ARTERIAL BLOOD GAS ANALYSIS

1. ARTERIAL BLOOD GAS
ANALYSIS

2. What is an ABG?
• Arterial Blood Gas
• Drawn from artery- Radial, Brachial, Femoral
• It is an invasive procedure

3. Why to order an ABG?
• Assess adequacy of ventilation and oxygenation
• Aids in establishing a diagnosis and severity of respiratory
failure
• Assess changes in acid- base homeostasis
• Helps to guide treatment plan
• Helps in management of ICU patients.

4. Components of an ABG
– pH
– PaCO2
– PaO2
– HCO3
– O2saturation
– BE

5. Others include
• Haemoglobin
• Hematocrit
• Na
• K
• Glucose
• Standard bicarbonate
• Buffer base
• Standard base excess
• TCO2

6. • Base Excess: It indicates increase in the amount
of buffer base.
• It is the number of mmol of strong acid needed
to adjust pH to 7.4 at PCO2 40 mm Hg.
• Base Deficit: It indicates decrease in the
amount of buffer base.

7. • Standard bicarbonate
It is the bicarbonate conc. In plasma in a completely
oxygenated blood sample at Pco2 of 40 mm Hg at 370C .
SBC > 24 mmol/l indicates metabolic alkalosis
SBC<24 mmol/l indicates metabolic acidosis
Buffer base
It is the total equivalent conc. of all anion buffer
components of blood . Normal value =48 mmol/L

8. • Standard base excess
• It gives a view of the base excess of the entire extracellular
fluid.
• It indicates average Hb of the fluid space through which
bicarbonate distributes.
• standard base excess is the value when the hemoglobin is
at 5 g/dl.
Total plasma CO2 (T-CO2)
Total content of the CO2 normal value= 27 meq/L

9. Normal Values
– pH - 7.35 - 7.45
– PaCO2 - 35-45 mmHg
– PaO2 - 80-100 mmHg
– HCO3 - 22-26
– O2sat - 95-100%
– Base Excess - +/-2 m Eq/L

10. HOW TO DRAW AN ABG..???
• Equipments
• Site Selection
• Contraindication
• Puncture procedure
• Post puncture procedure
• Sample handling

11. Equipments
1. One 1 cc to 5 cc vented, pre-heparinized, plastic syringe
2. One 20 - 25 gauge 1 –1 1/2” needle
Longer needles for brachial and femoral artery puncture
3. One Biohazard labelled plastic bag
4. . Two 1 x 1 inch sterile gauze

12. • 5. Alcohol prep pad
• 6. Specimen/Patient label
• 7. Iodine pad
• 8. One adhesive bandage
• 9. Lab Form
• 10. Ice

13. Site Selection
• Radial Artery - 45 insertion angle
• Brachial Artery - 60 - 90 insertion angle
• Femoral Artery - 90 insertion angle
• Dorsalis Pedis Artery
• Posterior Tibial artery

14. KK

15. Contraindication
• No absolute contraindications
• Dialysis shunt – choose another site
• Mastectomy – use opposite side
• Patient on anticoagulant/aspirin therapy – may have to hold
pressure on puncture site longer than normal

16. Site specific contraindication
Radial : Buergers disease
Raynauds
Absent Ulnar collateral circulation
AV dialysis shunt
Femoral: Local infection

17. Puncture procedure
1. Check for orders
2.Explain the patient about compression of puncture site
3. Make positive patient I.D.
4. Put on gloves
5. Assemble needle to syringe
a. keep needle sterile
b. eject excess heparin and air bubbles
c. pull back syringe plunger to at least 1 cc

18. 4 things that “hurt”
1. Needle through skin (sharp)
2. Needle through arterial wall (blunt)
3. Miss & catch nerve (shooting)
4. Miss & hit periostium (sharp)

19. Site selection
1. Radial artery is always the first choice because it provides
collateral circulation.
• A. Palpate the right and left radials arterial pulse and
visualize the course of the artery.
• B. Pick strongest pulse
i. if radial pulse weak on right, move to left
ii. if pulse on left weak, then try brachial
• 2. Brachial used as alternative site
• 3. Femoral is the last choice in normal situations
Highest complication rate

