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Background: Hyperkalemia is an electrolyte disorder commonly encountered in the emergency department that can result in significant morbidity and mortality. While sodium bicarbonate is often used for acute lowering of serum potassium, its efficacy is not well established. The purpose of this study was to evaluate and quantify the amount of potassium reduction in emergency department patients who received intravenous sodium bicarbonate as part of treatment for hyperkalemia compared with those who did not., Methods: A retrospective electronic chart review was conducted on adult patients who presented to the emergency department with initial potassium concentration greater than or equal to 5.4 mMol/L and received intravenous insulin as part of hyperkalemia treatment. Patients who received intravenous sodium bicarbonate in addition to intravenous insulin were included in the sodium bicarbonate group. The control group included patients who did not receive intravenous sodium bicarbonate. The primary objective of this study was to compare the absolute reduction in serum potassium between initial and second concentrations in patients from the sodium bicarbonate group and those in the control group., Results: A total of 106 patients were included in this study with 38 patients in the sodium bicarbonate group and 68 patients in the control group. Median initial potassium concentration was 6.6 mMol/L in the sodium bicarbonate group and 6.1 mMol/L in the control group (P = 0.009). Absolute reduction of potassium at first repeat was 1 and 0.9 mMol/L in sodium bicarbonate group and control group respectively (P = 0.976)., Conclusions: The addition of sodium bicarbonate therapy to intravenous insulin in the treatment of hyperkalemia did not offer statistically significant added efficacy in potassium lowering. Larger studies are needed to further validate the result findings., Competing Interests: Declaration of Competing Interest Shiyi Geng: none. Emily Green: none. Jessica Rivera: none. Michael Kurz: funded by NIH 5U01DK096037 (Site PI); K23AG038548 (Site PI); R01GM101197 (Site PI); R01GM103799 (Site PI), American Heart Association, Society for Critical Care Medicine, Emergency Medicine Foundation, Rapid Pathogen Screening Inc, Boehringer-Ingelheim, Abbott, Zoll Medical Corporation, and Stryker Corporation to the University of Alabama at Birmingham., (Copyright © 2021 Elsevier Inc. All rights reserved.)

We report a case of a 74-year-old lady admitted to the emergency department with a very broad QRS complex caused by flecainide intoxication due to acute renal failure. Appropriate recognition of the ECG changes and symptoms provoked by flecainide intoxication permitted quick directed treatment with intravenous administration of high dose sodium bicarbonate, which resolved the QRS elongation., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Purpose: Sodium bicarbonate is frequently used for patients unresponsive to cardiopulmonary resuscitation (CPR). Its use may be associated with longer resuscitation duration as well as more severe metabolic acidosis. We applied a new analytical method based on a matched case-control study design to control for the potential confounders., Basic Procedures: Out-of-hospital cardiac arrest patients resuscitated in an emergency department for at least 20 minutes, unless there was any return of spontaneous circulation (ROSC) within the time frame, were analyzed. Patients without ROSC for 20 minutes of CPR were matched to those with ROSC based on initial bicarbonate level categorized using cutoff points of 10, 15, 20, 25, and 30 mEq/L, and their observation durations were trimmed to match their pairs. The association between sodium bicarbonate and ROSC was examined using conditional logistic regression analysis., Main Findings: Two matched groups, one with ROSC and the other without (both n = 258), were generated. Sodium bicarbonate administration and its total cumulative dose were significantly associated with an increased ROSC, with odds ratios for ROSC of 1.86 (95% confidence interval [CI], 1.09-3.16; P = .022) and 1.18 (per 20 mEq; 95% CI, 1.04-1.33; P = .008), respectively. The positive associations remained unchanged after multivariable adjustment, with odds ratios for ROSC of 2.49 (95% CI, 1.33-4.65; P = .004) and 1.27 (95% CI, 1.11-1.47; P = .001), respectively., Principal Conclusion: Sodium bicarbonate administration during CPR in emergency department was associated with increased ROSC., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Flecainide is a Class Ic antiarrythmic agent associated with adverse events due to its pro-arrythmic effects. We report the case of a 33-year-old female presenting in cardiac arrest after a flecainide overdose treated with intravenous fat emulsion (IFE), sodium bicarbonate (NaHCO₃), and extracorporeal membrane oxygenation (ECMO). This case reviews the pathophysiology and management of flecainide toxicity including novel strategies of IFE and ECMO.

