Metabolic acidosis- pathophysiology and treatment - Gafacom (For health. For knowledge)

Metabolic acidosis- pathophysiology and treatment

Metabolic acidosis- pathophysiology and treatmentMetabolic acidosis is characterized by decreased pH and serum HCO3− concentrations, which can result from adding organic acid to extracellular fluid (e.g., lactic acid and ketoacids), loss of HCO3− stores (e.g., diarrhea), or accumulation of endogenous acids due to impaired renal function (e.g., phosphates and sulfates).

Serum anion gap (SAG) can be used to elucidate the cause of metabolic acidosis. SAG is calculated as follows:
SAG = [Na+] − [Cl−] − [HCO3−]
The normal anion gap is approximately 9 mEq/L (9 mmol/L), with a range of 3 to 11
mEq/L (311 mmol/L). SAG is a relative rather than an absolute indication of the cause of metabolic acidosis.

The primary compensatory mechanism is to decrease Paco2 by increasing the respiratory rate.


• Relatively asymptomatic; major manifestations are bone demineralization with the development of rickets in children and osteomalacia and osteopenia in adults. 
Acute severe metabolic acidemia (pH below than7.2) involves the cardiovascular, respiratory, and central nervous systems. Hyperventilation is often the first sign of metabolic acidosis. Respiratory compensation may occur as Kussmaul respirations (ie, deep, rapid respirations characteristic of diabetic ketoacidosis).
• Alkali therapy can be used to treat patients with acute severe metabolic acidosis due to hyperchloremic acidosis, but its role is controversial in patients with lactic acidosis.

Therapeutic options include sodium bicarbonate and tromethamine.

Sodium bicarbonate is recommended to raise arterial pH to 7.2. However, no controlled clinical studies have demonstrated reduced morbidity and mortality compared with general supportive care. If IV sodium bicarbonate is administered, the goal is to increase, not normalize, pH to 7.2 and HCO3− to 8 to 10 mEq/L (810mmol/L).

Tromethamine, a highly alkaline solution, is a sodium-free organic amine that acts as a proton acceptor to prevent or correct acidosis. However, no evidence exists that tromethamine is beneficial or more efficacious than sodium bicarbonate. The usual empiric dosage for tromethamine is 1 to 5 mmol/kg administered IV over 1 hour, and an individualized dose can be calculated as follows:
Dose of tromethamine (in mL) = 1.1 × body weight (in kg) × (normal [HCO3−] – current [HCO3−])

Metabolic acidosis- pathophysiology and treatment Metabolic acidosis- pathophysiology and treatment Reviewed by gafacom on June 07, 2019 Rating: 5

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