Blood gas analysis is a commonly used diagnostic tool to evaluate the partial pressures of gas in blood and acid-base content. Understanding and use of blood gas analysis enable providers to interpret respiratory, circulatory, and metabolic disorders. 
A "blood gas analysis" can be performed on blood obtained from anywhere in the circulatory system (artery, vein, or capillary). An arterial blood gas (ABG) tests explicitly blood taken from an artery. ABG analysis assesses a patient's partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2). PaO2 provides information on the oxygenation status, and PaCO2 offers information on the ventilation status (chronic or acute respiratory failure). PaCO2 is affected by hyperventilation (rapid or deep breathing), hypoventilation (slow or shallow breathing), and acid-base status. Although oxygenation and ventilation can be assessed non-invasively via pulse oximetry and end-tidal carbon dioxide monitoring, respectively, ABG analysis is the standard.
When assessing the acid-base balance, most ABG analyzers measure the pH and PaCO2 directly. A derivative of the Hasselbach equation calculates the serum bicarbonate (HCO3) and base deficit or excess. This calculation frequently results in a discrepancy from the measured due to the blood CO2 unaccounted for by the equation. The measured HCO3 uses a strong alkali that liberates all CO2 in serum, including dissolved CO2, carbamino compounds, and carbonic acid. The calculation only accounts for dissolved CO2; this measurement using a standard chemistry analysis will likely be called a "total CO2". For that reason, the difference will amount to around 1.2 mmol/L. However, a larger difference may be seen on the ABG, compared to the measured value, especially in critically ill patients. 
The calculation has been disputed as both accurate and inaccurate based on the study, machine, or calibration used and must be interpreted appropriately based on your institutional standards.
Arterial blood gases are frequently ordered by emergency medicine, intensivist, anesthesiology, and pulmonology clinicians but may also be needed in other clinical settings. Many diseases are evaluated using an ABG, including acute respiratory distress syndrome (ARDS), severe sepsis, septic shock, hypovolemic shock, diabetic ketoacidosis, renal tubular acidosis, acute respiratory failure, heart failure, cardiac arrest, asthma, and inborn errors of metabolism.
By obtaining an ABG and analyzing the pH, partial pressures, comparing it to measured serum bicarbonate in a sick patient, multiple pathological conditions can be diagnosed. The alveolar-arterial oxygen gradient is a useful measure of lung gas exchange, which can be abnormal in patients with a ventilation-perfusion mismatch.
Specimen Requirements and Procedure
Whole blood is the required specimen for an arterial blood gas sample. The specimen is obtained through an arterial puncture or acquired from an indwelling arterial catheter. A description of these procedures is beyond the scope of this article; please refer to the StatPearls article “arterial lines” and other references for more information. Once obtained, the arterial blood sample should be placed on ice and analyzed as soon as possible to reduce the possibility of erroneous results. Automated blood gas analyzers are commonly used to analyze blood gas samples, and results are obtained within 10 to 15 minutes. Automated blood gas analyzers, directly and indirectly, measure specific components of the arterial blood gas sample (see above).
pH = measured acid-base balance of the blood
PaO2 = measured the partial pressure of oxygen in arterial blood
PaCO2 = measured the partial pressure of carbon dioxide in arterial blood
HCO3 = calculated concentration of bicarbonate in arterial blood
Base excess/deficit = calculated relative excess or deficit of base in arterial blood
SaO2 = calculated arterial oxygen saturation unless a co-oximetry is obtained, in which case it is measured
A modified Allen test is a must before an ABG is drawn from either of the upper extremities to check for adequate collateral flow. Alternatively, pulse oximetry and duplex ultrasound can be used too. The arterial site commonly used is the radial artery, as it is superficial and easily palpable over the radial styloid process. The next most common site is the femoral artery. The test is performed on the unilateral upper extremity chosen for the procedure (Please look at the attached image for graphical illustration). The selected upper extremity is flexed at the elbow, and the patient requested to clench the raised fist for 30 seconds. Then pressure is applied over the ulnar and radial arteries with the intent to occlude the blood flow. After five seconds, unclench the raised fist. The palm will now appear pale, white, or blanched. Then pressure over the ulnar artery is released while the radial artery compression is maintained. In 10 to 15 seconds, the palm returns to its original color, indicating adequate Ulnar collateral blood flow. If the palm does not return to its actual color, it is an abnormal test and unsafe to puncture the radial artery. Similarly, the radial collateral blood flow is assessed by maintaining ulnar artery pressure and releasing the radial artery pressure. 