Background: This study was performed to determine the effects of sodium bicarbonate injection during prolonged cardiopulmonary resuscitation (for >15 minutes)., Methods: The retrospective cohort study consisted of adult patients who presented to the emergency department (ED) with the diagnosis of cardiac arrest in 2009. Data were retrieved from the institutional database., Results: A total of 92 patients were enrolled in the study. Patients were divided into 2 groups based on whether they were treated (group1, n = 30) or not treated (group 2, n = 62) with sodium bicarbonate. There were no significant differences in demographic characteristics between groups. The median time interval between the administration of CPR and sodium bicarbonate injection was 36.0 minutes (IQR: 30.5-41.8 minutes). The median amount of bicarbonate injection was 100.2 mEq (IQR: 66.8-104.4). Patients who received a sodium bicarbonate injection during prolonged CPR had a higher percentage of return of spontaneous circulation, but not statistical significant (ROSC, 40.0% vs. 32.3%; P = .465). Sustained ROSC was achieved by 2 (6.7%) patients in the sodium bicarbonate treatment group, with no survival to discharge. No significant differences in vital signs after ROSC were detected between the 2 groups (heart rate, P = .124; systolic blood pressure, P = .094). Sodium bicarbonate injection during prolonged CPR was not associated with ROSC after adjust for variables by regression analysis (Table 3; P = .615; odds ratio, 1.270; 95% confidence interval: 0.501-3.219), Conclusions: The administration of sodium bicarbonate during prolonged CPR did not significantly improve the rate of ROSC in out-of-hospital cardiac arrest., (Copyright © 2013 Elsevier Inc. All rights reserved.)

A 23-month-old boy was brought to the emergency department of an adult and pediatric tertiary care center 1 hour after an inadvertent “double dose” of 120 mg flecainide (9.2 mg/kg). His electrocardiogram revealed sinus rhythm with a terminal R wave in aVR greater than 7 mm, a bifascicular block, and prolonged QRS and QTc intervals. A dramatic improvement in the bifascicular block and terminal R wave occurred after the administration of sodium bicarbonate. He was discharged after 36 hours with no complications. This case demonstrates that flecainide can cause significant cardiac conduction disturbances in doses much lower than previously described. All supratherapeutic ingestions should be assessed in hospital.

Severe hyperkalemia (>7 mmol/L) is a medical emergency because of possible fatal arrhythmias. We here report the case of a 58-year-old woman surviving extreme hyperkalemia (>10 mmol/L). The patient with a history of congestive heart failure, a DDD pacemaker and mild chronic renal insufficiency was admitted with progressive weakness and sudden onset of hypotension and bradycardia in the absence of any pacemaker action. Laboratory tests revealed an extreme serum potassium level of 10.1 mmol/L, with a slightly elevated serum creatinine of 149 μmol/L. Treatment with norepinephrine, sodium bicarbonate, and insulin improved both the hemodynamic situation and the serum potassium with subsequent regaining pacemaker actions even before additional hemodialysis normalized the potassium level. A thorough investigation demonstrated that several mechanisms contributed to the extreme potassium level: urinalysis and a low transtubular potassium gradient in the presence of metabolic acidosis with normal anion gap pointed to preexisting interstitial nephritis, with renal tubular acidosis type IV as the predisposing factor, whereas several drugs and acute impairment of renal function contributed to the dangerous situation. Despite the odds for fatal outcome, the patient recovered completely, and long-term management was initiated to prevent recurrent hyperkalemia.

