Sodium Bicarbonate Infusion Side Effects
Sodium bicarbonate infusion causes multiple serious adverse effects including metabolic alkalosis, hypernatremia, hyperosmolarity, paradoxical intracellular acidosis from excess CO2 production, hypokalemia, hypocalcemia, impaired oxygen delivery, and tissue necrosis if extravasated. 1, 2
Metabolic and Electrolyte Disturbances
Alkalosis and pH Derangements
- Metabolic alkalosis is the most common complication of overly aggressive sodium bicarbonate therapy, manifesting with muscular twitching, irritability, and tetany 2
- Extracellular alkalosis shifts the oxyhemoglobin saturation curve, inhibiting oxygen release to tissues and potentially worsening tissue hypoxia 1, 3
- Providers should avoid extremes of alkalemia, keeping serum pH below 7.50-7.55 3
Electrolyte Abnormalities
- Hypernatremia and hyperosmolarity occur from the high sodium load, with guidelines recommending serum sodium not exceed 150-155 mEq/L 1, 3, 4
- Hypokalemia develops during alkalemia as potassium shifts intracellularly, requiring monitoring and treatment 3, 4
- Hypocalcemia is frequently observed, particularly in critically ill patients 5
Paradoxical Acidosis
Intracellular and Tissue Acidosis
- Excess CO2 production from bicarbonate metabolism freely diffuses into myocardial and cerebral cells, paradoxically contributing to intracellular acidosis despite correcting blood pH 1, 3
- Central venous acidosis can be exacerbated by bicarbonate administration 1
- Cerebrospinal fluid acidosis may develop, potentially causing neurologic dysfunction 6
This paradoxical effect is particularly concerning because the CO2 generated crosses cell membranes more readily than bicarbonate, worsening the very acidosis clinicians are attempting to treat 1, 7.
Cardiovascular Effects
Hemodynamic Compromise
- Reduced systemic vascular resistance may compromise coronary perfusion pressure (CPP), particularly problematic during cardiac arrest 1
- Catecholamine inactivation occurs when bicarbonate is administered simultaneously with vasopressors, reducing their effectiveness 1, 3
- Never mix sodium bicarbonate with vasoactive amines or calcium-containing solutions 3
Local Tissue Injury
Extravasation Complications
- Chemical cellulitis with tissue necrosis, ulceration, or sloughing can occur at infiltration sites due to the alkalinity of hypertonic bicarbonate solutions 2
- Prompt elevation of the affected area, warmth application, and local injection of lidocaine or hyaluronidase are recommended to reduce tissue damage 2
- For pediatric patients under 2 years, the 8.4% solution must be diluted 1:1 with normal saline to achieve 4.2% concentration to reduce this risk 3
Clinical Context and Outcomes
Limited Efficacy with Potential Harm
- The majority of studies show no benefit or found relationships with poor outcomes when bicarbonate is used routinely in cardiac arrest 1
- In the BICAR-ICU trial, metabolic alkalosis, hypernatremia, and hypocalcemia were observed more frequently in the bicarbonate group, though no life-threatening complications were reported 5
- Recent evidence suggests bicarbonate use in diabetic ketoacidosis does not improve outcomes and may cause harm in pediatric patients 8
Specific Scenarios Where Benefits May Outweigh Risks
Despite these adverse effects, bicarbonate remains indicated for specific conditions including preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdose, and other sodium channel blocker toxicity 1, 3. In these scenarios, the life-threatening nature of the primary condition justifies accepting the risk of side effects with careful monitoring.
Monitoring Requirements
When bicarbonate therapy is necessary, close monitoring is essential 3:
- Serial arterial blood gases to guide dosing and avoid overcorrection
- Serum sodium levels to prevent dangerous hypernatremia
- Serum potassium levels to detect and treat hypokalemia
- Serum calcium levels, particularly in critically ill patients
- Acid-base status throughout therapy
The key principle is that bicarbonate therapy should be guided by laboratory values rather than empiric dosing, and providers should not attempt complete correction of calculated base deficit to minimize iatrogenic alkalosis 1.