- Clinical science
Acid-base disorders are a group of conditions characterized by changes in the concentration of hydrogen ions (H+) or bicarbonate (HCO3-), which lead to changes in the arterial blood pH. These conditions can be categorized as acidoses or alkaloses and have a respiratory or metabolic origin, depending on the cause of the imbalance. Diagnosis is made by arterial blood gas (ABG) interpretation. In the setting of metabolic acidosis, calculation of the anion gap is an important resource to narrow down the possible causes and reach a precise diagnosis. Treatment is based on identifying the underlying cause.
|Respiratory acidosis||Respiratory alkalosis||Metabolic acidosis||Metabolic alkalosis|
|PCO2||↑||↓||↓ (compensation)||↑ (compensation)|
|HCO3-||↑ (compensation)||↓ (compensation)||↓||↑|
|Mechanism|| || || |
|Common causes|| || |
pH and pCO2 are the most important lab values to assess the acid-base status in any patient.
- pH: A logarithmic scale that expresses the acidity or alkalinity of a solution based on the concentration of hydrogen ions (pH = -log[H+]). The neutral value of pH is 7, with lower values being acidic and higher values being basic.
- The Henderson-Hasselbalch equation allows for calculation of HCO3- from pH and pCO2; : pH = 6.1 + log ([HCO3-] / 0.03 x pCO2)
Start with an and then proceed in the following order
- Evaluate blood pH
- Evaluate pCO2 (partial pressure of carbon dioxide in blood, reference range: 33–45 mm Hg) to determine whether the primary is respiratory or metabolic
- pH and pCO2 change in the opposite direction → respiratory disorder
- pCO2 and pH change in the same direction → metabolic disorder
- Suspect a mixed acid-base disorder if
- Evaluate HCO3- (Reference range: 22–28 mEq/L)
- Evaluate pO2
- Definition: physiological changes that occur in acid-base disorders in an attempt to maintain normal body pH
- Compensatory changes
|Primary disorder||Compensatory process||Expected compensation*|
|Metabolic alkalosis|| |
|Respiratory acidosis||Acute compensation|| || |
|Chronic compensation|| |
|Respiratory alkalosis||Acute compensation|| || |
|Chronic compensation|| |
|*If the expected compensation does not occur, a secondary acid-base disturbance will be present in addition to the primary disorder|
- Definition: difference between the concentration of unmeasured anions and the concentration of unmeasured cations
Anion gap = [Unmeasured cations] - [Unmeasured anions]
- [Unmeasured cations] = [Total cations] - [Routinely measured cations]
- [Unmeasured anions] = [Total anions] - [Routinely measured anions]
- Since [Total cations] ≈ [Total anions] to maintain electrical neutrality, the formula can be rewritten as Anion gap = [Routinely measured cations] – [Routinely measured anions]
- If potassium concentration is normal, anion gap ≈ [Na+] - ([Cl-] + [HCO3-]) (Reference range: 6–12 mmol/L)
- In European countries, calculation of the anion gap usually also accounts for potassium, in which case the anion gap = ([Na+] + [K+]) - ([Cl-] + [HCO3-]) (Reference range: 10–16 mmol/L)
- In certain conditions (see “” below), the unmeasured anions increase → ↑ anion gap
- Anion gap = [Unmeasured cations] - [Unmeasured anions]
Normal anion gap metabolic acidosis (also known as hyperchloremic acidosis)
- Primary loss of HCO3- compensated with ↑ Cl- → unchanged anion gap
- Further evaluation: measure urine anion gap = [Urine Na+] + [urine K+] - [urine Cl-]
High anion gap metabolic acidosis
- Increased concentration of organic acids such as lactate, ketoacids (beta-hydroxybutyrate, acetoacetate), oxalic acid, formic acid, or glycolic acid; → no compensatory increase of Cl- → ↑ anion gap
- Normal anion gap metabolic acidosis (also known as hyperchloremic acidosis)
Causes of high anion gap acidosis (MUDPILES): M – methanol intoxication, U – uremia, D – diabetic ketoacidosis, P – paraldehyde, I – isoniazid or iron overdose, inborn error of metabolism, L – lactic acidosis, E – ethylene glycol intoxication, S – salicylate intoxication
Causes of normal anion gap acidosis (FUSEDCARS): F – Fistula (biliary, pancreatic), U – ureterogastric conduit, S – saline administration, E – endocrine (Addison's disease, hyper-PTH), D – diarrhea, C – carbonic anhydrase inhibitor, A – ammonium chloride, R – renal tubular acidosis, S – spironolactone
A neGUTive urine anion gap implies GI loss of bicarbonate.
Treatment of acid-base disorders should always address the underlying cause. Some steps in urgent management are listed below.
- Respiratory acidosis: treat underlying cause; (see “Treatment” of , , )
- Respiratory alkalosis: treat underlying cause; in the event of hyperventilation syndrome; , patients benefit from reassurance and rebreathing into a paper bag.
- Acute severe metabolic acidosis (pH < 7.1): intravenous sodium bicarbonate
- Chronic metabolic acidosis: oral sodium bicarbonate along with treatment of the underlying cause (e.g., diarrhea, renal tubular acidosis)
- Electrolyte disturbances: correct (e.g., see “Treatment” in hyperkalemia).
- See individual articles for the management of , .
- Metabolic alkalosis