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Richard Stretton Respiratory Registrar

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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?


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