The document discusses arterial blood gas (ABG) analysis. It provides 3 key points: 1. ABG analysis aids in establishing diagnoses and assessing the severity of respiratory failure by measuring oxygenation, ventilation, and acid-base balance. 2. The normal values for pH, PCO2, PO2, HCO3, and other components are outlined. 3. A step-wise approach to interpreting an ABG report is described, including assessing whether it indicates a respiratory or metabolic disorder, whether compensation is adequate, and evaluating other acid-base parameters like anion gap.

1. ARTERIAL BLOOD
GAS (ABG) ANALYSIS
BY- PAWAN KUMAR RAY
DR.RMLIMS LUCKNOW

2. Contents
 Uses
 Contraindications
 ABG procedure and precautions
 Normal values
 Interpretation
-Oxygenation
-Acid base balance
Definitions and terminologies
Regulation of acid base balance
Step wise interpretation of ABG
Causes

3. Why it is important to know about
ARTERIAL BLOOD GASES?
Blood pH <6.8 or >7.8 not compatible with
life and indicates irreversible cell damage or
death.
Aids in establishing a diagnosis and severity of
respiratory failure.
 Assess adequacy of ventilation and oxygenation
Adequacy of CO2 excretion
Assess changes in acid- base homeostasis
Helps to guide treatment plan.
Helps in management of ICU patients.

4. Contraindication
 Cellulitis or other infections over puncture site.
 Absence of palpable arterial pulse.
 Negative result of an Allen test/modified Allen test
 Coagulopathies / anticoagulant therapy.
 History of arterial spasm following previous puncture.
 Severe PVD
 Arterial grafts.
 Dialysis shunt – choose another site.

5. Site Selection
Radial Artery - 45 insertion angle
Brachial Artery - 60 - 90 insertion
angle
Femoral Artery - 90 insertion angle
Dorsalis Pedis Artery
Posterior Tibial artery
(Ideally)

6. ABG – Procedure and Precautions
 Pre-heparinised ABG syringes
Syringe should be FLUSHED with 0.05ml to 0.1ml of 1:1000 Heparin
solution and emptied.
DO NOT LEAVE EXCESSIVE HEPARIN IN THE SYRINGE
HEPARIN DILUTIONAL HCO3
EFFECT PCO2
 Use only 2ml or less syringe.

7.  Ensure No Air Bubbles. Syringe must be sealed immediately after
withdrawing sample.
 Contact with AIR BUBBLES
Air bubble = PO2 150 mm Hg , PCO2 0 mm Hg
Air Bubble + Blood = PO2 PCO2
 ABG Syringe must be transported at the earliest to the laboratory for
EARLY analysis via COLD CHAIN

9. ABG Analyser is controlled for Normal Body temperatures
 Sample of hyperthermic patient >37°C, Measured values of PaO2
and PaCO2 are less than actual.
 Hypothermic patient < 37°C measured values of PaO2 and PaCO2
are more than the actual values.
Every 1◦C ↓in temperature PCO2↓
pH ↑
Every1◦C ↑in temperature PCO2 ↑
pH ↓
Body temperature

10. ABG Sample should always be sent with relevant
information regarding O2, FiO2 status and Temp .
Before you withdraw a sample for ABG
After any change in FiO2 wait for 20min
And wait for 30 min after any change in ventilatory
parameters to ensure steady state.

11. Complications:
 Pain
 Bruising and haematoma
 Nerve damage
 Aneurysm
 Spasm
 AV fistula
 Infection
 Air or thromboembolism
 Anaphylaxis from local anaesthetic

12. Normal Values
ANALYTE Normal Value Units
pH 7.35 - 7.45
PCO2 35 - 45 mm Hg
PO2 72 – 104 mm Hg`
[HCO3] 22 – 30 meq/L
SaO2 95-100 %
Anion Gap 12 + 4 meq/L
∆HCO3 +2 to -2 meq/L

13. Blood Gas Norms
pH pCO2 pO2 HCO3 BE
Arterial 7.35-7.45 35-45 80-100 22-26 -2 to +2
Venous 7.30-7.40 43-50 ~45 22-26 -2 to +2

