged in patients who are CYP2D6 poor metabolizers.

Introduction: Bupropion is a commonly used antidepressant, and overdose can lead to both neurologic and cardiovascular toxicity, including agitation, seizure, tachycardia, QT and QRS prolongation, and rhythm disturbances., Methods: We developed this simulation case for attendings, fellows, nurse practitioners, and nurses in the pediatric emergency department (ED). The scenario involved a 13-year-old male presenting to the ED with altered mental status and a generalized tonic-clonic seizure shortly after arrival. The team needed to quickly perform primary and secondary surveys, manage his airway and breathing, and initiate treatment for seizure. The team had to obtain an abbreviated history and include ingestion in the differential. The patient then developed pulseless ventricular tachycardia, and the team needed to respond with high-quality CPR, defibrillation, and advanced airway management. Preparatory materials, a debriefing guide, and scenario evaluation forms assisted with facilitation., Results: Twenty-eight physicians, 56 nurses, 10 nurse practitioners, four pharmacists, two students, and one respiratory therapist completed this simulation in 13 sessions. On a 5-point Likert scale, participants agreed with the stated objective of ability to manage a patient with a bupropion overdose ( M = 4.09; range, 2-5). The scenario was rated as highly relevant ( M = 4.93) and the debriefing as very effective ( M = 4.85)., Discussion: This scenario is a complete educational resource for setting up, implementing, and debriefing in an interprofessional setting. It was well received by learners from diverse professional backgrounds working together in actual care teams in the pediatric ED., Competing Interests: None to report., (Copyright © 2019 Hartford et al.)

Risperidone and paliperidone palmitate are two antipsychotic drugs well tolerated in the management of schizophrenia and other psychiatric conditions. There have been few reports of tachycardia induced by either drugs. Here, we report on a 21-year-old man, with a history of schizophrenia, and who developed persistent sinus tachycardia after he was restarted on risperidone, which later worsened after administration of paliperidone palmitate for long-term management. He had no cardiovascular risk factors other than obesity, and a prior well-tolerated risperidone treatment. Clinicians must be aware of the possibility of patients developing sinus tachycardia due to autonomic instability from a prior risperidone treatment, even though overall, these drugs are well tolerated., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Case Presentation: A 91-year-old woman was transferred to our Emergency Medical Center and Poison Center with somnolence, hypertension (186/61 mm Hg), and repeated vomiting. Three hours later, 10 transdermal patches, each containing 18 mg of rivastigmine (9.5 mg/24 h), were found on her lower back and both thighs, when miosis, facial and trunk sweating, enhanced bowel sound, hypertension, and sinus tachycardia were noted. She was diagnosed with acute cholinergic syndrome due to rivastigmine poisoning. Her hypertension and sinus tachycardia peaked 8 and 5 h after all the patches were removed, respectively. Her symptoms subsided spontaneously after 17 h., Discussion: In the present case, our patient was presented with acute cholinergic syndrome due to carbamate intoxication after massive transdermal exposure to rivastigmine. Toxicological analysis revealed a remarkably high estimated serum rivastigmine concentration (150.6 ng/ml) and notably low serum butyrylcholinesterase activity (35 IU/l) on admission, with a markedly prolonged calculated elimination half-life of 6.5 h., Conclusions: Emergency physicians should consider acetylcholinesterase inhibitor exposure (e.g., rivastigmine) when patients are present with acute cholinergic syndrome.

Nedaplatin (NDP) is a second-generation platinum derivative that was developed in Japan. Nowadays, it is being widely used in the management of lung cancer, esophageal cancer, head and neck cancers, especially when cisplatin and carboplatin cannot be tolerated or show drug resistance. To the best of our knowledge, there are few reported cases of NDP-induced bradycardia in the relevant medical literature. The current report presents three patients treated with NDP chemotherapy-induced serious arrhythmias. The three cases developed sinus tachycardia and atrial premature beats, complete left bundle branch block, and bigeminy ventricular premature contraction, in the second, sixth and second cycle, respectively. No one died of cardiac toxicity. These were treated with dexamethasone, 5 mg intravenous injection and diphenhydramine 20 mg, intramuscular injection. The heart rhythm returned to normal in 30 minutes, a day, and four days, respectively.

