Unexpected deterioration of sick patient Hypoxaemia on sats monitoring Reduced conscious level Exacerbation of COPD Monitoring of ventilated patient Sepsis Metabolic or electrolyte problem e.g. DKA Drug Overdose
Normal PaO2 11.5-13.5 kPa ON AIR› Correct hypoxaemia immediately (target SpO2)
Respiratory failure defined as PaO2 <8kPa (SpO2 <93%)› Type I – normal PaCO2
› Type 2 – elevated PaCO2 (ventilatory failure)
Significant respiratory failure may be present despite ‘normal’ or high PaO2
› Predicted PaO2 normally ~10kPa below FiO2
› e.g. 40% venturi, PaO2 should be ~30kPa
› Document oxygen use on ABG result!
Look at the pH (normal range 7.35-7.45)
pH <7.35 = acidaemia/acidosis
pH >7.45 = alkaemia/alkalosis
Acidosis or alkalosis may still be present with a ‘normal’ pH if the body has already buffered = compensation
CO2 is acidic and HCO3- is alkaline
Normal compensation for acidosis is to decrease CO2
(rapid) and increase HCO3- (takes longer)
Normal compensation for alkalosis is to decrease HCO3-
(and increase CO2)
Normal range for PaCO2 is 4.5-6.0kPa
Acidosis (pH <7.35)› PaCO2 >6.0kPa = respiratory acidosis
› PaCO2 <6.0kPa = metabolic acidosis
Alkalosis (pH >7.45)› PaCO2 >4.5kPa = metabolic alkalosis
› PaCO2 <4.5kPa = respiratory alkalosis
Normal range for HCO3- is 22-26mmol/L
› Normal range for base excess (BE) is -2 to +2
Acidosis (pH <7.35)› HCO3
- <22mmol/L (BE < -2) = metabolic acidosis
› HCO3- >22mmol/L (BE > -2) = respiratory acidosis
Alkalosis (pH >7.45)› HCO3
- >26mmol/L (BE > +2) = metabolic alkalosis
› HCO3- <26mmol/L (BE < +2) = respiratory alkalosis
What is the primary disturbance?
Is there any compensation?
Is there a mixed picture?
e.g. in acidosis (pH <7.35)
› PaCO2 >6.0kPa with HCO3- >26mmol/L =
› Respiratory acidosis with partial metabolic compensation
› PaCO2 >6.0kPa with HCO3- <22mmol/L =
› Mixed respiratory and metabolic acidosis
Lactate (normal range 0-2mmol/L)
› Elevated levels often associated with acidosis
› tissue hypoperfusion/anaerobic metabolism, liver/renal failure or drugs (e.g. metformin)
› Degree of elevation correlates directly with mortality in sepsis
› Response to fluids also important
Haemoglobin (Hb)
Potassium (K+) and Sodium (Na+)
Glucose (not on AMU analyzer)
78-year-old male admitted with IECOPD becomes more drowsy and confused whilst on AMU. Oxygen is being delivered via a non-rebreathe bag and mask.
FiO2 0.4 (40%) 0.21 (air)pH 7.21 7.35-7.45PaO2 15.7kPa 11.5-13.5kPa
PaCO2 8.9kPa 4.5-6.0kPa
HCO3- 31mmol/L 22-
26mmol/LBE +8 -2 to +2Lactate 1.8mmol/L <2.0mmol/L
Relative hypoxaemia (PaO2 should be ~30kPa) Respiratory failure = type 2 (elevated PaCO2) Acidosis (pH <7.35) High PaCO2 = respiratory acidosis
High HCO3- = partial metabolic compensation
(likely chronic) Acute-on-chronic type 2 respiratory failure with
respiratory acidosis and partial metabolic compensation
29-year-old female with type 1 diabetes. Admitted with 48h history of diarrhoea and vomiting. Rapid respiratory rate. CBG 27mmol/L and blood ketones 4.9mmol/L.
FiO2 0.21 (21%) 0.21 (air)pH 7.36 7.35-7.45PaO2 13.7kPa 11.5-13.5kPa
PaCO2 3.2kPa 4.5-6.0kPa
HCO3- 14mmol/L 22-
26mmol/LBE -12 -2 to +2Lactate 2.8mmol/L <2.0mmol/L
Normal PaO2 on air i.e. no respiratory failure Normal pH however; Low HCO3
- and BE with high lactate and ketones = metabolic acidosis
Low PaCO2 = respiratory compensation (Kussmaul respiration)
Fully compensated metabolic acidosis due to DKA
36-year-old male with alcohol dependence and ALD. Admitted to AMU following a staggered co-codamol overdose. GCS 8/15 with small pupils and respiratory rate of 10/min.
FiO2 0.35 (35%) 0.21 (air)pH 7.19 7.35-7.45PaO2 11.7kPa 11.5-13.5kPa
PaCO2 7.5kPa 4.5-6.0kPa
HCO3- 17mmol/L 22-
26mmol/LBE -8 -2 to +2Lactate 4.2mmol/L <2.0mmol/L
Relative hypoxaemia (PaO2 should be ~25kPa)
Respiratory failure = type 2 (elevated PaCO2) Acidosis (pH <7.35) High PaCO2 = respiratory acidosis
Low HCO3- and BE = metabolic acidosis
Mixed respiratory and metabolic (lactic) acidosis Hypoventilation due to reduced GCS (hepatic
encephalopathy) and opiate overdose Lactic acidosis due to liver failure/drug overdose
56-year-old female admitted with acute breathlessness. Recent marital stress. Heart rate 120/min, respiratory rate 28/min, SpO2 96% on air. Chest clear. Looks anxious ++
FiO2 0.21 (40%) 0.21 (air)pH 7.49 7.35-7.45PaO2 10.1kPa 11.5-13.5kPa
PaCO2 3.8kPa 4.5-6.0kPa
HCO3- 25mmol/L 22-
26mmol/LBE +2 -2 to +2Lactate 0.7mmol/L <2.0mmol/L
Hyperventilation with respiratory alkalosis
No metabolic compensation
May be due to anxiety/panic attack but relative hypoxaemia in this case suggests alternative cause e.g. PE, pneumonia, acute asthma
Cannot be used to assess pO2 or pCO2 › Normal pCO2 on VBG excludes hypercapnia
Good correlation with ABG for other parameters › pH, lactate, BE, HCO3
-, electrolytes, Hb
› except if patient shocked/peri-arrest
VBG usually adequate in all other situations› Obtain VBG in all acutely unwell patients› Especially sepsis, DKA, UGIB, AKI, overdose
Sample must not be shaken and should be analysed immediately (<10min) to prevent haemolysis › lowers pH and increases K+
K+ up to 0.5mmol lower than lab value
Na+ up to 6mmol lower than lab value
Hb 5g/L higher than lab value on average
Acid Base Disorder pH pCO2 HCO3- Examples
Metabolic Acidosis ↓ ↔ ↓Sepsis, shock,
AKI, drugs, DKA
Metabolic Acidosis with Respiratory Compensation
↔ ↓ ↓ DKA with Kussmaul’s
Respiratory Acidosis ↓ ↑ ↔ COPD, LVF, reduced GCS
Respiratory Acidosis with Metabolic Compensation
↔ ↑ ↑ COPD with chronic T2RF
Metabolic Alkalosis ↑ ↔ ↑ Prolonged vomiting
Respiratory Alkalosis ↑ ↓ ↔Anxiety, PE, pneumonia,
asthma