Arterial Blood Gas Interpretation
March 4th, 2023
The arterial blood gas is useful for assessing a patient's oxygenation, and identify acid-base disorders. This section outlines an approach to interpreting ABGs.
While oxygen saturations are a useful non-invasive test for assessing a patient's oxygenation, greater information can be gained by assessing a patient's arterial blood gas.
A venous blood gas is not of use in assessing a patient's oxygen status.
- Normal Ranges
- Arterial partial pressure of oxygen (PaO₂) - 80 - 100mmHg (room air)
- Oxyhaemoglobin (HbO₂) - >90%
Arterial Partial Pressure of Oxygen (PaO₂)
- The PaO₂ is the partial pressure of oxygen dissolved in plasma. This is a marker of the amount of oxygen available to be delivered to tissues.
Normally, the PaO₂ is between 80 - 100mmHg, though this can be less in patients with chronic respiratory disease.
- Hypoxia, suggested by a reduced PaO₂, may occur in the context of many causes that can be roughly broken into four groups:
- Low partial pressure of oxygen - high altitude
- Hypoventilation - drugs, chronic obstructive pulmonary disease, obstructive sleep apnoea, encephalopathy, neuromuscular disease, chest wall abnormalities
- V/Q mismatch - physiological shunt (atelectasis, APO, pneumonia), anatomical (intracardiac) shunt, dead space ventilation (airways disease, PE)
- Decreased diffusion capacity (rare)
- Oxyhaemoglobin (HbO₂) refers to the percentage of haemoglobin that is bound to oxygen. This is the same concept as the peripheral oxygen saturation, and these two measures should be equivalent - if not, then this suggests a sampling error with one of the measurements.
A reduction in the level of haemoglobin saturated by oxygen (reduced oxyhaemoglobin) may be due to any cause of hypoxia.
- If the PaO₂ is normal but the HbO₂ is reduced, , then hypoxia is not the issue at hand. The potential causes for this are:
- Right shift of the oxygen dissociation curve - acidaemia, hyperthermia, high 2,3-DPG
- Carbon monoxide poisoning
- Haemoglobinopathy - methaemoglobinaemia, foetal haemoglobin
This diagram is the oxyhaemoglobin dissociation curve, which describes the relationship between PaO₂ and HbO₂.
At high PaO₂ (e.g. at the alveolar-capillary membranes in the lung), oxygen readily binds to haemoglobin; at low PaO₂ (e.g. at the systemic capillaries), oxygen is readily released from haemoglobin.
As the curve shifts to the left, oxygen will more readily bind to haemoglobin. This may occur in the context of alkalaemia (high pH), hypothermia, or decreased 2,3-DPG.
As the curve shifts to the right, oxygen will more readily be released from haemoglobin. This may occur in the setting of acidaemia (low pH), hyperthermia or increase 2,3-DPG.
Taking the FiO2 into Account
- The PaO₂ on an arterial blood is only relevant for assessing for hypoxia when the patient is on room air. If they are receiving supplemental oxygen this will artificially increase the PaO₂ which may appear normal.
PF Ratio =
The PF ratio is an assessment of PaO2₂ taking into account the FiO₂ - correcting for this discrepancy. If the PaO₂ divided by the FiO₂ is <400, then this suggests that the patient's oxygenation is insufficient despite the oxygen they are recieving.
The A-a Gradient
- The alveolar-arterial gradient is a comparison of the partial pressure of O₂ in the alveoli and in arterial blood. The alveolar O₂ partial pressure (PAO₂) is calculated using the following simplified equation:
A-a gradient = ( FiO₂ x 713 ) -
To see how and why this equation is simplified, read more about the A-a gradient.
- An elevated A-a gradient indicates that the partial pressure of O₂ is higher in the alveoli than in arterial blood, indicating a V/Q mismatch. This may occur due to:
- Dead space ventilation - pneumonia, asthma, COPD, pulmonary embolismVentilation without perfusion
- Left to right shunt - pulmonary oedema, ARDS, pneumoniaPerfusion without ventilation
- Alveolar hypoventilation - pulmonary fibrosis, interstitial lung disease
The second major role of the arterial blood gas is to assess a patient's acid-base balance.
