Metabolic Acidosis

Mechanism

Classification Based on Anion Gap

The initial diagnostic differentiation requires discerning between acidosis with elevated Anion Gap and hyperchloremic acidosis with normal Anion Gap:

High Anion Gap Acidosis (HAGMA)

It occurs secondary to the consumption of chemical buffers due to the tissue accumulation of unmeasured acids of metabolic or toxicological origin:

• Lactic Acidosis: Tissue hypoperfusion or shock of septic, cardiogenic or distributive origin (Acidosis type A), or due to mitochondrial cell dysfunction, drugs such as metformin or neoplasms (Acidosis type B).
• Ketoacidosis: Diabetic, alcoholic or secondary to extreme prolonged starvation.
• Severe uremia: Advanced renal failure with accumulation of phosphates and sulfates.
• Toxic Ingestion: Methanol, ethylene glycol or salicylates.

Normal Anion Gap Acidosis (NAGMA)

It occurs due to the net loss of bicarbonate directly from the body, which generates a compensatory elevation of the plasma chlorine ion to preserve electrical neutrality:

• Gastrointestinal Losses: Severe secretory diarrhea or digestive fistulas of biliary or pancreatic origin.
• Renal Tubular Acidosis (RTA): Specific dysfunction in the regeneration of bicarbonate or secretion of hydrogen ions in the renal tubule.

Indicators and dose

Diagnostic Differentiation of Renal Tubular Acidoses (RTA)

Use of Sodium Bicarbonate in Metabolic Acidosis

Sodium bicarbonate infusion in metabolic acidosis is a topic of ongoing clinical debate and its widespread use is not recommended due to potential deleterious cellular effects.

Specific Clinical Indications of Sodium Bicarbonate

The use of sodium bicarbonate is restricted exclusively to rigorously selected clinical scenarios:

• Severe Hyperchloremic Metabolic Acidosis (with pH < 7.15 and cardiovascular instability): Useful because the pathophysiological etiology is associated with the absolute depletion of the bicarbonate buffer reserve without concurrent production of cellular lactate.
• Advanced Chronic Kidney Disease: To maintain basal serum bicarbonate levels above 22 mEq/L, slowing the progression of renal osteodystrophy and skeletal muscle catabolism.
• Intoxication by Salicylates or Tricyclic Antidepressants: To selectively alkalinize urine (promoting renal ionization and excretion of salicylates) or to stabilize cardiac sodium channels in tricyclic toxicity.

Calculation of Sodium Bicarbonate Deficiency for Controlled Infusion:

Bicarbonate Deficiency (mEq) = 0.5 · Body weight (kg) · ( [HCO₃^-]_target - [HCO₃^-]_measured )

The initial correction objective should be partial, aiming to raise plasma bicarbonate only to a safe value of 15 to 18 mEq/L, initially administering half of the deficit calculated to pass in a slow period of 4 to 6 hours.

Security

Physiological Alert: Paradox of Intracellular Acidosis and Hemoglobin Curve

The rapid administration of Sodium Bicarbonate (NaHCO₃) to correct metabolic acidemia can paradoxically aggravate the intracellular acidosis of the target organs:

HCO₃^- + H⁺ H₂CO₃ Carbonic Anhydrase CO₂ + H₂O

When exogenous bicarbonate joins with plasma hydrogen ions, carbon dioxide (CO₂) and free water are immediately generated. Unlike electrically charged bicarbonate, carbon dioxide is a highly soluble and lipophilic gas that freely crosses the cell plasma membrane into the interior of cells (especially in the myocardium and brain parenchyma).

Once inside the cellular cytosol, carbon dioxide is hydrated with intracellular water, again releasing free hydrogen ions locally, inducing a deep acute intracellular acidosis that decreases myocardial contractility and perpetuates shock.

In addition, the correction of extracellular pH abruptly shifts the oxyhemoglobin dissociation curve to the left, increasing the affinity of oxygen for the transporter and preventing its normal physiological delivery to hypoxic peripheral tissues.