Lecture notes on ABG interpretation and case examples

1. Introduction to Arterial Blood
Gases
Dr G Abraham

2. ECG Quiz
• What is the relationship of p waves to qrs.
• What is the diagnosis?

3. CXR Quiz
• 33 year old man, otherwise fit and well, acute shortness of breath
and hypotension presents to ED.

4. Acid base homeostasis
• pH is a logarithmic scale of the concentration of
hydrogen ions in a solution. It is inversely proportional
to the concentration of hydrogen ions.
• Normally the body’s pH is closely controlled at
between 7.36 – 7.42. This is achieved through buffering
and excretion of acids.
• Buffering involves reversible binding of hydrogen ions
• Bicarbonate and ammonia are extracellular buffers.
• Proteins and phosphate act as intracellular buffers

5. The Bicarbonate buffering system
• 𝐻2 𝑂 + 𝐶𝑂2 ⇌ 𝐻2 𝐶𝑂3 ⇌ 𝐻𝐶𝑂3 + 𝐻+
• Thus decreasing 𝐶𝑂2 by increasing minute ventilation
buffers excess hydrogen ions (Le Chatelier’s principle)
• Derived Henderson Hasselbalch Equation for blood pH:
• 𝑝𝐻 = 6.1 + 𝑙𝑜𝑔10
[𝐻𝐶𝑂3]
0.0307 × 𝑝𝐶𝑂2
Acid dissociation constant of
carbonic acid
Solubility of carbon dioxide in blood

6. Effect of ventilation
• Decreasing 𝐶𝑂2 by increasing minute
ventilation buffers excess hydrogen ions.
• Ventilation is a function of respiratory rate and
tidal volume.
• Hyperventilation is when alveolar ventilation
of C𝑂2 exceeds the body’s production of C𝑂2.
• Hypoventilation is the converse.

7. Renal Solute exchange
• By Haisook at English Wikipedia, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=2945979

8. Renal Physiology
• In response to acidosis, tubular cells reabsorb
more bicarbonate from the tubular fluid.
• Collecting duct cells secrete more hydrogen and
generate more bicarbonate, and ammonia-
genesis leads to increased formation of the NH3
buffer.
• In response to alkalosis, the kidney may excrete
more bicarbonate by decreasing hydrogen ion
secretion from the tubular epithelial cells
• Lower rates of glutamine metabolism (to
produce ammonium) and ammonium excretion

9. Acid-Base disorders
• Occur when a significant
insult overwhelms
capacity of ventilation
and renal system to
compensate.
• Include respiratory
acidosis and alkalosis
• Metabolic acidosis and
alkalosis.

10. Partial Pressure
• The amount of pressure a particular
gas contributes to the total pressure.
For example, we normally breathe air
which at sea level has a pressure of
100kPa, oxygen contributes 21% of
100kPa, which corresponds to a
partial pressure of 21kPa.
• Henry’s law states that when a gas is
dissolved in a liquid, its partial
pressure (i.e. concentration of gas)
within the liquid is the same as in the
gas in contact with the liquid.
Therefore you can measure the
partial pressure of gases in the blood.
• PaO2 is the partial pressure of oxygen
in arterial blood
• PaCO2 is the partial pressure of
carbon dioxide in arterial blood.

11. Base Excess
• This is the amount of strong base which would
need to be added or subtracted from a substance
in order to return the pH to normal (7.40).
• A value outside of the normal range (-2 to +2
mEq/L) suggests a metabolic cause for the
acidosis or alkalosis.
• In terms of basic interpretation:
• A base excess more than +2 mEq/L indicates a
metabolic alkalosis.
• A base excess less than -2 mEq/L indicates a
metabolic acidosis.

12. Anion Gap
• The anion gap is the difference between primary measured
cations (sodium and potassium) and the primary measured
anions (chloride and bicarbonate). It is calculated by
subtracting the concentrations of chloride and bicarbonate
(anions) from the concentrations of sodium and potassium
(cations):
• Anion gap = ([Na+] + [K+]) − ([Cl−] + [HCO3−])
• Reference range usually 7–16 mEq/L (but varies between
hospitals)
• Potassium is commonly left out of the equation as
potassium concentrations, being very low, usually have
little effect on the gap. This leaves the following equation:
• Anion gap = [Na+] − ([Cl–] + [HCO3−])

13. Typical values in an analyser
• pH: 7.35 – 7.45
• pO2: 10 – 14kPa
• pCO2: 4.5 – 6kPa
• Base excess (BE): -2 – 2 mmol/l
• HCO3: 22 – 26 mmol/l
• 1kPa = 7.5mmHg.

14. ‘Never Forget’
• Electrolytes – sodium, potassium
• Lactate – a marker of tissue
perfusion as raised in anaerobic
respiration.
• Glucose
• Hb although unreliable
• Carbon Monoxide - >10%
suggests CO poisoning
• MetHb – Methaemaglobinemia
– oxidised form of Hb – toxins eg
nitrates, dapsone, inborn errors
of metabolism

15. Oxygen dissociation curve

16. Respiratory compensation
• If a metabolic acidosis
develops the change is
sensed by
chemoreceptors
centrally in the
medulla oblongata and
peripherally in the
carotid bodies.
• The body responds by
increasing depth and
rate of respiration
therefore increasing
the excretion of CO2 to
try to keep the pH
constant.

17. Metabolic compensation
• In response to a
respiratory acidosis
eg CO2 retention in
COPD, the kidneys
will retain more
HCO3 in order to
correct the pH.
• Slower process
typically occurring
over several hours
to several days.

