1. An arterial blood gas (ABG) analysis can provide information about oxygenation, ventilation, and acid-base status. It answers questions like how severe hypoxia or hypercarbia is and what acid-base abnormalities may be present. 2. The document provides templates for interpreting ABG results and analyzing acid-base disturbances and their compensation. It also includes several case scenarios where ABG results are used to diagnose conditions like respiratory acidosis from narcotic overdose or metabolic acidosis and hyperventilation from pneumonia. 3. Key steps in ABG interpretation involve checking for hypoxemia and quantifying any shunt fraction, evaluating ventilation and dead space, identifying primary acid-base disturbances and compensation

1. ARTERIAL BLOOD GAS
ANALYSIS
DR UNNIKRISHNAN
PRATHAPADAS
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3. Questions that an ABG can answer
How is oxygenation: is there any hypoxia?
Cause? How severe?
How is ventilation: any hypercarbia?
Any Acid Base abnormalities? Compensation?
Mixed?

4. SUMMARY of compensation
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5. At the end of the day…
Clinical condition
Interpret PaO2 with the knowledge of FiO2, A-a Gradient and
P/F ratio- PvO2 if needed
Interpret PCO2 with the knowledge that, it depends on CO2
production and alveolar ventilation & Dead space ventilation
Primary acid-base disturbances: See the pH, PaCO2 and
SBE
Look for compensation / mixed imbalances
Anion gap for metabolic acidosis

6. Case Scenario 1
A 24 year-old woman is found unconcious by some
bystanders. The medics are called and, upon arrival, find her
with an oxygen saturation of 88% on room air and pinpoint
pupils on exam. She is brought into the ER where a room air
arterial blood gas is performed and reveals:
pH 7.25,
PCO2 60 mmHg
PO2 65 mmHg
HCO3 – 26 mEq/L
Base Excess 1.22

7. Case Scenario:1
Acid-base status:• The patient has a low pH (acidemia)• The
PCO2 is high (respiratory acidosis) and the SBE is normal.
The low pH and high PCO2 imply that the respiratory
acidosis the primary process
PaO2/FiO2= 325 , 550-325= 225=10%
PAO2=713x0.2-1.25x60=68
pAO2-paO2=3 mm of Hg.. Normal, which tells us that her
hypoxemia is entirely due to hypoventilation

8. Sorry.. Foreign ABG
There is no compensation happening
The respiratory acidosis implies that the patient is
hypoventilating. This fact, in combination with the pinpoint
pupils suggests the patient is suffering from an acute narcotic
overdose.
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9. Case Scenario:2
Patient presenting to casualty with tachypnoea, sweating &
agitation. He is disoriented and agitated. ABG in RA:
pH 7.22,
pCO2 24 mmHg
pO2 60 mmHg
HCO3 8 mEq/L
SBE -20,
SpO2 96%,
CXR: R lower lobe pneumonia and creatinine 2.0.

10. Case Scenario:2
How a good interpretation can help a patient?
 Patient presenting to casualty with tachypnoea, sweating &
agitation. He is disoriented and agitated. ABG in RA: pH
7.22, pCO2 24, pO2 60, HCO3 8, SBE -20, SpO2 96%, CXR:
R lower lobe pneumonia and creatinine 2.0. Please use the
template to solve this ABG
 PAO2 = 713 x 0.2 – 1.25 x 24 = 112
 A-a gradient = 52
 P/F= 300
 Metabolic acidosis
 Pneumonia V/Q mismatch
 Gas exchange issues + Metabolic acidosis
Hyperventilation-⬆️ WOB
 Will he tolerate the extra 20% of VO2 demand by respiratory
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11. Case Scenario:3
55 yr old male came to ER with h/o fall. The trainee took
ABG sample, value are as follows:
pH= 7.36,
PaO2 40 mmHg
PCO2 = 42 mmHg,
SaO2 72%,
SpO2 95%
SBE = -6 mEq/L
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12. Case Scenario:3
pH= 7.36, SBE = -6 mEq/L , PaO2 40, SaO2 72%, PCO2 =
42 mmHg, SpO2 95%
Metabolic acidosis. Compensation? PaCO2=SBE
marked metabolic acidosis with mild respiratory
compensation.
Wrong answer
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13. Don’t satisfy the criteria for OCD
Even stable patients on ventilator can show variability in
PaO2 in the range of 2-37 mm of Hg and in PCO2 in the
range of 1-12 mm of Hg…should be considered as normal
Unnecessary repeating of ABGs will create confusion
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15. Key Step: Oxygenation- any shunt or
dead space ventilation?
V/Q mismatch is the commonest cause
What alters the Ventilation-perfusion match?
Dead space is wasted ventilation
Shunt is wasted perfusion: No rise in SpO2 with
⬆️ in FiO2, Wide A-a O2 gradient, low
PaO2/FiO2
Different diseases have varying proportion of
shunt & dead space ventilation: eg ARDS* &
emphysema*

