The purpose of this course is reinforcing arterial blood gas interpretation skills; raise awareness and understanding of the various aspects of arterial blood gases, and provide a comfort level with the care of the patient by increasing the knowledge base.
After completion of this course, the learner will:
A study conducted in Illinois at Freeport Health Network Memorial Hospital and Swedish American Hospital demonstrated that a computer based module aided nurses to learn ABG interpretation (Schneiderman, Corbridge, & Zerwic, 2009).
Short educational modules for nurses in arterial blood gas analysis can have significant impact on improving the knowledge of the nurse. A recent study showed that 98% of nurses believed that this training was useful (De Sliva, Stephens, Welch, Sigera, DeAlwis, Athapattu, Dharmagunawardene, Olupeliyawa, De Abrew, Peiris, Siriwardana, Karunathilake, Dondorp & Haniffa, 2015).
Whatever the underlying cause for the acid-base disturbance, one must gain knowledge for interpretation of the ABG to establish the best course of treatment. Therefore, the healthcare provider will determine the limitations of therapy based on the results of the ABG.
Another recent analysis showed that teaching a stepwise approach to evaluating ABGs and using case studies, tables and figures could enhance the ability of the nurse to interpret ABG (Barnett & Kautz, 2013).
ABG sampling is a procedure that involves the direct puncture of an artery. It is associated with a low incidence of complication and is used to determine gas exchange levels in the blood and assesses renal, metabolic and respiratory function.
Understanding the significance of the findings for the arterial blood gases (ABG) is the first step in the interpretation of them. Without this understanding, the nurse cannot be expected to realize the implication of the results.
Adult students demonstrate various methods of learning to better enhance their knowledge base. Finding the best education method for the individual is the first step to success in clinical competence.
ABG reflect the physiologic state of the patient at the time the test was done. The radial artery is typically the preferred site because it has collateral circulation and is accessible. When the radial artery is not feasible the femoral or brachial artery can be used. The femoral artery is a deeper artery and there is greater risk of damage to adjacent structures. It is close to the femoral vein and nerve. When the femoral artery is sampled it requires monitoring and is often only done in an inpatient setting.
The brachial artery is also a deep artery and is more difficult to identify. There are multiple problems with the brachial artery. It is a small caliber vessel, it does not have good collateral circulation and attaining hemostasis is more difficult.
Repeated punctures increase the risk of artery laceration, inadvertent venous sampling, hematoma and scaring. When frequent sampling is needed the use of an indwelling arterial catheter may be beneficial.
When it is difficult to identify sampling sites such as those who have weak pulses, distorted anatomic landmarks or when a deep vascular artery is being accessed, the use of ultrasound-guided ABG sampling may be done. This allows more accurate placement of the needle and reduced the risk of damage to the surrounding structures.
Absolute contraindications to ABG include:
Relative contraindications to ABG include:
Pulses that cannot be identified easily
Difficult to position the patient
Obesity – because of subcutaneous fat over access areas/obscures landmarks
Vascular disease leading to rigidity in vessel walls
Poor distal perfusion – heart failure, hypovolemia, vasopressor therapy
Air bubbles can increase PaO2 and lower PaCO2
Heparin may lower PaCO2
Gas may diffuse though a plastic syringe
Acid-base balance may be inaccurate in arterial blood in those with reduced cardiac output (CPR/circulatory failure).
Prior to getting a sample of blood from the radial artery, collateral circulation should be assessed. This is commonly done with the Allen or modified Allen test.
The modified Allen’s test is used to assure ulnar artery collateral circulation and palmar arch patency. It is unknown if it can predict ischemic complications with radial artery occlusion (Theodore, 2015).
In the modified Allen test the patient holds the hand high and clenches the fist while the clinician compressing the radial and ulnar arteries. The hand is lowered, the fist is opened and pressure is removed off the ulnar artery. Within 5-15 seconds the color should return to the hand. This suggests that the ulnar artery and the superficial palmar arch are patent. If it takes more than 15 seconds the test is abnormal.
The Allen test (from which the modified Allen test evolved) is performed identically, except the Allen test is done two times. One time the pressure is released from the radial artery and once from the ulnar artery.
