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Richard Stretton
Respiratory Registrar
Arterial Blood Gases
Seen as complicated
 Misunderstood
 Important
 An easy way and a hard way

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
What Are We Measuring?
pH
 pO2
 pCO2
 HCO3
 Base Excess

Acid Base Balance

pH is carefully controlled

Enzymatic Function relies on pH control

Buffers
○ Haemoglobin
○ BICARBONATE
○ Ammonium
○ Phosphate
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+
5-step approach
1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component
4. Determine the metabolic component
5. Which is primary and which is secondary
5-step approach
1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component
4. Determine the metabolic component
5. Which is primary and which is secondary
5-step approach
1. 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 <3
A-a Gradient = PAO2 – (PaO2 + PaCO2/0.8)
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
5-step approach
1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component
4. Determine the metabolic component
5. Which is primary and which is secondary
5-step approach
2. Determine Acid-Base Deficit
 pH>7.45 alkalaemia
 pH<7.35 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.
5-step approach
1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component
4. Determine the metabolic component
5. Which is primary and which is secondary
5-step approach
3. Determine the respiratory component
Does this explain the acid-base deficit?
 PaCO2:

>6.0 kPa - respiratory acidosis
<4.7kPa - respiratory alkalosis
5-step approach
1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component
4. Determine the metabolic component
5. Which is primary and which is secondary
5-step approach
4.
Determine the metabolic component.
Does this explain the acid-base deficit?
 HCO3 <22 mmols/l - metabolic acidosis
>26 mmols/l - metabolic alkalosis
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+
5-step approach
1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component
4. Determine the metabolic component
5. Which is primary and which is secondary
5-step approach
5.
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

5-step approach
1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component
4. Determine the metabolic component
5. Which is primary and which is secondary
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

Respiratory Acidosis
Any cause of hypoventilation
 CNS depression
 Neuromuscular disease
 Acute or chronic lung disease
 Cardiac arrest
 Ventilator malfunction
Respiratory Alkalosis
Any cause of hyperventilation
 Hypoxia
 Acute lung conditions
 Anxiety
 Fever
 Pregnancy
 Hepatic failure
 Some central CNS lesions
Metabolic Acidosis
Added Acid
•
•
•
•
Renal failure
Ketoacidosis
Lactic acidosis
Salicylate/Tricyclic overdose
Loss of Bicarbonate
•
•
•
•
•
Renal tubular acidosis
Diarrhoea
Carbonic anhydrase
inhibitors
Ureteral diversion
Chloride administration
Metabolic Alkalosis
Loss of acid or gaining alkali
 Vomiting
 Diarrhoea
 Diuretics (and hypokalaemia generally)
 Ingestion of alkali
Reminder of normal values





pH
7.35 – 7.45
pO2
10 - 13
pCO2
4.6 - 6.0
HCO3
25 - 35
Base excess ± 2.0
(H+ = 35 -45)
kPa on air
kPa
mmols/l
Lets get going……..

Working out acidosis/alkalosis and
compensation is usually the bit people
struggle with

So…..
Outcome codes
Outcome
Code
Outcome
Code
pH
High
Alkali
Low
Acid
pCO2
High
Acid
Low
Alkali
HCO3
High
Alkali
Low
Acid
Translate
Value
Code
Translate
Opinion
pH
7.1
Low
Acid
Acidaemia
pCO2
5.3
Normal
Normal
Normal
HCO3
16
Low
Acid
Primary
Uncompensated Metabolic Acidosis
Translate
Value
Code
Translate
Opinion
pH
7.1
Low
Acid
Acidaemia
pCO2
8.3
High
Acid
Primary
HCO3
26
Normal
Normal
Normal
Uncompensated Respiratory Acidosis
Translate
Value
Code
Translate
Opinion
pH
7.56
High
Alkali
Alkalaemia
pCO2
2.3
Low
Alkali
Primary
HCO3
25
Normal
Normal
Normal
Uncompensated Respiratory Alkalosis
Translate
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
Translate
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
Translate
Value
Code
Translate
Opinion
pH
7.21
Low
Acid
Acidaemia
pCO2
12
High
Acid
Primary
HCO3
32
High
Alkali
Secondary
Decompensated Respiratory Acidosis
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
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
Case 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
Case 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
Case 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

Case 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

Case 4

Middle aged man post cardiac arrest.
Breathing spontaneously on
endotracheal tube
pO2
pH
PaCO2
HCO3

35 on 15l via reservoir mask
6.9
8.9
13
Mixed metabolic and respiratory acidosis
Case 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

Case 6

Young diabetic male admitted with chest
infection, vomiting and drowsiness
pO2
pH
PaCO2
HCO3

12 on air
7.31
1.6
6.0
Acute metabolic acidosis with
respiratory compensation
Case 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
Case 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
Questions
?
The 6th step…
6.
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
Anion Gap
 Anion Gap = [Na+K] –[CL+HCO3]
 Normal anion gap 10-18
Metabolic Acidosis

Increased anion gap (added acid)
 Renal failure
 Ketoacidosis
 Lactic acidosis
 Salicylate/Tricyclic overdose
Metabolic Acidosis

Decreased anion gap (loss of
bicarbonate)
 Renal tubular acidosis
 Diarrhoea
 Carbonic anhydrase inhibitors
 Ureteral diversion
 Chloride administration
High Anion Gap

A

M

U

D

P

I

L

E

S
High Anion Gap

Alcohol (Alcohol dissociates to become a week acid)

M

U

D

P

I

L

E

S
High Anion Gap

Alcohol (Alcohol dissociates to become a week acid)

Methanol (See alcohol. Causes blindness)

U

D

P

I

L

E

S
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
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
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
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
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
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
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)
Normal Anion Gap
Addison’s Disease
 High Output Fistulas
 RTA I, II, IV
 Acetazolamide Therapy
 Diarrhoea

Any more Questions?