Introduction: Mexedrone, 3-methoxy-2-(methylamino)-1-(4-methylphenyl)propan-1-one, is the alpha-methoxy-derivative of mephedrone (4-methyl-N-methyl cathinone). Mexedrone inhibits the re-uptake of serotonin and dopamine in a dose-dependent manner and has affinity for serotonin and dopamine membrane transporters and receptors (5-HT2 and D2 receptors), producing sympathomimetic effects similar to amfetamines. To date there are no published clinical reports on mexedrone use that are analytically confirmed., Objective: To characterise the features of mexedrone use in patients who presented to our hospital after using a variety of psychoactive substances including mexedrone, with analytical confirmation in each case., Methods: This is an observational case series. Urine toxicological screening using ultra-performance liquid chromatography with tandem mass spectrometry and exact mass time of flight was employed in all patients., Results: A total of 305 cases were screened and mexedrone was identified in 11 urine samples. Agitation was the most common presenting feature in 10 of 11 patients. This was marked to the extent of aggression in some cases, with six patients requiring sedation and/or physical restraint. Delusions and hallucinations, often with paranoia, were observed in three cases with a prominent supernatural/demonic theme. None of these individuals had a history of psychosis. Seven of 11 patients were tachycardic >100 bpm. The median length of stay was 20 hours (range 2-77; IQR 4-33). Mexedrone alone is only likely to have been responsible for these clinical features in 2 cases; in two others mexedrone was found in high concentration along with substantial amounts of other stimulants. In 7 other cases other stimulants detected more likely explained the features. However, comprehensive analytical data enabled us to identify the full complement of agents contributing to the clinical presentation., Conclusions: Agitation was the predominant clinical feature in this case series and was often accompanied by a sinus tachycardia; mexedrone was primarily responsible in 2 patients but contributed substantially in two others. Patients typically recovered fully within 24 hours, unless they required sedation.

Introduction: Exposure to metallic mercury can cause severe accidental intoxications in children, whose clinical symptoms can vary depending on the route of administration, the dose, as well as the time and duration of the exposure. It has become unusual in France, yet it must be considered when taking a patient's medical history in cases of multisystemic involvement without a clear explanation., Clinical Case: We report the case of a 12-year-old patient hospitalized because of a cough, poor general condition, chills, night sweats, psychomotor retardation, and skin lesions that had been developing for several weeks. The initial clinical examination also revealed sinus tachycardia, arterial hypertension, and abolition of osteotendinous reflexes. Complementary examination results were normal apart from a glomerular proteinuria without renal failure. When interviewing the mother, she reported that the child had played with mercury balls 3 months earlier. The suspicion of poisoning was confirmed by blood and urine analysis as well as renal biopsy showing an aspect of membranous glomerulonephritis with IgG and C3 depositions. An intoxication via a transdermal route being unlikely on healthy skin, the Regional Health Agency's survey concluded that chronic intoxication had occurred by inhalation of the mercury spread on the floor at the time of the exposure, which was then vacuum cleaned and released again by the contaminated vacuum cleaner. The patient's outcome was favorable within a few weeks after initiating DMSA chelation therapy., Conclusion: Mercury poisoning should be considered in cases of a multisystemic disorder without clear explanation, in order to intervene quickly and thus prevent irreversible renal and neurological consequences., (Copyright © 2016 Elsevier Masson SAS. All rights reserved.)

We report the case of a 50-year-old obese man (115 kg body mass at 1.77 m height), who started taking 2,4-dinitrophenol (DNP) for weight reduction 44 days before his death. After 43 days of taking DNP, the man showed signs of intoxication with nausea, vomiting, and attacks of sweating. After admission to a hospital where the man concealed his DNP intake, sinus tachycardia, tachypnea, and general unrest were noted. The patient died 9 h after the onset of those symptoms. Upon autopsy, a yellowing of palms and soles was striking. The initially uncertain cause of death could only be clarified by the forensic toxicological examinations and subsequent police investigations. Finally, the man had a total intake of 12.3 g of DNP in 44 days which is relatively high compared to other lethal DNP intoxications.