28. Check for:
• a. Bleeding
• b. movement of fingers and tingling sensation
• c. pulse distal to puncture

29. Post puncture procedure
1. Remove any air bubbles from sample and cap
syringe
• Dispose of needle in sharps container
2. Roll syringe to mix heparin with sample
3. Immerse in ice
4. On lab slip indicate:
a. FIO2
b. Patient temperature
c. Ventilator parameters
5. Deliver to lab

30. Sample handling
Sample should be analyzed as soon as possible
– If iced sample can be stored
» Glass syringe – 1 hour
» Plastic syringe – 15 minutes
Remember: Blood is living tissue that continues to
consume O2 and produce CO2

31. ABG Specimen Collection/Handling
• Transport specimen to laboratory in a biohazard container
• Analyze specimen on an instrument that has been recently
calibrated
• Temperature correction specimen in analyzer
• Increase in patient temp: PO2, PCO2, pH
• Decrease in patient temp: PO2, PCO2, pH

32. Blood Gas Analyzer

34. Technical Causes of Abnormal Results
• 1. Room air mixed with sample
• a. PaO2 will equilibrate to above 160
• 2. CO2 will be lower due to equilibration
• 3. Delay in running sample
• O2 consumption will continue as will CO2 production –
pH decreases
• Iced, sample will last an hour without a change in the result
• un-iced, ABG's can be significantly changed after 10 minutes

35. • 4. Venous sample drawn
• a. Usually this in patients with shock
• b. Should doubt when PO2 is significantly lower than expected
• i. draw venous blood to check comparison or
• ii. redraw sample

36. • 5. Heparin
• a. Sodium Heparin 1% solution should be used
• b. ammonium heparin will alter pH
• c. dry lithium heparin is OK
• • All unnecessary heparin should be ejected from syringe, excess
can effect results

37. • 6. Patient pain
• a. Can cause hyperventilation or breath holding
• b. An anaesthetic may be injected prior to stick for pain
• • Usually 2% lidocaine
• • CAUTION – some people allergic to “caines”
• 7. Machine errors
• a. Improper calibration
• b. Air bubbles in electrode

38. Acid-Base Physiology
• pH is the negative logarithm to the base 10 of the hydrogen ion
concentration in mmol/L
• pH = - log10[H+]
• An increase in pH indicates a proportionate decrease in the [H+] and
a decrease in the pH indicates a proportionate increase in the [H+].
• H2CO3 generates 12,500 mmol H+ per day.
• Normal metabolism of proteins and nucleotides generates about 100
mmol H+ per day in the form of sulphuric and phosphoric acids.

39. Calculation of pH
• pH is calculated from Henderson-Hasselbalch
equation .
• pH = pK + log acid/bas
• pH = 6.1 + log HCO3-
H2CO3
Kassirer and Bliech modified equation
• H+ = 24 x PCO2/HCO3-

40. Regulation of pH
pH is maintained in narrow range by
• 1) In seconds: buffer systems
• 2)In minutes: CO2 excretion by the lungs
• 3)In hours to days: renal excretion of H+,
reabsorption of HCO3

41. Regulation of arterial pH
• 1.BUFFERS –Buffer systems minimize the change in pH resulting from
production of acid .
• Main buffer system in humans is HCO3- in ECF and protein and
phosphate buffers in ICF.
2.ROLE OF THE RESPIRATORY SYSTEM–Elimination of volatile acid CO2.
• a. Respiratory centers in the brain respond to changes in pH of
CSF and blood to affect ventilatory rate.
• b. Ventilation directly controls the elimination of CO2.

42. 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%

43. Carbon dioxide transport
• In Dissolved form : Carbon dioxide is twenty times more soluble in
water than oxygen.
• 100 ml of plasma with a PCO2 of 40 mmHg carries about 2.4 mlCO2
in solution. 5% of total CO2 carriage.
• As carbamino compounds : 5 -10% of CO2 carriage
• Bicarbonate: The remaining 85 -90% of carbon dioxide is carried by
blood in the form of bicarbonate ions.

