sodium-bicarbonate and Long-QT-Syndrome

Cocaine use is common in many areas of the world, particularly the United States and Western Europe. Toxicity following the use of cocaine is associated with a wide range of clinical features. In this review, we will focus on the cocaine-associated cardiac arrhythmias and, in particular, some of the controversies in their etiology and management. Cocaine can produce arrhythmias either through the production of myocardial ischemia or as a direct result of ion channel alterations. Excessive catecholamines, combined with sodium and potassium channel blockades, give rise to a wide variety of supra-ventricular and ventricular rhythms. The animal and human evidence for ion channel dysfunction is reviewed, and the effects of catecholamines are followed from the cardiac action potential to the development of arrhythmias. Finally, theoretical constructs are combined with existing evidence to develop a rational treatment strategy for patients with cocaine-induced cardiac arrhythmias. In particular, we review the evidence concerning the controversies relating to the use of lidocaine in comparison with sodium bicarbonate, in terms of QRS prolongation secondary to sodium channel blockade.

Topics: Action Potentials; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Cocaine; Cocaine-Related Disorders; Humans; Lidocaine; Long QT Syndrome; Myocardium; Potassium Channels; Sodium Bicarbonate; Sodium Channels

Sodium bicarbonate therapy (SBT) is currently indicated for the management of a variety of acute drug poisonings. However, SBT effects on serum potassium concentrations may lead to delayed QTc prolongation (DQTP), and subsequent risk of adverse cardiovascular events (ACVE), including death. Emergency department (ED)-based studies evaluating associations between SBT and ACVE are limited; thus, we aimed to investigate the association between antidotal SBT, ECG changes, and ACVE.. This was a secondary data analysis of a consecutive cohort of ED patients with acute drug overdose over 3 years. Demographic and clinical data as well as SBT bolus dosage and infusion duration were collected, and outcomes were compared with an unmatched consecutive cohort of patients with potential indications for SBT but who did not receive SBT. The primary outcome was the occurrence of ACVE, and secondary outcomes were delayed QTc (Bazett) prolongation (DQTP), and death. Propensity score and multivariable adjusted analyses were conducted to evaluate associations between adverse outcomes and SBT administration. Planned subgroup analysis was performed for salicylates, wide QRS (> 100 ms), and acidosis (pH < 7.2).. Out of 2365 patients screened, 369 patients had potential indications for SBT, of whom 31 (8.4%) actually received SBT. In adjusted analyses, SBT was found to be a significant predictor of ACVE (aOR 9.35, CI 3.6-24.1), DQTP (aOR 126.7, CI 9.8-1646.2), and death (aOR 11.9, CI 2.4-58.9). Using a propensity score model, SBT administration was associated with ACVE (OR 5.07, CI 1.8-14.0). Associations between SBT and ACVE were maintained in subgroup analyses of specific indications for sodium channel blockade (OR 21.03, CI 7.16-61.77) and metabolic acidosis (OR: 6.42, 95% CI: 1.20, 34.19).. In ED patients with acute drug overdose and potential indications for SBT, administration of SBT as part of routine clinical care was an independent, dose-dependent, predictor of ACVE, DQTP, and death. This study was not designed to determine whether the SBT or acute overdose itself was causative of ACVE; however, these data suggest that poisoned patients receiving antidotal SBT require close cardiovascular monitoring.

Topics: Action Potentials; Adolescent; Adult; Aged; Aged, 80 and over; Antidotes; Dose-Response Relationship, Drug; Drug Overdose; Emergency Service, Hospital; Female; Heart Conduction System; Heart Rate; Humans; Long QT Syndrome; Male; Middle Aged; Risk Assessment; Risk Factors; Sodium Bicarbonate; Time Factors; Treatment Outcome; Young Adult

Topics: Antidotes; Humans; Long QT Syndrome; Sodium Bicarbonate

Topics: Antidotes; Humans; Long QT Syndrome; Sodium Bicarbonate

We report a rare fatal case of acute metformin overdose in a 19-year-old woman.

