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 (±2)
- 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 (N[normal] AGMA)?
- 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 : 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-
- Take normal AG as 12 and normal HCO3- as 24
- ΔAG-ΔHCO3- = (AG-12)-(24-HCO3-) = Na+ - Cl- - 36
Na+ - Cl- - 36
- <-6 = Mixed high and normal anion gap acidosis
- -6 to 6 = Only a high anion gap acidosis exists
- >+6 = Mixed high AG acidosis and metabolic alkalosis
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
Resp. compensation in Metab acidosis:
Expected PaCO2 = (1.5*bicarbonate) + 8
In mmHg .... 7.xx rule (mmHg) : PaCO2 = decimal digits of pH ± 5 mmHg
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 Resp. acidosis - Δ HCO3- = 1 mmol/l for each 1 kPa change in pCO2
- Chronic Resp. 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 Resp. alkalosis - Δ HCO3- = 2 mmol/l for each 1 kPa change in pCO2
- Chronic Resp. 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
- Each pH ↓, K+ should ↑ by from 5mmol/L by 0.5 mmol/L
- E.g. Expect K+ for pH 7.2 = 5.0 + 2 = 6.0 mmol/L
- Na+ + (Glucose -5)/3
A-a oxygen gradient [P(A-a)O2]
Approx. FiO2 on O2 flow rate in a rigid mask:
|Flow rate l/min||4||6||8||10||12||15|
Approx. FiO2 on O2 flow rate nasal cannulae
|Flow rate l/min||1||2||3||4||5||6|
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
- ↓ PiO2
- Low mixed venous oxygen content