Arterial blood gases

1. ARTERIAL BLOOD GAS ANALYSIS
PRESENTED BY: DR TETIKCHA GURUNG
MODERATED BY : DR RAM RAI

2. INTRODUCTION
 ABG provides rapid information on three physiological processes:
i. Ventilation( reflected by PaCO2)
ii. Oxygenation status( assessed primarily by PaO2 andSaO2
iii. Acid Base Balance
 ABG analysis  essential for diagnosing and managing the patient’s
oxygenation status , ventilation failure and acid base balance.

3. INDICATION
 Assess the ventilatory setting, oxygenation and acid base status.
 Assess the response to an intervention.
 Regulate electrolyte therapy.
 Establish preoperative baseline parameters.

4. CONTRAINDICATION
 An abnormal modified Allen’s test.
 Local infection or distorted anatomy at puncture site.
 Severe peripheral vascular disease of the artery.
 Active Raynaud’s Syndrome

5. SITE
 Radial artery ( most common )
 Brachial artery
 Femoral artery
 Radial is the most preferable site used
because:
i. It is easy to access
ii. It is not a deep artery which facilitate
palpation,
stabilization and puncturing
iii. The artery has a collateral blood
circulation

6. EQUIPMENTS
Blood gas kit OR
 1ml syringe
 23-26 gauge needle
 Stopper or cap
 Alcohol swab
 Disposable gloves
 Plastic bag & crushed
ice
 Lidocaine (optional)
 Vial of heparin
(1:1000)
 Bar code or label

7. METHODOLOGY
PREPARATORY PHASE:
 Record patient inspired oxygen concentration.
 Explain the procedure to the patient.
 Heparinize the needle.
• Donot leave excess heparin in the syringe
• ↑↑ heparin  ↑↑ dilutional effect  ↓↓ HCO3
−
and ↓↓pCO2
 Wait at least 20 minutes before drawing blood for ABG after changing
settings of mechanical ventilation, after suctioning the patient or after
extubation.

8.  After preparing the site, the artery is palpated for maximum pulsation
 In case of radial artery , Modified Allen test is done.
 Skin and subcutaneous tissue may be infiltrated with local anesthetic agent if
needed
 The needle is inserted at 45 in radial, 60 in brachial and 90 in femoral.
• Ensure no air bubble
Air Bubble has pO2 − 150 mm Hg and pCO2 −0 mmHg
Air Bubble + Blood = ↑↑ pO2 and ↓↓ pCO2
 Place the capped syringe in the container of ice immediately
 Maintain firm pressure on the puncture site for 5 minutes.

9. MODIFIED ALLEN’S TEST
 Test to determine collateral circulation is present from the ulnar
artery in case thrombosis occur in the radial artery.

10.  ABG syringe must be transported at the earliest to the laboratory for early
analysis via cold chain
 ABG sample should always be sent with relevant information regarding
O2, FiO2 status and Temperature.

11. COMPLICATION
 Arteriospasm
 Infection
 Hematoma
 Hemorrhage
 Distal Ischemia
 Gangrene
 AV Fistula

12. ACID BASE BALANCE
 Acid base balance is defined by the concentration of hydrogen ion
 The hydrogen ion concentration in aqueous solution is expressed by pH
which is defined as negative logarithm( base 10 ) of [H+
].
pH = log(1/ [H+
]) = -log [H+
].

13. The acid base equilibrium is described using Henderson Hasselbach Equation:

14.  BICARBONATE BUFFER
SYSTEM
 Acts within few seconds
 RESPIRATORY
REGULATION
 Acts within few minutes
 RENAL REGULATION
 Acts in hours to days

15. CHEMICAL BUFFER
 Buffer = base molecule and its weak conjugate acid.
 pKa= dissociation ionization constant  pH at which acid is 50 %
dissociated and 50% undissociated.
 pKA indicates strength of the acid
 There are 2 buffer system:
i. Extracellular buffer system
ii. Intracellular buffer system

16. EXTRACELLULAR BUFFER SYSTEM
 It includes : Bicarbonate buffer system(pKa=6.1) and Phosphate buffer
system(pKa=6.8).
1. Bicarbonate Buffer System(H2CO3/HCO3
−
)
The base = bicarbonate and its weak acid conjugate= carbonic acid
CO2 + H2O carbonic anhydrase H2CO3 H+ + HCO3
-

17. INTRACELLULAR BUFFER
 It includes :
i. Hemoglobin buffer(HbH/Hb)
ii. Other protein buffer(PrH/Pr−)
iii. Phosphate buffer(H2PO4 −/HPO4 2−),

