An acceptable normal range of ABG values of ABG components are the following,[5][6] noting that the range of normal values may vary among laboratories, and in different age groups from neonates to geriatrics:

• pH (7.35-7.45)
• PaO2 (75-100 mmHg)
• PaCO2 (35-45 mmHg)
• HCO3 (22-26 meq/L)
• Base excess/deficit (-4 to +2)
• SaO2 (95-100%)

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.[7][5][6][8]  This method assists with determining 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, and <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[6]:  ABG : pH = 7.39, PaCO2 = 51 mm Hg, PaO2 = 59 mm Hg, HCO3 = 30 mEq/L and SaO2 = 90%, on room air.

1. pH is in the normal range, so use 7.40 as a cutoff point, in which case it is <7.40 so acidosis is present.
2. The PaCO2 is elevated indicating a respiratory acidosis, and the HCO3 is elevated indicating a metabolic alkalosis. 
3. 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 primary disorder that is not acute because it takes days for metabolic compensation to be effective.   
4. 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[6]:  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.

1. pH is in the normal range. Using 7.40 as a cutoff point, it is >7.40 so alkalemia is present.
2. The PaCO2 is decreased indicating a respiratory alkalosis and the HCO3 is normal but on the low end of normal. 
3. 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.  
4. Last, the PaO2 is within the normal range, so there is no abnormality in oxygenation. 

When evaluating the acid-base status of a patient, 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 a persistent metabolic acidosis due to a 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 largely replaced by non-invasive monitoring, it is still useful in the confirmation and calibration of non-invasive monitoring techniques. 

In the intensive care unit (ICU) and emergency room settings, evaluation of oxygenation is most commonly 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 cause of hypoxemia within a general category.  For example, the presence or absence of a gradient can help determine whether the abnormality in oxygenation is potentially due to hypoventilation, a shunt, V/Q mismatch or impaired diffusion.  The equation for 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 are not contributing 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.[1]  For simplicity, assessment of 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 the assessment of oxygenation as the discrepancy between venous admixture and the P/F ratio, at a given shunt fraction, is dependent on the delivered FiO2.[1]  For research purposes, the P/F ratio has also been used to categorize disease severity in ARDS.[9]

Another parameter commonly used in ICU’s 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 as it includes the level of invasive ventilatory support required to maintain oxygenation.[10]  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 calculated OI is commonly used to guide management, such as initiating inhaled nitric oxide, administration of surfactant and defining the potential need for extracorporeal membrane oxygenation.[11]

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.[5]  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 ventilation of the pulmonary units increases relative to their perfusion and when shunting increases.  Hence, pulmonary dead space is an excellent bedside indicator of lung function, as well as one of the best prognostic factors in patients with ARDS.[1]  Pulmonary dead space fraction may also be helpful in the diagnosis of other conditions such as pulmonary embolism.[12]   

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 a 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.

An arterial blood gas can be analyzed as a point-of-care test, along with electrolytes (often called a Shock panel).  It is important that these machines are calibrated/standardized appropriately to ensure accurate and precise results for clinical decisions. Please refer to the appropriate user manuals to ensure your device is calibrated appropriately and at proper time intervals, or discuss with your clinical laboratory team. 

Blood gas analysis is recommended for evaluating a patient’s ventilatory, acid-base, and/or oxygenation status. (Level 1A)[13]  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)[13]  Despite its clinical value, erroneous or discrepant values are a potential drawback of blood gas analysis so elimination of potential sources of error is paramount.[5]  Therefore, attention to detail in 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 a majority of errors, in point of care analysis, of ABG’s attributable to clinical providers.[5]  Several important pre-analytic steps must be followed in order to obtain a valid, interpretable ABG.[5]  In most hospital settings, ABG analysis is a process that involves multiple healthcare providers (e.g. physicians, respiratory therapists and/or 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.[13]  Notable sources of erroneous values, at the time of blood draw, include abnormal or misstated FiO2, barometric pressures, or temperatures. Temperature is a particularly important variable as it leads to PaO2 and O2 saturation discrepancies as does acid-base disturbances.  Several physiological and clinical conditions, such as hyperleukocytosis and dyshemoglobinemias, can also lead to discrepancies in PaO2 and O2 saturation.  Sample dilution can be an additional source of error, with both liquid heparin and saline as potential culprits.[14]  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.[14]  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 in a timely manner, for rapid analysis can help to minimize erroneous values.[14]