Reference ranges of serum bicarbonate vary by age in both males and females.
In males, ranges are as follows:
Age 12-24 months: 17-25 mmol/L
Age 3 years: 18-26 mmol/L
Age 4-5 years: 19-27 mmol/L
Age 6-7 years: 20-28 mmol/L
Age 8-17 years: 21-29 mmol/L
Age 18 years or older: 22-29 mmol/L
In females, ranges are as follows:
Age 1-3 years: 18-25 mmol/L
Age 4-5 years: 19-26 mmol/L
Age 6-7 years: 20-27 mmol/L
Age 8-9 years: 21-28 mmol/L
Age 10 years or older: 22-29 mmol/L
Arterial blood pH
The reference range of the pH of arterial blood is 7.35-7.45.
Arterial blood partial pressure of carbon dioxide
The reference range of the partial pressure of carbon dioxide (pCO2) of arterial blood is 35-45 mm Hg.
A 3-step approach is used to assess the acid-base disorder: (1) establishment of a primary disturbance, (2) determination of the serum anion gap, and (3) evaluation of compensation.
Establishment of primary disturbance
The pH, obtained from arterial blood gas (ABG), should be the first value analyzed upon suspicion of an acid-base disorder. A low blood pH is referred to as an acidemia; acidemia results when an acid-generating process, known as an acidosis, creates an excess of H+ ions. Similarly, an alkalemia refers to elevated blood pH when an alkalosis is present.
The changes in pH, bicarbonate (HCO3-), and carbon dioxide (CO2) expected to be seen in the primary processes are as follows:
Metabolic acidosis: Decreased pH, decreased HCO 3 -
Metabolic alkalosis: Increased pH, increased HCO 3 -
Respiratory acidosis: Decreased pH, increased CO 2
Respiratory alkalosis: Increased pH, decreased CO 2
Serum anion gap determination
When a metabolic acidosis is found, the anion gap should be calculated. The anion gap represents the "unmeasured" anions in the blood, which are formed from organic acids that have dissociated in blood. Unmeasured refers to the fact that these anions are not reported in a standard metabolic panel or ABG but are contributing to the acidosis.
Serum anion gap = Na - (Cl + HCO3)
Some clinicians may also include the serum potassium value in the formula, during which the normal range increases by approximately 4 mEq/L, as follows:
Serum anion gap = (Na + K) - (Cl + HCO3)
The newer autoanalyzers measure a higher serum chloride concentration, which lowers the normal range of the anion gap to 3-9 mEq/L (previously 7-13 mEq/L). Because these machines are not yet universal, it is essential to interpret individual results in the context of the laboratory’s reference range.
Evaluation of compensation
The degree of compensation should be assessed to see if the patient is responding appropriately to their altered pH.
Metabolic acidosis is divided into anion gap metabolic acidosis and non–anion gap metabolic acidosis; these two categories have different etiologies and treatments.
In patients with metabolic acidosis, it is important to determine if respiratory compensation is adequate or if the patient has a concurrent respiratory acidosis or alkalosis. Winter formula is used to determine if the change in PCO2 is appropriate.
Winter formula: Expected pCO2 = 1.5 (HCO3 -) + 8 ± 2
If a patient’s pCO2 is higher than the range expected from Winter formula, a concomitant respiratory acidosis is present. If a patient’s pCO2 is lower than expected, a respiratory alkalosis is also present.
Metabolic alkalosis most commonly results from either diuretic use or gastrointestinal losses, such as in vomiting. If the etiology of the alkalosis is unclear from the examination, a urinary chloride concentration may be measured. Gastrointestinal losses are noted to have low urinary chloride levels (< 20 mEq/L), while patients currently on diuretic therapy present with high urinary chloride levels (>20 mEq/L). A complete list of differential diagnoses and workup may be found at metabolic alkalosis .
Respiratory acidosis and respiratory alkalosis can be assessed further to determine if the condition is acute or chronic; chronic changes in CO2 allow the renal compensatory mechanism more time to adjust bicarbonate and pH accordingly.
Table 1. Indicators of Chronic and Acute Respiratory Acidosis and Respiratory Alkalosis (Open Table in a new window)
|For every ↑ 10 mm Hg CO2||↑ 4 mmol/l HCO3-||↑ 1 mmol/l HCO3-|
|For every ↓ 10 mm Hg CO2||↓ 4 mmol/l HCO3-||↓ 2 mmol/l HCO3-|
Table 2. Compensatory Acid-Base Disorders Characterized by Changes in pH, HCO3-, and CO2 (Open Table in a new window)
|Primary Disturbance||Compensatory Change||pH||HCO3-||CO2|
|Metabolic acidosis||Respiratory alkalosis||Decreased||Decreased|
|Metabolic alkalosis||Respiratory acidosis||Increased||Increased|
|Respiratory acidosis||Metabolic alkalosis||Decreased||Increased|
|Respiratory alkalosis||Metabolic acidosis||Increased||Decreased|
Compensatory changes do not entirely correct the primary acid-base disorder. If an individual has a primary acidosis, his or her compensatory mechanism will not normalize the pH.
An additional acid-base disorder (ie, a mixed acid-base disorder is present) is suggested by the presence of inappropriate compensation. A normal pH in the setting of abnormal bicarbonate and CO2 levels suggests a mixed acid-base disorder.