Objective: This study evaluates the effect of early administration of an empirical (1 mEq/kg) sodium bicarbonate dose on survival from prehospital cardiac arrest within brief (<5 minutes), moderate (5-15 minutes), and prolonged (>15 minutes) down time., Methods: Prospective randomized, double-blinded clinical intervention trial that enrolled 874 prehospital cardiopulmonary arrest patients managed by prehospital, suburban, and rural regional emergency medical services. Over a 4-year period, the randomized experimental group received an empirical dose of bicarbonate (1 mEq/kg) after standard advanced cardiac life support interventions. Outcome was measured as survival to emergency department, as this was a prehospital study., Results: The overall survival rate was 13.9% (110/792) for prehospital arrest patients. There was no difference in the amount of sodium bicarbonate administered to nonsurvivors (0.859 +/- 0.284 mEq/kg) and survivors (0.8683 +/- 0.284 mEq/kg) (P = .199). Overall, there was no difference in survival in those who received bicarbonate (7.4% [58/420]), compared with those who received placebo (6.7% [52/372]) (P = .88; risk ratio, 1.0236; 0.142-0.1387). There was, however, a trend toward improved outcome with bicarbonate in prolonged (>15 minute) arrest with a 2-fold increase in survival (32.8% vs 15.4%; P = .007)., Conclusion: The empirical early administration of sodium bicarbonate (1 mEq/kg) has no effect on the overall outcome in prehospital cardiac arrest. However, a trend toward improvement in prolonged (>15 minutes) arrest outcome was noted.

Severe cocaine toxicity causes acidemia and cardiac dysfunction. These manifestations are described in 4 patients who presented with seizures, psychomotor agitation, and cardiopulmonary arrest. Their initial laboratory values demonstrated acidemia and electrocardiographic findings that included a prolonged QRS complex and QTc duration and a rightward T40 ms axis deviation. Treatment of the patients with hyperventilation, sedation, active cooling, and sodium bicarbonate infusion led to the normalization of their blood pHs and reversal of their cardiac conduction disorders. Acidemia can contribute to cocaine cardiac disorders by promoting conduction delays, dysrhythmias, and depressed myocardial contractility. Good supportive care corrects the blood pH and cardiac conduction disorders and remains the major focus in the management of patients with cocaine toxicity.

The tricyclic antidepressant (TCA) agents are recognized for their potentially lethal cardiovascular and neurological effects in poisoned patients. The 12-lead electrocardiogram (ECG) has emerged as a popular bedside tool in the evaluation of TCA toxicity. Although the history and physical examination play a key role in the assessment of the patient with potential TCA poisoning, the presence or absence of features of the TCA toxidrome are not sufficient to detect or exclude toxicity from this class of drugs. A variety of ECG findings occur with TCA toxicity. Aside from the sinus tachycardia due principally to anticholinergic effects, TCA-toxic changes seen on the ECG are attributable primarily to the sodium channel blockade caused by these agents. The majority of patients at significant risk for developing cardiac or neurological toxicity will have a QRS complex greater than 0.10 seconds or a rightward shift of the terminal 40 ms of the frontal plane QRS complex vector. The majority of these patients will also display these changes early in their emergency department stay. However, the appearance of these findings, either alone or in combination, does not mean the patient will develop significant cardiac or neurological toxicity. The ECG can neither unequivocally rule in nor rule out impending toxicity; recognizing these limitations, the emergency physician can use this bedside tool in combination with other clinical data during the assessment of the poisoned patient.

This report describes a patient with an acute intentional fluoxetine exposure who developed unique cardiovascular and neurovascular toxicity. The patient presented with lethargy and cardiac conduction delays (QRS 110 msec, QTc 458 msec) and developed a delayed seizure. On admission, therapy with intravenous sodium bicarbonate promptly narrowed the QRS to 90 msec. A comprehensive toxicology screen demonstrated only a serum fluoxetine concentration of 901 ng/mL (therapeutic range, 37-301), a serum norfluoxetine concentration of 451 ng/mL (29-329) and a serum acetaminophen concentration of 174 mg/L. Tricyclic antidepresants were specifically noted to be absent. A self-limiting generalized seizure was witnessed 16 hours after ingestion. At this time the bicarbonate infusion had been ceased and the QRS interval was not prolonged. The patient improved over time and no other apparent causes for the observed clinical effects could be discovered. Emergency physicians need to be aware of the uncommon occurrence of fluoxetine-induced cardiotoxicity and the potential benefit of sodium bicarbonate therapy.

