Metabolic acidosis refers to a condition characterized by a decrease in extracellular fluid pH caused by an increase in hydrogen ions (H⁺) and/or a loss of bicarbonate (HCO₃^-). It is defined by a primary reduction in plasma HCO₃^- concentration and is the most common type of acid-base imbalance in clinical practice.

Etiology

Excessive Loss of Alkaline Substances

Severe diarrhea, intestinal fistulas, pancreatic fistulas, and biliary drainage can result in significant loss of sodium bicarbonate (NaHCO₃).

Impaired Renal Acid Excretion and Bicarbonate Reabsorption

Renal failure or tubular dysfunction can hinder the excretion of fixed acids through urine and reduce HCO₃^- reabsorption in the proximal tubules. The use of carbonic anhydrase inhibitors, such as acetazolamide, can also suppress the activity of carbonic anhydrase in renal tubular epithelial cells, reducing hydrogen ion (H⁺) excretion and HCO₃^- reabsorption.

Excessive Production of Acidic Substances

Conditions like hypoxia and poor tissue perfusion can enhance anaerobic glycolysis, leading to lactic acidosis. In cases such as diabetes, severe starvation, or alcohol intoxication, accelerated fat breakdown can result in the formation of large amounts of ketone bodies, causing ketoacidosis.

Excessive Intake of Exogenous Fixed Acids

Consumption of substances like aspirin, ammonium chloride, arginine hydrochloride, or lysine hydrochloride can deplete HCO₃^- as it buffers the ingested acids.

Hyperkalemia

Elevated extracellular potassium (K⁺) concentration can drive the exchange of K⁺ with intracellular H⁺, leading to an increase in extracellular H⁺ concentration and metabolic acidosis.

During metabolic acidosis, the increased H⁺ in the blood is immediately buffered by the plasma buffering system, resulting in the consumption of alkaline buffers such as HCO₃^-. Additionally, the elevated H⁺ concentration stimulates chemoreceptors, activating the respiratory center to increase both the depth and frequency of breathing. As a result, carbon dioxide (CO₂) excretion is accelerated, reducing blood levels of carbonic acid (H₂CO₃), thereby maintaining a near-normal HCO₃^-/H₂CO₃ ratio and stabilizing blood pH. The kidneys also compensate by enhancing H⁺ and ammonium (NH₄⁺) excretion while increasing HCO₃^- reabsorption.

Clinical Manifestations

Mild metabolic acidosis may present without significant symptoms. Severe cases can manifest as fatigue, dizziness, drowsiness, impaired sensation, or agitation. The most pronounced symptom is deep and rapid breathing, referred to as Kussmaul respiration in typical cases. In diabetic ketoacidosis, breath may have a fruity odor due to the presence of ketones. Patients may exhibit flushed cheeks, an increased heart rate, and hypotension. Tendon reflexes may be diminished, consciousness may be impaired, and, in severe cases, coma can occur. Gastrointestinal symptoms such as mild abdominal pain, diarrhea, nausea, vomiting, and reduced appetite are also common.

Metabolic acidosis can reduce myocardial contractility and decrease vascular responsiveness to catecholamines, leading to arrhythmias, acute renal failure, and shock, conditions that tend to be difficult to correct and treat once established.

Diagnosis

The diagnosis of metabolic acidosis can be suspected in the presence of a history of severe diarrhea, intestinal fistulas, or shock, along with deep and rapid breathing. Arterial blood gas analysis and blood biochemical tests confirm the diagnosis and provide information on compensatory mechanisms and the severity of acidosis. Blood pH below 7.35 and significantly reduced HCO₃^- concentration indicate metabolic acidosis. During the compensatory phase, blood pH may remain within the normal range, but reductions in HCO₃^-, base excess (BE), and arterial carbon dioxide pressure (PaCO₂) are observed. Blood gas parameters in metabolic acidosis include decreased levels of standard bicarbonate (SB), actual bicarbonate (AB), and buffer base (BB), an increased negative BE value, a reduced pH, and a secondary reduction in PaCO₂, with AB less than SB.

Treatment

Treatment primarily involves addressing the underlying cause. For lactic acidosis, correcting circulatory disturbances, improving tissue perfusion, and managing infections are critical. Diabetic ketoacidosis requires timely fluid replacement, insulin administration for glycemic control, and correction of electrolyte imbalances. The body has a strong capacity to regulate acid-base balance, and once the underlying cause is resolved, mild metabolic acidosis can often resolve spontaneously with supplementary fluids to correct dehydration. Mild metabolic acidosis caused by hypovolemic shock can resolve following fluid replacement and blood transfusion to correct the shock state.

In severe cases, where plasma HCO₃^- concentration falls below 10 mmol/L, immediate fluid replacement and the administration of alkaline agents are necessary. Sodium bicarbonate (NaHCO₃) solution is commonly used. Upon entering bodily fluids, this solution dissociates into Na⁺ and HCO₃^-. HCO₃^- combines with H⁺ in the fluid to form H₂CO₃, which further dissociates into H₂O and CO₂, with CO₂ exhaled via the lungs. This process reduces the body's H⁺ levels, improving acidosis. The retained sodium (Na⁺) also increases extracellular fluid osmotic pressure and expands blood volume.

Clinicians typically administer an initial dose of 100–250 mL of 5% NaHCO₃ solution via intravenous infusion, followed by a re-evaluation of arterial blood gas and plasma electrolyte levels within 2–4 hours to determine the need for continued treatment. Given that the 5% NaHCO₃ solution is hypertonic, excessive or rapid administration can lead to hypernatremia and hyperosmolarity, which should be avoided. Correction of acidosis may also result in hypokalemia and hypocalcemia, requiring careful monitoring and appropriate intervention to manage these conditions.