This page focuses on providing some possible causes for the various disturbances that may be seen on an ABG. Although not an exhaustive list, it attempts to outline the main headings for possible pathology.
It covers acid-base disturbance, respiratory failure, and a small summary for some other derangements.
Causes of disturbance
Respiratory acidosis1
Respiratory acidosis is caused by inadequate alveolar ventilation leading to CO2 retention.
Ventilation rate = tidal volume * respiratory rate
Therefore anything that affects tidal volume or respiratory rate, may affect the amount of CO2 retained.
Selected etiologies of respiratory acidosis:
Figure 1: Respiratory acidosis outline
Figure 2: Respiratory alkalosis outline
Respiratory alkalosis1
Respiratory alkalosis is caused by excessive alveolar ventilation (hyperventilation) resulting in more CO2 than normal being exhaled. Often this is related to the fact that CO2 is more easily exchanged than O2, therefore the body may still be able to exhale excessive amounts of CO2, even when it is struggling to maintain a normal PaO2. As a result, PaCO2 is reduced and pH increases causing alkalaemia.
Selected etiologies of respiratory alkalosis:
Metabolic acidosis1
Metabolic acidosis can occur as a result of either:
Selected etiologies of metabolic acidosis:
Determining which one of these main headings is a fault, can be done through the use of the 'anion gap' calculation, discussed in the 'extras' page.
Figure 3: Metabolic acidosis outline
Figure 4: Metabolic alkalosis outline
Metabolic alkalosis1
Metabolic alkalosis may occur as a result of decreased hydrogen ion concentration (by either the GI or renal system), leading to increased bicarbonate (as the bicarbonate buffer equation shifts to the right, to produce more H+ and HCO3-), or alternatively a direct result of increased bicarbonate concentrations.
Selected causes of metabolic alkalosis
Selected mixed and compensated acid-base disturbances
It must also be kept in mind that all of these conditions may occur in simultaneously, giving either mixed disorder (whereby two conditions act on the pH in the same direction), or compensated disorder (where the two conditions act in different directions on the pH).
A specific example a of a mixed disorder is cardiac arrest, whereby there is respiratory acidosis from respiratory arrest, and also metabolic acidosis from increased lactate from hypoperfusion.
An important example of a compensated disorder is ketoacidosis with vomiting, where there is a metabolic acidosis caused by increased ketoacids, as well as a metabolic alkalosis caused by the vomiting and loss of gastric acid.
Respiratory failure2
Respiratory failure can be split into Type 1 or Type 2 respiratory failure, depending on the value of PaCO2.
Type 1
Type 1 respiratory failure is caused by pathological processes which reduces the ability of the lungs to exchange oxygen, without changing the ability to excrete CO2, due to the different shape of the CO2 and O2 dissociation curves.
It involves hypoxia (PaO2 <8 kPa) with normocapnia (PaCO2 <6.0 kPa).
It occurs as a result of ventilation/perfusion mismatch; where the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lung tissue.
This may be due to either a reduction in ventilation, or a reduction in perfusion.
Examples of causes of type 1 respiratory failure are pulmonary embolus (reduced perfusion), pulmonary fibrosis, pneumonia, asthma/COPD, and pulmonary oedema (reduced ventilation), these may all further develop into type 2 respiratory failure.
Type 2
Type 2 respiratory failure involves hypoxia (PaO2 <8 kPa) with hypercapnia (PaCO2 >6.0 kPa).
Caused by a pathological process which affects the ability to both exchange oxygen and excrete CO2. It is due to inadequate alveolar ventilation.
Examples of causes:
Chronic type 2 respiratory failure, such as in COPD, must be managed carefully. Referred to as CO2 retainers, patients rely on their hypoxic drive to maintain ventilation, not on PaCO2, therefore when exposed to higher levels of O2 - as is often done when they present to A+E with increased breathlessness and low pulse oximeter readings - leads to a decrease in respiratory drive, and further alveolar hypoventilation, leading to extreme hypercapnia and acidosis. Therefore, only controlled methods of ventilation such as a Venturi mask should be used in these patients.
Common ABG patterns3
Other disturbances2
Lactate
Haemoglobin (Hb)
Glucose
Carbon monoxide (CO)
Methaemoglobin (metHb)
References
1. Kaufman, David A. Interpretation of Arterial Blood Gases (ABGs). American Thoracic Society. http://www.thoracic.org/professionals/clinical-resources/critical-care/clinical-education/abgs.php
2. Arterial Blood Gas (ABG) interpretation for medical students, OSCEs and MRCP PACES. Oxford Medical Education. [Online] http://www.oxfordmedicaleducation.com/abgs/abg-interpretation/
3. Mansbridge C. ABG interpretation. OSCEstop.com. [Online] http://www.oscestop.com/ABG_interpretation.pdf
Metabolic acidosis1
Metabolic acidosis can occur as a result of either:
Selected etiologies of metabolic acidosis:
Determining which one of these main headings is a fault, can be done through the use of the 'anion gap' calculation, discussed in the 'extras' page.