Background: Clozapine is an efficacious treatment for treatment-resistant schizophrenia; however its use can be limited by side effect intolerability. Sinus tachycardia is a common adverse event associated with clozapine treatment. Various pharmacological treatments are used to control heart rate increase due to clozapine use and can include a decreased rate of clozapine titration, a switch to a different antipsychotic, or treatment with negative chronotropic drugs., Objectives: To assess the clinical effects and efficacy of pharmacological interventions for clozapine-induced sinus tachycardia.To systematically review the adverse events associated with pharmacological interventions for clozapine-induced sinus tachycardia., Search Methods: On 23 March 2015, we searched the Cochrane Schizophrenia Group's Study-Based Register of Trials, which is based on regular searches of CINAHL, BIOSIS, AMED, EMBASE, PubMed, MEDLINE, PsycINFO and registries of clinical trials. There are no language, date, document type or publication status limitations for inclusion of records in the register., Selection Criteria: Randomised controlled trials comparing pharmacological interventions, at any dose and by any route of administration, for clozapine-induced tachycardia., Data Collection and Analysis: We independently screened and assessed studies for inclusion using pre-specified inclusion criteria., Main Results: The electronic searches located three references. However, we did not identify any studies that met our inclusion criteria., Authors' Conclusions: With no studies meeting the inclusion criteria, it is not possible to arrive at definitive conclusions. There are currently insufficient data to confidently inform clinical practice. We cannot, therefore, conclude whether specific interventions, such as beta-blockers, are less effective or more effective than standard courses of alternative treatments for tachycardia. This lack of evidence for the treatment of clozapine-induced tachycardia has implications for research and practice. Well-planned, conducted and reported randomised trials are indicated. One trial is currently underway. Current practice outside of well-designed randomised trials should be clearly justified.

We present a case of acute clenbuterol toxicity following ingestion of 20 μg of clenbuterol, resulting in symptoms of sympathetic activation, sinus tachycardia and electrolyte derangement. The patient was managed conservatively with fluid resuscitation, electrolyte replacement and monitoring, and discharged following a 5-day stay in hospital., (2016 BMJ Publishing Group Ltd.)

A 30-year-old man was admitted to the intensive care unit after a suicide attempt with respiratory difficulties, tremor, sinus tachycardia and significant hypokalemia. On examination, the patient was lucid, fully conscious and did not exhibit positive symptoms. Sings were not typical for overdosing olanzapine, alprazolam and alcohol as declared by the patient. Additional anamnesis revealed high doses of ingested clenbuterol, a selective β2-adrenergic agonist. Due to its anabolic and lipolytic properties, clenbuterol has become a commonly abused drug in bodybuilding industry and is not routinely detected by toxicology screens. This is the first known report of suicide attempt by clenbuterol overdosing., (© 2015 MEDPRESS.)

