Correcting Metabolic Acidosis

Initial Assessment and Diagnosis

Obtain arterial blood gas (ABG) to determine pH and PaCO2, along with a basic metabolic panel to measure serum bicarbonate and electrolytes. 1 Venous pH (typically 0.03 units lower than arterial pH) can be used for ongoing monitoring once the diagnosis is established, as repeat arterial blood gases are generally unnecessary. 2

Calculate the Anion Gap

Anion gap = [Na+] - ([HCO3-] + [Cl-]), with normal values being 10-12 mEq/L. 2, 3
An elevated anion gap (>12 mEq/L) indicates accumulation of unmeasured anions such as lactate, ketoacids, uremic toxins, or ingested toxins. 2, 3
A normal anion gap (hyperchloremic acidosis) suggests bicarbonate loss from GI tract or renal tubular acidosis. 3, 4

Common pitfall: In critically ill patients, 98% have unmeasured strong anions present, and multiple underlying mechanisms frequently coexist—don't assume a single cause. 5

Treatment Based on Underlying Cause

Diabetic Ketoacidosis (DKA)

Bicarbonate therapy is NOT indicated in DKA unless pH falls below 6.9-7.0. 2, 1 The primary treatment is insulin therapy and fluid resuscitation, which corrects the underlying ketoacidosis. 2, 1

Administer isotonic saline (0.9% NaCl) at 15-20 ml/kg/h during the first hour to restore intravascular volume. 2, 1
Start continuous IV regular insulin at 0.1 units/kg/h after excluding hypokalemia (K+ >3.3 mEq/L). 2
When plasma glucose reaches 250 mg/dl, decrease insulin to 0.05-0.1 units/kg/h and add dextrose (5-10%) to IV fluids. 2
If bicarbonate therapy is necessary (pH <6.9), administer calculated amounts to bring pH up to 7.2, NOT to normalize it. 1, 6
Monitor venous pH and anion gap every 2-4 hours to assess resolution of acidosis. 2

Resolution criteria: Glucose <200 mg/dl, serum bicarbonate ≥18 mEq/L, and venous pH ≥7.3. 2

Lactic Acidosis from Sepsis or Shock

Do NOT use sodium bicarbonate to treat metabolic acidosis from tissue hypoperfusion in sepsis—focus on restoring tissue perfusion with fluid resuscitation and vasopressors. 1 The acidosis may have protective effects, and bicarbonate effectiveness in septic shock is uncertain. 1

Aggressive volume expansion with isotonic saline is the cornerstone of initial management. 1
Monitor blood gases, plasma osmolarity, arterial lactate, hemodynamics, and cardiac rhythm. 6

Chronic Kidney Disease (CKD)

Maintain serum bicarbonate ≥22 mmol/L to prevent protein catabolism, bone disease, and CKD progression. 1

Treatment Algorithm by Bicarbonate Level:

Bicarbonate ≥22 mmol/L: Monitor monthly, no pharmacological intervention needed. 1
Bicarbonate 18-22 mmol/L: Consider oral sodium bicarbonate 0.5-1.0 mEq/kg/day (typically 2-4 g/day or 25-50 mEq/day) divided into 2-3 doses, OR increase fruit and vegetable intake. 1
Bicarbonate <18 mmol/L: Initiate pharmacological treatment with oral sodium bicarbonate immediately. 1

Alternative approach: Increasing fruit and vegetable intake provides potassium citrate salts that generate alkali, and may additionally reduce systolic blood pressure and body weight compared to sodium bicarbonate alone. 1

Critical caveat: Avoid citrate-containing alkali in CKD patients exposed to aluminum-containing phosphate binders, as citrate increases aluminum absorption and worsens bone disease. 1

Intravenous Sodium Bicarbonate Dosing

Cardiac Arrest

Administer one to two 50 mL vials (44.6-100 mEq) rapidly initially, then continue at 50 mL (44.6-50 mEq) every 5-10 minutes as indicated by arterial pH and blood gas monitoring. 6 In cardiac arrest, the risks from acidosis exceed those of hypernatremia. 6

Less Urgent Metabolic Acidosis

Infuse 2-5 mEq/kg body weight over 4-8 hours, with therapy planned in a stepwise fashion since the degree of response is not precisely predictable. 6

Target goal: Achieve total CO2 content of approximately 20 mEq/L at the end of the first day of therapy, which will usually be associated with normal blood pH. 6
Do NOT attempt full correction to normal values within the first 24 hours, as this may be accompanied by unrecognized alkalosis due to delayed readjustment of ventilation. 6
Monitor blood gases, plasma osmolarity, arterial lactate, hemodynamics, and cardiac rhythm during therapy. 6

Monitoring During Treatment

Essential Parameters

Serum electrolytes (Na+, K+, Cl-, HCO3-): Every 2-4 hours during acute treatment. 2
Venous pH and anion gap: Every 2-4 hours to monitor resolution of acidosis. 2
Serum potassium: Monitor frequently, as alkalinization drives potassium intracellularly and can precipitate life-threatening hypokalemia. 1, 7
Blood pressure and volume status: Ensure bicarbonate therapy doesn't cause hypertension, hyperkalemia, or volume overload. 1

Chronic CKD Monitoring

Monthly bicarbonate monitoring initially after starting treatment, then at least every 4 months once stable. 1
Avoid sodium bicarbonate in patients with advanced heart failure with volume overload, severe uncontrolled hypertension, or significant edema. 1

Special Clinical Scenarios

Compensated Chronic Respiratory Acidosis

Do NOT treat elevated bicarbonate in patients with chronic hypercapnia and normal pH—the elevated bicarbonate is protective and physiologically appropriate. 1 Target oxygen saturation of 88-92% rather than attempting to correct the bicarbonate level. 1

Hospitalization Criteria for CKD Patients

Hospitalize if:

Bicarbonate <18 mmol/L with severe metabolic acidosis requiring close monitoring. 1
Acute illness or catabolic state (critical illness, major surgery, acute kidney injury). 1
Symptomatic complications (protein wasting, severe muscle weakness, altered mental status, inability to maintain oral intake). 1
Severe electrolyte disturbances (hyperkalemia, severe hypocalcemia). 1

Outpatient management is appropriate for:

Bicarbonate 18-22 mmol/L with oral alkali supplementation. 1
Stable CKD without intercurrent illness and adequate oral intake. 1

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