44. Acid base disorders
• Acidemia –pH less than 7.35
• Acidosis – A process that would cause
acidemia, if not compensated
• Alkalemia–pH greater than 7.45
• Alkalosis – A process that would cause
alkalemia if not compensated

45. Four primary acid-base disorders
• Metabolic acidosis
• Metabolic alkalosis
• Respiratory acidosis
• Respiratory alkalosis

46. SIMPLE VS. MIXED ACID-BASE DISORDER
Simple acid-base disorder – a single primary
process of acidosis or alkalosis.
Mixed acid-base disorder – presence of more
than one acid base disorder simultaneously

47. COMPENSATION
The normal response of the respiratory system
or kidneys to change in pH induced by a primary
acid-base disorder

48. Compensation
• In the presence of acidosis or alkalosis, regulatory
mechanisms occur which try to maintain arterial
pH.
• Disturbances in HCO3- result in respiratory
compensation
• Changes in CO2 are counteracted by renal
compensation

49. a. Renal compensation – kidneys adapt to alterations
in pH by changing the amount of HCO3-
generated/excreted.
Full renal compensation takes 2-5 days
b. Respiratory compensation – alteration in ventilation
allow immediate compensation for metabolic acid-
base disorders

50. Characteristics of  acid-base disorders
DISORDER PRIMARY RESPONSES COMPENSATORY
RESPONSE
Metabolic
acidosis
 [H+]  PH  HCO3
-  pCO2
Metabolic
alkalosis
 [H+]  PH  HCO3
-  pCO2
Respiratory
acidosis
 [H+]  PH  pCO2  HCO3
-
Respiratory
alkalosis
 [H+]  PH  pCO2  HCO3
-

51. Prediction of compensation
Metabolic acidosis PaCO2= (1.5 x HCO3
-) + 8 ± 2
Metabolic alkalosis
PaCO2 will↑ 0.75 mmHg per
mmol/L ↑ in [HCO3
-]
Respiratory
acidosis
Acute
[HCO3
-] will ↑ 0.1 mmol/L per
mmHg in PaCO2
Chronic
[HCO3
-] will ↑ 0.4 mmol/L per
mmHg in PaCO2
Respiratory
alkalosis
Acute
[HCO3
-] will ↑ 0.2 mmol/L per
mmHg in PaCO2
Chronic
[HCO3
-] will ↑ 0.4 mmol/L per
mmHg in PaCO2

52. Anion Gap
• Anion gap used to assess acid-base status in
D/D of meabolic acidosis
Anion gap based on principle of electro
neutrality:
• Total Serum Cations = Total Serum Anions
• Na – (HCO3 + Cl) = Anion gap
• Normal Anion gap – 10 +/- 2meq/L

53. • 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}

54. Delta gap
• Difference between
– Change in anion gap ( AG)
– Change in bicarbonate ( HCO3
- )
• Based on assumption that for each 1 meq/L
increase in AG, HCO3 will fall by 1 meq/L , to
maintain a stable anion content.
• Usual range: -6 to +6 meq/L ; should be 0

55.  AG =  HCO3
-  Pure High AG Met Acidosis
 AG > HCO3
- ( Gap >6)  HCO3- does not
decrease as expected.
Associated Metabolic Alkalosis or respiratory acidosis
 AG <  HCO3
- ( Gap < -6)  HCO3- does not
increase as expected
Associated N AG Met Acidosis or rarely respiratory
alkalosis
Delta ratio may also be calculated

56. PLASMA OSMOLAR GAP
 Calculated Plasma Osmolarity = 2[Na+] + [Gluc]/18 +
[BUN]/2.8
Normal Measured Plasma Osmolarity > Calculated
Plasma Osmolarity (upto 10 mOsm/L)
 Measured Plasma Osmolarity - Calculated Plasma
Osmolarity > 10 mOsm/kg indicates presence of abnormal
osmotically active substance
Ethanol
Methanol
Ethylene glycol

57. 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.