18. HEMOGLOBIN BUFFER SYSTEM

19. RESPIRATORY REGULATION

21. RENAL REGULATION
 Occurs via 3 mechanism:
i. reabsorption of the filtered HCO3
−
ii. excretion of titratable acids,
iii. production of ammonia

23. 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 9 + 3 meq/L
B.E +2 to -2 meq/L

24. DEFINITIONS
 ACID: molecule that can act as a proton (H+) donor
 BASE: molecule that can act as a proton acceptor.
 ACIDEMIA:A blood pH less than 7.35
 ALKALKEMIA : a blood pH greater than 7.45
 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
-

25.  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
The Compensatory responses to a primary Acid Base disturbance are never
enough to correct the change in pH they only act to reduce the severity.
 Mixed Acid Base Disorder – Presence of more than one acid base disorder
simultaneously .

26.  Buffer Base:
 It is total quantity of buffers in blood including both volatile(Hco3) and non
volatile (as Hgb,albumin,Po4)
 Base Excess/Base Deficit:
 Amount of strong acid or base needed to restore plasma pH to 7.40 at a Pa
CO2 of 40 mm Hg,at 37*C.
 Calculated from pH, PaCO2 and HCT
 Negative BE also referred to as Base Deficit
 True reflection of non respiratory (metabolic) acid base status
 Normal value: -2 to +2mEq/L

27.  The H+ In extracellular fluid is determined by balance between the pCO2 and HCO3
- in the
fluid.
 This relationship is expressed as
H+ = 24 x (pCO2/ HCO3 )

28. STEPWISE APPROACH TO ACID BASE ANALYSIS

29.  STEP 1: Check for authenticity
 STEP 2: : Identify the primary Acid Base disorder
 STEP 3: Evaluate the Secondary Response
 STEP 4: Calculate Anion Gap

30. STEP 1 : CHECH FOR AUTHENTICITY
 [H+] neq/l = 24 X (PCO2 / HCO3)
Calculate it from the ABG report and if this value
is equal to H+ in the report,the ABG report is
authentic.
 Alternatively subtract the last two digits of the
pH(e.g 20 in Ph 7.20) from 80, this value is
approximately equal to the H+ concentration in
the ABG report.
 𝐻𝐶𝑂3
−
= 24 x
𝑝𝐶𝑂2
𝐻+ = ± 2 of 𝐻𝐶𝑂3
−
of venous
blood ; ifnot then the ABG is invalid and not
compatible
H+ ion 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

31. STEP 2 : IDENTIFY THE PRIMARY ACID BASE DISORDER.
 RULE 1 : If the 𝑃𝑎𝐶𝑂2 and /or pH is outside the normal range acid base
disorder
 RULE 2: if the 𝑃𝑎𝐶𝑂2 and pH are both abnormal, compare the directional
change
 2a: if 𝑡ℎ𝑒 ↑ 𝑃𝑎𝐶𝑂2 and ↑pH or ↓ 𝑃𝑎𝐶𝑂2 and ↓pH  primary metabolic acid
base disorder
 2b : if 𝑡ℎ𝑒 ↑ 𝑃𝑎𝐶𝑂2 and↓pH or ↑ pH and ↓ 𝑃𝑎𝐶𝑂2 primary respiratory acid
base disorder

32.  RULE 3: if the 𝑃𝑎𝐶𝑂2 or pH is abnormal, the condition is a mixed metabolic
and respiratory disorder.
 3a: if 𝑃𝑎𝐶𝑂2 is abnormal, directional change in 𝑃𝑎𝐶𝑂2  type of respiratory
disorder
 3b: if pH is abnormal , the directional change in pH metabolic disorder.

33. STEP 3 : EVALUATE THE SECONDARY RESPONSE

34.  RULE 4: For a primary metabolic acidosis , if
measured 𝑃𝑎𝐶𝑂2 is higher than expected secondary respiratory acidosis and
measured 𝑃𝑎𝐶𝑂2 is less than expected  secondary respiratory alkalosis.

35.  Metabolic Acidosis
 Winter’s formula: Expected pCO2 = 1.5[HCO3] + 8 ± 2
OR
 pCO2 = 1.2 ( HCO3)
 If serum pCO2 > expected pCO2 -> additional respiratory acidosis and vice versa

36. EXPECTED CHANGES IN ACID-BASE DISORDERS
Primary Disorder Expected Changes
Metabolic acidosis PCO2 = 1.5 × HCO3 + (8 ± 2)
Metabolic alkalosis PCO2 = 0.7 × HCO3 + (21 ± 2)
Acute respiratory acidosis delta pH = 0.008 × (PCO2 - 40)
Chronic respiratory acidosis delta pH = 0.003 × (PCO2 - 40)
Acute respiratory alkalosis delta pH = 0.008 × (40 - PCO2)
Chronic respiratory alkalosis delta pH = 0.003 × (40 - PCO2)
From: THE ICU BOOK - 2nd Ed. (1998) [Corrected]

