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Cardiac arrest Only in selected cases (prolonged arrest, known acidosis) Routes of Administration Intravenous sodium bicarbonate (acute/severe cases) Oral bicarbonate (chronic metabolic acidosis, CKD) Adverse Effects Metabolic alkalosis Hypokalemia Hypernatremia Fluid overload (especially in heart or renal failure) Paradoxical intracellular acidosis Reduced oxygen delivery (left shift of oxyhemoglobin curve) Contraindications / Cautions Respiratory acidosis Metabolic alkalosis Hypocalcemia Congestive heart failure Renal impairment (risk of sodium overload) Bicarbonate in AcidBase Disorders Low Bicarbonate Metabolic acidosis DKA Diarrhea Renal tubular acidosis Lactic acidosis High Bicarbonate Metabolic alkalosis Vomiting Diuretic use Excess bicarbonate intake Primary extracellular buffer Normal range: 2228 mmol/L Treats metabolic acidosis and hyperkalemia Overuse metabolic alkalosis Not routinely used in DKA unless severe acidosis Summary Bicarbonate is the main extracellular buffer maintaining blood pH, clinically used to treat severe metabolic acidosis and hyperkalemia, but must be used cautiously due to risks of alkalosis and sodium overload

Together with the genetic evidence showing GLR3.3 is required for both GSH- and Glu-triggered systemic [Ca 2+ ] cyt transmission (Fig
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Placenta as a protecting barriersome properties of glutathione-S-transferase [PMID: 1441828] Laboratory literature summary: Placenta as a protecting barriersome properties of glutathione-S-transferase