Hemodynamic Instability and Abnormal Vasopressor Responsiveness in the Setting of Severe Metabolic Acidosis Treated With Adapted Alkalinization and Continuous Renal Replacement Therapy in the Emergency Department

Background: Whereas laboratory data and clinical experience suggest that metabolic acidosis deleteriously affects certain cardiovascular functions and may contribute to hemodynamic compromise, treatment of acidemia itself with alkalinization therapy, predominantly in the form of bolus dosing of intravenous sodium bicarbonate, has not been shown to improve hemodynamics or patient-oriented outcomes in clinical trials. Detailed examination of the biochemical effects of standard sodium bicarbonate administration reveals a possible explanation: ionized serum hypocalcemia, serum hypercarbia, and a paradoxical decrease in intracellular pH occur when bicarbonate is given alone and rapidly, without adjustment in minute ventilation or calcium supplementation. "Adapted alkalinization" treatment countering these side effects through hyperventilation, calcium supplementation, and slower sodium bicarbonate infusion has been studied in animals, but not yet described in humans.

Case report: We report a case of successful treatment of severe hemodynamic instability and vasopressor hyporesponsiveness in the setting of profound metabolic acidosis with such an adapted alkalinization approach, plus short-term continuous renal replacement therapy, in a critically ill patient, all performed in the emergency department. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Emergency physicians encounter patients with severe metabolic acidosis, shock, and hemodynamic instability despite vasopressor agents. Adapted alkalinization therapy with sodium bicarbonate, hyperventilation, and calcium administration may promote hemodynamic stability in such patients and allow for successful treatment of the underlying disease process.