Background: Opioid dependence remains a significant public health problem worldwide with only three FDA-approved treatments, all targeting the mu-opioid receptor. Dronabinol, a cannabinoid (CB) 1 receptor agonist, is currently under investigation as a novel opioid withdrawal treatment. This study reports on safety outcomes of dronabinol among adults in opioid withdrawal., Methods: Twelve adults physically dependent on short-acting opioids participated in this 5-week within-subject, randomized, double blind, placebo-controlled inpatient study. Volunteers were maintained on oral oxycodone 30 mg qid. Double-blind placebo substitutions occurred for 21 h before each of 7 experimental sessions in order to produce opioid withdrawal. A single oral test dose was administered each session (placebo, oxycodone 30 and 60 mg, dronabinol 5, 10, 20, and 30 mg [decreased from 40 mg]). Heart rate, blood pressure, respiratory outcomes and pupil diameter were assessed repeatedly., Results: Dronabinol 40 mg produced sustained sinus tachycardia accompanied by anxiety and panic necessitating dose reduction to 30 mg. Sinus tachycardia and anxiety also occurred in one volunteer after dronabinol 20mg. Compared to placebo, dronabinol 20 and 30 mg produced significant increases in heart rate beginning 1h after drug administration that lasted approximately 2h (p<0.05). Dronabinol 5 and 10mg produced placebo-like effects. Oxycodone produced prototypic mu-opioid agonist effects (e.g., miosis)., Conclusion: Dronabinol 20mg and higher increased heart rate among healthy adults at rest who were in a state of opioid withdrawal, raising concern about its safety. These results have important implications for future dosing strategies and may limit the utility of dronabinol as a treatment for opioid withdrawal., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Tacrolimus is a potent immunosuppressive agent widely used after organ transplantation. In this present study we present eight patients who complained of palpitation after kidney transplantation. Eight out of 31 patients who received tacrolimus after kidney transplantation suffered from tachycardia. Resting electrocardiography, 24 hours Holter monitorization, echocardiography were performed, and serum levels of cardiac troponin T, creatine kinase, CKMB, brain natriuretic peptide and tacrolimus were measured. The median time to palpitation after kidney transplantation was 30 days in seven patients, and one patient complained of palpitation five years after transplantation. Cardiovascular assessment revealed sinus tachycardia in all patients. Beta-blocker was instituted in five patients. After two months all patients were asymptomatic and their pulse rates were within normal limits. Transient sinus tachycardia is a frequent adverse event during tacrolimus therapy in children and young adults, at therapeutic levels. Patients may benefit from beta-blockers.

K2 is a synthetic cannabinoid that has potential cardiovascular side effects, including myocardial ischemia, myocardial infarction, and arrhythmias. Cardiac testing of pediatric patients is often not performed owing to a lack of symptomatology. We report a series of pediatric patients with concern for myocardial ischemia temporally associated with K2 exposure., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Introduction: We report the case of a multiple drug interaction involving clozapine, antifungals and oral contraceptives, which resulted in an increased clozapine plasma level, pericarditis with pericardial effusion and eosinophilia in a young Caucasian woman. These symptoms and signs disappeared a few days after discontinuation of clozapine. At present, we are not aware of reports of clozapine-antifungals interaction, whereas there is only one other case report on the interaction between oral contraceptives and clozapine. The purpose of this case report is to show the risk of potentially serious adverse effects stemming from drug interactions involving medications routinely used in clinical practice., Case Presentation: A 29-year-old Caucasian woman diagnosed with a schizoaffective disorder was admitted to a psychiatric unit for acute psychosis (hallucinations, delusions and catatonic behavior). She denied smoking tobacco products and was on long-term oral contraceptives. During the first month of hospitalization she was treated with antipsychotics and for 1 week she took simultaneously fluconazole and miconazole gel, after being diagnosed with oral candidiasis. On the last day of antifungals treatment, 29 days after admission, clozapine was started with resolution of psychotic symptoms. After 3 weeks, her clozapine plasma level had increased to 542 ng/mL and eosinophilia was observed. She complained of nausea, vomiting and palpitations; echocardiography showed echocardiographic abnormalities and pericardial effusion. Oral contraceptives were discontinued and after 1 week clozapine was interrupted, with a complete resolution of side effects and pericardial effusion within 4 days., Conclusions: Clozapine is metabolized by cytochrome P450. The use of inhibitors or other substrates of cytochrome P450, such as antifungals and oral contraceptives, can cause long-lasting interactions and clozapine toxicity. The Naranjo algorithm shows clozapine is a definite cause of pericarditis (score 9) and both clozapine-antifungals and clozapine-contraceptives interactions resulted probable (score 5) in Drug Interaction Probability Scale. A good knowledge on drugs that act as substrates, inhibitors or inducers of cytochrome P450 is mandatory. When those drugs are used in patients taking clozapine, blood level monitoring of clozapine should be recommended, since a lower dose of clozapine might be required to prevent clozapine toxicity.

