What are the treatments for different types of acidosis?

Treatment of Acidosis by Type

Primary Classification and Treatment Algorithm

The treatment of acidosis fundamentally depends on whether it is metabolic or respiratory in origin, with metabolic acidosis requiring treatment of the underlying cause and potential bicarbonate supplementation when pH <7.2, while respiratory acidosis demands improved ventilation to reduce CO2 levels. 1

Metabolic Acidosis

Initial Assessment and Diagnosis

• Calculate the anion gap [(Na+ + K+) - (Cl- + HCO3-)] to differentiate between high anion gap and normal anion gap (hyperchloremic) metabolic acidosis 2, 3
• High anion gap causes include lactic acidosis, ketoacidosis, renal failure, and toxic ingestions (ethylene glycol, methanol, salicylates) 3
• Normal anion gap causes include gastrointestinal bicarbonate loss, renal tubular acidosis, early renal failure, and drug-induced hyperkalemia 3

Treatment Thresholds and Approach

For chronic kidney disease-related metabolic acidosis:

• Monitor serum bicarbonate monthly and maintain levels ≥22 mmol/L 4
• Consider oral alkali supplementation when bicarbonate is 18-22 mmol/L 4
• Initiate pharmacological treatment with oral sodium bicarbonate (0.5-1.0 mEq/kg/day divided into 2-3 doses) when bicarbonate falls below 18 mmol/L 4
• Target bicarbonate levels toward but not exceeding the normal range (22-26 mmol/L) 4

For acute severe metabolic acidosis:

• Bicarbonate therapy is indicated when pH falls below 7.0-7.2 4, 2
• In cardiac arrest, administer 1-2 vials (44.6-100 mEq) IV rapidly, then 50 mL every 5-10 minutes as guided by arterial pH 5
• For less urgent situations, give 2-5 mEq/kg over 4-8 hours 5
• Avoid attempting full correction in the first 24 hours—target total CO2 of approximately 20 mEq/L initially to prevent overshoot alkalosis 5

For diabetic ketoacidosis (DKA):

• Primary treatment is insulin therapy and fluid resuscitation, NOT bicarbonate 6, 4
• In youth with ketoacidosis, initiate subcutaneous or IV insulin to rapidly correct hyperglycemia and metabolic derangement 6
• Once acidosis resolves, start metformin while continuing subcutaneous insulin 6
• Bicarbonate therapy is generally NOT indicated unless pH falls below 6.9-7.0 4
• Monitor arterial or venous blood gases to assess treatment response 6

For lactic acidosis:

• The only effective treatment is cessation of acid production via improvement of tissue oxygenation 3
• Focus on restoring tissue perfusion with fluid resuscitation and vasopressors 4
• Sodium bicarbonate should NOT be used to treat metabolic acidosis from tissue hypoperfusion in sepsis 4
• Bicarbonate administration has not reduced morbidity or mortality in clinical studies despite improving acid-base parameters 3, 7

Critical Monitoring During Treatment

• Monitor blood pressure, serum potassium, and fluid status regularly—bicarbonate therapy can cause hypertension, hyperkalemia, or volume overload 4
• Measure arterial blood gases in complex cases to determine pH and PaCO2 4
• Monitor plasma osmolarity and hemodynamics in shock-associated acidosis 5
• Plasma potassium should be monitored closely as pH changes alter potassium concentrations 2

Important Clinical Caveats

• Avoid sodium bicarbonate in patients with advanced heart failure with volume overload, severe uncontrolled hypertension, or significant edema 4
• Citrate-containing alkali should be avoided in CKD patients exposed to aluminum salts as they increase aluminum absorption 4
• In pediatric CKD patients, treat more aggressively (even when bicarbonate >18 mmol/L) to optimize growth and bone health 4
• Increasing fruit and vegetable intake can help treat metabolic acidosis and may decrease blood pressure and body weight compared to sodium bicarbonate alone 4

Respiratory Acidosis

Pathophysiology and Diagnosis

• Characterized by elevated PaCO2 (>46 mmHg) and low blood pH (<7.35) resulting from hypoventilation and CO2 retention 4, 8
• Acute causes include Type II respiratory failure from pulmonary edema, COPD/asthma exacerbations, pleural disease, chest wall abnormalities, neuromuscular disorders, or CNS depression 8
• Chronic respiratory acidosis shows sustained PaCO2 elevation with renal compensation (elevated bicarbonate as a secondary response, not the primary disorder) 4, 8
• About 20% of patients with acute COPD exacerbations have respiratory acidosis 1

Treatment Approach

• Focus treatment on managing the underlying respiratory disorder to improve ventilation and reduce CO2 levels 4, 1
• Mechanical ventilation may be required in acute respiratory acidosis to improve ventilation 1
• Use careful oxygen therapy in chronic respiratory acidosis—target oxygen saturation of 88-92% to avoid worsening hypercapnia in COPD patients 4
• Do NOT treat the compensatory elevated bicarbonate in chronic respiratory acidosis—this is an appropriate renal response 4

Key Distinction from Metabolic Alkalosis

• In chronic respiratory acidosis, elevated bicarbonate represents renal compensation for CO2 retention, not primary metabolic alkalosis 4
• To differentiate, obtain arterial blood gas showing significantly elevated PaCO2 (>46 mmHg) with elevated bicarbonate 4
• Treatment targets the respiratory problem, not the bicarbonate level 4

Hospitalization Criteria for Metabolic Acidosis

Admit patients with:

• Severe metabolic acidosis (bicarbonate <18 mmol/L) requiring pharmacological treatment and close monitoring 4
• Acute illness or catabolic state (critical illness, major surgery, acute kidney injury on CKD) 4
• Symptomatic complications (protein wasting, severe muscle weakness, altered mental status, inability to maintain oral intake) 4
• Severe electrolyte disturbances (hyperkalemia, severe hypocalcemia, life-threatening metabolic derangements) 4
• Need for kidney replacement therapy initiation 4

Manage as outpatient:

• Bicarbonate levels 18-22 mmol/L with oral alkali supplementation 4
• Stable CKD without intercurrent illness 4
• Adequate oral intake maintained 4