Transcript Slide 1

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
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Value
Code
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Opinion
pH
7.1
Low
Acid
Acidaemia
pCO2
5.3
Normal
Normal
Normal
HCO3
16
Low
Acid
Primary
Uncompensated Metabolic Acidosis
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Value
Code
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Opinion
pH
7.1
Low
Acid
Acidaemia
pCO2
8.3
High
Acid
Primary
HCO3
26
Normal
Normal
Normal
Uncompensated Respiratory Acidosis
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Value
Code
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Opinion
pH
7.56
High
Alkali
Alkalaemia
pCO2
2.3
Low
Alkali
Primary
HCO3
25
Normal
Normal
Normal
Uncompensated Respiratory Alkalosis
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Value
Code
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Opinion
pH
7.37
Normal
Normal
Normal
pCO2
2.1
Low
Alkali
????
HCO3
14
Low
Acid
????
Compensated Metabolic Acidosis or
Compensated Respiratory Alkalosis
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Value
Code
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Opinion
pH
7.40
Normal
Normal
Normal
pCO2
8
High
Acid
????
HCO3
35
HIgh
Alkali
????
Compensated Respiratory Acidosis or
Compensated Metabolic Alkalosis
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Value
Code
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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?