14.  Determination of PaO2
PaO2 is dependent upon Age, FiO2, Patm
As Age the expected PaO2
• PaO2 = 109 - 0.4 (Age)
As FiO2 the expected PaO2
• Alveolar Gas Equation:
• PAO2= (PB-P h2o) x FiO2- pCO2/R
O
X
Y
G
E
N
A
T
I
O
N
PAO2 = partial pressure of oxygen in alveolar gas, PB = barometric pressure
(760mmHg), Ph2o = water vapor pressure (47 mm Hg), FiO2 = fraction of
inspired oxygen, PCO2 = partial pressure of CO2 in the ABG, R = respiratory
quotient (0.8)

15.  Determination of the PaO2 / FiO2 ratio
Inspired Air FiO2 = 21%
PiO2 = 150 mmHg
PalvO2 = 100 mmHg
PaO2 = 90 mmHg
O2CO2
(along with other criteria)
P/F ratio

16. PaO2/ FiO2 ratio ( P:F Ratio )
 Gives understanding that the patients
OXYGENATION with respect to OXYGEN
delivered is more important than simply the PO2
value.
Example,
Patient 1
On Room Air
Patient 2
On MV
PaO2 60 90
FiO2 21% (0.21) 50% (0.50)
P:F
Ratio
285 180

17. Oxygen content of blood
CaO2 = (Hb x 1.34 x SaO2 ) + (.003 x PaO2 )

18. Acid Base Balance
BICARBONATE
BUFFER
SYSTEM
Acts in few seconds
RESPIRATORY
REGULATION
Acts in few minutes
RENAL
REGULATION
Acts in hours to days

19. Regulation of Acid Base
 Bicarbonate Buffer System
CO2 + H2O carbonic anhydrase H2CO3 H+ + HCO3
-
In Acidosis - Acid = H+
H+ + HCO3 H2CO3 CO2 + H2O
In Alkalosis
HCO3
- + H+ H2CO3

20.  Respiratory Regulation of Acid Base Balance-
H+
H+
ALVEOLAR
VENTILATION
ALVEOLAR
VENTILATION
PaCO2
PaCO2

21. ROLE OF KIDNEY
It retains and regenerate HCO3- thereby regenerating the body
buffer with the net effect of eliminating the non-volatile acid
load
a. H+ secretion
1. Free urinary H+ - minimal contribution
2. Ammonia
3. Phosphorus
b. HCO3- reabsorption
1. Proximal tubule – 90%
2. Distal tubule -10%

22. Assessment of ACID BASE Balance
 Definitions and Terminology
 ACIDOSIS – presence of a process which tends to
 pH by virtue of gain of H + or loss of HCO3
-
 ALKALOSIS – presence of a process which tends to  pH
by virtue of loss of H+ or gain of HCO3
-
If these changes, change pH, suffix ‘emia’ is added
 ACIDEMIA – reduction in arterial pH (pH<7.35)
 ALKALEMIA – increase in arterial pH (pH>7.45)

23.  Simple Acid Base Disorder/ Primary Acid Base disorder – a
single primary process of acidosis or alkalosis due to an initial
change in PCO2 and HCO3.
 Compensation - The normal response of the respiratory
system or kidneys to change in pH induced by a primary acid-
base disorder
 Mixed Acid Base Disorder – Presence of more than one acid
base disorder simultaneously .

24. BASE EXCESS
 Base excess is the amount of acid or base (expressed in mEq/L)
that must be added for blood pH to return to 7.40 and Paco2 to
return to 40 mm Hg at full O2 saturation and 37°C.
 The metabolic component of an acid–base disturbance.
 A positive value indicates metabolic alkalosis.
 whereas a negative value reveals metabolic acidosis.

