What is the cause of a low bicarbonate (HCO3) level of 19.2 mmol/L in an arterial blood gas (ABG) result indicating metabolic acidosis?

Causes of Low Bicarbonate (19.2 mmol/L) on ABG

A bicarbonate level of 19.2 mmol/L indicates metabolic acidosis, which requires immediate investigation of the underlying cause through systematic evaluation of the anion gap, clinical context, and associated laboratory findings. 1, 2

Understanding the Measurement

• Metabolic acidosis is characterized by primary reduction in serum bicarbonate (<22 mmol/L), associated with blood pH <7.35, and the body attempts to compensate by increasing ventilation to eliminate CO2. 1, 2
• Low serum bicarbonate concentrations almost always indicate metabolic acidosis, with normal range being 22-26 mmol/L. 1
• The bicarbonate level of 19.2 mmol/L falls below the critical threshold of 22 mmol/L, confirming metabolic acidosis that warrants further evaluation and potential treatment. 3, 1

Diagnostic Algorithm: Determining the Cause

Step 1: Calculate the Anion Gap

• Calculate anion gap as [Na+] - ([HCO3-] + [Cl-]) to classify into elevated anion gap or normal (hyperchloremic) anion gap categories. 2
• This classification guides differential diagnosis, though categories can overlap. 2

Step 2: Elevated Anion Gap Causes

• Acute overproduction of organic acids such as ketoacids (diabetic ketoacidosis, starvation, alcoholic) or lactic acid (tissue hypoxia, sepsis, shock states). 2
• Renal failure with impaired hydrogen ion excretion and ammonia synthesis leading to acid accumulation. 1
• Drug toxicity including metformin-associated lactic acidosis, particularly with concomitant use of carbonic anhydrase inhibitors. 4
• Tissue ischemia from conditions like air embolism post-cardiac surgery causing anaerobic metabolism and lactate accumulation. 5

Step 3: Normal Anion Gap (Hyperchloremic) Causes

• Chronic kidney disease (CKD stages 3-5) with impaired renal acidification and bicarbonate wasting. 3, 1
• Renal tubular acidosis with specific defects in renal acid handling. 3
• Gastrointestinal bicarbonate losses from diarrhea, fistulas, or ureterosigmoidostomy. 2
• Recovery phase from diabetic ketoacidosis when anion gap normalizes but bicarbonate remains low. 1

Step 4: Assess Clinical Context

• In CKD patients, chronic metabolic acidosis results from impaired hydrogen ion excretion, reduced ammonia synthesis, and dietary acid load from high animal protein intake with low fruit/vegetable consumption. 1
• In critically ill patients, evaluate for sepsis, shock states, or tissue hypoperfusion causing lactic acidosis. 5, 6
• Review medication list for carbonic anhydrase inhibitors (topiramate, zonisamide, acetazolamide), which frequently cause non-anion gap metabolic acidosis and can potentiate metformin-associated lactic acidosis. 4
• Assess for diabetic ketoacidosis with typical presentation of hyperglycemia, ketonuria, and characteristic symptoms. 1

Clinical Significance and Management Implications

When to Treat

• Bicarbonate levels between 18-22 mmol/L (which includes 19.2 mmol/L) can typically be managed as outpatients with oral alkali supplementation in stable CKD patients. 1
• Pharmacological treatment with sodium bicarbonate is strongly recommended when bicarbonate drops below 18 mmol/L. 1
• The treatment goal is to increase bicarbonate toward but not exceeding the normal range (≥22 mmol/L). 3, 1

Indications for Hospitalization with Bicarbonate 19.2 mmol/L

• Acute illness or catabolic state such as critical illness, major surgery, or acute kidney injury superimposed on CKD. 1
• Symptomatic complications including protein wasting, severe muscle weakness, altered mental status, or inability to maintain oral intake. 1
• Severe electrolyte disturbances such as hyperkalemia or life-threatening metabolic derangements. 1
• Suspected diabetic ketoacidosis (bicarbonate 15-18 mmol/L indicates mild DKA). 1

Adverse Effects of Untreated Acidosis

• Chronic metabolic acidosis causes increased protein catabolism and muscle wasting, bone demineralization contributing to renal osteodystrophy, and growth retardation in children. 3, 1, 2
• Acute metabolic acidosis causes decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impaired immune response. 2
• Chronic acidosis alters calcium-PTH-vitamin D homeostasis, exaggerating bone dissolution. 3

Common Pitfalls to Avoid

• Do not assume obesity hypoventilation syndrome (OHS) is the cause, as bicarbonate <27 mmol/L has very high negative predictive value (99%) for ruling out OHS. 3
• Do not overlook mesenteric ischemia in post-cardiac surgery patients with unexplained acidosis, as this requires urgent surgical evaluation. 5
• Avoid citrate-containing alkali salts in CKD patients exposed to aluminum, as citrate increases aluminum absorption and worsens bone disease. 3, 1
• Do not administer bicarbonate therapy in diabetic ketoacidosis unless pH falls below 6.9-7.0; instead focus on insulin therapy and fluid resuscitation. 1
• Do not use sodium bicarbonate to treat metabolic acidosis from tissue hypoperfusion in sepsis; restore tissue perfusion with fluid resuscitation and vasopressors instead. 1

Monitoring Requirements

• Measure arterial blood gases to determine pH and PaCO2 for complete acid-base assessment in complex cases. 1
• In CKD patients, monitor serum bicarbonate monthly initially, then at least every 4 months once stable. 1
• After initiating treatment, monitor blood pressure, serum potassium, and fluid status regularly to ensure treatment doesn't cause hypertension or hyperkalemia. 1
• Serial measurements of lactate, base deficit, and pH provide valuable information about shock severity and response to treatment in critically ill patients. 5