The patient should not overextend the hand or spread the fingers wide as it may lead to false-normal results.
Much debate has been held regarding the necessity to obtain an Allen Test prior to obtaining an ABG. Many believe the Allen Test is a standard of care and as such is written into policy at facilities across the country.
Because the definition of an abnormal Allen Test is difficult at least to describe, criteria for determining abnormality is challenging. In a study led by Jarvis the conclusion was that the Allen Test was only accurate about 80% of the time (Barone & Madlinger, 2006). Since the Allen Test is controversial, hospital policy must be adhered to at all times.
Determine the site to be sampled
The site is prepped in a sterile fashion
Consider local analgesia before to arterial puncture as it reducespain without negatively impacting the procedure
Use an ABG kit
Palpate the artery with the nondominate hand
Puncture the artery with the needle at a 45 degree angle relative to the skin
The syringe should fill on its own – get 2-3 mL of blood
Hold pressure on the site for 5-10 minutes
Prior to performing ABG the patient should be educated about the procedure including the risks and benefits of the procedure. The patient should let the health care provider know if there is new/worsening pain, reduced movement, numbness/tingling in the limb or active bleeding after the procedure is performed.
To get a sample from the radial artery the patient should lie supine with the forearm supinated on a hard surface. The wrist is extended 20-30 degrees; a small roll may be put under the wrist to make the radial artery more superficial. If a sample is to be taken from the femoral artery the patient is supine with the leg in a neutral position. If blood is taken from the brachial artery the arm is on a firm surface and the shoulder slightly abducted with the forearm supinated and the elbow extended.
When performing an ABG sampling the provider should wear gloves and eye protection. The site should be cleaned with an antiseptic solution. The non-dominate hand locates the arterial pulse with the second and third fingers with both fingers proximal to the desired puncture site.
The needle is inserted at a 45 degree angle aiming at the artery with the needle bevel facing upwards. When the needle is angled it reduced vessel trauma and allows the muscle fibers to seal the puncture site after the puncture.
When the blood starts filling the syringe remove the nondominate hand. After 2-3 ml is obtained the needle is removed and gauze is placed over the site with the nondominate hand to hold pressure for five minutes. For those at risk for bleeding, pressure may need to be held for longer periods of time. Afterwards, an adhesive dressing should be placed over the puncture site.
The excess air should be removed from the syringe, the syringe capped and placed in ice while it is awaiting analysis. No air bubbles should be present as this may underestimate the PaC02 and overestimate the PaO2.
The nurse must monitor for complications. Active profuse bleeding from the puncture site suggests that there is vessel laceration. Compartment syndrome may result from an expanding hematoma that compromising circulation. Compartment syndrome is suggested by the six P’s: pain, pallor, paresthesia, paralysis, poikilothermia, and pulselessness. Ischemia from a thrombus, vasospasm or arterial occlusion presents as pulselessness, color change and distal coldness. A nerve injury may present with paresis and persistent pain. Infection presents with fever and local erythema.
When interpreting the ABG results, one must first know the five major components of the ABG to be addressed: oxygen saturation (SaO2), partial pressure of oxygen (PaO2), acidity or alkalinity (pH), partial pressure of carbon dioxide (PaCO2), and bicarbonate ions concentration (HCO3).
Definitions important to know when Interpreting ABG:
Acidemia – arterial pH less than 7.35
Acidosis – lowering of the extracellular fluid pH caused by an elevated PCO2 or a reduced HCO3
Metabolic acidosis – reduction in pH and serum HCO3
Respiratory acidosis – Reduction in pH with an elevation of the arterial PCO2
Alkalemia – arterial pH above 7.45
Alkalosis – elevation of the extracellular fluid pH caused by an fall in PCO2 or a rise in HCO3
Metabolic alkalosis - elevation in pH and serum HCO3
Respiratory alkalosis – an elevation of the pH with a reduction in the arterial PCO2
Mixed acid-base disorder – more than one acid-base disorder at the same time
Anion gap = (Na) - (Cl + HCO3)
Normal range is 8-16 mEq/L
The four main acid-base disorders are metabolic alkalosis, metabolic acidosis, respiratory alkalosis and respiratory acidosis. Respiratory alkalosis and acidosis may be classified as acute or chronic as it takes up to five days for the renal system to compensate for respiratory disorders.