18. Pa𝑂2/Fi𝑂2
• Relationship of expected arterial oxygen value to
the inspired oxygen concentration.
• Widely used clinical indicator of hypoxaemia eg in
ARDS, though its diagnostic utility is disputed
especially if PaCO2 is abnormal.
• At sea level normal is > 500mmHg
• Can be used as a rough guide to whether there is
a significant A-a gradient present: PaO2 should =
FiO2 x 500 (e.g. 0.21 x 500 = 105 mmHg = 14kPa)
• A-a gradient = alveolar pO2 – arterial pO2

19. Suggested plan for interpretation
• Look at the clinical context
• Look at pH – is it an acidosis or alkalosis?
• Is CO2 abnormal?
• Is HCO3 abnormal?
• Are these changes in keeping with the expected
effect on pH?
• If so, this is the primary abnormality.
• If it is the opposite of what you would expect, it
suggests a compensatory change.

20. Presenting the results
• State that this is an arterial
blood gas sample
• State the patients name and brief
clinical context
• State the time the sample was
taken and how much inspired
oxygen the patient was on at the
time.
• Present any abnormal findings or
important negatives from the
rest of the values.
• A one line summary of your
findings

21. Case 1
• You are called to see a 54 year old lady on the
ward. She is three days post-cholecystectomy and
has been complaining of shortness of breath. Her
ABG on room air is as follows:
• pH: 7.49 (7.35-7.45)
• pO2: 7.5 (10–14)
• pCO2: 3.9 (4.5–6.0)
• HCO3: 22 (22-26)
• BE: -1 (-2 to +2)
• Other values within normal range

22. Case 1
• Respiratory alkalosis and type 1 respiratory
failure
• Differential diagnosis: PE, pneumonia, pleural
effusion, pneumothorax, pulmonary oedema

23. Causes of respiratory alkalosis
• CNS – Stroke, SAH, meningitis
• Anxiety
• Pregnancy
• High altitude
• Salicylate poisoning (phase 1 due to
respiratory activation)

24. Case 2
• A 75 year old gentleman living in the community is
being assessed for home oxygen. His ABG on room air
is as follows:
• pH: 7.36 (7.35-7.45)
• pO2: 8.0 (10–14)
• pCO2: 7.6 (4.5–6.0)
• HCO3: 31 (22-26)
• BE: +5 (-2 to +2)
• Other values within normal range

25. Case 2
• Respiratory acidosis
with full metabolic
compensation
(chronic)
• Note no acidemia –
pH normal
• Seen in chronic lung
disease, eg COPD

26. Causes of respiratory acidosis
Pulmonary problems Mechanical problems Central problems
COPD Chest wall trauma Opiate overdose
Pulmonary oedema Muscular dystrophies Acute CNS disease
Pneumonia Motor neurone disease
Myasthenia Gravis
• Describe presence of type 1 and type 2 respiratory failure
• Type 1 – paO2< 8
• Type 2 – paO2 <8 and PaCO2 > 6

27. Case 3
• A 32 year-old man presents to the emergency department having
been found collapsed by his girlfriend.
• pH: 7.25 (7.35-7.45)
• pO2: 11.1 (10–14)
• pCO2: 3.2 (4.5–6.0)
• HCO3: 11 (22-26)
• BE: -15 (-2 to +2)
• Potassium: 4.5
• Sodium: 135
• Chloride: 100
• Other values within normal range

28. Case 3
• Raised anion gap metabolic acidosis
• Anion gap = 139.5 – 111 = 28.5

29. Raised anion gap metabolic acidosis
Increased endogenous acids Diabetic ketoacidosis
Lactic acidosis
Increased exogenous acids Methanol
Ethylene Glycol
Decreased excretion of acid Chronic renal failure

30. Normal anion gap metabolic acidosis
Loss of bicarbonate GI loss diarrhoea
ileostomy
Intestinal, pancreatic,
biliary fistula
Renal Type 2 proximal renal
tubular acidosis
Carbonic anhydrase
inhibitors
Impaired renal excretion Type 1 distal renal tubular
acidosis
Reduced action of
aldosterone
Type 4 renal tubular
acidosis

31. Case 4
• A 67 year-old man with a history of peptic ulcer
disease presents with persistent vomiting.
• pH: 7.56 (7.35-7.45)
• pO2: 10.7 (10–14)
• pCO2: 5.0 (4.5–6.0)
• HCO3: 31 (22-26)
• BE: +5 (-2 to +2)
• Other values within normal range

32. Case 4
• Metabolic alkalosis due
to vomiting
• Pathophysiology
involves:
1) ECF depletion
2) Activation of
renin/angiotensin/
aldosterone
1) Reabsorption of sodium
at the expense of 𝐻+

33. Causes of metabolic alkalosis
• Vomiting
• Aspiration
• Diuretics
• Hyperaldosteronism
• Cushing’s Syndrome
• Hypokalemia (acid
shifted into cells to
maintain neutrality)

34. Summary
• ABG interpretation
requires a systematic
approach – look at pH and
then expected findings of
HCO3 or paCO2.
• Decide which is
predominantly
responsible and which is a
compensatory change
• Consider the clinical
context and the likely
cause

35. References
• http://www.oxfordmedicaleducation.com/abg
s/abg-interpretation/
• Oxford Handbook of Critical care
• http://lifeinthefastlane.com/
• Uptodate.com