25. STEP WISE APPROACH
to
Interpretation Of
ABG reports

26.  STEP 0- IS THIS ABG AUTHENTIC?
 STEP1- ACIDEMIA OR ALKALEMIA
 STEP2-RESPIRATORY OR METABOLIC
 STEP3- IF RESPIRATORY-ACUTE OR CHRONIC?
 STEP4- IS COMPENSATION ADEQUATE?
 STEP5-IF METABOLIC- ANION GAP?
 STEP6- IF HIGH ANION GAP METABOLIC
ACIDOSIS- Δ GAP?

27. Is this ABG authentic ?
 pH = - log [H+]
Henderson-Hasselbalch equation
pH = 6.1 + log HCO3
-
0.03 x PCO2
pHexpected = pHmeasured = ABG is authentic

28.  Reference table for pH v/s [H+]
[H+] neq/l = 24 X (PCO2 / HCO3)
H+ ion (neq/l) pH
100 7.00
79 7.10
63 7.20
50 7.30
45 7.35
40 7.40
35 7.45
32 7.50
25 7.60

29.  Look at pH
<7.35 - acidemia
>7.45 – alkalemia
STEP1- ACIDEMIA OR ALKALEMIA

30. IS PRIMARY DISTURBANCE RESPIRATORY OR
METABOLIC?
pH PCO2 or pH PCO2 METABOLIC
pH PCO2 or pH PCO2 RESPIRATORY
In primary respiratory disorders, the pH and PaCO2 change
in opposite directions; in metabolic disorders the pH and
PaCO2 change in the same direction.
STEP2-RESPIRATORY OR METABOLIC

31. STEP3- IS COMPENSATION ADEQUATE?
 pH within normal range- No acid base disorder,
Fully compensated
or mixed disorder.
 pH out of the range- uncompensated
or partially compensated.

32. Compensation
• PCO2 = (1.5 X [HCO3
-])+8 ±2
• For every 1mmol/l in HCO3 the PCO2 falls
by 1.25 mm Hg
METABOLIC
ACIDOSIS
• PCO2 = (0.7 X [HCO3
-])+ 21± 2
• For every 1mmol/l in HCO3 the PCO2 by
0.75 mm Hg
METABOLIC
ALKALOSIS
Metabolic Disorders – Compensation in these disorders leads to
a change in PCO2

33. Acute respiratory disorder ∆pH(e-acute) = 0.008x ∆Pco2
Chronic respiratory disorder ∆pH(e-chronic)= 0.003x ∆Pco2
Compare, ∆ pHmeasured (pHm) v/s ∆ pHexpected (pHe)
∆pH(m) = ∆pH(e- acute)
∆pH(m) =
between ∆pH(e- acute)
& ∆pH(e- chronic)
∆pH(m) =∆ pH(e-chronic)
ACUTE RESPIRATORY
DISORDER
PARTIALLY
COMPENSATED
CHRONIC RESPIRATORY
DISORDER
STEP4- IF RESPIRATORY-ACUTE OR
CHRONIC?

34. In Respiratory Disorders
Compensation begins to appear in 6 – 12 hrs and is fully developed
only after a few days.
1.ACUTE
Before the onset of compensation
Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.1meq/l
Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.2
meq/l

35. After compensation is fully developed
Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.4meq/l
Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.4meq/l
2.CHRONIC (>24 hrs)

36. Characteristics of ACID BASE Disorders
PRIMARY
DISORDER
PRIMARY RESPONSES COMPENSATORY
RESPONSESpH Primary
Defect
Metabolic
Acidosis pH HCO3
PCO2
Alveolar
Hyperventilation
Metabolic
Alkalosis pH HCO3
PCO2
Alveolar
Hypoventilation
Respiratory
Acidosis pH PCO2 HCO3
Respiratory
Alkalosis pH PCO2 HCO3

37. Mixed Acid-base Disorders are Common
 In chronically ill respiratory patients, mixed disorders are probably
more common than single disorders, e.g., RAc + MAlk, RAc + Mac,
Ralk + MAlk.
 In renal failure combined MAlk + MAc is also encountered.
Clues to a mixed disorder:
 Normal pH with abnormal HCO3 or CO2
 PaCO2 and HCO3 move in opposite directions
 pH changes in an opposite direction for a known primary disorder