16. V/Q MISMATCH : The shunt!
Shunt doesn’t affect pCO2 because of the stimulation of
respiration by chemoreceptors
Shunt fraction Consequence
2-3% Normal
10% Tolerated by a healthy person
25-45% Life threatening: Requires
mechanical ventilation, PEEP,
recruitment, positioning, FOB
and suctioning

17. Key Step: Check the validity of PaO2,
look for the gradient & quantify the
shunt if present
Clinical context
Use the Alveolar Gas Equation
Know the alveolar PO2 (PAO2)
Know the arterial PO2 (PaO2)
Find PaO2/FiO2 ratio
Quantification of the shunt fraction

18. pAO2 from Alveolar Gas Equation
PAO2 =[(PB – PH2O) FiO2 ] – (PaCO2 / RQ)
Atmospheric pressure is 760 mm Hg at sea level
PH2O is vapor pressure of water at 37°C and is equal to 47
mmHg
713 x FiO2 – 1.25 x PaCO2
The respiratory quotient or respiratory coefficient (RQ) is the
ratio of CO2 produced divided by the O2 consumed, and its
value is typically 0.8 (RQ = CO2 eliminated / O2 consumed).
R is taken as 1 @FiO2> 0.6
PB – PH2O is known as PiO2 713
Simplified as
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PAO2 = 713 x FiO2 – 1.25 x
PaCO2