58. 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

59. METABOLIC ACIDOSIS

60. Causes of High AG Met Acidosis
1. Ketoacidosis:
Diabetic
Alcoholic
Starvation
2. Lactic Acidosis:
Type A (Inadequate O2 Delivery to Cells)
Type B (Inability of Cells to utilise O2)
Type D (Abn bowel anatomy)
3. Toxicity:
Salicylates Paraldehyde
Methanol Toluene
Ethylene Glycol
4. Renal Failure
5. Rhabdomyolsis

61. CAUSES OF NORMAL ANION GAP
METABOLIC ACIDOSIS
1. HCO3 loss:
GIT Diarrhoea
Pancreatic or biliary drainage
Urinary diversions
(ureterosigmoidostomy)
Renal Proximal (type 2) RTA
Ketoacidosis (during therapy)
Post-chronic hypocapnia

62. 2. Impaired renal acid excretion:
Distal (type 1) RTA
Hyperkalemia (type 4) RTA
Hypoaldosteronism
3. Misc:
Acid Administration (NH4Cl)
Hyperalimentation
Cholestyramine Cl
HCl therapy (Rx of severe met alkalosis)

63. METABOLIC ALKALOSIS

64. CAUSES OF METABOLIC
ALKALOSIS
1. EXOGENOUS HCO3- LOADS
Acute alkali administration
Milk – alkali syndrome
2. Effective ECFV contraction, normotention, K+ deficiency and
secondary Hyperreninemic hyperaldosteronism:
GI LOSS: Vomiting
Gastric Aspiration
Villous adenoma

65. RENAL LOSS : Diuretics
Post hypercapnic state
Hypercalcaemia
Recovery from LA/KA
Mg2+ deficiency
Bartters/Gitelmans syndr
Nonreabs anions – penicill
3. ECFV expansion, hypertension,K+ deficiency,
and mineralocorticoid excess:
HIGH RENIN : RAS
Accelerated hypertension
Renin sec tumor

66. LOW RENIN :
PRIMARY ALDOSTERONISM –
Adenoma, hyperplasia , carcinoma
ADRENAL ENZYME DEFECTS –
11 b Hydroxylase, 17 alfa Hydr def
CUSHINGS SYNDROME OR DIS.
OTHERS- licorice, carbenoxolone
4. Gain of function mutation of renal sodium channel
with ECF expansion , hypertension , K+ deficiency
and hyporeninemic hypoaldosteronism :
LIDDLES SYNDROME

67. RESPIRATORY ACIDOSIS

68. Causes of Respiratory Acidosis
1. CENTRAL :
Drugs( anesthetics, morphine , sedatives)
Stroke
Infection
2. AIRWAY :
Obstruction
Asthma
3. PARENCHYMA :
Emphysema
Pneumoconiosis
Bronchitis
ARDS
Barotrauma

69. • 4. NEUROMUSCULAR :
• Poliomyelitis
• Kyphoscoliosis
• Myasthenia
• Muscular dystrophies
5. MISCELLANEOUS
• Obesity
• Hypoventilation
• Permissive Hypercapnia

70. Respiratory Alkalosis

71. Causes of Respiratory Alkalosis
1.CENTRAL NERVOUS SYSTEM STIMULATION
Structural Causes Non Structural Causes
Head trauma Pain
Brain tumor Anxiety
CVA Fever
Meningitis, encephalitis Psychosis
2. HYPOXEMIA OR TISSUE HYPOXIA
Pneumonia, pulm oedema
Aspiration
High Altitude

72. 3. STIMULATION OF CHEST RECEPTORS :
• Hemothorax
• Flail chest
• Cardiac failure
• Pulmonary embolism
4. MIXED/UNKNOWN MECHANISMS:
Drugs – Salicylates Nicotine
Progesterone Thyroid hormone
Catecholamines
Xanthines (Aminophylline & related compounds)
Cirrhosis
Gram –ve Sepsis
Pregnancy
Heat exposure
Mechanical Ventilation

73. A Stepwise
Approach
to Solving
Acid-Base
Disorders

74. Step – 1 : Check for ERRORS
Have the required parameters been correctly
fed..???
 Patient’s Temperature
 Fi O₂ : specially if patient is in ventilator
 Hemoglobin : some machines may not measure it
 Barometric pressure : some machines may not measure it

75. Effect of temperature

77. Effect of barometric pressure (Pb)

78. Sampling error..??
Arterial, veinous or mixed…???

79. pH is inversely related to [H+]; a pH change of 1.00
represents a 10-fold change in [H+]
pH [H+] in nanomoles/L
7.00 100
7.10 80
7.30 50
7.40 40
7.52 30
7.70 20
8.00 10
Relation b/w pH & H+ conc.
Assessment of validity of test results

80. Assessment of validity of test results
• H+ in nmol/L = 24 × PCO₂/HCO₃
• If there is a discripancy between the 2
results, the blood should be reanalyzed.

