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ABG Interpretation
Author: Pam Dugle


ABG Interpretation | Copyright 2010



The purpose of this course will be to remove the mystery behind the interpretation of the arterial blood gases (ABG); raise awareness and understanding of the various aspects of the ABG, and provide a comfort level with care of the patient by increasing the knowledge base.



After completion of this course, the learner will:

  Demonstrate the ability to distinguish between acidosis and alkalosis
  Interpret ABG results
  Discuss the causes of respiratory acidosis and alkalosis
  Discuss the causes of metabolic acidosis and alkalosis
  Identify the role of the ABG in a trauma assessment



Understanding the significance of the findings for the arterial blood gases (ABG) is the first step in interpretation of them. Without this understanding, the nurse cannot be expected to realize the implication of the results.

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). Many 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.

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 (Kellum, 2007).


ABG Interpretation

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) (Pruitt & Jacobs, 2004).

Let us begin by looking at the pH of the blood. The acid-base balance of the blood is maintained by two areas of the body: the respirations and the kidneys. The lower pH represents acidosis and the higher pH represents alkalosis. The normal range is 7.35-7.45.

The PaO2 evaluates the oxygen in plasma and has a normal range of 80-95 mm Hg. This 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 should be above 90%.

PaCO2 evaluates the ventilation component. The normal range is 35-45. 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 (Pruitt & Jacobs, 2004).

HCO3 is regulated by the kidneys and evaluates the metabolic component. The normal range is 22-26 mEq/L. Below 22 is considered to be acidosis and above 26 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 (Pruitt & Jacobs, 2004).


Normal Value

pH 7.35-7.45
HCO3 22-26
PaCO2 35-45
PaO2 80-95 mm Hg
SaO2 95-99%

Four conditions are evaluated based on the ABGs: 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

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.

The ABG values one would see with respiratory acidosis would be: pH < 7.35; PaCO2 > 45 mmHg; and HCO3 > 26 mEq/L if compensating.

Respiratory Acidosis Compensation

  Acidosis Alkalosis
pH 7.35 7.45
PaCO2 45 35
HCO3 22→ → → → 26 (increases)


Respiratory Alkalosis

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; PaCO
2 < 35 mm Hg; and HCO3 < 22 mEq/L if compensating.

Respiratory Alkalosis Compensation

  Acidosis Alkalosis
pH 7.35 → → → → 7.45 (increases)
PaCO2 45 → → → → → 35 (decreases)
HCO3 22 ← ← ← ← ← 26 (decreases)


Metabolic Acidosis

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; 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.

Metabolic Acidosis Compensations

  Acidosis Alkalosis
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 testing to include the ABG. Results of the ABG revealed: a pH of 7.32, PaCO2 45, and HCO3 21. Understanding that without treatment metabolic acidosis will only become progressively worse, and steps will be needed to bring the patient into a compensatory mode to recovery.


Metabolic Alkalosis

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.

ABG values one would see with metabolic alkalosis would be: pH > 7.45; HCO3 > 26 mEq/L and PaCO2 > 45 Hg if compensating.

Metabolic Alkalosis Compensation

  Acidosis Alkalosis
pH 7.35 → → → 7.45 (increases)
PaCO2 45 ← ← ← ← 35 (increases)
HCO3 22 → → → → 26 (increases)


Systematically reviewing the pH, HCO3, and PaCO2

An easy way to remember what is going on in the body with acid and alkaline and compensation is to think of it like this: acid is regulated by the respiratory system, alkaline is regulated by metabolic and if compensated everything shifts in the opposite direction.

  Low High Normal
pH Acidosis Alkalosis  
PaCO2 Alkalosis Acidosis  
HCO3 Acidosis Alkalosis Uncompensated

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. 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


Role of ABG in Trauma Assessment

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 study conducted by Kaplan and Kellum of trauma patients revealed the trauma survivors had lactic acidosis (Kaplan & Kellum, 2008).

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.


Eyes Open Spontaneous 4
To verbal command 3
To pain 2
No response 1
Best Motor Response to verbal command Obeys 6
Best Motor Response to painful stimulus Localizes pain 5
Flexion-withdrawal 4
Flexion-abnormal 3
Extension 2
No response 1
Best Verbal Response Oriented and converse 5
  Disoriented and converses 4
  Inappropriate words 3
  Incomprehensible sounds 2
  No response 1

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, obey 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 leaving the GCS to be a poor indicator of patient condition.

Take for example the 50 year old female who arrives via ambulance who was the driver of a vehicle that ran head on into the median underpass on the interstate. She was wearing a seat belt and collapsed 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; 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.



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.



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.

Kaplan, L. J., & Kellum, J. A. (2008). Comparison of acid base models for prediction of hospital mortality following trauma. Shock, 00(00), 1-6.

Kellum, J. A. (2007). Disorders of acid-base balance. Critical Care Medicine, 35(11), 2630-2636.

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. 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. Clinical Nurse Specialist, 23(3), 151-155.