Title: Arterial Blood Gases
1Arterial Blood Gases
- Richard Stretton
- Respiratory Registrar
2Arterial Blood Gases
- Seen as complicated
- Misunderstood
- Important
- An easy way and a hard way
3Objectives
- 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 its
significance in the acutely unwell
4What Are We Measuring?
- pH
- pO2
- pCO2
- HCO3
- Base Excess
5Acid Base Balance
- pH is carefully controlled
- Enzymatic Function relies on pH control
- Buffers
- Haemoglobin
- BICARBONATE
- Ammonium
- Phosphate
6Striking the Balance
- H HCO3- ? H2CO3 ? CO2 H2O
- When youve got too much H, lungs blow off CO2
- When you cant blow off CO2, kidneys try to get
rid of H
75-step approach
- Assess Oxygenation
- Determine Acid-Base Deficit
- Determine the respiratory component
- Determine the metabolic component
- Which is primary and which is secondary
85-step approach
- Assess Oxygenation
- Determine Acid-Base Deficit
- Determine the respiratory component
- Determine the metabolic component
- Which is primary and which is secondary
95-step approach
- Assess Oxygenation
- pO2 10 -13 kPa on air
- 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 lt3
- A-a Gradient PAO2 (PaO2 PaCO2/0.8)
10I shouldnt 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
115-step approach
- Assess Oxygenation
- Determine Acid-Base Deficit
- Determine the respiratory component
- Determine the metabolic component
- Which is primary and which is secondary
125-step approach
- Determine Acid-Base Deficit
- pHgt7.45 alkalaemia
- pHlt7.35 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.
135-step approach
- Assess Oxygenation
- Determine Acid-Base Deficit
- Determine the respiratory component
- Determine the metabolic component
- Which is primary and which is secondary
145-step approach
- Determine the respiratory component
- Does this explain the acid-base deficit?
- PaCO2 gt6.0 kPa - respiratory acidosis
- lt4.7kPa - respiratory alkalosis
155-step approach
- Assess Oxygenation
- Determine Acid-Base Deficit
- Determine the respiratory component
- Determine the metabolic component
- Which is primary and which is secondary
165-step approach
- Determine the metabolic component.
- Does this explain the acid-base deficit?
- HCO3 lt22 mmols/l - metabolic acidosis
- gt26 mmols/l - metabolic alkalosis
17Remember
- H HCO3- ? H2CO3 ? CO2 H2O
- When youve got too much H, lungs blow off CO2
- When you cant blow off CO2, kidneys try to get
rid of H
185-step approach
- Assess Oxygenation
- Determine Acid-Base Deficit
- Determine the respiratory component
- Determine the metabolic component
- Which is primary and which is secondary
195-step approach
- Which is primary and which is secondary?
- Remember
- Compensation doesnt always completely restore pH
to the normal range - A mixed picture may be present
205-step approach
- Assess Oxygenation
- Determine Acid-Base Deficit
- Determine the respiratory component
- Determine the metabolic component
- Which is primary and which is secondary
21Assumptions
- 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
22Respiratory Acidosis
- Any cause of hypoventilation
- CNS depression
- Neuromuscular disease
- Acute or chronic lung disease
- Cardiac arrest
- Ventilator malfunction
23Respiratory Alkalosis
- Any cause of hyperventilation
- Hypoxia
- Acute lung conditions
- Anxiety
- Fever
- Pregnancy
- Hepatic failure
- Some central CNS lesions
24Metabolic 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
25Metabolic Alkalosis
- Loss of acid or gaining alkali
- Vomiting
- Diarrhoea
- Diuretics (and hypokalaemia generally)
- Ingestion of alkali
26Reminder of normal values
- pH 7.35 7.45 (H 35 -45)
- pO2 10 - 13 kPa on air
- pCO2 4.6 - 6.0 kPa
- HCO3 25 - 35 mmols/l
- Base excess 2.0
27Lets get going..
- Working out acidosis/alkalosis and compensation
is usually the bit people struggle with - So..
28Outcome codes
Outcome Code Outcome Code
pH High Alkali Low Acid
pCO2 High Acid Low Alkali
HCO3 High Alkali Low Acid
29Translate
Value Code Translate Opinion
pH 7.1 Low Acid Acidaemia
pCO2 5.3 Normal Normal Normal
HCO3 16 Low Acid Primary
Uncompensated Metabolic Acidosis
30Translate
Value Code Translate Opinion
pH 7.1 Low Acid Acidaemia
pCO2 8.3 High Acid Primary
HCO3 26 Normal Normal Normal
Uncompensated Respiratory Acidosis
31Translate
Value Code Translate Opinion
pH 7.56 High Alkali Alkalaemia
pCO2 2.3 Low Alkali Primary
HCO3 25 Normal Normal Normal
Uncompensated Respiratory Alkalosis
32Translate
Value Code Translate Opinion
pH 7.37 Normal Normal Normal
pCO2 2.1 Low Alkali ????