Antiepileptic medications have been reported to cause disturbances in cardiac conduction. Lacosamide decreases seizure burden by modulating sodium channels. Although it has been demonstrated to have few side effects, there have been reports of clinically significant cardiac conduction disturbances. We report the case of a child with hypoplastic left-heart syndrome and well-controlled multifocal atrial tachycardia who developed haemodynamically significant atrial tachycardia after receiving two doses of lacosamide.

We report the case of a 32-year-old man with Myotonic Dystrophy type 1 showing adenosine-induced sinus tachycardia during transesophageal electrophysiological evaluation.

In recent years, intravenous lipid emulsion (ILE) therapy has emerged as a new rescue antidote for treatment of certain toxicities, including cyclic antidepressants, and as the primary treatment of toxic manifestations after local anesthetic exposure. We present a case of a 13-year-old girl who developed delayed seizures and cardiac arrest after amitriptyline ingestion. As part of the treatment, she was treated with ILE therapy. The patient's laboratories were not interpretable for several hours after the lipid emulsion. The patient developed pancreatitis after the ILE therapy. This case is unique; not only is it one of the first reported cases of lipid emulsion being used in a pediatric patient, but in that the patient developed delayed toxicity and iatrogenic harm from the ILE.

Introduction: Diphenhydramine is an antihistamine commonly implicated in overdose. It has many pharmacologic effects, including sodium channel blockade. Overdoses in toddlers causing QRS prolongation are only rarely reported and never with effective use of sodium bicarbonate. We report a diphenhydramine overdose in a toddler with multiple markers of sodium channel blockade effectively treated with sodium bicarbonate., Methods: A 13-month-old infant girl was brought in by the emergency medical service for a witnessed tonic-clonic seizure. Two hours previously, the child had been found with an open bottle of 25-mg diphenhydramine tablets, 24 of which were missing. Midazolam was administered with seizure resolution. Examination revealed 4-mm reactive pupils; nystagmus; warm, dry, flushed skin; and altered mental status. Initial electrocardiograms revealed sinus tachycardia at a rate of 180 beats per minute, a prolonged QRS of 130 milliseconds (from a baseline of 65 milliseconds), and a positive terminal R wave in aVR, which later resolved after sodium bicarbonate treatment. The patient was discharged home the following day with no sequelae., Results and Discussion: Diphenhydramine toxicity is a common poisoning in children. Toxicity typically presents with signs and symptoms of the anticholinergic toxidrome. Diphenhydramine also has sodium channel-blocking properties, and this can be shown in the form of prolonged QRS and a terminal R wave in aVR. QRS prolongation and aVR abnormalities from diphenhydramine ingestion in a toddler have been reported, but effective use of sodium bicarbonate has not., Conclusions: Electrocardiographic finding consistent with sodium channel blockade should be recognized as a complication of pediatric diphenhydramine overdose, and they seem responsive to hypertonic sodium bicarbonate.

Life-threatening complications may occur in body-packers and the rupture of a single packet containing cocaine may lead to fatality. We report the case of a 35-year-old body-packer who developed at the airport clinical signs of cocaine toxicity. There was evidence of bowel obstruction. The plasma concentration of cocaine, benzoylecgonine (BZE) and ecgonine methyl ester (EME) was determined 1 h after symptoms onset, during surgery and postoperative period. The measured peak value at 1 h was 594 ng/ml for cocaine, 9423 ng/ml for BZE and 3261 ng/ml for EME. We confirm the following order BZE > EME > cocaine for peak plasma concentrations. A rebound in plasma levels was found during surgery, together with electrocardiographic changes. A total of 107 packets were eliminated, and the patient survived., (Copyright © 2011. Published by Elsevier Ltd.)