Figure 3: Metabolic acidosis outline
This page focuses on providing some possible causes for the various disturbances that may be seen on an ABG. Although not an exhaustive list, it attempts to outline the main headings for possible pathology.
It covers acid-base disturbance, respiratory failure, and a small summary for some other derangements.
Causes of disturbance
Respiratory acidosis1
Respiratory acidosis is caused by inadequate alveolar ventilation leading to CO2 retention.
Ventilation rate = tidal volume * respiratory rate
Therefore anything that affects tidal volume or respiratory rate, may affect the amount of CO2 retained.
Selected etiologies of respiratory acidosis:
Respiratory alkalosis1
Respiratory alkalosis is caused by excessive alveolar ventilation (hyperventilation) resulting in more CO2 than normal being exhaled. Often this is related to the fact that CO2 is more easily exchanged than O2, therefore the body may still be able to exhale excessive amounts of CO2, even when it is struggling to maintain a normal PaO2. As a result, PaCO2 is reduced and pH increases causing alkalaemia.
Selected etiologies of respiratory alkalosis:
Metabolic acidosis1
Metabolic acidosis can occur as a result of either:
Selected etiologies of metabolic acidosis:
Determining which one of these main headings is a fault, can be done through the use of the 'anion gap' calculation, discussed in the 'extras' page.
Metabolic alkalosis1
Metabolic alkalosis may occur as a result of decreased hydrogen ion concentration (by either the GI or renal system), leading to increased bicarbonate (as the bicarbonate buffer equation shifts to the right, to produce more H+ and HCO3-), or alternatively a direct result of increased bicarbonate concentrations.
Selected causes of metabolic alkalosis
Selected mixed and compensated acid-base disturbances
It must also be kept in mind that all of these conditions may occur in simultaneously, giving either mixed disorder (whereby two conditions act on the pH in the same direction), or compensated disorder (where the two conditions act in different directions on the pH).
A specific example a of a mixed disorder is cardiac arrest, whereby there is respiratory acidosis from respiratory arrest, and also metabolic acidosis from increased lactate from hypoperfusion.
An important example of a compensated disorder is ketoacidosis with vomiting, where there is a metabolic acidosis caused by increased ketoacids, as well as a metabolic alkalosis caused by the vomiting and loss of gastric acid.
Respiratory failure2
Respiratory failure can be split into Type 1 or Type 2 respiratory failure, depending on the value of PaCO2.
Type 1
Type 1 respiratory failure is caused by pathological processes which reduces the ability of the lungs to exchange oxygen, without changing the ability to excrete CO2, due to the different shape of the CO2 and O2 dissociation curves.
It involves hypoxia (PaO2 <8 kPa) with normocapnia (PaCO2 <6.0 kPa).
It occurs as a result of ventilation/perfusion mismatch; where the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lung tissue.
This may be due to either a reduction in ventilation, or a reduction in perfusion.
Examples of causes of type 1 respiratory failure are pulmonary embolus (reduced perfusion), pulmonary fibrosis, pneumonia, asthma/COPD, and pulmonary oedema (reduced ventilation). These may all further develop into type 2 respiratory failure.
Type 2
Type 2 respiratory failure involves hypoxia (PaO2 <8 kPa) with hypercapnia (PaCO2 >6.0 kPa).
Caused by a pathological process which affects the ability to both exchange oxygen and excrete CO2. It is due to inadequate alveolar ventilation.
Examples of causes:
Chronic type 2 respiratory failure, such as in COPD, must be managed carefully. Referred to as CO2 retainers, they rely on their hypoxic drive to maintain ventilation, not on PaCO2, therefore when exposed to higher levels of O2 - as is often done when they present to A+E with increased breathlessness and low pulse oximeter readings - leads to a decrease in respiratory drive, and further alveolar hypoventilation, leading to extreme hypercapnia and acidosis. Therefore, only controlled methods of ventilation such as a Venturi mask should be used in these patients.
Common ABG patterns3
Other disturbances2
Lactate
Haemoglobin (Hb)
Glucose
Carbon monoxide (CO)
Methaemoglobin (metHb)
References
1. Kaufman, David A. Interpretation of Arterial Blood Gases (ABGs). American Thoracic Society. http://www.thoracic.org/professionals/clinical-resources/critical-care/clinical-education/abgs.php
2. Arterial Blood Gas (ABG) interpretation for medical students, OSCEs and MRCP PACES. Oxford Medical Education. [Online] http://www.oxfordmedicaleducation.com/abgs/abg-interpretation/
3. Mansbridge C. ABG interpretation. OSCEstop.com. [Online] http://www.oscestop.com/ABG_interpretation.pdf