38. Unmask the hidden metabolic
disorders
3 parameters need to be assessed
 Anion gap and its change from normal ΔAG
 Venous CO2 and its change from normal Δ CO2
 Bicarbonate gap

39.  Anion Gap= measured cations- measured anions
 ANION GAP(AG) = Na – (HCO3 + Cl)
Normal Value = 12 + 4 ( 8- 16 meq/l)
 ΔAG= MEASURED AG -12
IF ΔAG POSITIVE OR AG>16: METABOLIC ACIDOSIS
IF ΔAG NEGATIVE OR LOW AG:
Reduction in unmeasured anions (hypoproteinemia)
Excess of unmeasued cations(lithium toxicity)
Excessively abnormal positively charged
protien(multiple myeloma)
STEP5-IF METABOLIC- ANION GAP?

40.  Albumin is the major unmeasured anion
 The anion gap should be corrected if there are gross changes in
serum albumin levels.
AG (CORRECTED) = AG + { (4 – [ALBUMIN]) × 2.5}
If the anion gap is elevated, consider calculating the osmolal gap
in compatible clinical situations:
•Elevation in AG is not explained by an obvious case (DKA,
lactic acidosis, renal failure)
•Toxic ingestion is suspected

41. PLASMA OSMOLAR GAP
Cal. Plasma Osmolarity = 2[Na+] + [Gluc]/18 + [BUN]/2.8
 OSM gap = measured Osm – Cal. Plasma Osm
 The OSM gap should be < 10 mOsm/kg
Osm gap > 10 mOsm/kg indicates presence of abnormal osmotically
active substance
Ethanol
Methanol
Ethylene glycol

42. ∆ Anion Gap = Measured AG – Normal AG
Measured AG – 12
∆ HCO3 = Normal HCO3 – Measured HCO3
24 – Measured HCO3
Ideally, ∆Anion Gap = ∆HCO3
For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L
STEP6- IF HIGH ANION GAP METABOLIC
ACIDOSIS-DELTA RATIO/ DELTA GAP?
If an increased anion gap is present, assess the relationship between the
increase in the anion gap and the decrease in [HCO3-].
: unmask the co-existence of two metabolic disorders

43. DELTA GAP
 DELTA GAP = ΔAG-Δ HCO3
 DELTA GAP = (MEASURED AG-12) – (24-MEASURED HCO3)
 DELTA GAP = Na-Cl-36
 POSITIVE OR DELTA GAP > +6
METABOLIC ALKALOSIS
BICARBONATE RETENTION FOR RESPIRATORY ACIDOSIS
 NEGATIVE OR DELTA GAP < -6meq/l
NORMAL ANION GAP METABOLIC ACIDOSIS

44. DELTA RATIO
∆AG/ HCO3
- = 1  Pure High AG Met Acidosis
 AG/ HCO3
- > 1  Assoc Metabolic Alkalosis
 AG/ HCO3
- < 1  Assoc N AG Met Acidosis

45. High Anion Gap Metabolic Acidosis
M METHANOL
U UREMIA - ARF/CRF
D DIABETIC KETOACIDOSIS & other KETOSIS
P PARALDEHYDE, PROPYLENE GLYCOL
I ISONIAZIDE, IRON
L LACTIC ACIDOSIS
E ETHANOL, ETHYLENE GLYCOL
S SALICYLATE
Metabolic Acidosis

46.  1. Hypokalemic
a. GI losses of HCO3 –
i. Ureterosigmoidostomy
ii. Diarrhea, ingestion of CaCl2
iii. Ileostomy
 2. Normokalemic or hyperkalemic
a. Renal tubular disease
i. Acute tubular necrosis
ii. Chronic tubulointerstitial disease
iii. Distal RTA (type I and IV)
iv. Hypoaldesteronism
NORMALANION GAP METABOLIC ACIDOSIS
(hyperchloremic)
b. Renal losses of HCO3 –
i. proximal RTA
ii. carbonic Anhydrase
inhibitors
b. Pharmacological
i. Ammonium chloride
ii. Hyperalimentation
iii. Dilutional acidosis.