The acid-base balance of the blood is maintained by two areas of the body: the lungs and the kidneys. The lower pH represents acidosis and the higher pH represents alkalosis with the normal range of pH from 7.35-7.45.
The PaO2 evaluates the oxygen in plasma and has a normal range of 80-95 mm Hg. The PaO2 does not measure the amount of oxygen attached to the hemoglobin. SaO2 measures the amount of oxygen attached to the hemoglobin. The normal range is 95-99% and generally should be above 90%.
PaCO2 evaluates the ventilation component. The normal range is 35-45 mmHg. However, the value is inversely related to ventilation. For example, decreased ventilation has a higher value and increased ventilation has a lower value. Therefore, hyperventilation causes alkalosis because the patient is blowing off carbon dioxide and hypoventilation causes acidosis because the patient is retaining carbon dioxide. The body adjusts for these conditions by changing the respiratory rate (Kaufman, 2015)
HCO3 is regulated by the kidneys and evaluates the metabolic component. The normal range is 22-26 mEq/L. Below 22 mEq/L is considered to be acidosis and above 26 mEq/L is alkalosis. The body can adjust to the abnormalities in the HCO3 levels but not as quickly as it can to the abnormal PaCO2 levels. Several days could be required to make the necessary adjustments to bring the HCO3 levels to a normal range (Kaufman, 2015).
|PaCO2||35-45 mm Hg|
|PaO2||80-95 mm Hg|
Four conditions are evaluated based on the ABG: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. As we explore these conditions, the potential causes, the ABG values, and the compensatory mechanisms, we will gain a better understanding of what is happening within the body.
Respiratory acidosis is an attempt by the body to compensate for excessive PaCO2. The body excretes the extra hydrogen in the urine and exchanges it for bicarbonate ions. When this happens HCO3 rises to restore the body to a normal pH. Until the pH returns to normal, the PaCO2 may stay elevated.
Any situation that can cause the patient to develop a depressed respiratory status can cause this medical condition. Examples of these situations could be hypoventilation, asphyxia, central nervous system depression, chronic obstructive pulmonary disease, infection, and drug induced respiratory depression (Table 9).
The ABG values one would see with respiratory acidosis would be: pH < 7.35; PaCO2 > 45 mmHg; and HCO3 > 26 mEq/L if compensating.
In acute respiratory acidosis, to compensate the HCO3 increases approximately 1 mEq/L for each 10 mmHg in PaCO2. In chronic respiratory acidosis (after 3-5 days), the HCO3 will increase up to 5 mEq/L per 10 mmHg of PaCO2. If there is a mild-to-moderate chronic respiratory acidosis, suggested by a PaCO2 less than 70 mmHg, the pH may be in the low-normal range or slightly reduced. If the pH is significantly acidic in chronic acidosis there is typically a co-existent metabolic acidosis or an acute respiratory acidosis. If the pH is 7.40 or more than there is likely a co-existent acute respiratory alkalosis or a metabolic alkalosis.
|HCO3||22→ → → →||26 (increases)|
Respiratory alkalosis is a compensatory mechanism of the body aimed to increase excretion of HCO3 and retention of the hydrogen ions. Respiratory alkalosis lowers the HCO3 and restores pH to normal. Conditions that cause the respiratory system to be over stimulated can be extenuating factors in respiratory alkalosis such as hyperventilation.
The ABG values one would see with respiratory alkalosis would be: pH > 7.45; PaCO2 < 35 mm Hg; and HCO3 < 22 mEq/L if compensating.
In acute respiratory alkalosis the compensation is to lower the serum HCO3 by 2 mEq/L for every 10 mmHg reduction in PaCO2. In chronic respiratory alkalosis (after 3-5 days) the serum HCO3 falls about 4-5 mEq/L for every 10 mmHg reduction in PaCO2 (Emmett, 2015).
|pH||7.35 → → → →||7.45 (increases)|
|PaCO2||45 → → → → →||35 (decreases)|
|HCO3||22 ← ← ← ← ←||26 (decreases)|
When a patient is demonstrating metabolic acidosis his or her body is pulling the HCO3 into the cells as a buffer and therefore, depletes the plasma level. The body begins compensating by increasing the ventilation and thus renal retention of the HCO3 takes place.
