Overview

An arterial blood gas (ABG) is commonly performed in patients with respiratory failure, unconscious patients, patients with abnormal electrolytes and derangements of bicarbonate ions, and any other cause that may have acid-base abnormalities (e.g. heart failure, renal failure, diabetic ketoacidosis, sepsis, and burns).

An ABG generally measures the following (rough reference ranges are included):

  • pH – the hydrogen ion concentration (7.35 – 7.45)
  • pO2 – the partial pressure of oxygen (O2) (11 – 15 kPa)
  • pCO2 – the partial pressure of carbon dioxide (CO2) (4.6 – 6.4 kPa)
  • HCO3– – bicarbonate ion concentration (22 – 30 mmol/L)
  • Base excess (-2 to +2 mmol/L)

A blood sample is generally obtained by directly inserting a needle into the radial artery at the wrist.

It may be helpful to read about normal acid-base homeostasis.

Arterial Blood Gas Interpretation

Compensation

The acid-base balance is maintained via the respiratory system and renal and bicarbonate systems. Respiratory compensation occurs quickly over seconds to minutes when a metabolic disorder causes pH derangements (i.e. reduced or increased HCO3– causing acidosis or alkalosis):

  • Increased ventilation blows off more CO2, therefore less acid is retained in the blood, and this attempts to increase the pH.
  • Decreased ventilation ‘holds on to’ more CO2, therefore more acid is retained in the blood, and this attempts to decrease the pH.

Metabolic compensation takes a few days to occur when a respiratory disorder causes pH derangements (i.e. reduced or increased CO2 removal causing acidosis or alkalosis):

  • More HCO3– binds with more H+ and tries to reduce the amount of acid in the blood and increases pH.
  • Less HCO3– binds with less H+ and tries to increase the amount of acid in the blood and decreases the pH.

A balance of these two mechanisms is involved in acid-base homeostasis. Derangements in one may lead to another.

Clinical features

Before interpreting the results of an ABG, it is essential to compare pO2 and pCO2 to the patient briefly:

  • Normal pO2 in a patient with oxygen – this is misleadingly abnormal as they would not have a normal pO2 on room air
  • An unusually low pO2 in a completely well patient with normal O2 saturations – the sample is likely a venous blood sample, rather than arterial.

pO2

Is the patient hypoxic? In a healthy individual, the PaO2 is generally around 10 kPa lower than the inspired oxygen. For example, a patient breathing 40% inspired oxygen should have a pO2 of around 30 kPa. If this difference does not apply (e.g. a patient is breathing 50% inspired oxygen and their pO2 is 13 kPa) there is a problem.

Blood pH

Is the pH normal, acidotic (<7.35, more H+) or alkalotic (>7.45, less H+)? If the pH is normal or close to normal, this suggests a chronic condition with compensation. Compensation is either where the respiratory rate changes to alter CO2 levels and H+ if there is a metabolic disorder (problems with HCO3–), or where HCO3– levels change to alter H+ if there is a respiratory disorder.

As a general rule of thumb, the body does not overcompensate. If features suggest over-compensation, a mixed acid/base disorder may be present.

pCO2

Is this a respiratory problem? Derangements in pCO2 suggest a respiratory problem:

  • Low pH and high pCO2 suggest respiratory acidosis
  • High pH and low pCO2 suggest respiratory alkalosis

If the pH is normal or slightly high/low, this suggests compensation, therefore HCO3– should be looked at. If compensated, HCO3– is raised/lowered.

  • Normal/slightly low pH and high pCO2 and high HCO3– – respiratory acidosis with metabolic compensation
  • Normal/slightly high pH and low pCO2 and low HCO3– – respiratory alkalosis with metabolic compensation

Bicarbonate (HCO3–)

In summary, HCO3– binds to H+ and reduces their numbers. Therefore, a lower pH (more H+) would use up more HCO3– and reduce its levels, and a higher pH (less H+) would use up less and increase its levels. When interpreting bicarbonate, the following questions should be asked:

  • Is HCO3– normal?
    • If so, this suggests a respiratory problem without compensation
  • If abnormal, does it fit with the pH?
    • If the pH is lower (more H+), we would expect HCO3– to also be lower
    • If the pH is higher (less H+), we would expect HCO3– to also be higher
    • If it does not fit with the pH, it suggests compensation for a respiratory problem

Therefore, in summary:

  • Low pH, low HCO3– and normal pCO2 – metabolic acidosis
  • High pH, high HCO3– and normal pCO2 – metabolic alkalosis
  • Low pH, low HCO3– and low pCO2 – metabolic acidosis with respiratory compensation
    • The respiratory system is ‘getting rid’ of more H+ and acid via the removal of CO2 to try and compensate for metabolic acidosis. This usually manifests as hyperventilation.
  • High pH, high HCO3– and high pCO2 – metabolic acidosis with respiratory compensation
    • The respiratory system is ‘trying to hold on to’ more H+ and acid via less removal of CO2 to try and compensate for metabolic alkalosis. This usually manifests as hypoventilation.

Base Excess

The base excess describes the amount of base in the blood and is also used in interpreting metabolic acidosis or alkalosis:

  • A high base excess suggests increased HCO3– in the blood. This may be due to metabolic alkalosis or respiratory acidosis with metabolic compensation.
  • A low base excess suggests decreased HCO3– in the blood. This may be due to metabolic acidosis or respiratory alkalosis with metabolic compensation.

