Interpretation of Arterial Blood Gases
First Things First
Step 1: Properly obtaining ABG sample
- Values measured directly: PaCO2, PaO2, pH
- Values calculated: HCO3-
- PaO2 and PaCO2 must be corrected for temperature variations from the 37 degrees of the analyzer. Increased temperature decreases gas solubility and falsely increases the gas tensions. The opposite is true for lowering temperature.
- Sampling syringes should be glass or otherwise capable of limiting diffusion of the gases.
- Added heparin prevents blood from clotting.
- Samples should be free of air bubbles that allow equilibration of gases between the bubble and the blood sample, thereby lowering the measured gas tensions.
- Samples not analyzed immediately should be placed on ice to prevent metabolism of oxygen by platelets and leukocytes present in the blood sample. Room-temperature samples should be analyzed within 15 minutes.
- Iced samples can be analyzed up to an hour after acquisition.
Step 2: Oxygenation and PaO2
- PaO2 is directly measured by a Clark electrode and can be used to assess oxygen exchange through a few relationships.
- Normal PaO2 values = 80-100 mmHg
- Estimated normal PaO2 = 100 mmHg – (0.3) age in years
- Hypoxemia is PaO2 < 50 mmHg
- PaO2/FiO2
- The PaO2 rises with increasing FiO2. Inadequate or decreased oxygen exchange decreases the ratio.
- Normal PaO2/FiO2 is >400 mmHg
- Approximate PaO2 by multiplying FiO2 by 5 (eg, FiO2 = 21%, then PaO2 = 100 mmHg)
- A-a Gradient
- PaO2 is dependent on alveolar oxygen (PAO2), which is influenced by the FiO2, barometric pressure (high altitude), PaCO2 increase (respiratory depression), and the gradient between alveolar and arterial oxygen tension, which can be increased by ventilation and perfusion mismatch.
- A-a = (Pb-PH2O) x FiO2 – (PaCO2/0.8)
- Normal is < 10 mmHg
Step 3: Ventilation and PCO2
- Normal values for PaCO2 are usually 35-45 mmHg. The PaCO2 is directly measured and is used to estimate CO2 exchange.
- VD/VT = PaCO2 – PECO2/PaCO2:
- Normal values for the dead space to tidal volume ratio are 20-40%. As dead space increases, there is less equilibration between arterial and alveolar CO2 tensions and this ratio increases. However, this information is not readily available without sampling the exhaled volume and measuring CO2.
- Ve x PaCO2:
- The product of minute ventilation (Ve) and arterial CO2 can estimate changes in dead space.
- Spontaneous Ventilation: Ve x PaCO2 >200 L/min/mm
- Mechanical Ventilation: Ve x PaCO2 >400/L/min/mm
- The product of minute ventilation (Ve) and arterial CO2 can estimate changes in dead space.
Step 4: Acid–base disorders
- Respiratory disorders are due to hypercarbia or hypocarbia. A shift in the following equation leads to an increase or decrease in the number of hydrogen ions, changing the pH.
- H2O + CO2 < -> H+CO+ < -> [HCO3-] + H+
- Metabolic disorders are related to decreased losses, or increased ingestions or production of acids or bases. Metabolic disorders are reflected by a change in [HCO3-]
Step 4A: pH elevated or decreased
- pH is measured directly using an optical absorbance technique.
- Normal values 7.35-7.45
- Acidemia: pH < 7.35
- Acidosis: processes leading to acidemia
- Alkalemia: pH values >7.45
Step 4B: PaCO2 elevated for respiratory acidosis
- Failure to breathe off CO2 (poor ventilation) leads to acidemia. Compensation for increased CO2 is increased renal reabsorption of bicarbonate.
- pH will decrease 0.08 for every 10 mmHg the PaCO2 increases above 40 mmHg.
- Acute respiratory acidosis: [HCO3-] increases 1 mEq/L for every 10-mmHg rise of PaCO2 above 40 mmHg
- Chronic respiratory acidosis: [HCO3-] increases 4 mEq/L for every 10-mmHg rise of PaCO2 above 40 mmHg
Step 4C: Decreased PaCO2 for respiratory alkalosis
- An increase in ventilation rate or volume decreases CO2 and shifts the above equation to the left, decreasing the concentration of hydrogen ions, and alkalemia. Compensation is achieved by decreased renal bicarbonate absorption.
- pH increases 0.08 for every 10-mmHg decrease in PaCO2 below 40 mmHg.
