Metabolic Acidosis in the Hospitalized Patient: The Anion Gap, Bicarb Controversy, and Why Your Patient’s pH is Killing Their Heart

In this episode of Hospital Medicine Unplugged, we dive into metabolic acidosis—how to identify it quickly, match treatment to the underlying cause, and manage it effectively to avoid complications.

We start by confirming the diagnosis—check arterial blood gas (ABG) and serum electrolytes for a low pH and bicarbonate (HCO₃⁻). Next, calculate the anion gap (use the formula: [Na⁺] – [Cl⁻] – [HCO₃⁻]) to classify it as high anion gap (e.g., lactic acidosis, diabetic ketoacidosis, uremia, toxins) or normal anion gap (hyperchloremic) (e.g., gastrointestinal bicarbonate loss, renal tubular acidosis, saline overuse). A urine anion gap can help distinguish renal vs. extrarenal causes.

Now, let's treat the underlying cause:

• For high anion gap acidosis, you’ll need to address conditions like sepsis (with antibiotics), DKA (with insulin), or toxin ingestion (antidotes, possibly dialysis). In lactic acidosis, focus on correcting hypoperfusion and volume status.

• For normal anion gap acidosis, treat gastrointestinal losses (e.g., from diarrhea) or renal tubular acidosis. Saline overuse should be corrected with diuretics and reducing volume overload.

When it comes to sodium bicarbonate therapy, it’s controversial. Studies show mixed results in mortality improvement, but it may help in severe acidemia (pH <7.2), especially in patients with acute kidney injury (AKI) or vasopressor dependency. But beware of risks like intracellular acidosis, hypocalcemia, hypernatremia, and volume overload. It’s not about full correction; it’s about getting the pH up to 7.2—slowly, with infusions rather than boluses.

For severe or refractory cases, renal replacement therapy (RRT) is indicated, particularly in cases of lactic acidosis, severe renal dysfunction, or toxin clearance. Continuous modalities are ideal in unstable patients.

In chronic metabolic acidosis (like CKD), use oral sodium bicarbonate to avoid serum bicarbonate falling below 18 mmol/L. Though it’s effective at increasing bicarbonate, there’s no conclusive evidence that correcting this prevents kidney failure progression.

Don’t forget about monitoring—it’s key to assessing the response to therapy and managing electrolyte imbalances. Keep a close eye on potassium levels as correction of acidosis can cause hypokalemia. Regular assessment of ABG, lactate, and renal function helps guide the treatment.

For prognosis, severe acidosis (pH <7.2) has a high mortality rate—especially with lactic acidosis or in critically ill patients. Early identification and targeted treatment are key to improving outcomes.

We wrap up with a system move: automate the diagnosis with ABG and anion gap calculation, prioritize cause-specific treatment, and monitor closely for complications. If bicarbonate therapy is needed, slow infusions are the way to go—aiming for pH 7.2—and RRT for refractory cases.

Metabolic acidosis requires rapid, accurate diagnosis and a tailored treatment plan. With the right strategy, you can optimize patient outcomes and prevent life-threatening complications.