Results, Reporting, and Critical Findings
An acceptable normal range of ABG values of ABG components are the following, noting that the range of normal values may vary among laboratories and in different age groups from neonates to geriatrics:
PaO2 (75-100 mmHg)
PaCO2 (35-45 mmHg)
HCO3 (22-26 meq/L)
Base excess/deficit (-4 to +2)
Arterial blood gas interpretation is best approached systematically. Interpretation leads to an understanding of the degree or severity of abnormalities, whether the abnormalities are acute or chronic, and if the primary disorder is metabolic or respiratory in origin. Several articles have described simplistic ways to interpret ABG results. However, the Romanski method of analysis is most simplistic for all levels of providers. This method helps determine the presence of an acid-base disorder, its primary cause, and whether compensation is present.
The first step is to look at the pH and assess for the presence of acidemia (pH < 7.35) or alkalemia (pH > 7.45). If the pH is in the normal range (7.35-7.45), use a pH of 7.40 as a cutoff point. In other words, a pH of 7.37 would be categorized as acidosis, and a pH of 7.42 would be categorized as alkalemia. Next, evaluate the respiratory and metabolic components of the ABG results, the PaCO2 and HCO3, respectively. The PaCO2 indicates whether the acidosis or alkalemia is primarily from a respiratory or metabolic acidosis/alkalosis. PaCO2 > 40 with a pH < 7.4 indicates a respiratory acidosis, while PaCO2 < 40 and pH > 7.4 indicates a respiratory alkalosis (but is often from hyperventilation from anxiety or compensation for a metabolic acidosis). Next, assess for evidence of compensation for the primary acidosis or alkalosis by looking for the value (PaCO2 or HCO3) that is not consistent with the pH. Lastly, assess the PaO2 for any abnormalities in oxygenation.
Example 1: ABG : pH = 7.39, PaCO2 = 51 mm Hg, PaO2 = 59 mm Hg, HCO3 = 30 mEq/L and SaO2 = 90%, on room air.
pH is in the normal range, so use 7.40 as a cutoff point, in which case it is <7.40, acidosis is present.
The PaCO2 is elevated, indicating respiratory acidosis, and the HCO3 is elevated, indicating a metabolic alkalosis.
The value consistent with the pH is the PaCO2. Therefore, this is a primary respiratory acidosis. The acid-base that is inconsistent with the pH is the HCO3, as it is elevated, indicating a metabolic alkalosis, so there is compensation signifying a non-acute primary disorder because it takes days for metabolic compensation to be effective.
Last, the PaO2 is decreased, indicating an abnormality with oxygenation. However, a history and physical will help delineate the severity and urgency of required interventions, if any.
Example 2: ABG : pH = 7.45, PaCO2 = 32 mm Hg, PaO2 = 138 mm Hg, HCO3 = 23 mEq/L, the base deficit = 1 mEq/L, and SaO2 is 92%, on room air.
pH is in the normal range. Using 7.40 as a cutoff point, it is >7.40, so alkalemia is present.
The PaCO2 is decreased, indicating a respiratory alkalosis, and the HCO3 is normal but on the low end of normal.
The value consistent with the pH is the PaCO2. Therefore, this is a primary respiratory alkalosis. The HCO3 is in the range of normal and, thus, not inconsistent with the pH, so there is a lack of compensation.
Last, the PaO2 is within the normal range, so there is no abnormality in oxygenation.
