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Leah Lande - One of the best experts on this subject based on the ideXlab platform.
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Reversal of Citalopram‐Induced Junctional Bradycardia with Intravenous Sodium Bicarbonate
Pharmacotherapy, 2020Co-Authors: Michael Brucculeri, Joy Kaplan, Leah LandeAbstract:The cardiotoxicity of tricyclic antidepressants is a well-described phenomenon requiring serious consideration in patients who have taken an overdose. In patients who are at high risk for suicide attempts, selective serotonin reuptake inhibitors (SSRIs) were thought to constitute a safe alternative. However, evidence is accumulating that they, too, possess proarrhythmic properties, which must be reconciled in the setting of an overdose. An 82-year-old woman intentionally ingested citalopram 1.6 g. Several hours after presentation, she developed sinus arrest and junctional bradycardia that resolved after infusion of Intravenous Sodium Bicarbonate solution. Thereafter, she demonstrated no further electrocardiographic abnormalities and was safely transferred to the psychiatry service without the need for a temporary transvenous pacemaker. The dramatic effect of the Sodium Bicarbonate on the arrhythmia represents a probable event according to the Naranjo probability scale. Intravenous Sodium Bicarbonate may serve as an effective antidote to SSRI-induced bradyarrhythmias.
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reversal of citalopram induced junctional bradycardia with Intravenous Sodium Bicarbonate
Pharmacotherapy, 2005Co-Authors: Michael Brucculeri, Joy Kaplan, Leah LandeAbstract:The cardiotoxicity of tricyclic antidepressants is a well-described phenomenon requiring serious consideration in patients who have taken an overdose. In patients who are at high risk for suicide attempts, selective serotonin reuptake inhibitors (SSRIs) were thought to constitute a safe alternative. However, evidence is accumulating that they, too, possess proarrhythmic properties, which must be reconciled in the setting of an overdose. An 82-year-old woman intentionally ingested citalopram 1.6 g. Several hours after presentation, she developed sinus arrest and junctional bradycardia that resolved after infusion of Intravenous Sodium Bicarbonate solution. Thereafter, she demonstrated no further electrocardiographic abnormalities and was safely transferred to the psychiatry service without the need for a temporary transvenous pacemaker. The dramatic effect of the Sodium Bicarbonate on the arrhythmia represents a probable event according to the Naranjo probability scale. Intravenous Sodium Bicarbonate may serve as an effective antidote to SSRI-induced bradyarrhythmias.
Helmut Schiffl - One of the best experts on this subject based on the ideXlab platform.
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Sodium Bicarbonate infusion for prevention of acute kidney injury: No evidence for superior benefit, but risk for harm?
International Urology and Nephrology, 2015Co-Authors: Helmut SchifflAbstract:The best “treatment” of acute kidney injury (AKI) is prevention. Patients who are at high risk of AKI should have an assessment of their volume status and receive appropriate volume expansion. The most effective type of Intravenous fluid remains unclear. Innumerable studies have compared Sodium Bicarbonate and isotonic saline and have combined fluid hydration with pharmacological interventions, particularly N -acetyl-cysteine. However, abundant systematic reviews and meta-analyses have provided conflicting conclusions and have recognized a significant degree of heterogeneity between studies and publication bias. Most studies comparing Intravenous Sodium Bicarbonate and saline were small. They often enrolled patients with a low risk for AKI, yielding low serious events (renal replacement therapy), and used different protocols for administration of fluids. Based on current literature, Intravenous Sodium Bicarbonate does not seem to be more efficient than saline for the prevention of contrast-media-induced AKI, cardiac surgery-associated AKI, pigment nephropathy or septic AKI. However, some cohort studies or prospective randomized trials did track and report serious adverse events, such as higher rates of AKI or higher in-hospital mortality. At present, it should be concluded that the use of Intravenous Sodium Bicarbonate administration to prevent AKI should be evaluated further in multicenter randomized double-blind trials rather than adopted into routine clinical practice.
