Management of Bicarbonate Level of 37 mEq/L
A bicarbonate of 37 mEq/L represents metabolic alkalosis or compensated chronic respiratory acidosis, and you must obtain an arterial blood gas immediately to distinguish between these two fundamentally different conditions before initiating any treatment. 1
Initial Diagnostic Algorithm
Step 1: Obtain Arterial Blood Gas
- If PaCO2 is elevated with pH <7.40, this indicates chronic respiratory acidosis with appropriate renal compensation—the elevated bicarbonate is protective and should NOT be corrected 1
- If PaCO2 is normal or low with pH >7.45, this indicates primary metabolic alkalosis requiring treatment 1
Management Based on Etiology
If Chronic Respiratory Acidosis (Compensated)
Do NOT attempt to reduce the bicarbonate in this scenario. The elevated bicarbonate is an appropriate compensatory response to chronic CO2 retention, commonly seen in COPD patients. 1
Key Management Principles:
- Do not rapidly normalize bicarbonate in patients with chronic hypercapnia, as this can cause severe alkalemia and seizures 1
- Target oxygen saturation of 88-92% in COPD patients, not normalization of blood gases 1
- If initiating mechanical ventilation, reduce bicarbonate buffering capacity gradually through relative hyperventilation to allow urinary bicarbonate loss 1
- The higher the pre-morbid pCO2, the higher the target pCO2 should be 1
If Primary Metabolic Alkalosis
Treatment depends on severity and underlying cause:
Mild to Moderate Alkalosis (pH <7.55)
Address underlying causes first:
- Volume depletion/diuretic use: Administer normal saline to restore volume and provide chloride, which allows the kidney to excrete excess bicarbonate 2, 3
- Hypokalemia: Replete potassium deficits aggressively, as hypokalemia perpetuates metabolic alkalosis and alkalosis cannot be corrected with persistent potassium depletion 1, 2
- Diuretic-induced: Reduce or temporarily hold diuretics if bicarbonate rises significantly above 30 mmol/L and patient is volume depleted 4
Severe Alkalosis (pH >7.55)
Severe metabolic alkalosis with arterial pH ≥7.55 is associated with significantly increased mortality in critically ill patients. 5
Treatment approach:
- Continue aggressive potassium and chloride repletion 1, 2
- Consider acetazolamide 250-500 mg to promote renal bicarbonate excretion if pH >7.55 is causing hemodynamic compromise 1
- In extreme cases with kidney failure, low-bicarbonate dialysis may be necessary 2, 3
If Patient is on Hemodialysis
High bicarbonate in dialysis patients typically indicates malnutrition with low endogenous acid production. 6
Management approach:
- Evaluate for malnutrition as the primary intervention 1
- Consider lowering dialysate bicarbonate concentration from standard 35-40 mEq/L to 30-32 mEq/L if bicarbonate remains >28 mEq/L 1
- Monthly bicarbonate monitoring with assessment of nutritional status 1
If Patient is Taking Bicarbonate Supplements
Discontinue or reduce bicarbonate supplementation immediately. 1
- Bicarbonate supplementation is only indicated when serum bicarbonate is <22 mEq/L 4, 1
- Do not administer bicarbonate to patients who already have elevated bicarbonate levels 1
Critical Monitoring Parameters
- Serial ABGs every 2-4 hours when making interventions in patients with chronic CO2 retention 1
- Electrolytes including ionized calcium, as alkalemia decreases ionized calcium 1
- Serum potassium closely during treatment, as correction of alkalosis can cause potassium shifts 1
Common Pitfalls to Avoid
- Never rapidly correct chronic respiratory acidosis by aggressive ventilation—this can cause severe alkalemia and seizures 1
- Do not treat the number alone in asymptomatic patients with chronic compensated respiratory acidosis 1
- In metabolic alkalosis, correct hypokalemia first before attempting other interventions 1
- Avoid treating with bicarbonate in patients who already have elevated levels 1
- In sepsis with elevated bicarbonate, do not use bicarbonate therapy even if pH is low, as this worsens outcomes 1