Look at the patient and see and predict what should be going on based on clinical suspicion.
Then look at the blood gas.
"Gases" get confusing if you don't note (scribble down) each finding as you work through the printout.
VBG vs ABG
VBGs used in EDs in preference to ABGs.
Correlation good, apart from pO2.
pCO2 correlates well at normal ranges. Correlation worsens with sepsis/shock/rising pCO2.
pH = 7.4 (7.35-7.45)
PaCO2 = 4.7 - 6.0 kPa.
HCO3- = 24 mmol/l (22-26)
BE = 0
- Note (scribble down) if the patient has an acidaemia or an alkalaemia?
- What is the primary acidosis or alkalosis?
- If it is a Metabolic Acidosis (MA):
- Is the anion gap wide (R[raised] AGMA) or not (NAGMA)?
- If RAGMA check delta gap [see below] (to see if another problem)?
- Is the respiratory compensation as expected [see below]?
- If it is a metabolic alkalosis
- Is the respiratory compensation as expected? [See below]
- If it is a respiratory acidosis
- Is the metabolic compensation as expected?[see below]
- If the anion gap is wide there is probably a concurrent RAGMA
- If it is a respiratory alkalosis:
- Is the metabolic compensation as expected?
- If the pH is normal check the anion gap, the base excess, and the PaCO2 as there may be hidden disturbances
- Check the PaO2 and the A-a oxygen difference. is it what is expected given the FiO2?
- Check the Hb, the glucose, and the electrolytes
- Does the gas fit the patient?
Anion gap (AG) = ( Na+ ) - ( HCO3- + Cl- )
Upper limit normal is about 15 using (Na+) - (HCO3- + Cl-)
More than 20 definitely abnormal
Causes of a wide anion gap
- Lactic acidosis
- Non-ketotic hyperosmolar coma
- Uraemia (or other Organic acidosis)
- IgA myeloma
- Lactate or Citrate
Causes of a low anion gap
- Adjusted anion gap = observed anion gap + 0.25 (normal albumin - observed albumin): Where albumin concentrations are in g/l
- IgG myeloma
- Lithium intoxication
- Analytical error: hypernatraemia, hyperlipidaemia
Anion gap : K+ + Na+ - Cl- - HCO3 = 8 - 16 mmol/l
with a high anion gap
with a normal AG
|C||CO (or Cyanide)|
|T||Toluene||P||Potassium sparing diuretics|
|D||DKA (and AKA)||M||Mineral Acids|
|P||Paraldehyde / Phenformin||E||Enterostomy|
|I||Iron / isoniazid||D||Diarrhoea|
|L||Lactic acidosis||I||Intestinal fistula|
- If a wide-anion-gap metabolic acidosis is the only disturbance, then the change in value of the anion gap should equal the change in bicarbonate (ie) ↑ AG = ↓ HCO3-
- The delta gap = increase AG - decrease HCO3-
- For purposes of calculation take normal AG as 12 and normal HCO3- as 24
- Shortcut calculation: Δ AG - Δ HCO3- = (AG -12) - (24 - HCO3-) = Na+ - Cl- - 36
- If the delta gap is < -6 there is also a non-anion gap metabolic acidosis.
- Other causes of a delta gap < -6 are a respiratory alkalosis (with compensating non-anion gap acidosis), or a low anion gap state
- If the delta gap > +6 there is a concurrent metabolic alkalosis.
- Other causes of a delta gap > +6 are respiratory acidosis (with compensating metabolic alkalosis), or a non-acidotic high anion gap state
Expected PaCO2 = (1.5*bicarbonate) + 8
PaCO2 = decimal digits of pH ± 5 mmHg
Respiratory compensation for metabolic acidosis
Causes of respiratory acidosis
Disorders of gas exchange
- Pulmonary oedema
- Foreign body aspiration
- Mechanical ventilation
- Prolonged pneumonia
Respiratory muscle abnormalities
- Chest wall trauma
- Tension pneumothorax
- Familial periodic paralysis
- Muscle weakness
- Myasthenia gravis
- Amyotrophic lateral sclerosis
- Pickwickian syndrome
Respiratory centre abnormalities
- General anaesthesia
- Cardiac arrest
- CNS abnormalities
Metabolic compensation for respiratory acidosis
- Acute respiratory acidosis - Δ HCO3- = 1 mmol/l for each 1 kPa change in pCO2
- Chronic respiratory acidosis - Δ HCO3- = 4 mmol/l for each 1 kPa change in pCO2
Causes of respiratory alkalosis
- CNS diseases
- Anxiety / hysteria
- Hypermetabolic states
- Hepatic insufficiency
- Assisted ventilation
Metabolic compensation for resp. alkalosis
Respiratory acidosis and alkalosis are characterized by a primary change in pCO2. Secondary physiological compensation is seen in blood gas results as a change (Δ) in bicarbonate concentration (↑ in the case of acidosis and ↓ in alkalosis). So expect:
- Acute respiratory alkalosis - Δ HCO3- = 2 mmol/l for each 1 kPa change in pCO2
- Chronic respiratory alkalosis - Δ HCO3- = 3 mmol/l for each 1 kPa change in pCO2
Causes of metabolic alkalosis
(urine chloride < 10 mmol/l ) .. hypovolaemia
- Vomiting, NG suctioning
- Following respiratory acidosis
- Exogenous alkalis
- Contraction alkalosis
Saline unresponsive . normovolaemia
- Hyperaldosteronism ( primary, secondary, exogenous )
- Cushing's syndrome
- Severe hypokalaemia
- Milk alkali syndrome
- Metabolism of organic anions
- Massive blood transfusion
- Nonparathyroid hypercalcaemia
Respiratory compensation for metabolic alkalosis
Expected PaCO2 = (0.9 x bicarb) + 9 OR Expected PaCO2 = decimal digits of pH ± 5 mmHg
PaO2 and age
The normal value for the partial pressure of arterial oxygen (PaO2) irrespective of age is >10.6 kPa.
The normal PaO2 for a given age can be predicted from:
- Seated PaO2 = 13.8 kPa - 0.27 x age
- Supine PaO2 = 13.8 kPa - 0.42 x age
If PaO2 is < 10.7 kPa, the patient has arterial hypoxemia.
Causes of a low PaO2
- Shunt (pulmonary, cardiovascular)
- Ventilation perfusion imbalance
- Diffusion block
- Decreased PiO2
- Low mixed venous oxygen content
A-a oxygen difference [P(A-a)O2]
- PAO2 is estimated from the alveolar gas equation
- PaO2 is measured in the blood gases
- P(A-a)O2 at sea level = (FiO2 x 713) - 1.2(PaCO2) - PaO2 (Drop the 1.2 correction factor if FiO2 > 0.6)
- The predicted A-a oxygen difference is 5-15 mmHg in youth, 15-25 mmHg in the elderly
- The A-a oxygen difference can be 10-110 mmHg for individuals breathing >60% oxygen
- The A-a oxygen difference should be measured with the patient upright
Approximate FiO2 based on oxygen flow rate in a rigid mask:
|Flow rate l/min||4||6||8||10||12||15|
Approximate FiO2 based on oxygen flow rate with nasal cannulae
|Flow rate l/min||1||2||3||4||5||6|