The routine use of sodium bicarbonate in patients with cardiac arrest has been discouraged, with the benefit of outcome evaluation. Current recommendations include an elaborate stratification of circumstances in which bicarbonate is to be used. The physiological and clinical aspects of bicarbonate administration during cardiopulmonary resuscitation in animal and human studies were reviewed. The onset of significant acidemia or alkalemia is associated with adverse system specific effects. The administration of bicarbonate may mitigate the adverse physiological effects of acidemia, improve response to exogenously administered vasopressor agents, or simply increase venous return due to an osmolar effect, resulting in increased coronary perfusion pressure. Likewise, bicarbonate may have adverse effects in each of these areas. The preponderance of evidence suggests that bicarbonate is not detrimental and may be helpful to outcome from cardiac arrest. An objective reappraisal of the empirical use of bicarbonate or other buffer agents in the appropriate "therapeutic window" for cardiac patients may be warranted.

Flecainide occasionally produces incessant ventricular tachycardia that is difficult to treat. Reports of uncontrolled clinical studies have suggested a therapeutic role for hypertonic sodium bicarbonate (NaHCO3). To test this observation, spontaneous and pacing-induced arrhythmia canine models were designed. In the spontaneous model, flecainide was infused at 0.5 mg/kg/min until ventricular tachycardia occurred spontaneously. In the pacing-induced model, flecainide was infused at 1.0 mg/kg/min load (0.5 mg/kg/min maintenance) stepwise until the QRS was widened 50%, 75%, and 100%, with programmed ventricular stimulation at each step until ventricular arrhythmia was induced. Dogs who developed spontaneous arrhythmia were treated blindly with three doses of either NaHCO3 (3 mEq/kg/dose, with 1 minute between doses) or normal saline. Dogs who were induced in the second model were treated with the same three doses, 10 minutes apart, with programmed stimulation between each dose. Before unblinding in both protocols, dogs were classified as "responders" or "nonresponders" to therapy. In the spontaneous model, of 14 dogs with spontaneous ventricular tachycardia, all 7 dogs treated with NaHCO3 showed response, compared with only 1 of 7 dogs treated with saline (P < .01). Ventricular QRS complexes/min were reduced by NaHCO3 in that protocol. In the induced arrhythmia protocol, of 14 dogs with inducible arrhythmia, 6 of 7 responded to NaHCO3, and 1 of 7 responded to placebo (P < .05). In both protocols, arterial pH and the serum sodium concentration were increased by NaHCO3 but not by normal saline control treatment. QRS interval duration was shortened by NaHCO3 therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

The objective of this study was to characterize the effect of intravenous hypertonic sodium bicarbonate (NaHCO3) administration in patients with moderate-to-severe cyclic antidepressant (CA) overdose. We reviewed charts of all 91 patients given the diagnosis of CA overdose in the University of California Los Angeles (UCLA) Emergency Medicine Center (EMC), who either died in the EMC or were admitted to the medical intensive care unit (MICU), and who received NaHCO3 in the EMC between 1980 and 1988. Twenty-four other patients with the same EMC diagnosis were admitted to the MICU during this period but did not receive NaHCO3. The response of blood pressure, electrocardiographic parameters, and mental status to serum alkalinization with NaHCO3 were evaluated. Major morbidity and mortality were recorded for all patients. Hypotension was corrected within 1 hour in 20 of 21 (96%) patients, QRS prolongation corrected in 39 of 49 (80%), and mental status improved in 40 of 85 (47%). There was one death, in a patient who was moribund on arrival to the EMC. No complications were attributable to the administration of NaHCO3. NaHCO3 seems to improve hypotension and normalize QRS duration rapidly in most patients treated, and improve mental status changes in almost one half. Serum alkalinization with NaHCO3, in conjunction with appropriate supportive care, seems to limit major morbidity and mortality effectively in patients with serious CA overdose.