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