Arterial blood gases help to identify acid-base balance disturbances. Measurements include hydrogen ion concentration (pH), partial pressure of carbon dioxide (PaCO2), bicarbonate ions (HCO3), partial pressure oxygen (PaO2), oxygen saturation (SaO2), and base excess/deficit (BE) (Wotton, 2013).



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pH: This reflects the amount of hydrogen ions present in the blood. The normal range is 7.35-7.45. Less than 7.35 means there are too many hydrogen ions in the blood (acidic) and more than 7.45 means there are not enough hydrogen ions in the blood (alkalotic) (Hryciw & Bonner, 2015).

PaCO2: This is the amount of dissolved carbon dioxide within the blood. It provides information on how effective respiration and gas exchange are. The normal range is 35-45. The rate of respiration will affect PaCO2 levels. Tachypnea (hyperventilation) will cause excessive CO2 loss resulting in respiratory alkalosis (<35). Bradypnea (hypoventilation) can cause respiratory acidosis from CO2 retention (>45). Respiration can also be used as a buffering system and the amount present can identify whether it is partially compensating, fully compensating, or not compensating at all for metabolic acidosis/alkalosis (Brookside Associates, 2008; Hryciw & Bonner, 2015).

HCO3: Bicarbonate ions are an important acid-base buffering substance regulated by the kidneys. Alterations to this reflect metabolic processes within the body. The normal range is 22-26. <22 means there is not enough bicarb to buffer acid (metabolic acidosis). >26 means there is too much bicarb (metabolic alkalosis) (Hryciw & Bonner, 2015).

BE: This provides a measurement of the amount of buffering compounds in the blood. The normal range is -2 to +2. >2 indicates an increase in HCO3 (alkalosis) and <-2 indicates a decrease in HCO3 (acidosis) (Brookside Associates, 2008; Wotton, 2013).



Respiratory Acidosis: is a result of excess carbon dioxide in the body (hypercapnia). It is characterised by <7.35 pH and >45 PaCO2. When this occurs, there is inefficient gas exchange at the alveoli. The kidneys try to compensate the increase of acid by increasing production of bicarbonate ions. Bicarb levels >26 suggest the body is trying to compensate. Respiratory depression can be caused from an overdose of opiates, respiratory centre damage, or chronic obstructive pulmonary disorder (COPD). Symptoms of respiratory acidosis are headaches, dizziness, slow respirations, and warm, flushed skin (Hryciw & Bonner, 2015; Wotton, 2013).




Respiratory Alkalosis: occurs when there is not enough carbon dioxide in the blood (hypocapnia). An excess of carbon dioxide is being exhaled which increases pH >7.45 and there is <35 PaCO2. This can occur through hyperventilation from an anxiety attack or an asthma attack. Symptoms of respiratory alkalosis are rabid breathing, muscle spasms (tetany), dizziness, and confusion (Hryciw & Bonner, 2015; Wotton, 2013).




Metabolic Acidosis: is caused by an increased loss of bicarbonate or an increase of metabolic acids (ketones or lactic acid). pH will decrease <7.35 and HCO3 <22. Diabetic ketoacidosis and kidney failure can cause metabolic acidosis. The presenting symptoms are kassmaul breathing, lethargy, nausea and diarrhoea (Hryciw & Bonner, 2015; Wotton, 2013).




Metabolic Alkalosis: occurs when there is an increased bicarbonate level >26, or if there is an increase in metabolic acid loss, pH >7.45. Some causes for this are diarrhoea, vomiting, or ingestion of excessive bicarbonate. Slow, shallow breathes may be a symptom as the lungs try to retain CO2 to buffer the increased bicarbonate levels. Other symptom include muscle cramps, numbness of the toes and fingers, tetany, and confusion (Hryciw & Bonner, 2015; Wotton, 2013).






Brookside Associates. (2008). Arterial blood gas (ABG). Retrieved April 21, 2016 from

Hryciw, D., & Bonner, A. (2015). Fluids and electrolytes, acids and bases. In J. Craft & C. Gordon (Eds.), Understanding pathophysiology (2nd ed., pp. 843–870). Sydney, Australia: Mosby Elsevier.

Wotton, K. (2013). Fluid, electrolyte and acid-base balance. In J. Crisp, C. Taylor, C. Douglas, & G. Rebeiro (Eds.), Potter and Perry’s fundamentals of nursing (4th ed., pp. 1189–1254). Sydney, Australia: Mosby Elsevier.