- Normal Ranges
- pH - 7.35 - 7.45
- Bicarbonate (HCO₃) - 22 - 26
- Base Excess - -2 to +2
- Arterial partial pressure of CO₂ (PaCO₂) - 36 - 44
In understanding why the bicarbonate and PaCO₂ are important for assessing acid-base balance, remember the following equilibrium:
H⁺ + HCO₃⁻⇄ H₂CO₃ ⇄ H₂O + CO₂
Bicarbonate is the metabolic component, and is cleared by the kidneys; CO₂ is the respiratory component, and is cleared by the lungs.
- The first step is to assess the patient's pH. This is a measure of the acidity of alkalinity of the blood, based on an inverse log of the hydrogen ion concentration.
A reduced pH is referred to as acidaemia, while an increased pH is an alkalaemia - remember that acidosis and alkalosis are processes, not measurements, and cannot be identified based on pH alone.
Bicarbonate is one of the major alkali present in the blood, and plays a crucial role in acid-base balance through renal metabolism. Significant derangement suggests the presence of a metabolic process:
- An elevated bicarbonate suggests a metabolic alkalosis (primary process) or metabolic compensation for respiratory acidosis (secondary process).
- A reduced bicarbonate suggests a metabolic acidosis (primary process) or metabolic compensation for respiratory alkalosis (secondary process)
Base Excess (BE)
- The bicarbonate level is significantly influenced by acid-base buffering system, and can by affected by the presence of a respiratory process. The base excess is an indicator of a metabolic process that is independent of this buffering system.
A base excess of greater than +2 suggests the presence of a metabolic alkalosis, while a base excess of less than -2 suggests a metabolic acidosis.
Arterial Partial Pressure of CO₂ (PaCO₂)The PaCO₂ is the arterial partial pressure of carbon dioxide. An increase or decrease in the PaCO₂ level suggests the presence of a respiratory process causing an acid-base imbalance:
- An elevated PaCO₂ suggests a respiratory acidosis (primary process) or respiratory compensation of metabolic alkalosis (secondary process).
- A reduced PaCO₂ suggests a respiratory alkalosis (primary process) or respiratory compensation of metabolic acidosis (secondary process).
The Anion Gap
- The anion gap is used to further assess someone with a metabolic acidosis. It is a calculation of the unmeasured anions and cations in the blood, based on anions and cations that we can measure (sodium, chloride and bicarbonate).
Anion Gap = Na⁺ - ( Cl⁻ + HCO₃⁻ )
The normal range of the anion gap is 8 - 16.
A normal anion gap metabolic acidosis (NAGMA) suggests that loss of bicarbonate is ocurring, either due from the gastrointestinal tract (e.g. diarrhoea) or kidneys (e.g. Addison's, renal tubular acidosis, acetazolamide).
A high anion gap metabolic acidosis (HAGMA) suggests that there is an excess of acid within the blood - this may be lactate (lactic acidosis), ketones (diabetic, alcoholic or starvation ketoacidosis), nitrogenous wastes (uraemia) or exogenous acids like methanol, ethanol, salicylates or carbon monoxide.
The Gap-Gap Ratio
- The gap-gap ratio is used to further assess patients with a high anion gap metabolic acidosis (HAGMA).
The calculation essentially checks whether the change in anion gap from normal is equivalent to the change in the bicarbonate from normal - i.e. that all of the bicarbonate change is accounted for by a high anion gap process.
Gap-gap ratio =
anion gap - 12 24 - HCO₃
- If a HAGMA is the only process present, then the value will be 1 (unity).
- If there is a concomitant HAGMA and a NAGMA present, then the value will be <1.
- If there is both a metabolic acidosis and a metabolic alkalosis present, then the value will be >1.
Serum lactate is an important marker of prognosis and resolution in many critical illnesses. It is produced via pyruvate metabolism under both anaerobic and aerobic glycolytic conditions, and is mainly metabolised by the liver.
- An elevated serum lactate reflects an imbalance between production and clearance of lactate. Accumulation of lactate is associated with acidosis; lactic acidosis is a high anion gap metabolic acidosis.
Anaerobic lactate buildup occurs in the context of excess lactate production without sufficient oxygen delivery; aerobic lactate buildup occurs when there is shunting of pyruvate into lactate despite adequate oxygen delivery (e.g. due to β2 stimulation or pyruvate dehydrogenase deficiency).