HCO3 14 Low Acid ????
Compensated Metabolic Acidosis or Compensated
Respiratory Alkalosis
33Translate
Value Code Translate Opinion
pH 7.40 Normal Normal Normal
pCO2 8 High Acid ????
HCO3 35 HIgh Alkali ????
Compensated Respiratory Acidosis or Compensated
Metabolic Alkalosis
34Translate
Value Code Translate Opinion
pH 7.21 Low Acid Acidaemia
pCO2 12 High Acid Primary
HCO3 32 High Alkali Secondary
Decompensated Respiratory Acidosis
35What 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
36Nomenclature
- 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
37Case 1
- Young female admitted with overdose of unknown
tablets and smelling of alcohol - pO2 12 kPa on air
- pH 7.24
- PaCO2 2.5
- HCO3 8
- Metabolic Acidosis with respiratory compensation
38Case 2
- Elderly male admitted from nursing home with one
week history of fever and vomiting - pO2 12 kPa on 4l by mask
- pH 7.49
- PaCO2 6.3
- HCO3 35
- Metabolic alkalosis with respiratory
compensation
39Case 3a
- Middle aged man admitted with cough sputum and
haemoptysis. Life-long smoker - pO2 4 on air
- pH 7.19
- PaCO2 9.7
- HCO3 28
- Acute respiratory acidosis with no time for
metabolic compensation
40Case 3b
- Middle aged man admitted with cough sputum and
haemoptysis. Life-long smoker - pO2 6 on air SpO2 92
- pH 7.32
- PaCO2 10.0
- HCO3 39
- Acute respiratory acidosis with no time for
metabolic compensation
41Case 4
- Middle aged man post cardiac arrest. Breathing
spontaneously on endotracheal tube - pO2 35 on 15l via reservoir mask
- pH 6.9
- PaCO2 8.9
- HCO3 13
- Mixed metabolic and respiratory acidosis
42Case 5
- Elderly lady with congestive cardiac failure
- pO2 9 on 40 oxygen
- pH 7.64
- PaCO2 3.5
- HCO3 29
- Respiratory alkalosis secondary to pulmonary
oedema. - Acute as no metabolic compensation
-
43Case 6
- Young diabetic male admitted with chest
infection, vomiting and drowsiness - pO2 12 on air
- pH 7.31
- PaCO2 1.6
- HCO3 6.0
- Acute metabolic acidosis with respiratory
compensation
44Case 7
- 54 yr-old lady post MI. Acutely unwell, cold,
clammy, hypotensive and oliguric - pO2 10 on 60 oxygen
- pH 6.99
- PaCO2 7.8
- HCO3 14
- Mixed pattern of respiratory and metabolic
acidosis
45Case 8
- 50 yr-old man admitted with exacerbation of
long-standing bronchial asthma. Respiratory rate
of 18 - pO2 5.1 on 60 oxygen
- pH 7.39
- PaCO2 5.8
- HCO3 26
- Severe type I respiratory failure
46Questions
47The 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
48Anion Gap
- Anion Gap NaK CLHCO3
- Normal anion gap 10-18
49Metabolic Acidosis
- Increased anion gap (added acid)
- Renal failure
- Ketoacidosis
- Lactic acidosis
- Salicylate/Tricyclic overdose
50Metabolic Acidosis
- Decreased anion gap (loss of bicarbonate)
- Renal tubular acidosis
- Diarrhoea
- Carbonic anhydrase inhibitors
- Ureteral diversion
- Chloride administration
51High Anion Gap
52High Anion Gap
- Alcohol (Alcohol dissociates to become a week
acid) - M
- U
- D
- P
- I
- L
- E
- S
53High Anion Gap
- Alcohol (Alcohol dissociates to become a week
acid) - Methanol (See alcohol. Causes blindness)
- U
- D
- P
- I
- L
- E
- S
54High 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
55High 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
56High 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
57High 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
58High 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
59High 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
60High 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)
61Normal Anion Gap
- Addisons Disease
- High Output Fistulas
- RTA I, II, IV
- Acetazolamide Therapy
- Diarrhoea
62Any more Questions?