The changes in pH in mixed acid-base disturbances are as follows:
Metabolic acidosis: Normal or significantly decreased pH
Metabolic alkalosis: Normal or significantly increased pH
Respiratory acidosis: Normal or significantly decreased pH
Respiratory alkalosis: Normal or significantly increased pH
The mixed disorders include combinations of metabolic disorders, such as vomiting-induced metabolic alkalosis with hypovolemia-induced lactic acidosis; combinations of respiratory disorders, such as COPD related respiratory acidosis with simultaneous opioid-induced hypoventilation; or mixed metabolic and respiratory disorders, such as metabolic acidosis and respiratory alkalosis in salicylate intoxication, among numerous others.
Frequently, the patient’s clinical presentation suggests the cause of the disturbance, and other laboratory values (eg, urine drug screen, serum metabolic panel, serum osmolarity) are used to guide interpretation of the acid-base disturbance.
Collection and Panels
Specimen type: Serum
Specimen volume: 0.5 mL, minimum volume 0.25 mL
Container/tube: Serum gel preferred, red-top tube (pictured below) acceptable
Patient information: Patient sex and age are required
Reject of the specimen in cases of gross hemolysis or bacterial contamination.
Specimen stability: Serum can be refrigerated for a maximum of 24 hours
Arterial blood gas
Prior to performing radial artery cannulation for blood gas determination, a modified Allen test should be performed to ensure adequate perfusion by the ulnar artery.
The use of nonsterile gloves is acceptable, but the puncture site should not be touched after the area is cleaned.
The sample is collected using a standard syringe with a 25-gauge needle and a 3-mL capacity. A higher-capacity syringe may be difficult to maneuver, and smaller needles can possibly increase the risk of traumatic hemolysis, which would decrease the accuracy of the hemoglobin and potassium values.
Aspirate 1-2 mL (1000 U/mL) of heparin into the syringe through the needle, and then push it out; leave the plunger depressed to allow arterial blood flow to fill the syringe.
Alternatively, a prefilled heparinized syringe with a protective needle sleeve and a syringe cap are provided with some ABG kits. The sleeve, while still attached to the syringe, locks the needle within itself to prevent direct contact between the operator and needle. A vented plunger is available with some syringe models, which allows the operator to preset a specific amount of blood to be drawn. The plunger is placed at the midway point of the syringe but is not pulled back while the puncture is performed. Prior to the procedure, the prefilled heparin is expelled and the vented plunger is then repositioned at the 2-mL mark.
The ABG syringe kit contains the following:
Antiseptic skin solution - Commonly used solutions are chlorhexidine and povidone-iodine
Syringe cap (usually included in the ABG syringe kit)
Sterile gauze (2 X 2-inch)
Bag with ice
Local anesthesia with epinephrine-free lidocaine may be used for patient comfort.
Maintenance of the acid-base balance is a coordinated effort by the kidneys and lungs. Combined, these organs excrete approximately 15,000 mmol of CO2 and 50-100 mEq of nonvolatile acid daily. Considerably more CO2 is excreted with exercise. Additionally, CO2 can combine with water via carbonic anhydrase to produce carbonic acid and ultimately bicarbonate. The nonvolatile acid excreted in greatest quantity is sulfuric acid, produced from the metabolism of sulfur-containing amino acids.
The kidney excretes acid by combining hydrogen ions with urinary buffers to form titratable acids, mainly phosphate (HPO42- + H+ → H2 PO4-), or with ammonia to form ammonium (NH3 + H+ → NH4+).  When the kidney must excrete excessive amounts of acid, the major adaptive response is increased ammonium production and secretion.
The following formula is used to evaluate acid-base status by measuring the components of the HCO3- –carbon dioxide buffer system in blood:
Dissolved CO2 + H2 O ↔ H2 CO3 ↔ HCO3- + H+
Most commonly, specific electrodes are used to measure both the pCO2 and the pH. Then, the Henderson-Hasselbalch equation, in which pCO2 is measured in mm Hg and HCO3- is measured in mEq/L, is used to calculate the serum HCO3- concentration, as follows:
pH = 6.10 + log ([HCO3-]/[0.03 x pCO2])
In the Henderson-Hasselbalch equation above, the pH is equal to (-log [H+]); 6.10 is the negative log of Ka (-log Ka), which is the dissociation constant for the reaction; 0.03 is the solubility coefficient for CO2 in blood; and the pCO2 is the partial pressure of CO2 in blood.
Acid-base interpretation is used to assess the 4 primary acid-base disorders, which include the following:
Diagnostic evaluation of an acid-base disturbance is not confirmed based solely on the serum HCO3; ABG evaluation for pH and pCO2 also are required. For example, low bicarbonate levels can represent metabolic acidosis or the renal compensation to respiratory alkalosis. High values can represent metabolic alkalosis or the renal compensation to respiratory acidosis.
In hypoalbuminemia, the anion gap decreases by approximately 2.30-2.5 mEq/L for every 1 g/dL reduction in serum albumin concentration from normal (4 g/dl). Patients with low albumin may have deceptively normal uncorrected anion gaps. In hyperalbuminemia, the opposite is true.