/ABG

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:

  • Airway obstruction
    • Upper
    • Lower
      • COPD; Asthma (near-fatal); Other obstructive lung disease
  • CNS depression: Opiates; Head trauma
  • Sleep disordered breathing (OSA or OHS)
  • Neuromuscular impairment/mechanical lung dysfunction
    • Guillain–Barré (paralysis leads to an inability to adequately ventilate); Obesity; Myasthenia gravis; deformity such as severe scoliosis.
  • Increased CO2 production: rigors; seizures; malignant hyperthermia
  • Iatrogenic: incorrect mechanical ventilation settings

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:

  • CNS stimulation: anxiety (panic attack), fever, pain, fear, CVA, cerebral oedema, brain trauma, brain tumour, CNS infection – causing increased respiratory rate
  • Hypoxia: lung disease, asthma (moderate/severe - hyperventilating), profound anaemia, low FiO2 – resulting in increased alveolar ventilation in an attempt to compensate
  • Stimulation of chest receptors: pulmonary oedema, pleural effusion, pneumonia, pneumothorax, pulmonary embolus
  • Drugs/hormones: salicylates, catecholamines, medroxyprogesterone, progestins
  • Conditions: Pregnancy, liver disease, sepsis, hyperthyroidism
  • Iatrogenic (excessive mechanical ventilation)

Metabolic acidosis1

Metabolic acidosis can occur as a result of either:

  • Increased H + production or ingestion
    • HCO3- concentrations decrease by acting as a buffer. The HCO3- is consumed by the H+ - to produce CO2 and H2O - resulting in a high pH.
  • GI or renal HCO 3 - loss
    • Where a decrease in HCO3- is the primary pathology, causing the acidaemia.

 

Selected etiologies of metabolic acidosis:

  • Increased H+ production or ingestion: (MUDPILES acronym)
    • Methanol intoxication
    • Uremia
    • Diabetic ketoacidosis (common), alcoholic ketoacidosis, starvation ketoacidosis
    • Paraldehyde toxicity/propylene glycol
    • Isoniazid/iron
    • Lactic acidosis (metformin) (common)
      • Due to either tissue ischemia or altered cellular metabolism
    • Ethanol or ethylene glycol intoxication
    • Salicylate (aspirin) intoxication
  • HCO 3 - loss
    • GI loss
      • Diarrhea, ileostomy, proximal colostomy, ureteral diversion
    • Renal loss
      • Proximal renal tube acidosis
      • Carbonic anhydrase inhibitor (acetazolamide)
    • Renal tubular disease (dysfunction)
      • Acute tubular necrosis
      • Chronic renal disease
      • Distal renal tube acidosis
      • Aldosterone inhibitors or absence (+Addison’s disease)
      • NaCl infusion, TPN, NH4+ administration

 

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

  • GI loss of H+
  • Vomiting / diarrhoea (with Cl- rich fluid)
  • Renal loss H +
    • Loop and thiazide diuretics
    • Oedematous states (heart failure, cirrhosis, nephrotic syndrome)
    • Hyperaldosteronism (+Conn’s syndrome),
    • Exogenous steroids
    • Severe hypokalemia (H+/K+ exchange)
  • Burns
  • Iatrogenic: alkali/bicarbonate administration (milk alkali syndrome)

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:

  • Pulmonary problems e.g. COPD/asthma, pulmonary oedema, pneumonia
  • Mechanical problems e.g. Chest wall trauma/deformity, muscular dystrophies, motor neurone disease, myasthenia gravis, Guillain–Barré
  • Central problems (reduced breathing effort) e.g. Opiate overdose, acute CNS disease

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

  • Hyperventilation:
    • ↑pH  ↓PaCO2  ~HCO3-  ↑PaO2
    • Respiratory alkalosis
  • Chronic COPD:
    • ~pH  ↑PaCO2  ↑HCO3-  ↓PaO2
    • Type 2 respiratory failure; Fully compensated respiratory acidosis
  • Acute COPD exacerbation:
    • ↓pH  ↑↑PaCO2  ↑HCO3-  ↓↓PaO2
    • Type 2 respiratory failure; Partially compensated respiratory acidosis
  • Asthma exacerbation (life-threatening):
    • ↑pH  ↓PaCO2  ~HCO3-  ↓PaO2
    • Respiratory alkalosis (wheeze → anxiety → increased respiratory rate → hyperventilation → decreased PaCO2; on a background of increased airway resistance → decreased PaO2, despite the hyperventilation)
  • Decreased respiratory drive: (near-fatal) e.g. exhausted asthmatic exacerbation patient, opiate overdose)
    • ↓pH  ↑PaCO2  ~HCO3-  ↓PaO2
    • Type 2 respiratory failure; Respiratory acidosis
  • Pulmonary embolism (may vary depending on RR):
    • ↑pH  ↓PaCO2  ~HCO3-  ↓PaO2
    • Type 1 respiratory failure; Respiratory alkalosis (hyperventilation causes hypocapnia, but is unable to correct hypoxia due to VQ mismatch).
  • Other important presentations include heart failure, acute pulmonary oedema, and diabetic ketoacidosis.

