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Procedural Skills (SLO6)
Question 29 of 127
You are asked to review an arterial blood gas (ABG) that has been performed by a junior colleague. The ABG shows a normal anion gap metabolic acidosis. Which of the following is a cause of a normal anion gap metabolic acidosis?
Answer:
- A normal anion gap indicates decreased acid excretion or loss of bicarbonate (FUSED CARS)
- Fistula (pancreaticoduodenal)
- Ureteroenteric conduit
- Saline administration
- Endocrine (hyperparathyroidism)
- Diarrhoea
- Carbonic anhydrase inhibitors (e.g. acetazolamide)
- Ammonium chloride
- Renal tubular acidosis
- Spironolactone
Arterial Blood Gas Analysis
Procedural Skills (SLO6)
Last Updated: 16th February 2023
Normal ABG values
RCEM defines the normal values for blood gases as:
- pH = 7.35 - 7.45
- pO2 (on air) = 11 - 14 kPa
- pCO2 = 4.5 - 6.0 kPa
- HCO3- = 24 - 30 mmol/L
- BE = +/- 2 mmol/L
Base Excess
- Base excess is defined as the amount of strong acid that must be added to each litre of fully oxygenated blood to return the pH to 7.40 at a temperature of 37 °C and a pCO2 of 40 mmHg (5.3 kPa). A negative base excess (a base deficit) can be correspondingly defined in terms of the amount of strong base that must be added.
- A typical reference range for base excess is -2 to +2 mmol/L.
- A base excess higher than +2 mmol/L indicates:
- Primary metabolic alkalosis or
- Compensation for primary respiratory acidosis
- A base excess more negative than -2 mmol/L (a base deficit) indicates:
- Primary metabolic acidosis or
- Compensation for primary respiratory alkalosis
Interpretation of ABG Results
- Assess the patient clinically
- Assess PaO2 (in the context of any supplemental oxygen)
- As a rule of thumb the PaO2 should be numerically about 10 less than the inspired oxygen concentration (%); if there is a difference of greater than 10 between the two values, there is a defect in oxygenation, proportional to the magnitude of the difference (so a patient breathing room air should have a PaO2 10.0 - 13.0 kPa)
- PaO2 < 10 kPa on air = hypoxaemia
- Assess pH
- pH < 7.35 = acidaemia
- pH > 7.45 = alkalaemia
- Assess PaCO2
- pH < 7.35 and PaCO2 > 6.0 kPa = respiratory acidosis
- pH > 7.45 and PaCO2 < 4.7 kPa = respiratory alkalosis
- Assess base excess (BE) and bicarbonate
- pH < 7.35 and BE < - 2 mmol/L and/or bicarbonate < 22 mmol/L = metabolic acidosis
- pH > 7.45 and BE > +2 mmol/L and/or bicarbonate > 26 mmol/L = metabolic alkalosis
Respiratory Failure
- Type 1 respiratory failure
- Hypoxaemia (PaO2 <8 kPa) with normocapnia (PaCO2 <6.0 kPa)
- Caused by ventilation/perfusion (V/Q) mismatch
- The volume of air flowing in and out of the lungs is not matched with the flow of blood to the lung tissue. As a result of the VQ mismatch, PaO2 falls and PaCO2 rises. The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shape of the CO2 and O2 dissociation curves.
- For example in:
- Reduced ventilation and normal perfusion e.g. pulmonary oedema, bronchoconstriction
- Reduced perfusion and normal ventilation e.g. pulmonary embolism
- Type 2 respiratory failure
- Hypoxaemia (PaO2 <8 kPa) with hypercapnia (PaCO2 >6.0 kPa)
- Caused by alveolar hypoventilation
- The volume of air flowing in and out of the lungs is not enough for the patient to adequately oxygenate and eliminate CO2 from their blood.
- For example in:
- Increased resistance as a result of airway obstruction e.g. COPD
- Reduced compliance of the lung tissue/chest wall e.g. pneumonia, rib fractures, obesity
- Reduced strength of the respiratory muscles e.g. Guillain-Barré, motor neurone disease
- Drugs acting on the respiratory centre reducing overall ventilation e.g. opiates
Acid-Base Disturbance ABG Results
| Acid-base disturbance | pH | PaCO2 | HCO3-/BE |
|---|---|---|---|
| Respiratory acidosis | ↓ | ↑ | ↔ |
| Respiratory alkalosis | ↑ | ↓ | ↔ |
| Respiratory acidosis with metabolic compensation | ↓/↔ | ↑ | ↑ |
| Respiratory alkalosis with metabolic compensation | ↑/↔ | ↓ | ↓ |
| Metabolic acidosis | ↓ | ↔ | ↓ |
| Metabolic alkalosis | ↑ | ↔ | ↑ |
| Metabolic acidosis with respiratory compensation | ↓/↔ | ↓ | ↓ |
| Metabolic alkalosis with respiratory compensation | ↑/↔ | ↑ | ↑ |
| Mixed respiratory and metabolic acidosis | ↓ | ↑ | ↓ |
| Mixed respiratory and metabolic alkalosis | ↑ | ↓ | ↑ |
Compensation
- Respiratory acidosis/alkalosis (changes in CO2) can be metabolically compensated by increasing or decreasing the levels of HCO3- in an attempt to move the pH closer to the normal range.