81. Analyse the adequacy of oxygenation..

82.  STEP -2 : Comprehensive history and physical
examination.
 STEP -3 : Acidosis or alkalosis..???
See the pH (<7.35 or >7.45)
 STEP -4 : Identify the primary disorder
See the change in PCo2 & HCO3
 STEP -5 : Calculate the compensatory response
Is adequately compensated???

83.  STEP -6 : Calculate anion gap
STEP -7 : Calculate the delta gap (unmask hidden
mixed disorders)
STEP -8 : Calculate the osmolar gap (for high AG
acidosis)
 STEP -9 : Calculate the urinary anion gap (Non
AG metabolic acidosis)
 STEP -10 : Formulate differential diagnosis

84. Lets try…..

85. Case-1
• 60 years old M, presents to the ED with rapid
breathing and less responsive than usual. No
other history available.
ABG results
pH 7.31
PCO₂ 10
HCO₃ 5
Na 123
K 5
Cl 99

86. Stepwise interpretation
1. At pH 7.3 H+ conc. Should be ≈50nmol/L
– Calculated H+ = 24 × 10/5 = 24 × 2 = 48
– Both values corroborate, hence result is valid.
2. pH is 7.3 i.e Acidosis
3. HCO₃ value has gone down, primary process
is metabolic
4. Respiratory compensation:
– Calculated PCO₂ = (1.5 × 5)+8 ± 2 = 13.5 to 17.5
– Over compensated ; mixed disorder
– a/w respiratory alkalosis

87. 5. Anion gap: (123+5) – (99 + 5) = 19
– High anion gap metabolic acidosis
6. Delta gap :
– Change in AG = (19-10) = 9
– Change in HCO₃ = (24-5) = 19
– Delta gap = 9-19 = -10
Presence of non anion gap metabolic acidosis also.!!
7. Osmolar gap: data not provided.

88. Finally …
• Mixed acid base disorder, with presence of
both high AG & normal AG metabolic acidosis
and respiratory alkalosis.

89. Case-2
• A k/c/o COPD with cor pulmonale on
treatment presented with progressive
breathlessness.
ABG results
pH 7.42
PCO₂ 67
HCO₃ 42
Na 140
K 3.5
Cl 88

90. • pH is normal; but PCO₂ & HCO₃ both are
increased.
• Change in PCO₂ is 67-40 = 27
• Expected rise in HCO₃ should be 27 × 0.4 =
10.8
• Expected HCO₃ = 24+10.8 ≈ 35
• Actual HCO₃ = 42
• AG = 12 (N)
• Mixed disorder, both respiratory acidosis &
metabolic alkalosis.

91. Case -3
• A known case of case of chronic kidney disease,
discontinued MHD & presented to the emergency in
an altered state of sensorium. Attendants gave
history of repeated episodes of vomiting at home.
ABG results
pH 7.42
PCO₂ 40
HCO₃ 25
Na 140
K 3.0
Cl 95

92. • pH, PCO₂, HCO₃ all WNL
• AG = 23 (↑)
• Delta gap = 13 – 1 = 12 (↑)
• AG >> HCO3
–
• Mixed disorder with presence of both high AG
metabolic acidosis and metabolic alkalosis.

93. Case-4
• 65 yrs old M, past h/o AMI on medication, presented
with high grade fever with, cough & yellowish
expectoration for 5 days. Acute increase in shortness of
breath.
ABG results
pH 7.3
PCO₂ 38
HCO₃ 16
Na 136
K 4
Cl 102

94. • pH 7.3 = Acidosis
• HCO₃ is low ; primary disorder is metabolic
acidosis
• Expected PCO₂ = (1.5 × 16) + 8 = 32
• Calculated PCO₂ < estimated PCO₂
• AG = 22
• Delta gap = (10-8) = 2
• Mixed disorder with metabolic acidosis &
respiratory acidosis

95. Take home messages…

96. • ABG is a very useful diagnostic tool for our day
to day practice.
• Approach to interpret should be step wise & in
a systematic manner.
• Any abnormal result should be analyzed
cautiously in light of clinical context.
• Appropriate use of this tool using clinical
judgment is of paramount importance