Other disturbances2

Lactate

  • A raised lactate (lactic acid) can be caused by any anaerobic process.
  • Causes of lactic acidosis:
    • Hypoxic: Increased production of lactate e.g. DKA, starvation, cardiovascular/respiratory failure, severe sepsis
    • Non-hypoxic: A failure to break down lactate e.g. secondary to metformin or poisoning

Haemoglobin (Hb)

  • Haemoglobin acts as a guide but is often inaccurate. Lab samples should be sent to verify results.

Glucose

  • Especially relevant in patients with decreased consciousness or seizures; or known/suspected diabetes.
  • Glucose may also be disturbed in patients with sepsis.

Carbon monoxide (CO)

  • >10%: indicates poisoning, commonly from poorly ventilated boilers or old heating systems.
  • 10-20%: patient’s may experience symptoms such as nausea, headache, vomiting, and dizziness.
  • At higher levels: arrhythmias, cardiac ischaemia, respiratory failure, and seizures.

Methaemoglobin (metHb)

  • Methaemoglobin is a form of haemoglobin that contains the ferric [Fe3+] form of iron.
  • Levels of >2% are abnormal.
  • Symptoms include shortness of breath, cyanosis, altered mental state, headache, fatigue.
  • It may be caused by errors of metabolism or by exposure to toxins or certain medications such as nitrates.

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

 

/Abg

James Lloyd

Hull York Medical School

Metabolic acidosis1

Metabolic acidosis can occur as a result of either:

  • Increased H + production or ingestion
    • HCO3- concentrations decrease by acting as a buffer. The HCO3- is consumed by the H+ - to produce CO2 and H2O - resulting in a high pH.
  • GI or renal HCO 3 - loss
    • Where a decrease in HCO3- is the primary pathology, causing the acidaemia.

 

Selected etiologies of metabolic acidosis:

  • Increased H+ production or ingestion: (MUDPILES acronym)
    • Methanol intoxication
    • Uremia
    • Diabetic ketoacidosis (common), alcoholic ketoacidosis, starvation ketoacidosis
    • Paraldehyde toxicity/propylene glycol
    • Isoniazid/iron
    • Lactic acidosis (metformin) (common)
      • Due to either tissue ischemia or altered cellular metabolism
    • Ethanol or ethylene glycol intoxication
    • Salicylate (aspirin) intoxication
  • HCO 3 - loss
    • GI loss
      • Diarrhea, ileostomy, proximal colostomy, ureteral diversion
    • Renal loss
      • Proximal renal tube acidosis
      • Carbonic anhydrase inhibitor (acetazolamide)
    • Renal tubular disease (dysfunction)
      • Acute tubular necrosis
      • Chronic renal disease
      • Distal renal tube acidosis
      • Aldosterone inhibitors or absence (+Addison’s disease)
      • NaCl infusion, TPN, NH4+ administration

 

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

/Abg

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:

  • Airway obstruction
    • Upper
    • Lower
      • COPD; Asthma (near-fatal); Other obstructive lung disease
  • CNS depression: Opiates; Head trauma
  • Sleep disordered breathing (OSA or OHS)
  • Neuromuscular impairment/mechanical lung dysfunction
    • Guillain–Barré (paralysis leads to an inability to adequately ventilate); Obesity; Myasthenia gravis; deformity such as severe scoliosis.
  • Increased CO2 production: rigors; seizures; malignant hyperthermia
  • Iatrogenic: incorrect mechanical ventilation settings

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:

  • CNS stimulation: anxiety (panic attack), fever, pain, fear, CVA, cerebral oedema, brain trauma, brain tumour, CNS infection – causing increased respiratory rate
  • Hypoxia: lung disease, asthma (moderate/severe - hyperventilating), profound anaemia, low FiO2 – resulting in increased alveolar ventilation in an attempt to compensate
  • Stimulation of chest receptors: pulmonary oedema, pleural effusion, pneumonia, pneumothorax, pulmonary embolus
  • Drugs/hormones: salicylates, catecholamines, medroxyprogesterone, progestins
  • Conditions: Pregnancy, liver disease, sepsis, hyperthyroidism
  • Iatrogenic (excessive mechanical ventilation)

Metabolic acidosis1

Metabolic acidosis can occur as a result of either:

  • Increased H + production or ingestion
    • HCO3- concentrations decrease by acting as a buffer. The HCO3- is consumed by the H+ - to produce CO2 and H2O - resulting in a high pH.
  • GI or renal HCO 3 - loss
    • Where a decrease in HCO3- is the primary pathology, causing the acidaemia.

