Metabolic acidosis is defined as a plasma pH <7.35 that results from either an increase in nonvolatile acid production or loss of bicarbonate ions. It can:
Be acute, lasting minutes to days (common); or chronic, lasting weeks to months (less common).
Results when the body's multiple buffering and compensatory mechanisms are exhausted.
Metabolic acidosis is divided into a normal or increased anion gap and is useful in establishing a differential diagnosis. Anion gap is defined as the unmeasured anions present in the plasma; it does not imply that anions are missing, but only that they are not directly measured. It is calculated as follows:
Anion gap = [Na+] - ([Cl-] + [HCO3-]).
A normal anion gap is 6–10 mmol/L and is attributed to serum albumin, phosphates, and sulfates.
Perioperatively, the base excess is more commonly utilized in determining the extent of increased acid load. This is because metabolic acidosis is most commonly the result of anaerobic metabolism (lactic acidosis).
Epidemiology
Incidence
Acute metabolic acidosis is estimated to affect ~64% of ICU patients (1).
Prevalence
Chronic metabolic acidosis has an increased prevalence in patients with chronic kidney disease.
Morbidity
Primarily related to the underlying disease
Mortality
Primarily related to the underlying disease
Etiology/Risk Factors
Increased anion gap metabolic acidosis results from increased nonvolatile acid (2,3).
Type I and Type II (Gordon's syndrome) pseudoaldosteronism
Physiology/Pathophysiology
Normal acid production is 1 mmol/kg/day in adults and 1–3 mmol/kg/day in infants and children.
The hydrogen ion concentration is tightly regulated in the body to maintain a physiologic [H+] of 40 mEq/L. There are 3 key mechanisms:
Intracellular and extracellular buffering systems are the first-line mechanisms to remove excessive [H+].
Carbonic acid/bicarbonate system: [H+] + H2O + CO2. When the [H+] increases, the [HCO3-] declines as more H2CO3 forms. Carbonic anhydrase will convert H2CO3 to CO2 and H2O.
Phosphate: [H2PO4-] [H+] + [HPO44-]. The high intracellular concentration makes it an important intracellular buffer.
Hemoglobin
Plasma proteins
Alveolar ventilation and elimination of carbon dioxide (CO2)
Increases in [H+] stimulate chemoreceptors in the carotid body to increase minute ventilation and exhalation of CO2.
Winter's formula aids with identifying the presence of a mixed respiratory disorder: PaCO2 = (1.5 × [HCO3-]) + 8 ± 2. When the calculated and measured PaCO2 correspond, it suggests that the metabolic acidosis is an isolated disorder. If the measured PaCO2 is greater than the calculated PaCO2, a primary respiratory acidosis is also present; whereas, if the measured PaCO2 is lower than the calculated PaCO2, a primary respiratory alkalosis is also present.
Renal compensation:
Reabsorption and secretion. Filtered HCO3- is converted to CO2 in the lumen of the renal tubule; it then diffuses into proximal tubule cells and is subsequently reconverted to HCO3- and returned to the systemic circulation. Thus, for each HCO3- that is reabsorbed, an H+ is secreted into the urine by the renal tubular cell.
Effects on organ systems:
Cardiovascular
Impaired contractility of the myocardium
Increased pulmonary vascular resistance
Decreased systemic vascular resistance
Respiratory
Hyperventilation (compensatory mechanism)
Shift of oxygen dissociation curve to the right
Decreased 2,3-Diphosphoglycerate (DPG) in red cells leads to a decrease in hemoglobin's affinity to oxygen. There is a "left-shift" of the oxyhemoglobin curve.
Bone
Chronic acidosis, as is seen with renal disease, can result in increased mobilization of calcium from bone secondary to cellular effects on osteoclasts and osteoblasts and impaired bone matrix mineralization.
Prevantative Measures
Close monitoring of blood glucose levels in diabetics to prevent ketoacidosis.