When evaluating a patient's acid-base status, it is important to include an electrolyte imbalance or anion gap in your synthesis of the information. For example: In a patient who presents with Diabetic Ketoacidosis, they will eliminate ketones, close the anion gap but have persistent metabolic acidosis due to hyperchloremia. This is due to the strong ionic effect, which is beyond the scope of this article.
Arterial blood gas monitoring is the standard for assessing a patient’s oxygenation, ventilation, and acid-base status. Although ABG monitoring has been replaced mainly by non-invasive monitoring, it is still useful in confirming and calibrating non-invasive monitoring techniques.
In the intensive care unit (ICU) and emergency room settings, evaluation of oxygenation is frequently done in the context of severe sepsis, acute respiratory failure, and ARDS. Calculating an alveolar-arterial (A-a) oxygen gradient can aid in narrowing down the hypoxemia cause. For example, a gradient's presence or absence can help determine whether the abnormality in oxygenation is potentially due to hypoventilation, a shunt, V/Q mismatch, or impaired diffusion. The equation for the expected A-a gradient assumes the patient is breathing room air; therefore, the A-a gradient is less accurate at higher percentages of inspired oxygen. Determining the intrapulmonary shunt fraction, the fraction of cardiac output flowing through pulmonary units that do not contribute to gas exchange is the best estimate of oxygenation status. Calculating the shunt fraction is traditionally done at a delivered FiO2 of 1.0, but if performed at a FiO2 lower than 1.0, then venous admixture would be the more appropriate term. For simplicity, assessing oxygenation is more commonly performed by computing the ratio of PaO2 and fraction of inspired oxygen (PaO2/FiO2 or P/F ratio). However, there are limitations in using the P/F ratio in assessing oxygenation, as the discrepancy between venous admixture and the P/F ratio at a given shunt fraction depends on the delivered FiO2. For research purposes, the P/F ratio has also been used to categorize disease severity in ARDS.
Another parameter commonly used in ICUs to assess oxygenation is the oxygenation index (OI). This index is considered a better indicator of lung injury, particularly in the neonatal and pediatric population, compared to the P/F ratio. It includes the level of invasive ventilatory support required to maintain oxygenation. The OI is the product of the mean airway pressure (Paw) in cm H2O, as measured by the ventilator, and the FiO2 as the percentage divided by the PaO2. The OI is commonly used to guide management, such as initiating inhaled nitric oxide, administering surfactant, and defining the potential need for extracorporeal membrane oxygenation.
The presence of a normal PaO2 value does not rule out respiratory failure, particularly in the presence of supplemental oxygen. The PaCO2 reflects pulmonary ventilation and cellular CO2 production. It is a more sensitive marker of ventilatory failure than PaO2, particularly in the presence of supplemental oxygen, as it has a close relationship with the depth and rate of breathing. Calculation of the pulmonary dead space is a good indicator of overall lung function. Pulmonary dead space is the difference between the PaCO2 and mixed expired PCO2 (physiological dead space) or the end-tidal PCO2 divided by the PaCO2. Pulmonary dead space increases when the pulmonary units' ventilation increases relative to their perfusion and when shunting increases. Hence, pulmonary dead space is an excellent bedside indicator of lung function and one of the best prognostic factors in ARDS patients. The pulmonary dead space fraction may also help diagnose other conditions such as pulmonary embolism.
Acid-base balance can be affected by the aforementioned respiratory system abnormalities. For instance, acute respiratory acidosis and alkalemia result in acidemia and alkalemia, respectively. Additionally, hypoxemic hypoxia leads to anaerobic metabolism, which causes metabolic acidosis that results in acidemia. Metabolic system abnormalities also affect acid-balance as acute metabolic acidosis and alkalosis result in acidemia and alkalemia, respectively. Metabolic acidosis is seen in patients with diabetic ketoacidosis, septic shock, renal failure, drug or toxin ingestion, and gastrointestinal or renal HCO3 loss. Metabolic alkalosis is caused by conditions such as kidney disease, electrolyte imbalances, prolonged vomiting, hypovolemia, diuretic use, and hypokalemia.
