1. Richard Stretton Respiratory Registrar
Arterial Blood Gases
Richard Stretton
Respiratory Registrar

2. Arterial Blood Gases Seen as complicated Misunderstood Important
An easy way and a hard way

3. Objectives Develop an organised system for looking at blood gases
Be able to comment on the arterial pO2 in relation to the FiO2
Interpret acid base disturbance and it’s significance in the acutely unwell

4. What Are We Measuring? pH
pO2
pCO2
HCO3
Base Excess

5. Acid Base Balance BICARBONATE pH is carefully controlled
Enzymatic Function relies on pH control
Buffers
Haemoglobin
BICARBONATE
Ammonium
Phosphate

6. Striking the Balance H+ + HCO3-  H2CO3  CO2 + H2O
When you’ve got too much H+, lungs blow off CO2
When you can’t blow off CO2, kidneys try to get rid of H+

7. 5-step approach Assess Oxygenation Determine Acid-Base Deficit
Determine the respiratory component
Determine the metabolic component
Which is primary and which is secondary

8. 5-step approach Assess Oxygenation Determine Acid-Base Deficit
Determine the respiratory component
Determine the metabolic component
Which is primary and which is secondary

9. 5-step approach pO2 = 10 -13 kPa on air Assess Oxygenation
Is the patient hypoxic?
Is there a significant A-a Gradient?
A-a Gradient is the difference in concentration of oxygen between the Alveolus (A) and the artery (a)
Normal <3
A-a Gradient = PAO2 – (PaO2 + PaCO2/0.8)

10. I shouldn’t say this but…
v.v.v.v. rough guide
Inspired O2 - (pO2 + pCO2)
Add together pO2 and pCO2 from your blood gas
Take this away from the concentration of Oxygen the patient is breathing
With an upper limit of normal of about 5

11. 5-step approach Assess Oxygenation Determine Acid-Base Deficit
Determine the respiratory component
Determine the metabolic component
Which is primary and which is secondary

12. 5-step approach Determine Acid-Base Deficit pH>7.45 alkalaemia
pH< acidaemia
Acidosis - a process causing excess acid to be present in the blood. Acidosis does not necessarily produce acidaemia
Alkalosis - a process causing excess base to be present in the blood. Alkalosis does not necessarily produce alkalaemia.

13. 5-step approach Assess Oxygenation Determine Acid-Base Deficit
Determine the respiratory component
Determine the metabolic component
Which is primary and which is secondary

14. 5-step approach Determine the respiratory component
Does this explain the acid-base deficit?
PaCO2: >6.0 kPa - respiratory acidosis
<4.7kPa - respiratory alkalosis

15. 5-step approach Assess Oxygenation Determine Acid-Base Deficit
Determine the respiratory component
Determine the metabolic component
Which is primary and which is secondary

16. 5-step approach Determine the metabolic component.
Does this explain the acid-base deficit?
HCO3 <22 mmols/l - metabolic acidosis
>26 mmols/l - metabolic alkalosis

17. Remember…… H+ + HCO3-  H2CO3  CO2 + H2O
When you’ve got too much H+, lungs blow off CO2
When you can’t blow off CO2, kidneys try to get rid of H+

18. 5-step approach Assess Oxygenation Determine Acid-Base Deficit
Determine the respiratory component
Determine the metabolic component
Which is primary and which is secondary

19. 5-step approach Which is primary and which is secondary? Remember
Compensation doesn’t always completely restore pH to the normal range
A mixed picture may be present

20. 5-step approach Assess Oxygenation Determine Acid-Base Deficit
Determine the respiratory component
Determine the metabolic component
Which is primary and which is secondary

21. Assumptions CO2 changes are related to respiratory changes
HCO3 changes relate to metabolic changes
Overcompensation does not occur
Respiratory compensation is rapid
Metabolic compensation is slow

22. Respiratory Acidosis Any cause of hypoventilation CNS depression
Neuromuscular disease
Acute or chronic lung disease
Cardiac arrest
Ventilator malfunction

23. Respiratory Alkalosis
Any cause of hyperventilation
Hypoxia
Acute lung conditions
Anxiety
Fever
Pregnancy
Hepatic failure
Some central CNS lesions

24. Metabolic Acidosis Added Acid Loss of Bicarbonate Renal failure
Ketoacidosis
Lactic acidosis
Salicylate/Tricyclic overdose
Renal tubular acidosis
Diarrhoea
Carbonic anhydrase inhibitors
Ureteral diversion
Chloride administration

25. Metabolic Alkalosis Loss of acid or gaining alkali Vomiting Diarrhoea
Diuretics (and hypokalaemia generally)
Ingestion of alkali

26. Reminder of normal values
pH – 7.45 (H+ = )
pO kPa on air
pCO kPa
HCO mmols/l
Base excess ± 2.0

27. Lets get going……..
Working out acidosis/alkalosis and compensation is usually the bit people struggle with
So…..

28. Outcome codes
Outcome
Code pH
High
Alkali
Low
Acid
pCO2
HCO3

29. Translate Uncompensated Metabolic Acidosis Value Code Translate
Opinion pH
7.1
Low
Acid
Acidaemia
pCO2
5.3
Normal
HCO3 16
Primary
Uncompensated Metabolic Acidosis