When patients present with the following conditions, one must consider the patient could be a candidate for metabolic acidosis: HCO3 loss from diarrhea; shock; renal tubular acidosis; drug intoxication; salicylate poisoning; renal failure; diabetic ketoacidosis; and circulatory failure producing lactic acid.
ABG values one would see with metabolic acidosis would be: pH < 7.35; HCO3 < 22; and PaCO2 < 35 mm Hg if compensating.
Respiratory compensation for metabolic acidosis causes a reduction in the arterial PaCO2 by about 1.2 mmHg for every 1 mEq/L reduction in the serum HCO3. If compensation does not occur there is likely underlying neurologic or respiratory disease (Emmett, 2015).
Calculation of the serum anion gap should be determined in metabolic acidosis. In metabolic acidosis the anion gap may be high, normal or combined. Determining the anion gap will help determine the cause of the metabolic acidosis.
|pH||7.35 ← ← ←||7.45 (decreases)|
|PaCO2||45 → → → →||35 (decreases)|
|HCO3||22 ← ← ← ←||26 (decreases)|
One generally considers the ABG to be a test for respiratory conditions; however, a study of ABGs in Brazil to test patients for metabolic acidosis in relation to sepsis and shock was conducted. The study revealed a group whom were not able to clear their inorganic ions had a higher morbidity rate, whereas those who were able to correct their acidosis survived (Noritomi et al., 2009).
The severely septic patient who developed acute renal failure upon arrival to the intensive care unit (ICU) had a battery of tests including ABG. Results of the ABG revealed: a pH of 7.32, PaCO2 45, and HCO3 21. Without treatment metabolic acidosis will become progressively worse; steps need to be taken to bring the patient into a compensatory mode to recovery.
Treatment of metabolic acidosis is variable depending on the cause and whether it is acute or chronic. In severe metabolic acidosis, sodium bicarbonate is sometimes used.
With metabolic alkalosis one will see an increased level of HCO3. This could be caused by several factors such as too much bicarbonate during a code, excess hydrogen loss during vomiting or suctioning, potassium loss from diuretics or steroids, or excessive alkali ingestion. The kidneys will increase the HCO3 excretion trying to conserve the hydrogen and the respiratory system will compensate by decreasing the ventilations and conserving the CO2 and raising the PaCO2. Patients with normal kidney function are able to excrete excess bicarbonate in the urine so if a metabolic alkalosis is maintained there is an inability to excrete bicarbonate in the urine.
ABG values one would see with metabolic alkalosis would be: pH > 7.45; HCO3 > 26 mEq/L and PaCO2 > 45 Hg if compensating.
Respiratory compensation of metabolic alkalosis typically raises the PaCO2 approximately 0.7 mmHg for every 1 mEq/L increase in HCO3. The arterial PaCO2 rarely goes above 55 mmHg (Emmett, 2015).
|pH||7.35 → → →||7.45 (increases)|
|PaCO2||45 ← ← ← ←||35 (increases)|
|HCO3||22 → → → →||26 (increases)|
Acid-base disorders are typically associated with a compensatory response that lessens the change in the HCO3/ PaCO2 ratio and consequently in pH. For example, if there is a metabolic acidosis (a reduction in the serum HCO3) there should be respiratory compensation by moving the PaCO2 in the same direction as the serum HCO3 (falling). The respiratory compensation lessens the change in the ratio of the serum HCO3 to PaCO2 and consequently the pH. Respiratory compensation is a rapid adjustment. In metabolic acidosis the respiratory compensation starts within 30 minutes and is done in 12-24 hours.
A respiratory acid-base disorder leads to compensation in two phases: immediate and delayed. The immediate change is a small change in serum HCO3 in the same direction as the PaCO2. If the respiratory condition persists then the kidneys produce larger changes in the HCO3. This is meant to stabilize the pH.