Topics: Acidosis; Blood Gas Analysis; Cardiotonic Agents; Drug Overdose; Fatal Outcome; Female; Heart Arrest; Humans; Hypoglycemia; Hypoglycemic Agents; Hypotension; Long QT Syndrome; Metformin; Sodium Bicarbonate; Young Adult

Escitalopram is rarely associated with prolongation of the QTc interval; however, there are no reported cases of QRS complex widening associated with escitalopram overdose. We report a case of a patient who presented with both QRS complex widening and QTc interval prolongation after an escitalopram overdose.. A 16-year-old girl presented to the emergency department after ingestion of escitalopram, tramadol/acetaminophen, and hydrocodone/acetaminophen. Laboratory results were significant for 4-hour acetaminophen 21.1 μg/mL. Serum electrolytes including potassium, magnesium, and calcium were all normal. Initial electrocardiogram (ECG) revealed a widened QRS with an incomplete right bundle branch pattern. After administration of 100-mEq sodium bicarbonate, a repeat ECG revealed narrowing of the QRS complex and a prolonged QTc interval. Magnesium sulfate 2 g intravenous and sodium bicarbonate drip were initiated. A repeat ECG, 1 hour after the second, revealed normalization of the QRS complex and QTc interval.. Prolongation of the QTc interval is an expected effect of escitalopram. Both escitalopram and citalopram are metabolized to the cardiotoxic metabolite S-didesmethylcitalopram and didesmethylcitalopram, respectively, which have been implicated in numerous cardiac abnormalities including widening of the QRS complex. Although never previously described with escitalopram, this mechanism provides a reasonable explanation for the QRS complex widening and incomplete right bundle branch block that occurred in our patient.. Both QRS complex widening and QTc interval prolongation should be monitored in cases of escitalopram and citalopram overdoses.

Topics: Acetaminophen; Adolescent; Antidotes; Bradycardia; Bundle-Branch Block; Citalopram; Delayed Rectifier Potassium Channels; Drug Therapy, Combination; Electrocardiography; Emergencies; Female; Heart Conduction System; Humans; Hydrocodone; Long QT Syndrome; Magnesium Sulfate; Sodium Bicarbonate; Sodium Channels; Suicide, Attempted; Syncope, Vasovagal; Tramadol

Excited delirium is increasingly recognized as a risk factor for sudden death, though the specific pathophysiology of these deaths is typically unclear.. We describe a survivor of excited delirium that displayed a transient severe prolongation of the QT interval, suggesting unmasking of long QT syndrome as a possible mechanism of sudden death.. A 30-year-old man was arrested by police for violent assaultive behavior. Officers at the scene noted confusion, nonsensical speech, sweating, and bizarre agitated behavior; he was transported to the Emergency Department for medical evaluation of possible excited delirium. His initial electrocardiogram revealed a markedly prolonged corrected QT interval of over 600 ms. Intravenous hydration and sodium bicarbonate were administered, with normalization of the QT; he was admitted and recovered uneventfully.. We discuss the possible association between long QT syndrome and unexplained sudden deaths seen with excited delirium. Sodium bicarbonate may be considered when long QT syndrome is identified during or after agitated delirium, though its routine use cannot be recommended based on a case report.

Topics: Adult; Delirium; Electrocardiography; Emergency Service, Hospital; Fluid Therapy; Humans; Long QT Syndrome; Male; Police; Prisoners; Psychomotor Agitation; Sodium Bicarbonate

Intoxication caused by propafenone is very rare, and there is no case reported before propafenone and captopril intoxication together. There are few case reports in the literature about intoxication with more than 6 g of propafenone. We present the clinical manifestation and successfully treatment of 9 g of propafenone and 1 g captopril intoxication in an 18-year-old female. An 18-year-old female was brought to the emergency department approximately half an hour after she committed suicide with 30 propafenone tablets, 300 mg each, and 20 captopril tablets, 50 mg each. Her fist electrocardiography (ECG) shows a chaotic ventricular rhythm with a prolonged QRS complex. After fluid and sodium bicarbonate infusion and permanent pacemaker implantation, sinus rhythm was achieved. This case, to our knowledge, is the first in that it describes the successful recovery of a patient who ingested extensively large doses of propafenone (9 g) and captopril (1 g), both of which are known to have severe cardiac side effects.

Topics: Adolescent; Angiotensin-Converting Enzyme Inhibitors; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Captopril; Cardiopulmonary Resuscitation; Electrocardiography; Emergency Medical Services; Female; Fluid Therapy; Glasgow Coma Scale; Hemodynamics; Humans; Intubation, Gastrointestinal; Long QT Syndrome; Pacemaker, Artificial; Propafenone; Sodium Bicarbonate; Suicide, Attempted