Metabolic acidosis

Primary acid–base disturbance characterized by a reduction in serum HCO₃⁻ (bicarbonate), usually with compensatory drop in Pco₂; blood pH is low (<7.35) or sometimes near-normal if mixed disorders.

• Indicates serious underlying problems (e.g., DKA, shock/sepsis, renal failure) and can cause significant organ dysfunction. Acute severe acidosis (pH <7.20) carries high mortality if uncorrected, leading to impaired cardiac output, arrhythmias, and coma. Chronic metabolic acidosis (as in CKD) contributes to bone loss and muscle wasting but is treatable with alkali to improve outcomes.

• Often presents with nonspecific symptoms (fatigue, nausea, headache) or signs of the underlying cause. Moderate to severe acidemia causes Kussmaul respirations – deep, rapid breathing – as compensation. Patients may appear flushed and confused; severe acidosis can progress to hypotension and decreased level of consciousness.
• High anion gap acidosis scenarios: DKA (e.g., a type 1 diabetic with polyuria, abdominal pain, fruity odor breath, and Kussmaul breathing), lactic acidosis (shock or sepsis with hypotension and elevated lactate), or toxic alcohol ingestion (e.g., methanol causing visual blurring with anion gap acidosis, ethylene glycol causing acute renal failure with oxalate crystals). Renal failure (uremia in AKI/CKD) is another common high-gap cause.
• Normal anion gap (hyperchloremic) acidosis scenarios: GI bicarbonate loss (prolonged diarrhea or intestinal drainage leading to acidosis with normal gap) and renal tubular acidosis (defect in H⁺ excretion or HCO₃⁻ reabsorption) are most common. For example, a patient with chronic diarrhea and weakness may have a normal-gap metabolic acidosis from bicarbonate loss, whereas one with Type IV RTA (hypoaldosteronism) might have mild normal-gap acidosis with hyperkalemia.

1. Confirm metabolic acidosis on ABG: low pH (<7.35) with primary low HCO₃⁻ (and compensatory ↓Pco₂). Simultaneously check serum electrolytes to calculate the anion gap (AG = Na⁺ – [Cl⁻ + HCO₃⁻]).
2. Determine AG status: if high anion gap (>12), investigate MUDPILES causes (Methanol, Uremia, DKA, Propylene glycol, INH/Iron, Lactic acidosis, Ethylene glycol, Salicylates) – order tests for ketones, lactate, renal function, toxic alcohol levels, etc. If normal anion gap, suspect hyperchloremic acidosis – look for GI losses (history of diarrhea, fistula) or renal causes (urinalysis and renal panel for RTA, renal failure).
3. Apply Winter's formula to assess respiratory compensation: expected Pco₂ ≈ 1.5 × [HCO₃] + 8 ± 2. If measured Pco₂ is higher or lower than expected, a concurrent respiratory acidosis or alkalosis is likely present (mixed disorder). Also consider the delta gap (change in AG vs change in HCO₃⁻) to unmask mixed metabolic disturbances (e.g. coexistent metabolic alkalosis).
4. In normal-gap acidosis, use the urine anion gap (Na + K – Cl in urine) to differentiate renal vs extrarenal causes. A negative urine AG suggests appropriate renal acid excretion (implying extrarenal loss like diarrhea), whereas a positive urine AG indicates impaired ammonium excretion (renal tubular acidosis). Identifying the exact cause guides targeted therapy.