In respiratory alkalosis, urinary HCO3 and hydrogen ion secretion is reduced and in respiratory acidosis hydrogen ion secretion and HCO3 is increased to compensate. Renal compensation takes longer than respiratory compensation; it takes three to five days to complete compensation.
A look at a glance with the four disorders demonstrates what happens with the pH, what the initiating event causing the disorder, and the compensatory effect will be shown in the following table (Table 9). It is important to remember that compensating effects are seen in chronic conditions.
|Disorder||pH||Initiating Event||Compensating Effect|
|Respiratory Acidosis||↓||↑ PaCO2||↑ HCO3|
|Respiratory Alkalosis||↑||↓ PaCO2||↓ HCO3|
|Metabolic Acidosis||↓||↓ HCO3||↓ PaCO2|
|Metabolic Alkalosis||↑||↑ HCO3||↑ PaCO2|
Studies have shown that along with other indicators such as the Glasgow Coma Scale (GCS) the ABG results can serve as a strong indicator of a patient’s mortality during the hospital course. A recent study showed that acid base disturbances were predictors of death in major trauma patients (Shane, Robert, Arthur, Patson, & Moses, 2014).
Addressing the GCS of each trauma patient arriving in the ED is an important step in the assessment process. Using the information included in the following Glasgow Coma Scale, the nurse can assess eye opening, motor response, and verbal response.
|To verbal command||3|
|Best Motor Response to verbal command||Obeys||6|
|Best Motor Response to painful stimulus||Localizes pain||5|
|Best Verbal Response||Oriented and converses||5|
|Disoriented and converses||4|
Patients arriving in the Emergency Department (ED) post trauma receive a head to toe trauma assessment including the GCS. A GCS of < 8 indicates a severe head injury and generally has a poor outcome. The low GCS coupled with a strong ion gap according to Kaplan and Kellum (2008) is “a strong predictor of hospital mortality”. Therefore, vascular injury must be assessed along with other areas of assessment and fluid resuscitation initiated to prevent further decline.
However, a patient can arrive with a GCS of 15 indicating he or she has spontaneous eye opening, obeys verbal commands and he or she is oriented and conversing. This patient can be suffering from respiratory distress caused by a traumatic injury to the lungs, therefore when used alone the GCS may be a poor indicator of the patient’s condition.
A 50 year-old female arrives in the ED via ambulance. She was the driver of a vehicle that ran head on into the median underpass on the interstate. She was wearing a seat belt, but hit the steering wheel before the airbag deployed. When she arrived in the ED she had a GCS of 15 and was anxious. At initial inspection she had bruising to her chest from the seat belt, no visible head injury noted; and her vital signs were within normal limits. Shortly after arriving in the ED she began complaining of needing to have a bowel movement and difficulty breathing. Her oxygen saturation dropped to 88% on room air. An ABG was obtained with the following results: pH 7.32, PaCO2 47, and HCO3 28. Vital signs have now made a slight change from being within normal limits to: blood pressure 120/70, HR 88, and respiratory rate 30. Understanding the patient’s blood gas reveals a respiratory acidosis; preparations begin to treat the cause when the results of the x-ray reveal a left side pneumothorax.
|Causes of Respiratory Acidosis|
|Causes of Respiratory Alkalosis|
|Causes of Metabolic Acidosis|
|Causes of Metabolic Alkalosis|
A 45 year-old female presents to the emergency department with severe diarrhea for the last two days. She has the following ABG.
Arterial pH - 7.25
The pH is low and therefore the patient has acidemia. The low HCO3 suggests metabolic acidosis. The HCO3 is 12 mEq/L below the normal (which is 24 mEq/L). This should (and did) lead to respiratory compensation with a 14 mmHg fall in PaCO2 (the normal PaCO2 is 40 mmHg). Respiratory compensation for metabolic acidosis is when the arterial PaCO2 falls about 1.2 mmHg per 1 mEq/L reduction in the serum HCO3 concentration.
This patient has a partially compensated metabolic acidosis (the pH is not in the normal range – so it is only partially compensated). If the PaCO2 was significantly higher (above 26 mmHg) than expected there would be a concurrent respiratory acidosis (e.g., an obtunded patient).