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prevention of acute kidney injury by Intravenous Sodium Bicarbonate the end of a saga
Critical Care, 2014Co-Authors: Helmut SchifflAbstract:The systematic review and meta-analysis of prospective randomized trials reported by Tie and colleagues [1] in a previous issue of Critical Care provide evidence that Intravenous Sodium Bicarbonate (SBIC) administration does not reduce the incidence of cardiac surgery-associated (CSA) acute kidney injury (AKI) but prolongs the duration of mechanical ventilation and of hospital stay. The conclusions of the authors are corroborated by a recent comprehensive systematic review [2] demonstrating that the administration of SBIC to patients at risk for CSA-AKI, contrast-induced nephropathy, septic AKI, or pigment nephropathy has no additional benefit compared with saline but adds to in-hospital morbidity and mortality. The authors do not discuss the mechanisms underlying possible harms of SBIC. In cardiac patients, this type of fluid may precipitate volume overload and acute pulmonary edema. Alkalosis-induced hypoventilation may be associated with myocardial ischemia aggravating decreased cardiac contractility and may cause arrhythmia by inducing hypokalemia [3,4]. The principal intervention with proven efficacy for the prevention of AKI is adequate fluid administration. Definitively, SBIC is not the optimal fluid. Authors’ response Hong-Tao Tie, Qing-Chen Wu and Jing-Yuan Wan We appreciate Schiffl’s insightful commentary, which encourages us to expand on the mechanisms of SBIC in the prevention of CSA-AKI. The inefficacy of SBIC was due to the hypothesis that the significant increased power of hydrogen (PH) might not be adequate to prevent CSA-AKI. Nevertheless, the increased PH and subsequent disruption of homeostasis could cause possible harms. Firstly, arrhythmia and hypoventilation via inducing hypokalemia and alkalosis impair the cardiac function, as indicated by Schiffl. Moreover, hypocapnia by inducing alkalosis could reduce the cerebral blood flow and result in seizures and even coma or death [5]. Secondly, SBIC administration could impair the oxygenation and subsequently exacerbate the ischemia-reperfusion injury by aggravating the ischemia [4]. Thirdly, the induced intracellular alkalinization is associated with increased cell death, cell apoptosis, superoxide formation, pro-inflammatory cytokine release, blood lactate, and ketone bodies [6]. Finally, SBIC could cause decreased arterial blood pressure [7], an emergency situation for patients after cardiac surgery. Therefore, the risks overwhelm the benefits of SBIC for CSA-AKI prevention in patients undergoing cardiac surgery. However, the hypothesis that SBIC administration may precipitate volume overload and acute pulmonary edema seems irrational because each patient received the same solution (for example, 5% dextrose) and the same amount of fluid volume in each study. In short, the possible harms of SBIC should not be attributed to volume overload and acute pulmonary edema.
Michael Brucculeri - One of the best experts on this subject based on the ideXlab platform.
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Reversal of Citalopram‐Induced Junctional Bradycardia with Intravenous Sodium Bicarbonate
Pharmacotherapy, 2020Co-Authors: Michael Brucculeri, Joy Kaplan, Leah LandeAbstract:The cardiotoxicity of tricyclic antidepressants is a well-described phenomenon requiring serious consideration in patients who have taken an overdose. In patients who are at high risk for suicide attempts, selective serotonin reuptake inhibitors (SSRIs) were thought to constitute a safe alternative. However, evidence is accumulating that they, too, possess proarrhythmic properties, which must be reconciled in the setting of an overdose. An 82-year-old woman intentionally ingested citalopram 1.6 g. Several hours after presentation, she developed sinus arrest and junctional bradycardia that resolved after infusion of Intravenous Sodium Bicarbonate solution. Thereafter, she demonstrated no further electrocardiographic abnormalities and was safely transferred to the psychiatry service without the need for a temporary transvenous pacemaker. The dramatic effect of the Sodium Bicarbonate on the arrhythmia represents a probable event according to the Naranjo probability scale. Intravenous Sodium Bicarbonate may serve as an effective antidote to SSRI-induced bradyarrhythmias.