- Acute respiratory alkalosis: [HCO3-] decreases 2 mEq/l for every 10-mmHg drop in CO2 below 40 mmHg
- Chronic respiratory alkalosis: [HCO3-] decreases 5 mEq/L for every 10-mmHg drop in CO2 below 40 mmHg
Step 4D: Low pH and decreased PaCO2 for metabolic acidosis
- Decreased bicarbonate or excess acid load leads to metabolic acidosis. Compensation for the decrease in pH is achieved by respiratory CO2 elimination, and renal bicarbonate reabsorption. The expected PaCO2 can be derived three ways.
- PaCO2 = last two digits of the pH
- PaCO2 = 15 + [HCO3-]
- PaCO2 = 1.5[HCO3-] + 8 +/- 2
- Anion Gap
- The AG can provide information as to whether the acidosis is due to increased acid accumulation or bicarbonate loss. The AG is attributed to unmeasured anions and cations.
- AG = Na+ - [Cl- + HCO3-]. Normal AG = 3-11 mEq/L
- Plasma proteins provide a major buffering capacity; therefore, hypoalbuminemia can alter the AG, necessitating correction.
- Corrected AG = AG + 2.5(4 - Serum Albumin)
- The AG can provide information as to whether the acidosis is due to increased acid accumulation or bicarbonate loss. The AG is attributed to unmeasured anions and cations.
- High Anion Gap
- An increase of hydrogen ions in the ECF from increased production or decreased renal secretion. Common causes on the differential can be remembered by the mnemonic MUDPILES:
- Methanol, Uremia, Diabetic ketoacidosis (starvation/EtOH ketosis), Paraldehyde, Isoniazid/Iron, Lactic acidosis, Ethylene glycol (antifreeze), Salicylates
- An increase of hydrogen ions in the ECF from increased production or decreased renal secretion. Common causes on the differential can be remembered by the mnemonic MUDPILES:
- Normal Anion Gap
- A normal AG due to acidosis is attributed to bicarbonate loss or the accumulation of hydrogen ions by increased production or ingestion. Bicarbonate can be lost from both renal and extrarenal sources. Chloride is often retained in response to the bicarbonate loss. Normal AG acidosis is also referred to as hyperchloremic metabolic acidosis.
- Differential: large GI losses, type II RTA, dilutional with large volumes of saline
- Low Anion Gap
- Laboratory error is the most common cause, followed by hypoalbuminemia, since albumin constitutes up to 80% of the unmeasured anions. Other causes include halogen (iodine, bromide) intoxication, lithium excess, paraproteinemias, and polymyxin B therapy.
Step 4E: Elevated pH and increased PaCO2 for metabolic alkalosis
- Increases in bicarbonate or hydrogen ion loss define metabolic alkalosis.
- Increased alkali: citrate, acetate, antacids
- Hydrogen ion loss: emesis, aggressive GI suctioning, diuretics, volume depletion
- Compensation occurs with the retention of PaCO2.
- The expected PaCO2 can be derived from:
- PaCO2 = 0.7[HCO3-] + 20 +/- 2
Complications
- n/a
Author
Anna Crawford, MD, and Adebola Adesanya, MD
Last updated: April 28, 2010
Citation
"Interpretation of Arterial Blood Gases." Pocket ICU Management, PocketMedicine.com, Inc, 2010. Anesthesia Central, anesth.unboundmedicine.com/anesthesia/view/Pocket-ICU-Management/534207/all/Interpretation_of_Arterial_Blood_Gases.
Interpretation of Arterial Blood Gases. Pocket ICU Management. PocketMedicine.com, Inc; 2010. https://anesth.unboundmedicine.com/anesthesia/view/Pocket-ICU-Management/534207/all/Interpretation_of_Arterial_Blood_Gases. Accessed December 1, 2024.
Interpretation of Arterial Blood Gases. (2010). In Pocket ICU Management. PocketMedicine.com, Inc. https://anesth.unboundmedicine.com/anesthesia/view/Pocket-ICU-Management/534207/all/Interpretation_of_Arterial_Blood_Gases
Interpretation of Arterial Blood Gases [Internet]. In: Pocket ICU Management. PocketMedicine.com, Inc; 2010. [cited 2024 December 01]. Available from: https://anesth.unboundmedicine.com/anesthesia/view/Pocket-ICU-Management/534207/all/Interpretation_of_Arterial_Blood_Gases.
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