If the PaCO2 was significantly lower than expected (below 26 mmHg) than a concurrent respiratory alkalosis may be present. Respiratory alkalosis with metabolic acidosis is often seen in salicylate intoxication or septic shock.
The patient is noted to have a normal anion gap which is consistent with a metabolic acidosis caused by diarrhea.
Regardless of the condition of the patient, an important aspect of the ABG is to take a systematic approach to interpretation of the ABG and determining between the differential diagnoses. Know the patient history and begin treatment as soon as feasible to ensure the best possible outcomes. Placing the patient at the top of the pyramid is the absolute most significant step in the process.
Arogué, H. J., & Madias, N. E. (2010). Secondary responses to altered acid-base status: the rules of engagement. Journal of the American Society of Nephrology, 21, 920-3.
Barnett, L. & Kautz, D. D. (2013). Creative ways to teach arterial blood gas interpretation. Dimensions of Critical Care Nursing, 32(2), 84-7.
(Barone J E Madlinger R V 2006 Should an Allen Test be performed before radial artery cannulation?)Barone, J. E., & Madlinger, R. V. (2006). Should an Allen Test be performed before radial artery cannulation? The Journal of Trauma: Injury, Infection, and Critical Care, 61(2), 468-470.
De Sliva, A. P., Stephens, T., Welch, J., Sigera, C., DeAlwis, S., Athapattu, P., Dharmagunawardene, D., Olupeliyawa, A., De Abrew, A., Peiris, L., Siriwardana, S., Karunathilake, I., Dondorp, A. & Haniffa, R. (2015). Nursing intensive care skills training: a nurse led, short, structured, and practical training program, developed and tested in a resource-limited setting. Journal of Critical Care, 30(2), 438.e7-11.
Emmett, M. (2015). Simple and mixed acid-base disorders. Retrieved September 10, 2015 from: (Visit Source).
Kaplan, L. J., & Kellum, J. A. (2008). Comparison of acid base models for prediction of hospital mortality following trauma. Shock, 29(6):662-6.
Kaufman, D. A. (2015). Interpretation of Arterial Blood Gases. Retrieved September 10, 2015 from: (Visit Source).
(Noritomi D T Francisco G S Kellum J A Cappi S B Biselli P J Alexandre B L et al 2009 Metabolic acidosis in patients with severe sepsis and septic shock: A longitudinal quantitative study)Noritomi, D. T., Francisco, G. S., Kellum, J. A., Cappi, S. B., Biselli, P. J., Alexandre, B. L., et al. (2009). Metabolic acidosis in patients with severe sepsis and septic shock: A longitudinal quantitative study. Critical Care Medicine, 37(10), 1-7.
(Pruitt W C Jacobs M 2004 Interpreting arterial blood gases: Easy as ABC)Pruitt, W. C., & Jacobs, M. (2004). Interpreting arterial blood gases: Easy as ABC. Nursing, 34(8), 50-53
(Schneiderman J Corbridge S Zerwic J J 2009 Demonstrating the effectiveness of an online, computer-based learning module for arterial blood gas analysis)Schneiderman, J., Corbridge, S., & Zerwic, J. J. (2009). Demonstrating the effectiveness of an online, computer-based learning module for arterial blood gas analysis. Clinical Nurse Specialist, 23(3), 151-155.
Shane AI, Robert W, Arthur K, Patson M, & Moses G. (2014). Acid-base disorders as predictors of early outcomes in major trauma in a resource limited setting: An observational prospective study. The Pan African Medical Journal, 17, 2
Theodore, A.C. (2015). Arterial blood gasses. Retrieved September 10, 2015 from: (Visit Source).
This course is applicable for the following professions:
Advanced Registered Nurse Practitioner (ARNP), Certified Registered Nurse Anesthetist (CRNA), Clinical Nurse Specialist (CNS), Licensed Practical Nurse (LPN), Licensed Vocational Nurses (LVN), Registered Nurse (RN), Respiratory Therapist (RT)
Critical Care / Emergency Care, Medical Surgical