What is the role of bicarbonate (sodium bicarbonate) in cardiac arrest management?

Use of Sodium Bicarbonate in Cardiac Arrest

Sodium bicarbonate is NOT recommended for routine use during cardiac arrest, but should be considered in specific situations: hyperkalemia, tricyclic antidepressant/sodium channel blocker overdose, and prolonged arrest with documented severe metabolic acidosis (pH <7.1) after adequate ventilation is established. 1

Primary Recommendation Against Routine Use

The American Heart Association explicitly recommends against routine administration of sodium bicarbonate in cardiac arrest (Class III, Level of Evidence B). 2, 1 Multiple studies demonstrate no benefit or association with poor outcomes when used routinely during resuscitation. 1, 3

The fundamental problem is that bicarbonate does not improve the likelihood of defibrillation or survival rates in cardiac arrest. 1 In fact, a 2024 systematic review found that overall data revealed bicarbonate was associated with lower rates of return of spontaneous circulation (ROSC) and worse outcomes. 3

Why Bicarbonate Can Be Harmful in Cardiac Arrest

Physiologic Adverse Effects

• Paradoxical intracellular acidosis: Bicarbonate generates excess CO2 that diffuses into myocardial and cerebral cells, worsening intracellular acidosis even as extracellular pH improves. 2, 1

• Impaired oxygen delivery: Creates extracellular alkalosis that shifts the oxyhemoglobin dissociation curve leftward, inhibiting oxygen release to tissues. 2, 1

• Reduced coronary perfusion: May compromise coronary perfusion pressure by reducing systemic vascular resistance. 1

• Electrolyte disturbances: Produces hypernatremia, hyperosmolarity, hypokalemia, and hypocalcemia. 2, 1

• Catecholamine inactivation: Can inactivate simultaneously administered epinephrine and other vasopressors. 1

• Exacerbation of central venous acidosis: Worsens the acidosis in central venous blood. 1

Specific Indications Where Bicarbonate IS Recommended

1. Hyperkalemia-Associated Cardiac Arrest

Bicarbonate shifts potassium intracellularly and is indicated for life-threatening hyperkalemic cardiac arrest. 2, 1 This is one of the clearest indications supported by guidelines. 1

2. Tricyclic Antidepressant (TCA) Overdose

The American Heart Association gives a Class I (strong) recommendation for sodium bicarbonate in life-threatening cardiotoxicity from TCA poisoning. 1 Administer hypertonic solution (1000 mEq/L) as IV bolus of 50-150 mEq, targeting arterial pH 7.45-7.55 and QRS narrowing. 1

3. Sodium Channel Blocker Toxicity

Bicarbonate receives a Class IIa recommendation for other sodium channel blocker overdoses causing wide QRS (>120 ms) and hemodynamic instability. 1 Follow with continuous infusion of 150 mEq/L solution at 1-3 mL/kg/hour. 1

4. Prolonged Arrest with Severe Documented Acidosis

Consider bicarbonate only after:

• Effective ventilation is established (critical prerequisite) 2, 1
• First dose of epinephrine has been ineffective 1
• Documented severe metabolic acidosis with pH <7.1 and base excess <-10 2, 1
• Prolonged arrest duration with ongoing severe acidosis 1

The 1998 European Resuscitation Council guidelines specifically limited bicarbonate to "severe acidosis as defined in the previous guidelines (arterial pH <7.1 and base excess <-10)." 2

Dosing When Bicarbonate Is Indicated

Initial Dose

• Adults: 1-2 mEq/kg IV (typically 50-100 mEq or one to two 50 mL vials of 8.4% solution) given as slow IV push. 1, 4
• Pediatrics: 1-2 mEq/kg IV given slowly. 2, 1

Repeat Dosing

In cardiac arrest, may repeat 50 mL (44.6-50 mEq) every 5-10 minutes as indicated by arterial pH monitoring. 4 However, repeat dosing should be guided by arterial blood gas analysis, not given empirically. 1

Critical Administration Technique

• Flush IV line with normal saline before and after bicarbonate to prevent catecholamine inactivation. 1
• Administer as slow IV push, never rapid bolus. 1
• Never mix with calcium-containing solutions or vasoactive amines. 2, 1

The Correct Approach to Acidosis in Cardiac Arrest

The mainstay of acid-base restoration during cardiac arrest is NOT bicarbonate but rather:

1. High-quality chest compressions to support tissue perfusion 1
2. Appropriate ventilation with oxygen to eliminate CO2 1
3. Rapid achievement of ROSC 1

These interventions address the root cause of acidosis—inadequate circulation and ventilation—rather than attempting to buffer the consequences. 1

Common Clinical Pitfall

Despite clear guidelines, bicarbonate is administered in approximately 50% of in-hospital cardiac arrests. 5 A 2024 survey found physicians commonly cite "metabolic acidosis" and "prolonged arrest duration" as indications, even though these are not supported by American Heart Association guidelines unless meeting the specific criteria above. 5 Many clinicians use it as a "last ditch effort" in prolonged arrests, but this practice lacks evidence for benefit and may cause harm. 5

Monitoring Requirements When Bicarbonate Is Used

• Arterial blood gases every 2-4 hours to assess pH, PaCO2, and bicarbonate response 1
• Serum electrolytes every 2-4 hours (sodium, potassium, ionized calcium) 1
• Target pH 7.2-7.3, not complete normalization 1
• Avoid serum sodium >150-155 mEq/L 1
• Avoid pH >7.50-7.55 1
• Monitor and treat hypokalemia that develops from intracellular potassium shift 1

Special Consideration: Adequate Ventilation Is Mandatory

Before administering bicarbonate, effective ventilation must be established because bicarbonate produces CO2 that requires elimination. 2, 1 Without adequate ventilation, the CO2 generated will worsen intracellular acidosis despite improving arterial pH. 2, 1 This is a critical safety consideration that cannot be overlooked.