30. Translate Uncompensated Respiratory Acidosis Value Code Translate
Opinion pH
7.1
Low
Acid
Acidaemia
pCO2
8.3
High
Primary
HCO3 26
Normal
Uncompensated Respiratory Acidosis

31. Translate Uncompensated Respiratory Alkalosis Value Code Translate
Opinion pH
7.56
High
Alkali
Alkalaemia
pCO2
2.3
Low
Primary
HCO3 25
Normal
Uncompensated Respiratory Alkalosis

32. Translate Compensated Metabolic Acidosis or
Value
Code
Translate
Opinion pH
7.37
Normal
pCO2
2.1
Low
Alkali
????
HCO3 14
Acid
Compensated Metabolic Acidosis or
Compensated Respiratory Alkalosis

33. Translate Compensated Respiratory Acidosis or
Value
Code
Translate
Opinion pH
7.40
Normal
pCO2 8
High
Acid
????
HCO3 35
HIgh
Alkali
Compensated Respiratory Acidosis or
Compensated Metabolic Alkalosis

34. Translate Decompensated Respiratory Acidosis Value Code Translate
Opinion pH
7.21
Low
Acid
Acidaemia
pCO2 12
High
Primary
HCO3 32
Alkali
Secondary
Decompensated Respiratory Acidosis

35. What Now? Now you can determine any acid base pattern
Convert the numbers into high/low/normal
Convert that into acid/alkali
What is primary, what is compensation?
Distinguish between uncompensated, compensated, and decompensated

36. Nomenclature Uncompensated Respiratory Acidosis
Acute Type 2 Respiratory Failure
Compensated Respiratory Acidosis
Chronic Type 2 Respiratory Failure
Decompensated Respiratory Acidosis
Acute on Chronic Type 2 Respiratory Failure

37. Case 1
Young female admitted with overdose of unknown tablets and smelling of alcohol
pO kPa on air
pH 7.24
PaCO
HCO3 8
Metabolic Acidosis with respiratory compensation
Metabolic Acidosis with respiratory compensation and increased anion gap e.g. TCA overdose
A-a gradient 1.8

38. Case 2
Elderly male admitted from nursing home with one week history of fever and vomiting
pO kPa on 4l by mask
pH 7.49
PaCO
HCO3 35
Metabolic alkalosis with respiratory compensation
Metabolic alkalosis with respiratory compensation
A-a gradient 18 assuming FiO2 is 0.4
Possibilities include vomiting alone or atypical pneumonia with vomiting to account for increased A-a gradient and metabolic derangement

39. Case 3a
Middle aged man admitted with cough sputum and haemoptysis. Life-long smoker
pO2 4 on air
pH 7.19
PaCO
HCO3 28
Acute respiratory acidosis with no time for metabolic compensation
Acute respiratory acidosis with no time for metabolic compensation
A-a gradient 6.7
Candidates should say that the patient should receive a higher FiO2 and consider NIV.

40. Case 3b
Middle aged man admitted with cough sputum and haemoptysis. Life-long smoker
pO2 6 on air SpO2 92%
pH 7.32
PaCO
HCO3 39
Acute respiratory acidosis with no time for metabolic compensation
Practically fully compensated respiratory acidosis with hypoxia, but A-a gradient only 1.5
Increased FiO2 may not be necessary in this patient, AFTER the ABGs are known as this may be normal for them
The two cases can be used to highlight the difference between acute life-threatening hypoxia with hypoventilation and chronic type II respiratory failure

41. Case 4
Middle aged man post cardiac arrest. Breathing spontaneously on endotracheal tube
pO on 15l via reservoir mask
pH 6.9
PaCO
HCO3 13
Mixed metabolic and respiratory acidosis
Mixed metabolic and respiratory acidosis probably lactic, following cardiac arrest
A-a gradient 39.4
Candidate should recognise that gas exchange is not perfect despite that fact that the PaO2 is high
Patient needs to remain ventilated despite the good PaO2, to optimise Acid-base balance before extubation

42. Case 5 Elderly lady with congestive cardiac failure
pO2 9 on 40% oxygen
pH 7.64
PaCO
HCO3 29
Respiratory alkalosis secondary to pulmonary oedema.
Acute as no metabolic compensation
Respiratory alkalosis secondary to pulmonary oedema. Acute as no metabolic compensation
A-a gradient 24.6

43. Case 6
Young diabetic male admitted with chest infection, vomiting and drowsiness
pO on air
pH 7.31
PaCO
HCO3 6.0
Acute metabolic acidosis with respiratory compensation
Acute metabolic acidosis with respiratory compensation, presumable DKA, although lactic acidosis secondary to sepsis might be an alternative thought, or TCA overdose with the drowsiness
A-a gradient 3