Lactic acidosis results from tissue hypoxia (anaerobic metabolism) that is due to impaired perfusion or oxygen delivery
Maintain adequate volume in burn injuries, trauma, hemorrhage, diarrhea, bowel prep, third spacing
Maintain adequate perfusion with inotropes and vasopressors
Maintain adequate blood oxygen content via increasing the inspired oxygen fraction and possibly transfusing blood, if appropriate.
Arterial blood gas measurements provide values for pH, HCO3-, PaCO2, and base excess and are assessed in context with one another.
pH <7.35
[HCO3-] <24 mmol/L. Decreased from titration of nonvolatile anions or loss.
PaCO2: Assess for respiratory compensation or concurrent acidosis.
Base excess: More frequently utilized than the anion gap in the perioperative period; this is because metabolic acidosis is often the result of lactic acidosis secondary to anaerobic metabolism. Aids with determining the extent of the increased acid load, as opposed to aiding in the differential diagnosis.
Anion gap (AG) calculation aids with narrowing the diagnosis: AG = [Na+] - ([Cl-] + [HCO3-]). As mentioned above (1):
Increased AG signifies an accumulation of endogenous or exogenous acids.
Normal or non-anion gap metabolic acidosis reflects the loss of HCO3- anions from the kidneys or GI tract, the inability of the kidneys to excrete excess [H+], or overzealous fluid resuscitation with normal saline (hyperchloremic metabolic acidosis).
Urinary pH: Normally, the urine pH is less than 5. In patients with metabolic acidosis, urine pH becomes more acidic as the kidneys attempt to excrete the acid load.
Plasma glucose: The measurement is necessary to rule out diabetic ketoacidosis, along with urine ketones and glucose.
Hyperkalemia: Acidosis leads to intracellular shifting of hydrogen ions in exchange for potassium. The EKG may reveal peaked T waves, widening of the QRS complex, and reduction in the size of the P wave.
Differential Diagnosis
Respiratory acidosis:
Low pH
Increased PaCO2
Low [HCO3-]
Mixed metabolic and respiratory acidosis: Use Winter's formula as mentioned before.
Treatment⬆⬇
Diabetic ketoacidosis: Fluid and electrolyte replacement and insulin therapy, as well as inciting cause (e.g., infection, myocardial infarction).
Uremia: Dialysis, hemofiltration and renal replacement therapy.
Lactic acidosis: Identify and treat the underlying cause (hypovolemia, hypoxia, hypoperfusion).
Sodium bicarbonate administration: In the acidotic patient, inotropes and vasopressors may have decreased efficacy and hinder therapy aimed at the underlying cause.
NaHCO3 dissociates into a sodium and bicarbonate ion. The bicarbonate ion can bind with hydrogen ion to form H2CO3 which can be converted via carbonic anhydrase to water and carbon dioxide. CO2 can be exhaled via the pulmonary system.
The bicarbonate deficit can be calculated as follows: ([HCO3-]desired - [HCO3-]measured) × 0.6 × body weight in kg). Bicarbonate levels should not be corrected >12 mmol/L in the initial correction to prevent over treatment.
However, its use remains controversial and has not been shown to improve the outcome, even in patients in cardiopulmonary arrest. In addition, hyperosmolarity and hypernatremia can have deleterious effects. An inability to increase minute ventilation can result in a respiratory acidosis.
References⬆⬇
MacielAT, ParkM.Differences in acid–base behavior between intensive care unit survivors and nonsurvivors using both a physicochemical and a standard base excess approach: A prospective, observational study. J Crit Care. 2009;24(4):477–483.
MorrisCG, LowJ.Metabolic acidosis in the critically ill: Part 2. Causes and treatment. Anaesthesia. 2008;63(4):396–411.
MorrisCG, LowJ.Metabolic acidosis in the critically ill: Part 1. Classification and pathophysiology. Anaesthesia. 2008;63(3):294–301.
Additional Reading⬆⬇
See Also (Topic, Algorithm, Electronic Media Element)
Acidosis decreases protein binding of local anesthetics; therefore increasing the free fraction of the drug and its risk of systemic toxicity.
Propofol infusion syndrome should be suspected when metabolic acidosis develops in patients on a propofol infusion, combined with rhabdomyolysis and cardiac failure.