Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and gastrointestinal or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with arterial blood gas (ABG) and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Show Metabolic acidosis is acid accumulation due to
 The most common causes of a high anion gap metabolic acidosis are
Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis Diabetic Ketoacidosis (DKA) Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with... read more ), but it also occurs with chronic alcohol use disorder (see alcoholic ketoacidosis Alcoholic Ketoacidosis Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic... read more ), undernutrition Overview of Undernutrition Undernutrition is a form of malnutrition. (Malnutrition also includes overnutrition.) Undernutrition can result from inadequate ingestion of nutrients, malabsorption, impaired metabolism, loss... read more , and, to a lesser degree, fasting. In these conditions, the body converts from glucose metabolism to free fatty acid (FFA) metabolism; FFAs are converted by the liver into ketoacids, acetoacetic acid, and beta-hydroxybutyrate (all unmeasured anions). Ketoacidosis is also a rare manifestation of congenital isovaleric acidemia Isovaleric acidemia Valine, leucine, and isoleucine are branched-chain amino acids; deficiency of enzymes involved in their metabolism leads to accumulation of organic acids with severe metabolic acidosis. There... read more or congenital methylmalonic acidemia Methylmalonic acidemia Valine, leucine, and isoleucine are branched-chain amino acids; deficiency of enzymes involved in their metabolism leads to accumulation of organic acids with severe metabolic acidosis. There... read more . The most common causes of normal anion gap acidosis are
Normal anion gap metabolic acidosis is also called hyperchloremic acidosis because the kidneys reabsorb chloride (Cl−) instead of reabsorbing HCO3−. Many GI secretions are rich in HCO3− (eg, biliary, pancreatic, and intestinal fluids); loss due to diarrhea, tube drainage, or fistulas can cause acidosis. In ureterosigmoidostomy (insertion of ureters into the sigmoid colon after obstruction or cystectomy), the colon secretes and loses HCO3− in exchange for urinary chloride (Cl−) and absorbs urinary ammonium, which dissociates into ammonia (NH3+) and hydrogen ion (H+). Ion-exchange resin uncommonly causes HCO3− loss by binding HCO3−. Symptoms and SignsThe most characteristic sign is hyperpnea (long, deep breaths at a normal rate), reflecting a compensatory increase in alveolar ventilation; this hyperpnea is not accompanied by a feeling of dyspnea. Severe, acute acidemia predisposes to cardiac dysfunction with hypotension and
shock Shock Shock is a state of
organ hypoperfusion with resultant cellular dysfunction and death. Mechanisms may involve decreased circulating volume, decreased cardiac output, and vasodilation, sometimes... read more ,
ventricular arrhythmias
Overview of Arrhythmias The normal heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial... read more
The cause of an elevated anion gap may be clinically obvious (eg, hypovolemic shock, missed hemodialysis), but if not, blood testing should include
Salicylate levels can be measured in most laboratories, but methanol and ethylene glycol frequently cannot; their presence may be suggested by presence of an osmolar gap. Calculated serum osmolarity (2 [sodium] + [glucose]/18 + BUN/2.8 + blood alcohol/5, based on conventional units) is subtracted from measured osmolarity. A difference > 10 implies the presence of an osmotically active substance, which, in the case of a high anion gap acidosis, is methanol or ethylene glycol. Although ingestion of ethanol may cause an osmolar gap and a mild acidosis, it should never be considered the sole cause of a significant metabolic acidosis.
Treatment of acidemia with sodium bicarbonate (NaHCO3) is clearly indicated only in certain circumstances and is probably deleterious in others. When metabolic acidosis results from loss of HCO3− or accumulation of inorganic acids (ie, normal anion gap acidosis), bicarbonate therapy is generally safe and appropriate. However, when acidosis results from organic acid accumulation (ie, high anion gap acidosis), bicarbonate therapy is controversial; it does not clearly decrease mortality in these conditions, and there are several possible risks. With treatment of the underlying condition, lactate and ketoacids are metabolized back to HCO3−; exogenous HCO3− loading may therefore cause an “overshoot” metabolic alkalosis. In any condition, sodium bicarbonate may also cause sodium and volume overload, hypokalemia, and, by inhibiting respiratory drive, hypercapnia. Furthermore, because HCO3− does not diffuse across cell membranes, intracellular acidosis is not corrected and may paradoxically worsen because some of the added HCO3− is converted to carbon dioxide (CO2), which does cross into the cell and is hydrolyzed to H+ and HCO3−. Despite these and other controversies, most experts still recommend giving bicarbonate IV for severe metabolic acidosis (pH < 7.0). Treatment requires 2 calculations (same for both conventional and SI units). The first is the level to which HCO3− must be raised, calculated by the Kassirer-Bleich equation, using a target value for [H+] of 79 nEq/L (79 nmol/L), which corresponds to a pH of 7.10: 79 = 24 × Pco2/HCO3− or Desired HCO3−= 0.30 × Pco2 The amount of sodium bicarbonate needed to achieve that level is NaHCO3 required (mEq/mmol) = (desired [HCO3−] − observed [HCO3−]) × 0.4 × body weight (kg) For example, a 70-kg man has severe metabolic acidosis with a pH of 6.92, PCO2 40 mmHg and HCO3− of 8 mEq/L (8 mmol/L). The target bicarbonate level needed to achieve a pH of 7.10 is 0.30 × 40 = 12 mEq/L (12 mmol/L). This level is 4 mEq/L (4 mmol/L) more than his current bicarbonate level of 8. To increase bicarbonate by 4, multiply 4 by 0.4 times 70 (the body weight), giving a result of 112 mEq (112 mmol) of HCO3−. This amount of sodium bicarbonate is given over several hours. Blood pH and HCO3−levels can be checked 30 minutes to 1 hour after administration, which allows for equilibration with extravascular HCO3−. Alternatives to sodium bicarbonate include
These alternatives do not offer a proven benefit over sodium bicarbonate alone and can cause complications of their own. Potassium (K+) depletion, common in metabolic acidosis, should be identified through frequent serum K+ monitoring and treated as needed with oral or parenteral potassium chloride.
Click here for Patient Education Which acidIn patients with sepsis and septic shock, high anion gap metabolic acidosis is the dominant blood gas anomaly.
What is the most common type of acidMetabolic acidosis is the most common disorder encountered in clinical practice. The respiratory contribution to a change in pH can be determined by measuring PCO2 and the metabolic component by measuring the base excess.
Why is there mixed acidosis in shock?During hemorrhagic shock, metabolic acidosis is common and conventionally considered to be due essentially to hyperlactatemia. The increase in blood lactate generally originates from both increased lactate production and reduced lactate metabolism.
Is shock metabolic acidosis?Metabolic acidosis itself most often causes rapid breathing. Acting confused or very tired may also occur. Severe metabolic acidosis can lead to shock or death. In some situations, metabolic acidosis can be a mild, ongoing (chronic) condition.
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