Sodium Bicarbonate Drip Rate for Severe Metabolic Acidosis
For an adult with severe metabolic acidosis (pH < 7.20), administer an initial IV bolus of 50–100 mEq (50–100 mL of 8.4% solution) over several minutes, followed by a continuous infusion of 150 mEq/L solution at 1–3 mL/kg/hour (approximately 70–210 mL/hour for a 70 kg adult) if ongoing alkalinization is needed. 1, 2, 3
Initial Bolus Dosing
Administer 1–2 mEq/kg IV (typically 50–100 mEq or 50–100 mL of 8.4% solution) as a slow IV push over several minutes for severe metabolic acidosis with pH < 7.1 and base excess < -10. 1, 2, 3
The FDA label specifies that in less urgent forms of metabolic acidosis, the amount of bicarbonate given over a four-to-eight-hour period is approximately 2–5 mEq/kg body weight, depending on severity as judged by total CO₂ content, blood pH, and clinical condition. 3
Do not attempt rapid bolus administration in non-arrest situations; give slowly over several minutes to minimize complications including hyperosmolarity and paradoxical intracellular acidosis. 1, 3
Continuous Infusion Rate
After initial bolus, continue with an infusion of 150 mEq/L solution at 1–3 mL/kg/hour (70–210 mL/hour for a 70 kg adult) if ongoing alkalinization is needed. 1, 2
For a 70 kg adult, this translates to approximately 70 mL/hour at the lower end and 210 mL/hour at the upper end of the dosing range. 1
Prepare the 150 mEq/L solution by appropriately diluting 8.4% bicarbonate to achieve the target concentration for continuous infusion. 1
Preparation and Concentration Considerations
For volume-sensitive patients or those at risk for hyperosmolar complications, dilute 8.4% solution 1:1 with sterile water or normal saline to achieve 4.2% concentration before administration. 1
The 8.4% solution has an osmolality of 2 mOsm/mL, making it extremely hypertonic; isotonic formulations (4.2%) reduce the risk of hyperosmolar complications that can compromise cerebral perfusion. 1
No commercially available isotonic bicarbonate solutions exist in the United States, requiring pharmacy compounding and creating risk for preparation errors. 1
Target pH and Monitoring Requirements
Target a pH of 7.2–7.3, not complete normalization, as attempting full correction within the first 24 hours may be accompanied by unrecognized alkalosis due to delayed ventilatory readjustment. 1, 2, 3
Monitor arterial blood gases every 2–4 hours to assess pH, PaCO₂, and bicarbonate response during active therapy. 1, 2
Monitor serum electrolytes every 2–4 hours, specifically sodium (target < 150–155 mEq/L), potassium, and ionized calcium. 1, 2
Avoid serum sodium exceeding 150–155 mEq/L and pH exceeding 7.50–7.55 during therapy. 1, 2
Critical Safety Considerations
Ensure adequate ventilation before and during bicarbonate administration, as bicarbonate generates CO₂ that must be eliminated; giving it without adequate ventilation causes paradoxical intracellular acidosis. 1, 3
Never mix sodium bicarbonate with calcium-containing solutions or vasoactive amines (norepinephrine, dobutamine, epinephrine), as precipitation or catecholamine inactivation will occur. 1, 2
Flush the IV line with normal saline before and after bicarbonate administration to prevent inactivation of simultaneously administered catecholamines. 1
Monitor for hypokalemia, as bicarbonate shifts potassium intracellularly; replacement may be necessary during therapy. 1, 2
Specific Clinical Scenarios Requiring Different Rates
Sodium Channel Blocker/TCA Toxicity
- Administer initial bolus of 50–150 mEq using hypertonic solution (1000 mEq/L), titrated to resolution of QRS prolongation and hypotension. 1, 2
- Continue with infusion of 150 mEq/L solution at 1–3 mL/kg/hour, targeting arterial pH 7.45–7.55. 1
Diabetic Ketoacidosis
- For pH < 6.9: infuse 100 mmol sodium bicarbonate in 400 mL sterile water at 200 mL/hour. 1
- For pH 6.9–7.0: infuse 50 mmol sodium bicarbonate in 200 mL sterile water at 200 mL/hour. 1
- Bicarbonate is NOT indicated if pH ≥ 7.0 in DKA. 1
Cardiac Arrest
- In cardiac arrest, give 1–2 mEq/kg (44.6–100 mEq) as rapid IV bolus, repeatable every 5–10 minutes based on arterial pH monitoring. 2, 3
- The FDA label notes that in cardiac arrest, the risks from acidosis exceed those of hypernatremia, justifying more aggressive dosing. 3
Absolute Contraindications to Bicarbonate Therapy
Do NOT give bicarbonate for hypoperfusion-induced lactic acidemia with pH ≥ 7.15, as two blinded randomized controlled trials showed no difference in hemodynamic variables or vasopressor requirements compared to equimolar saline. 1, 2
Do NOT give bicarbonate routinely in sepsis-related acidosis when pH ≥ 7.15, as evidence shows no clinical benefit and potential harm including sodium/fluid overload, increased lactate, and decreased ionized calcium. 1
Do NOT use bicarbonate for respiratory acidosis; treat with ventilation instead. 1
Duration and Discontinuation Criteria
Discontinue bicarbonate when pH reaches 7.2–7.3, resolution of severe acidosis occurs, hemodynamic stability is achieved, or hypernatremia/excessive alkalemia develops. 1, 2
Therapy should be planned in a stepwise fashion since the degree of response from a given dose is not precisely predictable; initially infuse 2–5 mEq/kg over 4–8 hours, then adjust based on clinical response. 3
The FDA label emphasizes that it is unwise to attempt full correction of low total CO₂ content during the first 24 hours, as values brought to normal or above normal are very likely associated with grossly alkaline blood pH and undesired side effects. 3
Common Pitfalls to Avoid
Avoid rapid infusion of large quantities in non-emergent situations, as bicarbonate solutions are hypertonic and may produce undesirable rises in plasma sodium. 3
Do not calculate total deficit replacement and give it all at once; use a stepwise approach over 4–8 hours instead. 1
Do not exceed 6 mEq/kg total dose, as this commonly causes hypernatremia, fluid overload, metabolic alkalosis, and cerebral edema. 1
Do not ignore the underlying cause; bicarbonate buys time but does not treat the disease—focus on restoring adequate circulation and treating the primary disorder. 1, 4