History: A 3-year-old, 400 kg, gelding Quarter Horse was presented for investigation of epistaxis., Physical Examination: The horse was bright, alert and responsive with rectal temperature, heart rate and respiration rate within normal limits., Management: During a second general anaesthetic for surgical treatment of guttural pouch mycosis by balloon-tipped catheter occlusion of the right major palatine artery and ligation of the right external carotid artery, signs consistent with hyperkalaemic periodic paralysis (HYPP) were exhibited. These included concurrent hyperkalaemia, hypercapnoea, sinus tachycardia, and muscle fasciculations in the presence of normothermia. Stress associated with an acute haemorrhage pre-operatively, and intra-operative hypercapnoea may have precipitated the episode. There were no signs of HYPP during a general anaesthetic, 1 week earlier, when an initial attempt at surgical treatment of guttural pouch mycosis was performed. Treatment consisted of fluid therapy and administration of calcium gluconate (0.1-0.2 mg kg(-1) minute(-1)), dextrose 5% (5 mL kg(-1) hour(-1)) and insulin (0.05 IU kg(-1)). Treatment resulted in the resolution of clinical signs and an uneventful recovery., Follow-Up: The diagnosis of HYPP was confirmed by DNA analysis post-operatively., Conclusions: Clinical cases of intra-operative HYPP can present despite a previous history of uneventful general anaesthesia. Rapid diagnosis and treatment can result in the successful management of HYPP. This report documents an unusual presentation of HYPP, a disease that remains present in the Quarter Horse population., (© 2011 The Authors. Veterinary Anaesthesia and Analgesia © 2011 Association of Veterinary Anaesthetists and the American College of Veterinary Anesthesiologists.)

Despite above 40 years the presence of sulpride on the pharmaceutical market, the acute poisonings are poorly reported in the medical literature. The discussed case of sulpiride intoxication concerns ingestion probably dose of 12 g, that exceeded 10-fold maximum therapeutic dose. 16-year-old girl, with no previous sulpiride treatment, was admitted to the Toxicology Department about 3 hours after ingestion. In clinical picture she presented quantitative consciousness disturbances with maximum 10 scores in GCS scale, with tendency to low BP (minimum 88/45 mmHg) and episode of orthostatic hypotension. The ECG demonstrated: normogram, sinus tachycardia with a heart rate of 125 beats/min, PQ = 120 ms, QRS = 80 ms, prolongation of QTc to 519,6 ms and unspecific changes of ST-T syndrome. The qualitative toxicological test confirmed the presence of chlorprothixene in urine, but the serum therapeutic concentration (0.126 microg/ml) excluded the overdose. The quantitative determination of sulpiride serum concentration confirmed acute sulpiride poisoning. The measured sulpiride toxic concentration on admission and in the consecutive hours were from 13.2 to 8.2 microg/ml. Sulpiride toxicokinetic parameters such as t max = about 3 h, t 1/2 = 24.02 h, k(el) = 0.029 h(-1) were also estimated. They point out that the absorption rate is similar and the elimination is prorogated in sulpiride acute poisoning compared to therapeutic doses.

Capecitabine is an orally available fluoropyrimidine carbamate that selectively delivers fluorouracil (5-FU) to tissues expressing high levels of thymidine phosphorylase (TP) such as tumors. The drug has demonstrated efficacy in metastatic breast cancer, colorectal, and pancreatic cancer. Although these are considered safe drugs, a growing body of literature reports adverse cardiac effects. Clinical trials indicate that capecitabine has a cardiac toxicity similar to that of infused fluoropyrimidines such as 5-FU. Here, we review cardiotoxicity in the use of fluoropyrimidines, with particular attention toward capecitabine. We also describe a severe, reversible cardiac event that occurred in a 39-year-old woman, with no cardiac risk factors, treated with capecitabine for advanced breast cancer. This review and our experience confirm that fluoropyrimidine cardiotoxicity is an infrequent but documented side effect. Oncology patients under treatment should be closely observed and monitored for cardiac symptoms with particular attention in case of signs or symptoms of cardiovascular complications. The implementation of cardio-oncology interdisciplinary teams should, in the future, reduce the impact of cancer treatment-associated cardiotoxicity syndromes., (© 2010 Wiley Periodicals, Inc.)