47. 1. Hypoalbuminemia
2. Paraproteinemia (multiple myeloma)
3. Spurious hyperchloremia
4. Bromide intoxication
5. Hypermagnesemia.
Decreased anion gap acidosis

48. 1. Loss of H+ ions (e.g. vomiting, diuretics)
2. Increased reabsorption of bicarbonate – Low intravascular volume
– Hypokalemia
– High pCO2
– Increased mineralocorticoids
(aldosterone).
3. Administration of alkali (in setting of renal impairment) e.g. Ringer’s
lactate where lactate gets metabolised to bicarbonates in liver adding to
alkali pool.
METABOLIC ALKALOSIS

49. RESPIRATORY ACIDOSIS
1. Airway/pulmonary parenchymal disease
a. Upper airway obstruction
b. Lower airway obstruction
c. Pulmonary -
i. Cardiogenic pulmonary edema
ii. Pneumonia iii. ARDS
iv. Pulmonary perfusion defect—PE—air/fat/tumor
2. CNS depression -head injury ,medications such as narcotics, sedatives, or anesthesia
3. Neuromuscular disease and impairment
4. Ventilatory restriction—due to pain, chest wall injury/ deformity, or abdominal
distension.

50.  Increased CO 2 production
Large caloric loads
Malignant hyperthermia
Intensive shivering
Prolonged seizure activity
Thyroid storm
Extensive thermal injury (burns)

51. RESPIRATORY ALKALOSIS
1. CNS stimulation: Fever, pain, thyrotoxicosis, cerebrovascular
accidents.
2. Hypoxemia: pneumonia, pulmonary edema.
3. Drugs/hormones: Medroxyprogesterone, catecholamines, salicylates.
4. Miscellaneous: Sepsis, pregnancy
5. Psychological responses, such as anxiety or fear.

52. URINARY ANION GAP
 Urinary NH4
+ levels can be estimated by calculating the urine
anion gap (UAG)
 UAG = [Na+ + K+]u – [Cl–]u
 [Cl–]u > [Na+ + K+], the urine gap is negative by definition
 Helps to distinguish GI from renal causes of loss of HCO3 by
estimating Urinary NH4+ (elevated in GI HCO3 loss but low in
distal RTA).
 Hence a -ve UAG (av -20 meq/L) seen in former while +ve value
(av +23 meq/L) seen in latter.

53. Urine PH
 Non AG metabolic acidosis:
 If urine pH > 5.5 : Type 1 RTA
 If urine pH < 5.5 : Type 2 or Type 4 RTA
 Type 2 or Type 4 RTA can be later differentiated using serum
K+ level

55. References
1. Paul L.Marino – The ICU Book.
2. Millers anaesthesia- eighth edition.
3. Morgan and Mikhails’s – Clinical anaesthesiology 5th
edition
4. Prof. A. K. Sethi EORCAPS 2013
5. Davenport – The ABC of Acid Base Chemistry, 6th edition
6. Handbook of blood gas /Acid base interpretation- Ashfaq
Ahmed

56. THANK YOU!

57. STEWART APPROACH
Its variables are pCO2 , strong ion difference (SID) and Atot (Total weak acids)
– Respiratory disorders are due to alterations in pCO2 similar to the traditional
approach
– Metabolic disorders are due to primary alterations in strong ion difference
(SID) and Strong ion gap (SIG) or Atot
– The cations are Na+, K+, Ca++ and Mg++
– The anions are Cl– , Lactates and other strong ions
– SID apparent SIDa= (Na+k+Ca+Mg)–(Cl) –Lactate-other strong ions
– (Na + k + Ca + Mg) – (Cl)
Normal strong ion difference is about 40 mEq/L
– SID effective SIDe = (HCO3 ) + (A– ) where A– is the total concentration of
dissociated weak noncarbonic acids, mainly albumin and PO4 –
– Strong ion gap (SIG) or Atot = SIDa- SIDe.
Normal Strong ion gap is zero.