Quality Control and Lab Safety
An arterial blood gas can be analyzed as a point-of-care test, along with electrolytes (often called a Shock panel). It is essential that these machines are calibrated/standardized appropriately to ensure accurate and precise readings for clinical decisions. Please refer to the appropriate user manuals to ensure the appropriate device calibration at all times in discussion with the clinical laboratory team.
Enhancing Healthcare Team Outcomes
ABG is recommended for evaluating a patient’s ventilatory, acid-base, and oxygenation status. [Level 1A] Blood gas analysis is also recommended to evaluate a patient’s response to therapeutic interventions. [Level 2B] and for monitoring the severity and progression of documented cardiopulmonary disease processes. [Level 1A] Despite its clinical value, erroneous or discrepant values represent a potential drawback of blood gas analysis, so eliminating potential sources of error is paramount. Therefore, attention to detail in the sampling technique and processing is essential.
Rigorous quality control of the automated blood gas analyzers is also necessary for accurate results. However, advances in machine performance and quality assurance have now made most errors, in point of care analysis, of ABG’s attributable to clinical providers. Several necessary pre-analytic steps must be followed to obtain a valid, interpretable ABG. In most hospital settings, ABG analysis is a process that involves multiple healthcare providers (e.g., physicians, respiratory therapists, and nurses). Hence, interprofessional coordination, cooperation, and communication are vitally important.
The American Association for Respiratory Care has published Clinical Care Guidelines for Blood Gas Analysis and Hemoximetry that provides current best practices for sampling, handling, and analyzing ABG’s. Notable sources of erroneous values at the time of blood draw include abnormal or misstated FiO2, barometric pressures, or temperatures. Temperature is a significant variable as it leads to PaO2 and O2 saturation discrepancies, as do acid-base disturbances. Several physiological and clinical conditions, such as hyperleukocytosis and dyshemoglobinemias, can also lead to PaO2 and O2 saturation discrepancies. Sample dilution can be an additional error source, with both liquid heparin and saline as potential culprits. The mode of sample transportation is also of significance as discrepant values can result from air contamination after pneumatic tube system transport, compared with manual transport of the specimen, especially in the presence of inadvertent air bubbles. Therefore, procuring samples using suitable syringes filled with adequate amounts of blood without air bubbles, maintaining them at correct temperatures, and transporting them appropriately and promptly for rapid analysis can minimize erroneous values.
(Click Image to Enlarge)
Modified Allen Test. This test is used to check the overall blood supply to the hand.
Kim Y, Massie L, Murata GH, Tzamaloukas AH. Discrepancy between Measured Serum Total Carbon Dioxide Content and Bicarbonate Concentration Calculated from Arterial Blood Gases. Cureus. 2015 Dec 7:7(12):e398. doi: 10.7759/cureus.398. Epub 2015 Dec 7
[PubMed PMID: 26824002]
Pediatric Acute Lung Injury Consensus Conference Group. Pediatric acute respiratory distress syndrome: consensus recommendations from the Pediatric Acute Lung Injury Consensus Conference. Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies. 2015 Jun:16(5):428-39. doi: 10.1097/PCC.0000000000000350. Epub
[PubMed PMID: 25647235]
Rawat M, Chandrasekharan PK, Williams A, Gugino S, Koenigsknecht C, Swartz D, Ma CX, Mathew B, Nair J, Lakshminrusimha S. Oxygen saturation index and severity of hypoxic respiratory failure. Neonatology. 2015:107(3):161-6
[PubMed PMID: 25592054]
Kurt OK, Alpar S, Sipit T, Guven SF, Erturk H, Demirel MK, Korkmaz M, Hayran M, Kurt B. The diagnostic role of capnography in pulmonary embolism. The American journal of emergency medicine. 2010 May:28(4):460-5. doi: 10.1016/j.ajem.2009.01.031. Epub 2010 Jan 28
[PubMed PMID: 20466226]