The causes of hyperlactataemia may be broken into four major groups, as detailed below:
- AReduced tissue oxygen delivery - heavy exertion, shock, localised ischaemia, severe hypoxia
- B1Underlying disease - fulminant liver failure, endogenous β2 (stress, shock), impaired pyruvate dehydrogenase activity (sepsis), certain cancers
- B2Drugs / toxins - metformin (in renal failure), endogenous β2 (adrenaline, salbutamol), NRTIs, linezolid, cyanide
- B3Inborn errors of metabolism - e.g. pyruvate dehydrogenase deficiency
D-lactate is an isomer of lactate produced by bacteria that is not measured by conventional lactate testing.
Want more info like this?
- Your electronic clinical medicine handbook
- Guides to help pass your exams
- Tools every medical student needs
- Quick diagrams to have the answers, fast
- Quizzes to test your knowledge
Andersen L, Mackenhauer J, Roberts J, Berg K, Cocchi M, Donnino M. Etiology and Therapeutic Approach to Elevated Lactate Levels. Mayo Clin Proc. 2013;88:1127-1140.
Beasley R, McNaughton A, Robinson G. New look at the oxyhaemoglobin dissociation curve. The Lancet. 2006;367:1124-1126.Bellomo R. Bench-to-bedside review: lactate and the kidney. Critical Care 2002;6(4):1.Berend K, de Vries A, Gans R. Physiological Approach to Assessment of Acid-Base Disturbances. N Engl J Med. 2014;371:1434-1445.Brenner BE. Alveolar-arterial oxygen gradients. Ann Emerg Med. 1980;9:648-648.Brindley PG, Butler MS, Cembrowski G, Brindley DN. Falsely elevated point-of-care lactate measurement after ingestion of ethylene glycol. Canadian Medical Association Journal 2007;176(8):1097-9.Donnino MW, Carney E, Cocchi MN, Barbash I, et al. Thiamine deficiency in critically ill patients with sepsis. Journal of critical care 2010;25(4):576-81.Gore DC, Jahoor F, Hibbert JM, DeMaria EJ. Lactic acidosis during sepsis is related to increased pyruvate production, not deficits in tissue oxygen availability. Annals of surgery 1996;224(1):97.Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2014; 371: 2309-2319.Levraut J, Ciebiera JP, Chave S, Rabary O, et al. Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than overproduction. Am J RespirCrit Care Med. 1998; 157(4 Pt 1):1021-6.Levy B, Gibot S, Franck P, Cravoisy A, et al. Relation between muscle Na+ K+ ATPase activity and raised lactate concentrations in septic shock: a prospective study. The Lancet 2005;365(9462):871-5.Marino PL. Marino's the ICU Book. Fourthition. ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2014.McCarter FD, Nierman SR, James JH, Wang L, et al. Role of skeletal muscle Na+–K+ ATPase activity in increased lactate production in sub–acute sepsis. Life sciences 2002;70(16):1875-88.Moreau R, Hadengue A, Soupison T, Kirstetter P, et al. Septic shock in patients with cirrhosis: hemodynamic and metabolic characteristics and intensive care unit outcome. Critical care medicine 1992;20(6):746.Perriello G, Jorde R, Nurjhan N, Stumvoll M, et al. Estimation of glucose-alanine-lactate-glutamine cycles in postabsorptive humans: role of skeletal muscle. American Journal of Physiology-Endocrinology and Metabolism 1995;269(3):E443-50.Phypers B, Pierce JT. Lactate physiology in health and disease. Continuing education in Anaesthesia, critical care & pain. 2006 Jun 1;6(3):128-32.Stacpoole PW. Lactic acidosis. Endocrinol Metab Clin North Am 1993 Jun; 22(2) 221-45.
Tunney P, Chinnan NK. Serum Lactate in Intensive Care: Practical Points and Pitfalls. inflammation. 2016;6:7.Vary TC. Sepsis-induced alterations in pyruvate dehydrogenase complex activity in rat skeletal muscle: effects on plasma lactate. Shock 1996;6(2):89-94.Venkatesh B, Morgan T, Garrett P. Measuring the lactate gap. The Lancet 2001;358(9295):1806.