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reversal of citalopram induced junctional bradycardia with Intravenous Sodium Bicarbonate
Pharmacotherapy, 2005Co-Authors: Michael Brucculeri, Joy Kaplan, Leah LandeAbstract:The cardiotoxicity of tricyclic antidepressants is a well-described phenomenon requiring serious consideration in patients who have taken an overdose. In patients who are at high risk for suicide attempts, selective serotonin reuptake inhibitors (SSRIs) were thought to constitute a safe alternative. However, evidence is accumulating that they, too, possess proarrhythmic properties, which must be reconciled in the setting of an overdose. An 82-year-old woman intentionally ingested citalopram 1.6 g. Several hours after presentation, she developed sinus arrest and junctional bradycardia that resolved after infusion of Intravenous Sodium Bicarbonate solution. Thereafter, she demonstrated no further electrocardiographic abnormalities and was safely transferred to the psychiatry service without the need for a temporary transvenous pacemaker. The dramatic effect of the Sodium Bicarbonate on the arrhythmia represents a probable event according to the Naranjo probability scale. Intravenous Sodium Bicarbonate may serve as an effective antidote to SSRI-induced bradyarrhythmias.
Darrel W Hughes - One of the best experts on this subject based on the ideXlab platform.
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Intravenous Sodium Bicarbonate therapy in severely acidotic diabetic ketoacidosis
Annals of Pharmacotherapy, 2013Co-Authors: Bryson Duhon, Rebecca L Attridge, Crystal A Francomartinez, Pamela R Maxwell, Darrel W HughesAbstract:BACKGROUNDThe use of Intravenous Bicarbonate in diabetic ketoacidosis (DKA) may be considered for patients with a pH less than 6.9 according to the American Diabetes Association. The impact of this therapy on resolution of acidosis in patients with DKA is unclear.OBJECTIVETo determine whether the use of Intravenous Bicarbonate therapy was associated with improved outcomes in patients with severe DKA who were seen in the emergency department.METHODSThis review was conducted from 2007 to 2011 in the emergency department of a tertiary teaching hospital. Adults diagnosed with DKA with an initial pH less than 7.0 were included. Patients were stratified into 2 groups based on receipt of Intravenous Bicarbonate. The primary study outcome was time to resolution of acidosis, defined as return to pH greater than 7.2. Secondary outcomes included length of stay; continuous infusion insulin use; and Intravenous fluid, potassium, and insulin requirements within the first 24 hours of hospital admission, beginning upon a...
Haim Berkenstadt - One of the best experts on this subject based on the ideXlab platform.
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Intravenous Sodium Bicarbonate verifies Intravenous position of catheters in ventilated children.
Anesthesia and analgesia, 2012Co-Authors: Ilan Keidan, Erez Ben-menachem, Sno Ellen White, Haim BerkenstadtAbstract:Vascular access in children carries a significant risk of accidental extravasation of IV fluids and medications with the potential for tissue injury. In this prospective controlled study we assessed the diagnostic utility of using IV diluted Sodium Bicarbonate to confirm placement of IV catheters in ventilated children. Diluted Sodium Bicarbonate was created using undiluted standard 8.4% (1 mEq/mL) Sodium Bicarbonate mixed in a 1:3 and 1:5 ratio with sterile water to achieve a final diluted concentration of 2.1% (0. 