 

Selected etiologies of metabolic acidosis:

  • Increased H+ production or ingestion: (MUDPILES acronym)
    • Methanol intoxication
    • Uremia
    • Diabetic ketoacidosis (common), alcoholic ketoacidosis, starvation ketoacidosis
    • Paraldehyde toxicity/propylene glycol
    • Isoniazid/iron
    • Lactic acidosis (metformin) (common)
      • Due to either tissue ischemia or altered cellular metabolism
    • Ethanol or ethylene glycol intoxication
    • Salicylate (aspirin) intoxication
  • HCO 3 - loss
    • GI loss
      • Diarrhea, ileostomy, proximal colostomy, ureteral diversion
    • Renal loss
      • Proximal renal tube acidosis
      • Carbonic anhydrase inhibitor (acetazolamide)
    • Renal tubular disease (dysfunction)
      • Acute tubular necrosis
      • Chronic renal disease
      • Distal renal tube acidosis
      • Aldosterone inhibitors or absence (+Addison’s disease)
      • NaCl infusion, TPN, NH4+ administration

 

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

  • GI loss of H+
  • Vomiting / diarrhoea (with Cl- rich fluid)
  • Renal loss H +
    • Loop and thiazide diuretics
    • Oedematous states (heart failure, cirrhosis, nephrotic syndrome)
    • Hyperaldosteronism (+Conn’s syndrome),
    • Exogenous steroids
    • Severe hypokalemia (H+/K+ exchange)
  • Burns
  • Iatrogenic: alkali/bicarbonate administration (milk alkali syndrome)

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:

  • Pulmonary problems e.g. COPD/asthma, pulmonary oedema, pneumonia
  • Mechanical problems e.g. Chest wall trauma/deformity, muscular dystrophies, motor neurone disease, myasthenia gravis, Guillain–Barré
  • Central problems (reduced breathing effort) e.g. Opiate overdose, acute CNS disease

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

  • Hyperventilation:
    • ↑pH  ↓PaCO2  ~HCO3-  ↑PaO2
    • Respiratory alkalosis
  • Chronic COPD:
    • ~pH  ↑PaCO2  ↑HCO3-  ↓PaO2
    • Type 2 respiratory failure; Fully compensated respiratory acidosis
  • Acute COPD exacerbation:
    • ↓pH  ↑↑PaCO2  ↑HCO3-  ↓↓PaO2
    • Type 2 respiratory failure; Partially compensated respiratory acidosis
  • Asthma exacerbation (life-threatening):
    • ↑pH  ↓PaCO2  ~HCO3-  ↓PaO2
    • Respiratory alkalosis (wheeze → anxiety → increased respiration rate hyperventilation → decreased PaCO2; on a background of increased airway resistance → decreased PaO2, despite the hyperventilation)
  • Decreased respiratory drive: (near-fatal e.g. exhausted asthmatic exacerbation patient, opiate overdose)
    • ↓pH  ↑PaCO2  ~HCO3-  ↓PaO2
    • Type 2 respiratory failure; Respiratory acidosis
  • Pulmonary embolism (may vary depending on RR):
    • ↑pH  ↓PaCO2  ~HCO3-  ↓PaO2
    • Type 1 respiratory failure; Respiratory alkalosis (hyperventilation causes hypocapnia, but is unable to correct hypoxia due to VQ mismatch).
  • Other important presentations include heart failure, acute pulmonary oedema, and diabetic ketoacidosis.

Other disturbances2

Lactate

  • A raised lactate (lactic acid) can be caused by any anaerobic process.
  • Causes of lactic acidosis:
    • Hypoxic: Increased production of lactate e.g. DKA, starvation, cardiovascular/respiratory failure, severe sepsis
    • Non-hypoxic: A failure to break down lactate e.g. secondary to metformin or poisoning

Haemoglobin (Hb)

  • Haemoglobin acts as a guide but is often inaccurate. Lab samples should be sent to verify results.

Glucose

  • Especially relevant in patients with decreased consciousness or seizures; or known/suspected diabetes.
  • Glucose may also be disturbed in patients with sepsis.

Carbon monoxide (CO)

  • >10%: indicates poisoning, commonly from poorly ventilated boilers or old heating systems.
  • 10-20%: patient’s may experience symptoms such as nausea, headache, vomiting, and dizziness.
  • At higher levels: arrhythmias, cardiac ischaemia, respiratory failure, and seizures.

Methaemoglobin (metHb)

  • Methaemoglobin is a form of haemoglobin that contains the ferric [Fe3+] form of iron.
  • Levels of >2% are abnormal.
  • Symptoms include shortness of breath, cyanosis, altered mental state, headache, fatigue.
  • It may be caused by errors of metabolism or by exposure to toxins or certain medications such as nitrates.

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