37.  RULE 5: For a primary respiratory disorder,
a normal or near normal 𝐻𝐶𝑂3
−
 acute
 RULE 6: For a primary respiratory disorder where the 𝐻𝐶𝑂3
−
is abnormal , determine the
expected 𝐻𝐶𝑂3
−
for a chronic respiratory disorder
 6a : For a chronic respiratory acidosis, if
𝐻𝐶𝑂3
−
is lower than expected  incomplete renal response
𝐻𝐶𝑂3
−
is higher than expected secondary metabolic alkalosis
 6b : For a chronic respiratory alkalosis, if
𝐻𝐶𝑂3
−
is higher than expected incomplete renal response
𝐻𝐶𝑂3
−
is lower than expected  secondary metabolic alkalosis

38.  Respiratory Acidosis
 Acute (Uncompensated): for every 10 increase in pCO2 -> HCO3 increases by 1 and there is a decre
ase of 0.08 in pH
 Chronic (Compensated): for every 10 increase in pCO2 -> HCO3 increases by 4 and there is a decreas
e of 0.03 in pH
 Respiratory Alkalosis
 Acute (Uncompensated): for every 10 decrease in pCO2 -> HCO3 decreases by 2 and there is a increas
e of 0.08 in PH
 Chronic (Compensated): for every 10 decrease in pCO2 -> HCO3 decreases by 5 and there is a increas
e of 0.03 in PH

40. ANION GAP
 Normally, measured cation(MC) + unmeasured cation(UC) = measured anion(MA) + unmeasured
anion(UA).
 MC – MA = UA-UC
 Measured cation = 𝑁𝑎+
and Measured Anion = 𝐶𝑙−
and 𝐻𝐶𝑂3
−
 𝑁𝑎+ - (𝐶𝑙− + 𝐻𝐶𝑂3
−
) = UA –UC
 UA - UC = Anion Gap(AG)= 8-12mEq/L
 Corrected Anion Gap= Anion Gap + 2.5(4.5- albumin of patient)
 1g/dL of Albumin contribute to 3 mEq/L of Anion Gap

41. 1. HAGMA( High Anion Gap Metabolic Acidosis)
 Anion gap is high because fall in 𝐻𝐶𝑂3
−
is not compensated by 𝐶𝑙−
 Causes
K- Ketoacidosis due to endogenous causes/ acid  Diabetes, Alcohol , Starvation
U-Uremic Acidosis
S-Salicylate/Paraldehyde
M-Methanol
E-Ethylene Glycol
L-Lactic Acidosi

42. 2. NAGMA(Normal Anion Gap Metabolic Acidosis)
 A.k.a Hyperchloremic Metabolic Acidosis
 Fall in 𝐻𝐶𝑂3
−
is compensated by 𝐶𝑙−
 Causes:
Causes of nongap metabolic acidosis - DURHAM
Diarrhea, ileostomy, colostomy, enteric fistulas
Ureteral diversions or pancreatic fistulas
RTA type I or IV, early renal failure
Hyperailmentation, hydrochloric acid administration
Acetazolamide, Addison’s
Miscellaneous – post-hypocapnia, toulene, sevelamer, cholestyramine ingestion

43. CALCULATE ANION GAP
 𝑁𝑎+ - (𝐶𝑙− + 𝐻𝐶𝑂3
−
) = UA –UC; 𝑁𝑎+ = 140 and 𝐶𝑙− = 106
 UA - UC = Anion Gap(AG)= 8-12mEq/L
 In case of HAGMA, calculate Delta Ratio= 1-2
Delta Ratio =
∆𝐴𝐺
∆𝐻𝐶𝑂3
−
=
𝐴𝐺−12
24−𝐻𝐶𝑂3
−
 When Delta Ratio < 1 ; ∆ 𝐻𝐶𝑂3
−
increased disproportionately  HAGMA+NAGMA
 When Delta Ratio >2 ; ∆ 𝐻𝐶𝑂3
−
decreased disproportionately  HAGMA+ metabolic alkalosis
 When Delta Ratio 1-2  HAGMA

44.  If a patient has normal anion gap , cause may be
i. RTA
ii. GI loss of bicarbonate
 History to be noted
 If no history + , check for Urine Anion Gap
Urine Anion Gap( UAG) = Urine 𝑁𝑎+
+(Urine𝐾+
− 𝐶𝑙−
)
 In RTA UAG more positive
 In GI Loss of 𝐻𝐶𝑂3
−
 UAG negative.

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