- Metabolic acidosis/alkalosis (changes in HCO3-) can be compensated by the respiratory system retaining or blowing off CO2 in an attempt to move the pH closer to the normal range.
- Respiratory compensation for a metabolic disorder can occur quickly by either increasing or decreasing alveolar ventilation to blow off more CO2 ( to increase pH) or retain more CO2 (to decrease pH).
- Metabolic compensation for a respiratory disorder, however, takes at least a few days to occur as it requires the kidneys to either reduce HCO3– production (to decrease pH) or increase HCO3– production (to increase pH). As a result, if you see evidence of metabolic compensation for a respiratory disorder (e.g. increased HCO3-/base excess in a patient with COPD and CO2 retention) you can assume that the respiratory derangement has been ongoing for at least a few days, if not more.
- N.B. “Over-compensation” should never occur and therefore if you see something that resembles this you should consider other pathologies driving the change (e.g. a mixed acid/base disorder).
Respiratory Acidosis
Respiratory acidosis is caused by inadequate alveolar ventilation leading to CO2 retention.
Causes:
- Respiratory depression e.g. opiates
- Neurological, muscular or chest wall disease e.g. Guillain Barre
- Lung disease or injury e.g. asthma, COPD
- Iatrogenic (incorrect mechanical ventilation settings)
Respiratory Alkalosis
Respiratory alkalosis is caused by excessive alveolar ventilation (hyperventilation) resulting in more CO2 than normal being exhaled.
Causes:
- Anxiety/panic attack
- Pain
- Hypoxia
- Pulmonary embolism
- Pneumothorax
- Iatrogenic (excessive mechanical ventilation)
Metabolic Acidosis
Metabolic acidosis can occur due to:
- Increased acid production e.g. lactic acidosis, ketoacidosis (DKA, alcohol, starvation)
- Increased acid ingestion e.g. salicylate overdose, ethylene glycol poisoning
- Decreased acid excretion e.g. acute or chronic renal failure
- Increased gastrointestinal HCO3– loss e.g. chronic diarrhoea, ileal conduits, fistulae, small intestinal/pancreatic/biliary drains
- Increased renal HCO3– loss e.g. renal tubular acidosis
Anion Gap:
- The anion gap (AG) is a derived variable primarily used for the evaluation of metabolic acidosis to determine the presence of unmeasured anions. To work out if the metabolic acidosis is due to increased acid production or ingestion vs decreased acid excretion or loss of bicarbonate you can calculate the anion gap.
- Anion gap = (Na+ + K+) – (Cl- + HCO3-) or (Na+) – (Cl- + HCO3-)
- The normal anion gap varies with different assays but is typically between 4 to 12 mmol/L.
- A high anion gap indicates increased acid production or acid ingestion (MUDPILES)
- Methanol
- Uraemia (in renal failure)
- Diabetic ketoacidosis
- Propylene glycol overdose
- Infection/Iron overdose/Isoniazid/Inborn errors of metabolism
- Lactic acidosis
- Ethylene glycol overdose
- Salicylate overdose
- A normal anion gap indicates decreased acid excretion or loss of bicarbonate (FUSED CARS)
- Fistula (pancreaticoduodenal)
- Ureteroenteric conduit
- Saline administration
- Endocrine (hyperparathyroidism)
- Diarrhoea
- Carbonic anhydrase inhibitors (e.g. acetazolamide)
- Ammonium chloride
- Renal tubular acidosis
- Spironolactone
Metabolic Alkalosis
Metabolic alkalosis occurs as a result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations.
Causes:
- Gastrointestinal loss of H+ ions e.g. vomiting, diarrhoea, pyloric stenosis, NGT drainage
- Renal loss of H+ ions e.g. loop and thiazide diuretics, heart failure, nephrotic syndrome, cirrhosis, Conn’s syndrome
- Ingestion of HCO3- e.g. sodium bicarbonate, antacid overdose
- Iatrogenic (e.g. addition of alkali such as milk-alkali syndrome)
Mixed Acidosis/Alkalosis
- It is possible to have a mixed acidosis or alkalosis (e.g. respiratory and metabolic acidosis/respiratory and metabolic alkalosis).
- In these circumstances, the CO2 and HCO3- will be moving in opposite directions.
- Treatment is directed towards correcting each primary acid-base disturbance.
Causes of mixed respiratory and metabolic acidosis:
- Cardiac arrest
- Multi-organ failure
Causes of mixed respiratory and metabolic alkalosis:
- Liver cirrhosis in addition to diuretic use
- Hyperemesis gravidarum
- Excessive ventilation in COPD
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