Baclofen withdrawal syndrome is a rare and potentially life-threatening condition manifesting with autonomic dysreflexia, high fevers, spasticity, seizures, and multiorgan failure. Reversible cardiomyopathy due to this condition is extremely rare. A high level of suspicion is needed to recognize this condition and start an early intervention to improve patient outcome. Electrocardiographic ST-segment elevation in lead aVR was previously described in association with left main, left anterior descending, and triple-vessel coronary artery disease as well as Takotsubo cardiomyopathy. In this article we present a rare case of reversible cardiomyopathy due to baclofen withdrawal syndrome associated with diffuse ST-segment depressions and ST-segment elevation in lead aVR.

The optimum septic shock vasopressor support strategy is currently debated. This study was performed to evaluate the efficacy and safety of norepinephrine (NE) and dopamine (DA) as the initial vasopressor in septic shock patients who were managed with a specific treatment protocol. A prospective, randomized, open-label, clinical trial was used in a medical intensive care unit comparing DA with NE as the initial vasopressor in fluid-resuscitated 252 adult patients with septic shock. If the maximum dose of the initial vasopressor was unable to maintain the hemodynamic goal, then fixed-dose vasopressin was added to each regimen. If additional vasopressor support was needed to achieve the hemodynamic goal, then phenylephrine was added. The primary efficacy end point was all-cause 28-day mortality. Secondary end points included organ dysfunction, hospital and intensive care unit length of stay, and safety (primarily occurrence of arrhythmias). The 28-day mortality rate was 50% (67/134) with DA as the initial vasopressor compared with 43% (51/118) for NE treatment (P = 0.282). There was a significantly greater incidence of sinus tachycardia with DA (24.6%; 33/134) than NE (5.9%; 7/118) and arrhythmias noted with DA treatment (19.4%; 26/134) compared with NE treatment (3.4%; 4/118; P < 0.0001), respectively. Logistic regression analysis identified Acute Physiologic and Chronic Health Evaluation II score (P < 0.0001) and arrhythmia (P < 0.015) as significant predictors of outcome. In this protocol-directed vasopressor support strategy for septic shock, DA and NE were equally effective as initial agents as judged by 28-day mortality rates. However, there were significantly more cardiac arrhythmias with DA treatment. Patients receiving DA should be monitored for the development of cardiac arrhythmias (NCT00604019).

Background: The incidence of seizures after unintentional bupropion ingestion in children aged < 6 years has been reported as 0.2%. However, in many poison centers, > 80% of these patients are referred to the Emergency Department (ED) for evaluation., Objective: To evaluate if all unintentional pediatric bupropion ingestions require referral to a health care facility (HCF), or what fraction of these could be managed safely at home., Method: A retrospective chart review was conducted of all bupropion ingestions in children aged < 6 years for 2000-2006 from four regional poison centers. Exclusion criteria were lack of follow-up or multiple drug ingestion., Results: Of 407 patients, 209 (51%) were male. Mean age was 2.2 years (SD +/- 1.0). There were 329 patients (81%) seen in a HCF, of which 143 (35%) were hospitalized; 77 patients (19%) were observed at home. Symptoms occurred in 73 patients (18%): sinus tachycardia (n = 50), nausea/vomiting (n = 32), hyperactivity (n = 17), seizure (n = 3), hallucinations (n = 2), and hypertension (n = 2). The mean heart rate of patients with sinus tachycardia (n = 50, 12.3%) was 137 beats/min (SD +/- 13), with a range of 112-172 beats/min. Mean dosage of those with tachycardia was 24 mg/kg. In the 2 patients with hypertension, the maximum recorded blood pressures were 145/80 mm Hg (2-year-old boy) and 137/90 mm Hg (2-year-old girl), with heart rates of 122 and 125 beats/min, respectively. Dose ingested and patient weight was known for 218 patients. Mean dosage ingested was 12.2 mg/kg, with a range of 2.6-64 mg/kg. Eighty-eight percent of patients with a known dosage ingested < 20 mg/kg., Discussion: A high percentage of children continue to be seen in a HCF. Concern from the higher incidence of severe effects seen with intentional adult exposures may be one of the reasons for this cautious approach., Conclusion: Unintentional pediatric bupropion ingestions resulted in clinical effects that rarely required any HCF intervention. Isolated unintentional bupropion ingestion of