 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 PaO kPa ON AIR › Correct hypoxaemia immediately (target SpO 2 )  Respiratory failure defined as PaO 2 <8kPa (SpO 2 <93%) › Type I – normal PaCO 2 › Type 2 – elevated PaCO 2 (ventilatory failure)  Significant respiratory failure may be present despite ‘normal’ or high PaO 2 › Predicted PaO 2 normally ~10kPa below FiO 2 › e.g. 40% venturi, PaO 2 should be ~30kPa › Document oxygen use on ABG result!

 Look at the pH (normal range )  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  CO 2 is acidic and HCO 3 - is alkaline  Normal compensation for acidosis is to decrease CO 2 (rapid) and increase HCO 3 - (takes longer)  Normal compensation for alkalosis is to decrease HCO 3 - (and increase CO 2 )

 Normal range for PaCO 2 is kPa  Acidosis (pH <7.35) › PaCO 2 >6.0kPa = respiratory acidosis › PaCO 2 <6.0kPa = metabolic acidosis  Alkalosis (pH >7.45) › PaCO 2 >4.5kPa = metabolic alkalosis › PaCO 2 <4.5kPa = respiratory alkalosis

 Normal range for HCO 3 - is 22-26mmol/L › Normal range for base excess (BE) is -2 to +2  Acidosis (pH <7.35) › HCO 3 - <22mmol/L (BE < -2) = metabolic acidosis › HCO 3 - >22mmol/L (BE > -2) = respiratory acidosis  Alkalosis (pH >7.45) › HCO 3 - >26mmol/L (BE > +2) = metabolic alkalosis › HCO 3 - <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) › PaCO 2 >6.0kPa with HCO 3 - >26mmol/L = › Respiratory acidosis with partial metabolic compensation › PaCO 2 >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 PaO kPa kPa PaCO 2 8.9kPa kPa HCO mmol/L 22-26mmol/L BE to +2 Lactate 1.8mmol/L <2.0mmol/L

 Relative hypoxaemia (PaO2 should be ~30kPa)  Respiratory failure = type 2 (elevated PaCO2)  Acidosis (pH <7.35)  High PaCO 2 = respiratory acidosis  High HCO 3 - = 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.

FiO (21%) 0.21 (air) pH PaO kPa kPa PaCO 2 3.2kPa kPa HCO mmol/L 22-26mmol/L BE to +2 Lactate 2.8mmol/L <2.0mmol/L

 Normal PaO 2 on air i.e. no respiratory failure  Normal pH however;  Low HCO 3 - and BE with high lactate and ketones = metabolic acidosis  Low PaCO 2 = 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.

FiO (35%)0.21 (air) pH PaO kPa kPa PaCO 2 7.5kPa kPa HCO mmol/L22-26mmol/L BE-8-2 to +2 Lactate4.2mmol/L<2.0mmol/L

 Relative hypoxaemia (PaO 2 should be ~25kPa)  Respiratory failure = type 2 (elevated PaCO 2 )  Acidosis (pH <7.35)  High PaCO 2 = respiratory acidosis  Low HCO 3 - 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, SpO 2 96% on air. Chest clear. Looks anxious ++

FiO (40%) 0.21 (air) pH PaO kPa kPa PaCO 2 3.8kPa kPa HCO mmol/L 22-26mmol/L BE to +2 Lactate 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 pO 2 or pCO 2 › Normal pCO 2 on VBG excludes hypercapnia  Good correlation with ABG for other parameters › pH, lactate, BE, HCO 3 -, 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 DisorderpHpCO 2 HCO 3 - 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