44. Case 7
54 yr-old lady post MI. Acutely unwell, cold, clammy, hypotensive and oliguric
pO on 60% oxygen
pH 6.99
PaCO
HCO3 14
Mixed pattern of respiratory and metabolic acidosis
Mixed pattern of respiratory and metabolic acidosis due to cardiogenic shock
A-a gradient 37.3

45. Case 8
50 yr-old man admitted with exacerbation of long-standing bronchial asthma. Respiratory rate of 18
pO on 60% oxygen
pH 7.39
PaCO
HCO3 26
Severe type I respiratory failure
Could be venous sample!
Severe type I respiratory failure. A-a gradient 44.7
Presence of normal CO2 potentially very worrying if this all due to asthma. Is there something else contributing to this degree of hypoxia at the same time? PE for example
Candidates should be aware that a normal blood gas in acute severe asthma is either reassuring if the other features suggest that the asthma is not life-threatening. In the presence of other life-threatening features, this is a worrying blood gas

46. Questions ?

47. The 6th step…
If an acidosis is present work out the anion gap to help determine cause.
Anion Gap is the difference between the measured positive and negatively charged ions.
It gives an estimate of the unmeasured ions in the serum
Unmeasured – proteins, sulphates

48. Anion Gap
Anion Gap = [Na+K] –[CL+HCO3]
Normal anion gap 10-18

49. Metabolic Acidosis Increased anion gap (added acid) Renal failure
Ketoacidosis
Lactic acidosis
Salicylate/Tricyclic overdose

50. Metabolic Acidosis Decreased anion gap (loss of bicarbonate)
Renal tubular acidosis
Diarrhoea
Carbonic anhydrase inhibitors
Ureteral diversion
Chloride administration

51. High Anion Gap A M U D P I L E S

52. High Anion Gap Alcohol (Alcohol dissociates to become a week acid) M U

53. High Anion Gap Alcohol (Alcohol dissociates to become a week acid)
Methanol (See alcohol. Causes blindness) U D P I L E S

54. High Anion Gap Alcohol (Alcohol dissociates to become a week acid)
Methanol (See alcohol. Causes blindness)
Uraemia (Failure to reabsorb HCO3- and excrete H+) D P I L E S

55. High Anion Gap Alcohol (Alcohol dissociates to become a weak acid)
Methanol (See alcohol. Causes blindness)
Uraemia (Failure to reabsorb HCO3- and excrete H+)
DKA (Ketones are dehydrogenated alcohols, and dissociate to acid) P I L E S

56. High Anion Gap Alcohol (Alcohol dissociates to become a weak acid)
Methanol (See alcohol. Causes blindness)
Uraemia (Failure to reabsorb HCO3- and excrete H+)
DKA (Ketones are dehydrogenated alcohols, and dissociate to acid)
Paraquat (Very nasty poison, universally lethal) I L E S

57. High Anion Gap Alcohol (Alcohol dissociates to become a weak acid)
Methanol (See alcohol. Causes blindness)
Uraemia (Failure to reabsorb HCO3- and excrete H+)
DKA (Ketones are dehydrogenated alcohols, and dissociate to acid)
Paraquat (Very nasty poison, universally lethal)
Infection (Commonest cause. Localised tissue hypoxia leads to...) L E S

58. High Anion Gap Alcohol (Alcohol dissociates to become a weak acid)
Methanol (See alcohol. Causes blindness)
Uraemia (Failure to reabsorb HCO3- and excrete H+)
DKA (Ketones are dehydrogenated alcohols, and dissociate to acid)
Paraquat (Very nasty poison, universally lethal)
Infection (Commonest cause. Localised tissue hypoxia leads to...)
Lactic Acid (Product of anaerobic respiration, and tissue necrosis) E S

59. High Anion Gap Alcohol (Alcohol dissociates to become a weak acid)
Methanol (See alcohol. Causes blindness)
Uraemia (Failure to reabsorb HCO3- and excrete H+)
DKA (Ketones are dehydrogenated alcohols, and dissociate to acid)
Paraquat (Very nasty poison, universally lethal)
Infection (Commonest cause. Localised tissue hypoxia leads to...)
Lactic Acid (Product of anaerobic respiration, and tissue necrosis)
Ethylene Gylcol (Antifreeze. Quite a potent acid, no longer sold in UK) S

60. High Anion Gap Alcohol (Alcohol dissociates to become a weak acid)
Methanol (See alcohol. Causes blindness)
Uraemia (Failure to reabsorb HCO3- and excrete H+)
DKA (Ketones are dehydrogenated alcohols, and dissociate to acid)
Paraquat (Very nasty poison, universally lethal)
Infection (Commonest cause. Localised tissue hypoxia leads to...)
Lactic Acid (Product of anaerobic respiration, and tissue necrosis)
Ethylene Gylcol (Antifreeze. Quite a potent acid, no longer sold in UK)
Salicylates (Aspirin causes resp alkalosis, then metabolic acidosis)

61. Normal Anion Gap Addison’s Disease High Output Fistulas RTA I, II, IV
Acetazolamide Therapy
Diarrhoea

62. Any more Questions?