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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 BalanceStriking 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 approach1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component4. Determine the metabolic component5. Which is primary and which is secondary
5-step approach1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component4. Determine the metabolic component5. Which is primary and which is secondary
5-step approach1. 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 approach1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component4. Determine the metabolic component5. Which is primary and which is secondary
5-step approach2. 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 approach1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component4. Determine the metabolic component 5. Which is primary and which is secondary
5-step approach3. Determine the respiratory component
Does this explain the acid-base deficit?
PaCO2: >6.0 kPa - respiratory acidosis
<4.7kPa - respiratory alkalosis
5-step approach1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component4. Determine the metabolic component 5. Which is primary and which is secondary
5-step approach4. Determine the metabolic component.
Does this explain the acid-base deficit?
HCO3 <22 mmols/l - metabolic acidosis>26 mmols/l - metabolic
alkalosis
Remember……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 approach1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component4. Determine the metabolic component5. Which is primary and which is secondary
5-step approach5. 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 approach1. Assess Oxygenation
2. Determine Acid-Base Deficit
3. Determine the respiratory component4. Determine the metabolic component5. 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 hypoventilationCNS depressionNeuromuscular diseaseAcute or chronic lung diseaseCardiac arrestVentilator malfunction
Respiratory Alkalosis
Any cause of hyperventilationHypoxiaAcute lung conditionsAnxietyFeverPregnancyHepatic failureSome central CNS lesions
Metabolic AcidosisAdded Acid Loss of Bicarbonate
• Renal failure• Ketoacidosis• Lactic acidosis• Salicylate/Tricyclic overdose
• Renal tubular acidosis• Diarrhoea• Carbonic anhydrase
inhibitors• Ureteral diversion• Chloride administration
Metabolic Alkalosis
Loss of acid or gaining alkaliVomitingDiarrhoeaDiuretics (and hypokalaemia generally)Ingestion of alkali
Reminder 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
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 AcidAcidaemi
a
pCO2 5.3 Normal Normal Normal
HCO3 16 Low Acid Primary
Uncompensated Metabolic Acidosis
Translate
Value Code Translate Opinion
pH 7.1 Low AcidAcidaemi
a
pCO2 8.3 High Acid Primary
HCO3 26 Normal Normal Normal
Uncompensated Respiratory Acidosis
Translate
Value Code Translate Opinion
pH 7.56 High AlkaliAlkalaemi
a
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 orCompensated 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 airpH 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 35 on 15l via reservoir mask
pH 6.9
PaCO2 8.9
HCO3 13 Mixed metabolic and respiratory acidosis
Case 5 Elderly lady with congestive cardiac failure
pO2 9 on 40% oxygenpH 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 12 on air
pH 7.31
PaCO2 1.6
HCO3 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% oxygenpH 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?
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