19. The Alveolar –Arterial Oxygen Gradient
PAO2-PaO2
The expected paO2 will be 10-15 mm of Hg lower than that in
the alveoli: A-a O2 gradient
10-15 mm in young to middle aged
PaO2= 109- 0.43 [age in years]
It increases with increase in FiO2 [@FiO2 of 1,110!)
If higher than expected for age, shunt fraction is high
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20. The Alveolar –Arterial Oxygen Gradient
Hypoxemic respiratory failure with Normal A-a DO2
Hypoventilation**
High altitude
Fire
Inadvertent use of low O2 containing mixtures during anesthesia
Hypoxemic respiratory failure with widened A-a DO2
Increased shunt fraction
Increased dead space ventilation
Diffusion abnormality
Low cardiac output and increased O2 uptake
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21. PaO2 /FiO2
Normal  500-550
Used to diagnose ARDS (< 200) and ALI (< 300); 300-500 =
acceptable
Obtained value is subtracted from 550
For every difference of 100, the shunt fraction is  5%
Roughly, shunt %: 5005, 30015, 20020
Eg 68/0.4=170 , 550-170=380  20%
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22. Case Scenario 4
Patient breathing room air, has
PaO2 90 mm of Hg,
SpO2 96%, and
PaCO2 110 mm of Hg.
Check the validity
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23. Case Scenario 4
Patient breathing room air, has PaO2 90 mm of Hg, SpO2
96%, and PaCO2 110 mm of Hg. Check the validity (PaO2,
PaCO2 values reliable or not?)
Apply Alveolar Gas Equation
[713x0.2]-[1.2x110]= PAO2 is 18!, but SpO2 is 96. So one
among the value is wrong.
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24. Case Scenario 4
Patient on mechanical ventilation, has PaO2 150 mm of Hg,
FiO2 0.8, and PaCO2 30 mm of Hg. Check the validity and
find the gradient.
Apply Alveolar Gas Equation
[713x0.8]-[1.2x30]= PAO2 is 534. PaO2 is 150. A-a gradient
384
But please remember that the gradient increases with the
FiO2
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25. Case Scenario 5
Patient breathing room air. PaO2 125. PC02 50. Please find
the gradient?
[713x0.2]-[1.2x50]= PAO2 is 86.
PaO2 then cannot be 125
Air bubble?
MESSAGE: Isolated PaO2 value is meaningless without info
about FiO2 and PaCO2- so give enough importance for
’AGE’
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26. Case Scenario 5
Patient breathing room air. PaO2 125. PC02 50.
Please find the gradient?
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27. CaO2- Oxygen Content
Oxygen carried as oxyhemoglobin + dissolved O2
CaO2= [1.39 X Hb (gm/dl) X Saturation] + 0.003 X PaO2
If Hb=15 g/dl, SaO2 99%, 20.4 ml as oxy Hb + 0.3 ml in
plasma20.7
Anemia: will not affect saturation and evoke physiological
adaptations
Abnormal Hbs will decrease saturation and decrease O2
content; will not affect solubility and so PaO2 will be normal
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28. Case Scenario 6
24 years old male patient rescued from a burning house has
dyspnoea- was given O2 6l/min and shows SpO2 of 99%.
ABG: PaO2 125 mm of Hg PaCO2 of 35 mm of Hg.
Is the blood gas normal? Does he need supplemental O2?
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29. Case Scenario 6
24 years old male patient rescued from a burning house has
dyspnoea- was given O2 6l/min and shows SpO2 of 99%.
ABG: PaO2 125 mm of Hg PaCO2 of 35 mm of Hg. Is the
blood gas normal? Does he need supplemental O2?
Co-oximetry to find the amount of Carboxy Hb-SpO2 won’t be
correct
PaO2 will be normal
Give O2
Don’t rely on N PaO2
If metabolic acidosis/ disorientation Mechanical Ventilation
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30. Key Step: Check for Mixed Venous ‘Hypoxia’!
Decreased Cardiac Output (QT) in the presence of constant
O2 consumption (VO2)
Increased VO2 (shivering, fever)
Decrease mixed venous O2 content: CvO2= (1.39xHbx
SvO2)+(0.003xPvO2)
Normal: SvO2= 75% SvO2 ~ SaO2-[VO2/Hb x QT]
PvO2= 40 mm of Hg
In low CO states with continuing O2 extraction, PvO2 will be
low
Sample from a CVC [if no PAC] can identify low CO states
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31. Hypoventilation will cause hypoxia too
1.Hypoventilation shallow breathing  atelectasis 
reduce FRC
2.Hypoventilation  V decrease  overall V/Q of the lung
decrease
1+2 = Hypoxia
So hypoventilation = Hypercarbia + Hypoxia
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32. Also note hypoxia can occur even with
normal PaO2
Low Hb- Anemic hypoxia
Decreased O2 delivery- Stagnant hypoxia
Reduced utilization- Histotoxic hypoxia
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34. Key Step: Abnormal production/ alveolar
ventilation/ dead space?
Abnormality in Production OR Washout

35. Abnormal production?
? Increased production

36. Abnormal alveolar ventilation?
? High or low alveolar ventilation

37. Increased dead space?
Clues to increased dead space ventilation
Persisently high PCO2 despite high minute ventilation
PCO2-ETCO2 disparity > 5 mmof Hg
Increased dead space
Pulmonary vascular disease
Pulmonary embolism
Hypovolemia
Low cardiac output
COPD
ARDS
Pulmonary fibrosis