25 mEq/mL) and 1.05% (0.125 mEq/mL) Sodium Bicarbonate, respectively. In 18 ASA I-II mechanically ventilated children ages 1 to 8 years, the effects of 1 mL/kg of dilute 2.1%, 1.05% Sodium Bicarbonate, or 0.9% normal saline, injected in a randomized order, were analyzed. All children had oxygen saturation, arterial blood pressure, electrocardiograph, and end-tidal carbon dioxide (ETCO(2)) monitoring. In addition, venous blood samples were taken before injection and 10 minutes after the final injection for analysis of venous blood pH and electrolytes. In children, IV diluted 2.1% Sodium Bicarbonate resulted in significantly increased etco(2) (mean of 32.8 ± 3.4 mm Hg to 39.0 ± 3.5 mm Hg, P < 0.001), a mean increase of 6.2 mm Hg (95% prediction interval: 4.3 to 8.1 mm Hg) within 3 breaths. Intravenous diluted 1.05% Sodium Bicarbonate caused a less pronounced but still significant increase in etco(2) (33.4 ± 3.8 mm Hg to 36.3 ± 3.4 mm Hg, P < 0.001), a mean increase of 2.9 mm Hg (95% prediction interval: 1.8 to 4.1 mm Hg) within 3 breaths. Normal saline did not result in any significant changes, with a mean increase of 0.06 mm Hg (95% prediction interval: -1.3 to 1.4 mm Hg). Both concentrations of Sodium Bicarbonate were easily differentiated from normal saline injection by blinded anesthesiologists observing the change in etco(2) values immediately after injection. Analysis of pre- and postinjection venous pH, Bicarbonate, and Sodium levels could not detect clinically significant changes. A small but statistically significant increase in venous Bicarbonate was noted. The injection of 2.1% Sodium Bicarbonate in mechanically ventilated ASA I-II children identified intravascular placement and patency of an IV catheter by an increase in the exhaled CO(2) concentration. The injections did not have any clinically significant effects on blood pH, Bicarbonate, or Sodium concentration.
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Intravenous Sodium Bicarbonate verifies Intravenous position of catheters in ventilated patients
Anesthesia & Analgesia, 2011Co-Authors: Ilan Keidan, Erez Benmenachem, Aviv Barzilai, Haim BerkenstadtAbstract:BACKGROUND: Extravasation is the unintentional injection or leakage of fluids into the perivascular or subcutaneous space resulting in potential tissue injury. In this 2-part prospective, controlled study, we assessed the safety of subcutaneously injected Sodium Bicarbonate in rats first. In the second part, the diagnostic utility of using IV diluted Sodium Bicarbonate to confirm placement of IV catheters in endotracheally intubated and ventilated rats and patients was tested. Diluted Sodium Bicarbonate was created using undiluted standard 8.4% (1 mEq/mL) Sodium Bicarbonate mixed in a 1:1 ratio with sterile water to achieve a final diluted concentration of 4.2% (0.5 mEq/mL). METHODS: Sodium Bicarbonate (8.4% and 4.2%) was injected subcutaneously into 10 rats, and skin samples were evaluated. The hemodynamic and ventilatory effects of IV Bicarbonate (2 mL/kg) in ventilated rats were measured. Subsequently, in 20 ASA physical status I and II mechanically ventilated patients, the effects of 50 mL of diluted 4.2% Sodium Bicarbonate or 0.9% normal saline, injected in a randomized order, were analyzed. RESULTS: Part 1: Undiluted (8.4%) subcutaneous Sodium Bicarbonate resulted in a small area of skin necrosis in 10% of skin samples (3 of 30) taken from rats. Minimal effects (mild scale crust and foci of regenerative epidermis beneath) were detected when a diluted solution was used. In ventilated rats, IV injection of diluted Bicarbonate caused a significant increase in end-tidal carbon dioxide, whereas subcutaneous injection had no effect. In humans, diluted Bicarbonate resulted in an end-tidal carbon dioxide increase (mean of 38 ± 5 to 45 ± 7 mm Hg) within 7 breaths. Injected normal saline did not result in any changes. Sodium Bicarbonate was easily differentiated from normal saline injection by anesthesiologists observing the change in end-tidal carbon dioxide concentrations immediately after injection. CONCLUSION: The injection of diluted Sodium Bicarbonate (in mechanically ventilated patients) can be used to reliably identify the correct location of an IV catheter by an increase in the exhaled carbon dioxide concentration. Although we found no skin damage with 4.2% (0.5 mEq/mL) Sodium Bicarbonate, safety and efficacy should be further evaluated in future studies.