1. Address the underlying cause: e.g., IV insulin and fluids for DKA, aggressive IV fluids/pressors and oxygen for shock-induced lactic acidosis, dialysis for uremic acidosis or toxic alcohol ingestion (with antidotes like fomepizole for methanol/ethylene glycol), and cessation of offending drugs (e.g., metformin in lactic acidosis). Correct any precipitating factors (e.g., sepsis, ischemia, or hypoxia in lactic acidosis).
2. Use sodium bicarbonate judiciously. It is generally reserved for severe acidemia (pH <7.1) or specific situations (e.g., to stabilize cardiac membrane in hyperkalemia, or in certain poisonings like TCA overdose). Routine bicarb therapy in mild-to-moderate metabolic acidosis (pH ≥7.2) is not beneficial and may cause volume overload or alkalosis. If used, administer carefully and monitor blood gases.
3. Chronic metabolic acidosis (e.g., in CKD) is managed with oral alkali therapy. Give oral sodium bicarbonate or citrate to maintain HCO₃⁻ ≥22 mEq/L, alongside dietary measures (increasing fruits/vegetables) to reduce acid load. This helps protect bones/muscles and may slow progression of kidney disease. In Type 1 RTA, bicarbonate or Shohl's solution corrects the acidosis; in Type 4 RTA (hypoaldosteronism), address hyperkalemia and consider fludrocortisone.

• Mnemonic MUDPILES for high anion gap acidosis: Methanol, Uremia (renal failure), DKA (and other ketoacidoses), Propylene glycol (antifreeze solvent), Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates.
• Mnemonic HARDUPS for normal anion gap acidosis: Hyperalimentation, Acetazolamide (or Addison's disease), Renal tubular acidosis, Diarrhea (GI loss of HCO₃⁻), Ureterosigmoidostomy, Pancreatic fistula, Saline infusion.
• A salicylate (aspirin) overdose classically causes a mixed acid–base picture: an early respiratory alkalosis (from respiratory center stimulation) plus an anion gap metabolic acidosis. Always check for a mixed disorder when an AG acidosis has an inappropriately low Pco₂.
• Near-normal anion gap doesn't always mean pure hyperchloremic acidosis – it could be two processes offsetting each other (e.g., a high-gap acidosis plus a metabolic alkalosis can yield a near-normal AG). Use the delta gap and clinical context to catch such pitfalls in acid–base interpretation.

• Arterial pH <7.1 (or HCO₃⁻ <8): indicates life-threatening acidemia with risk of circulatory collapse, refractory arrhythmias, and coma. Requires ICU management – consider emergent IV bicarbonate, mechanical ventilation if respiratory compensation fails, or dialysis (especially if renal failure or toxin is involved).
• Signs of shock or organ failure in the context of metabolic acidosis (e.g., hypotension, oliguria, altered mental status in septic or cardiogenic shock) – this combination portends high mortality and demands immediate intervention (aggressive resuscitation, treating cause). Also, an anion gap acidosis with an unexplained osmolar gap suggests toxic alcohol ingestion (emergency antidote/dialysis needed).

1. pH <7.35 on ABG + low HCO₃⁻ → diagnose metabolic acidosis.
2. Calculate anion gap: if AG >12 → high-gap acidosis (search for MUDPILES causes); if AG normal → hyperchloremic acidosis (think GI losses or RTA).
3. Check compensation with Winter's formula: if measured Pco₂ deviates from expected, a mixed acid–base disorder is present (investigate further).
4. Identify the cause: review clinical context (DKA, shock, renal failure, toxins, diarrhea, etc.), get relevant labs (glucose, ketones, lactate, renal panel, toxicology, etc.).
5. Initiate cause-specific treatment promptly (e.g., insulin, fluids, antibiotics, dialysis). Reassess ABG and anion gap for improvement. If pH remains critically low (<7.1) despite therapy, escalate care (consider bicarbonate infusion or renal replacement therapy).

• Young type 1 diabetic with abdominal pain, vomiting, fruity odor on breath, and deep rapid respirations; lab shows AG metabolic acidosis and high glucose → diabetic ketoacidosis (high anion gap metabolic acidosis).
• Hospitalized septic shock patient with hypotension and tachycardia; labs: high lactate and anion gap metabolic acidosis → lactic acidosis due to tissue hypoperfusion.
• Patient with several days of profuse diarrhea, weakness, and lab showing non-anion gap metabolic acidosis (hyperchloremia, low HCO₃⁻) → bicarbonate loss from GI tract (normal-gap metabolic acidosis).