39. Metabolic and Respiratory acids
vs
Buffering & Compensation
LUNGS
2000mM
KIDNEYS
70 mM

40. SBE is a convenient representative
of all the buffer systems
The concept of Standard Base Excess (SBE)
puts all buffers into a single hypothetical system
Bring the pCO2 to 40 to negate the effect of
respiratory system and assume that the blood is
alkaline/acidic now
Base Excess/base deficit is the amount of
acid/alkali required to return the pH of the blood
to 7.4 and hence is the amount of ‘excess
base/acid’

41. Further exposing the SBE
SBE is the SB of ECF and SBa is that of blood
SBE is the perfect parameter as ECF is the
vehicle through which AB changes are
regulated
SBE normal range is +/- 2 mM/L
Other measures shown in the ABG like standard
pH, standard bicarbonate, buffer base, total
CO2 has been given up- no need to learn them

42. So when we arrange it in order, in response
to an acid base change
First defense: Buffering
Second: Respiratory : alteration in arterial pCO2
Third defense: Renal : alteration in HCO3 excretion
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43. NORMAL VALUES
.
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44. ARTERIAL Vs VENOUS BLOOD
.
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45. INDIVIDUAL ACID BASE
ABNORMALITIES AND
‘COMPENSATION’
mm

46. Compensation
In respiratory derangements the primary change
is in pCO2. Compensation is by kidneys which
reabsorb more bicarbonate, which increases the
SBE
In metabolic derangements, the primary change
is in SBE and compensatory changes are
provided by the lungs
For eg metabolic acidosis make SBE more
negative and lungs tries to excrete more CO2
(respiratory acid) to compensate this resulting in
a compensatory respiratory alkalosis

47. KEY STEP: ACUTE RESPIRATORY ACID BASE
CHANGES
PaCO2  pH SBE=0
• ACUTE RESPIRATORY ACIDOSIS[
buffering only; 99% in ICF]
PaCO2  pH
• ACUTE RESPIRATORY ALKALOSIS
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48. KEY STEP: CHRONIC RESPIRATORY ACIDOSIS
& ALKALOSIS
compensated by renal handling of bicarbonate; hence SBE
changes
pH return to 2/3 rd of normal
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 SBE = 0.4 PaCO2
• Direction of change of SBE is
same as that of direction of
change of PaCO2

49. Respiratory Acidosis :Causes
E.g. if PaCO2 is 60 mm of Hg and cause is chronic
respiratory acidosis, then the expected SBE is 0.4 X 20 = 8
mM/L
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CAUSES
Upper airway obstruction
Status asthmaticus
Pneumonia
Pulmonary edema
CNS depression
Neuro muscular impairment
Ventilatory restriction

50. Respiratory Alkalosis
Normal in mountain dwellers and pregnant women
pH>7.45 PaCO2<35 mm of Hg
Generally a poor prognostic sign, when present in critically ill
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CAUSES
Hypoxemia
Pulmonary embolism, asthma, pulmonary edema
CNS disorders
Hepatic failure
Sepsis
Salicylate toxicity
Anxiety- hyperventilation

51. Case Scenario:7
A patient with a long history of COPD presented to the
casualty with difficulty in breathing. He was conscious,
tachypneic with accessory muscle use. His pH is 7.35; PaO2
is 34 mm of Hg; PaCO2 of 72 mm of Hg, HCO3 37.5 mM/L
and SBE is 14 mM/L. He is given 4L O2 by mask and an
ABG drawn after 15 mins. Now his pH is 7.30, PaO2 is 70
mm of Hg, PaCO2 of 88 mm of Hg and SBE is 14 mM/L.
Analyse these 2 ABGs
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52. Case Scenario:7
A patient with a long history of COPD presented to the
casualty with difficulty in breathing. He was conscious,
tachypneic with accessory muscle use. His pH is 7.35; PaO2
is 34 mm of Hg; PaCO2 of 72 mm of Hg, HCO3 37.5 mM/L
and SBE is 14 mM/L. He is given 4L O2 by mask and an
ABG drawn after 15 mins. Now his pH is 7.30, PaO2 is 70
mm of Hg, PaCO2 of 88 mm of Hg and SBE is 14 mM/L.
Analyse these 2 ABGs
RA: A-a gradient-18; P/F-170
He is conscious!
Near normal pH.
O2 improves PaO2; but PaCO2 increases!
Despite a fall in pH, SBE is remaining same!
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53. Respiratory Acidosis: effects
 CBF and ICP
Arrhythmia
Hyperventilation
Hypoxemia
In patients breathing room air, PCO2 > 90 mm of Hg is not
compatible with life
If you acutely reduce CO2: accumulated HCO3 will remain
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54. KEY STEP: METABOLIC ACIDOSIS
Produced by increase in titratable hydrogen ion concentration
Diagnosis: pH low and SBE <-5 mM/L, HCO3 <20 mM/L
Respiratory compensation is immediate and return pH to one
third to half way normal
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PaCO2 = SBE