Anion Gap

Overview

The anion gap is the difference between positively charged ions (cations) and negatively charged ions (anions). It is typically used in metabolic acidosis and is calculated using (Na+ + K+) – (Cl– + HCO3–). Because K+ has a relatively small impact on the ion gap, it may be omitted in some scenarios, and the anion gap may be calculated using Na+ – (Cl– + HCO3–).

The number of cations should equal the number of anions so that the overall electrical charge is equal, however, tests performed do not measure all ions (such as albumin, lactate, and sulfate). Therefore, the anion gap represents all of the unmeasured ions left behind, which are generally anions, hence the name ‘anion gap’. A normal ion gap is generally considered to be 8-14 mmol/L.

Metabolic Acidosis: Causes

Metabolic acidosis with a normal anion gap

In metabolic acidosis with a normal gap, a decrease in HCO3– is the primary cause. However, when HCO3– is lost, it must be replaced with something of an equal charge to balance electrical charges. This is done by replacing the lost HCO3– with Cl–, hence, there is a normal ion gap.

Causes of HCO3– loss and hence, metabolic acidosis with a normal anion gap include:

  • Diarrhoea:
    • HCO3– is lost in the stool
  • Renal tubular acidosis:
    • The renal tubules cannot acidify urine, therefore HCO3– is used up to compensate
  • Addison’s disease:
    • Reduced aldosterone leads to urinary Na+ excretion and H+ retention in the serum, therefore HCO3– is used up to compensate
  • Some drugs (e.g. acetazolamide):
    • Acetazolamide is a carbonic anhydrase inhibitor, which is needed for combining CO2 and H2O to produce H2CO3, which dissociates into HCO3– and H+

Metabolic acidosis with a raised anion gap

Raised levels of acid due to an underlying cause bind to HCO3– to form H2CO3 which converts to CO2 and H2O. The HCO3– acts as a buffer, but is used up by the H+ without compensation, resulting in a high anion gap. Causes include:

  • Ketoacidosis: diabetic ketoacidosis, alcoholic ketoacidosis
    • Ketone acids lead to HCO3– consumption
  • Increased lactate: shock, hypoxia, metformin
    • Increased lactic acid leads to HCO3– consumption
  • Renal failure
    • Due to decreased acid excretion and HCO3– resorption
  • Salicylate overdose (i.e. aspirin overdose)
  • Methanol

Metabolic Alkalosis: Causes

Overview

Metabolic alkalosis occurs due to a loss of H+ from the body or an increase of HCO3–. The causes of metabolic alkalosis can be divided into:

  • Chloride-responsive alkalosis – loss of H+ by vomiting or dehydration
  • Chloride-resistant alkalosis – increased HCO3– due to retention

Chloride-responsive metabolic alkalosis

  • Vomiting – due to loss of gastric acid (hydrochloric acid, HCl)
  • Diuretic therapy – decreased blood volume triggers the renin-angiotensin-aldosterone system (RAAS). Aldosterone reabsorbs Na+ in exchange for H+ which is excreted in the urine while retaining HCO3–
  • Bicarbonate administration

Chloride-resistant metabolic alkalosis

  • Hyperaldosteronism – aldosterone promotes Na+ retention in exchange for H+ which is excreted in the urine while retaining HCO3–
  • Cushing’s syndrome – excess cortisol can bind to mineralocorticoid receptors and act like aldosterone, leading to similar effects mentioned above
  • Hypokalaemia – low serum K+ causes K+ to move from the cells into the blood. To maintain electrical neutrality, H+ moves into the cell, raising the blood pH

Respiratory Acidosis: Causes

Overview

Respiratory acidosis happens when problems with the respiratory system lead to ineffective carbon dioxide (CO2) clearance. It occurs due to an acute reduction in breathing or a significant increase in CO2 production that overwhelms normal homeostasis. These problems can include:

  • Diseases of the lung tissue itself (such as COPD)
  • Problems with chest wall mobility (such as obesity hypoventilation syndrome)
  • Neuromuscular disorders (such as Guillain-Barre syndrome or a myasthenic crisis)
  • Airway obstruction (such as foreign bodies, anaphylaxis, life-threatening asthma)
  • CO2 overproduction (e.g. sepsis and thyrotoxicosis)
  • Inadequate mechanical ventilation
  • Sedative drugs (e.g. benzodiazepines or opiate overdoses)

Respiratory Alkalosis: Causes

Overview

Respiratory alkalosis generally occurs secondary to tachypnoea (fast breathing). It may also be iatrogenic (such as improper ventilation settings). Some causes include:

  • Causes of hyperventilation (e.g. anxiety)
  • Pulmonary embolism – due to tachypnoea
  • Salicylate (e.g. aspirin) overdose – due to stimulation of the respiratory centres leading to alkalosis before metabolic acidosis follows
  • Focal neurological disorders – e.g. stroke, encephalitis, or intracranial bleeds
  • Pregnancy – progestogens stimulate the respiratory centres
  • High altitude – hypoxaemia may occur leading to tachypnoea

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