55. KEY STEP: FINDING THE ANION GAP
When all the commonly measured anions are substracted
from the cations, the result is a positive value of 12±4 mEq/L
Due to unmeasured anions
Corrected AG = Calculated AG + 2.5 [4.5-measured albumin
in g/dl]
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56. WIDE & NORMAL AG GAP ACIDOSIS
If AG > 20 suspect ; if > 25 confirmed
Some conditions generate anions these are neutralized by
bicarbonatebicarbonate falls
  AG widens
Some conditions lead to loss of bicarbonate this is
counterbalanced by gain in chloride gain in chloride exactly
matches loss of bicarbonate  AG is normal
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57. Metabolic Acidosis : Causes
Respiratory
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58. Metabolic Acidosis : Causes
.
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59. Case Scenario:8
A young woman suffering from fever 4 days has been
admitted in the ER. She is semi comatose and tachypnoeic.
Cool peripheries with BP of 90/30 mm Hg. SpO2- unreliable
trace. ABG on RA:
pH 7.19,
PaO2 100,
PaCO2 20,
HCO3 8,
SBE -17.7.
Serum electrolytes
Na 140 K 4.5 Cl 100
lactate 10
S creatinine 2.4
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60. Case Scenario:8
A young woman suffering from fever 4 days has been
admitted in the ER. She is semi comatose and tachypnoeic.
Cool peripheries with BP of 90/30 mm Hg. SpO2- unreliable
trace. ABG on RA: pH 7.19, PaO2 100, PaCO2 20, HCO3 8,
SBE -17.7. Serum electrolytes Na 140 K 4.5 Cl 100 lactate
10 S creatinine 2.4
No oxygenation issue
Metabolic acidosis
Lungs compensated it by increasing Mv. Pa CO2 20.
AG is 37 ( accumulated metabolic acids)
Lactate =10 = 10/ 17 is lactate; rest is by accumulation of
metabolites from renal failure
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61. Metabolic Acidosis : effects
Decreased strength of respiratory muscles
Hyperventilation
Myocardial depression
Sympathetic over activity
Decreased arrhythmia threshold
Resistance to catecholamines
Hyperkalemia
Increased metabolic demand [N:5% of VO2; in distress 25%]
Insulin resistance
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62. Metabolic Acidosis and Mechanical ventilation
Respiratory effect is hyper ventilation may not be tolerated
by patients with compromised cardiac or respiratory
reserve mechanical ventilation may be required in such
patients , till underlying metabolic acidosis is addressed
When on ventilator, try to mimic the natural compensation;
but don’t go < 30 mmof Hg of PaCO2
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63. NaHCO3 Therapy
Sodium bicarbonate should probably be administered to
intensive care patients with severe metabolic acidemia (pH ≤
7.20, PaCO2 < 45 mmHg) and moderate to severe acute
renal insufficiency
The administration of sodium bicarbonate could limit the
deleterious cardiovascular, respiratory, and cellular energy
effects of loss of bicarbonate .
Sodium bicarbonate should be administered carefully as it is
associated with a risk of hypokalemia, hypernatremia,
hypocalcemia, rebound alkalemia, and water–sodium
overload
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64. Respiratory Alkalosis : Effects
Increased neuromuscular irritability
Cerebral vasoconstriction
Decreased ICP
Increased cerebral excitability
Inhibition of respiratory drive
Hypokalemia
Respiratory alkalosis + abnormal respiratory muscle
activity? High ventilatory demand cautious decision
making regarding extubation
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65. Case Scenario:9
A 68 year-old man with a history of very severe COPD and
chronic carbon dioxide retention presents to the emergency
room complaining of worsening dyspnea and an increase in
the frequency and purulence of his sputum production over
the past 2 days. His oxygen saturation is 78% on room air.
Before he is placed on supplemental oxygen, a room air
arterial blood gas is drawn and reveals: pH 7.25, PCO2 68,
PO2 48, HCO3 31, SBE 6
Pao2/fio2=240, shunt fraction 15%, PAO2-PaO2=13
SBE=0.4 X paCO2= 11.2, Why only 6?
Acute on chronic respiratory failure with respiratory acidosis
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66. KEY STEP: METABOLIC ALKALOSIS
Produced by decrease in titratable hydrogen ion
concentration
Depress ventilation
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PaCO2 = 0.6 SBE
weaning

67. Metabolic Alkalosis
Generally pCO2 wont go > 55; if > 55, indicates severe
alkalosis OR combined metabolic alkalosis + respiratory
acidosis
Usually [HCO3-] prompt [HCO3-] excretion by kidney;
persistence requires additional process to impair [HCO3-]
excretion

68. Metabolic Alkalosis: Causes
.

69. Effects of Metabolic Alkalosis:
Reduced cerebral blood flow
Seizures
Tetany
Reduction in coronary blood flow
Predisposistion to refractory arrhythmias
Decreased contractility
Hypoventilation
Hypokalemia , Hypomagnesemia
Reduced ionized calcium
Promote anaerobic glycolysis lactate
Weaning failure, especially if HCO3 is >35

70. Impaired arterial oxygen content
Hypoventilation
Micro atelectasis
V-P mismatch
So assess for the requirement of supplemental
oxygen in metabolic alkalosis

71. Additional points- Metabolic alkalosis
Depresses respiration hypoxemia & hypercarbia
Effects on PaCO2 are seen only when HCO3> 35 Mm/L
Chloride responsive [Urinary Cl- < 15 mEq/L]: Rx is chloride-
volume-potassium repletion
Chloride resistant [Urinary Cl- >25 mEq/L]: Rx is correction of
the cause of mineralocorticoid excess and potassium
depletion and Acetazolamide
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72. You cant exist alone man; who is behind you?
Reduced GFR
Chloride depletion
Potassium depletion
ECF volume depletion
Because kidney has a large capacity to excrete bicarbonate
and return the plasma level to normal
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73. Case Scenario:10
10 years old boy who underwent occipital-C2 fusion for
complex Chiari malformation developed stress
cardiomyopathy on POD 1. After resuscitating the initial
decompensation using milrinone and diuretics, an ABG was
taken with FiO2 0.6: PCV- PC:13,PEEP:8, RR:20 MVe
3.8L/min PaO2 86 mm of Hg, PCO2 44, pH 7.26, SBE: -
7.4. How will you explain the changes? Do you think any
change in the ventilatory management would have been
more appropriate in this patient?
A-a gradient: 373-86=287
P/F: 86/0.6=143; 550-143=407shunt fraction 20%
Acidosis
Metabolic
Expected compensation: △PaCO2=SBE7.4Expected
PCO2-33Present PCO2-44-?

74. .

75. THANK YOU
The Lay Medical Man
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76. References :
Dr Suneel P.R., SCTIMST, Arterial blood gas
before, during and after mechanical ventilation,
Respiratory Care Update 2007
Arterial blood gases made easy, Ian A M
Hennessey, Alan G Japp
Lawrence Martin, All you really need to know to
interpret arterial blood gases, 2 nd edition
Simple as ABG, Ted &Larry’s
A. Hasan, Handbook of Blood Gas/Acid-Base
Interpretation, 2013
Standard Base Excess, T. J. MORGAN,
Australasian anesthesia 2003