ABG Analysis in pediatrics

1. Welcome To Seminar
on
Arterial Blood Gas Analysis
(ABG)
Dr. Momtahina Mou, Resident Year 1, Pediatric Hematology and Oncology
Dr. Renesha Islam, Resident Year 1, Pediatric Hematology and Oncology
Dr. Serajum Munira, Resident Year 2, Pediatric Cardiology

2. Outline of Presentation
Introduction
Indication of ABG
Procedure of arterial blood sampling
Pulmonary gas exchange
Acid base disorders
Stepwise approach to ABG analysis
ABG vs VBG

3. Introduction

4. Introduction
Arterial blood gas (ABG) analysis
refers to the measurement of pH
and the partial pressures of
oxygen (O2) and carbon dioxide
(CO2) in arterial blood.
acid–base
balance in
blood
pulmonary
gas
exchange

5. Normal values

6. Indications of ABG

7. Indications of ABG
Establishing diagnosis and assessing
illness severity
•Suspected hypercapnia (↑Pa CO 2 )
•Drowsiness, flapping tremor, bounding
pulses
•Clinical deterioration in a patient with
chronic type 2 respiratory impairment
Suspected severe hypoxaemia
•Very low or unrecordable O 2
saturation; cyanosis
•Severe, prolonged or worsening
respiratory distress
•Smoke inhalation Hyperventilation
(confirm ↓PaCO2, check for underlying
metabolic acidosis)
•Acute deterioration in consciousness
•Any severely unwell patient*
•Pulse oximetry unreliable or suspicious
result

8. Indications of ABG contd.
Guiding treatment and monitoring response
•Mechanically ventilated patients
•Patients receiving non-invasive assisted ventilation
•Patients with respiratory failure
•Patients with chronic hypercapnia receiving O2
•Critically ill patients undergoing surgery
•Candidates for long-term oxygen therapy

9. Procedure of arterial
blood sampling

10. Procedure of arterial blood sampling
Before sampling:
•Confirm the need for the ABG and identify any contraindications.
•Always record details of O2 therapy and respiratory support (e.g. ventilator settings).
•Allow at least 20 minutes after any change in O2 therapy before sampling (to achieve
a steady state).
•Obtain informed consent to proceed.
•Prepare necessary equipment (heparinized syringe with cap, 20–22G needle, gauze).
•Identify the site for sampling by palpation. For radial artery, perform a modified
Allen test to ensure adequate collateral circulation from the ulnar
artery.

11. Procedure of arterial blood sampling contd.
Site of arterial puncture:
Radial artery (1st choice)
Posterior tibial artery(2nd choice)
Arteria dorsal pedis
Femoral artery (should be preserved
for emergency situation)
Brachial artery (should not be used
unless absolutely necessary)

12. • Position the patient’s hand with
the wrist extended 20–30°.
• Identify the radial artery by
palpating the pulse.
• Clean the sampling site with an
alcohol wipe.
• Expel the heparin from the syringe.
Procedure of arterial blood sampling contd.

13. Procedure of arterial blood sampling contd.
• Insert the needle at 45 degrees,
bevel facing up.
• Insert the needle slowly to
minimize the risk of arterial spasm.
• When the needle is in the artery, a
flash of pulsatile blood will appear.
• Allow the syringe to fill under
arterial pressure.

14. Procedure of arterial blood sampling in children

15. Precautions for collection of blood sample
1. Heparin is acidic and lowers pH.
Use heparin of lower strength
2. Use small volume of heparinised
saline just for lubricating
syringe and plunger. If volume is
more, dissolved oxygen in
heparinised saline may increase
pO2.

16. Precautions (contd):
SAMPLE SHOULD NOT CONTAIN AIR BUBBLES OR BE LEFT OPEN TO
AIR:
•Presence of air will ↑ PO2 and ↓ PCO2 as ambient air contains
almost no CO2. Resulting pH will rise.
TEMPERATURE CORRECTION: (Body temp- 37°C)
•PaO2 ↑/↓ by 5mmHg for each degree Celsius temp. ↑/↓
•PaCO2 ↑/↓ by 2mmHg for each degree Celsius temp. ↑/↓

17. Precautions (contd):
SAMPLE SHOULD BE SEND WITH ICE:
•Without ice , analyze within 15 min.
•With ice, analyze within 1 hr.
The main effect of cellular metabolism is to ↓ PO2. Remarkable fall
in PaO2 if the blood contains WBC ≥100,000/mm3 (Leukocyte
larcency), even when the sample is on ice.

18. Contraindications
•Inadequate collateral circulation at the puncture site
•Should not be performed through a lesion or a surgical shunt
•Evidence of peripheral vascular disease distant to the puncture site
•A coagulopathy or medium- to high-dose anticoagulation therapy

19. Complications of Arterial Puncture
•Arteriospasm
•Hematoma
•Emboli (Air or clotted blood)
•Hemorrhage
•Trauma to vessel
•Arterial occlusion
•Vasovagal response and pain

20. Pulmonary gas exchange

21. Pulmonary gas exchange
Arterial blood gases (ABGs) help us to assess the effectiveness of gas exchange by
providing measurements of the partial pressures of O2 and CO2 in arterial blood
(i.e. the PaO2 and PaCO2).

22. Carbon dioxide elimination
• Diffusion of CO2 from the
bloodstream to alveoli is so
efficient that CO2 elimination
is limited by how quickly we
can ‘blow off’ the CO2 in our
alveoli
• The PaCO2 is determined by
alveolar ventilation.
Oxygenation
• PO2 measures the free,
unbound O2 molecules in
blood.
• Total amount of O2 in blood
depends on the following two
factors:
• 1. Hb concentration
• 2. Saturation of Hb with O2
(SO2): the percentage of
available binding sites on Hb
that contain an O2 molecule.

23. Acid Base Disorders

24. Acid Base Disorders
Chronic, mild derangements in acid–base status may interfere with normal
growth and development, whereas acute, severe changes in pH can be fatal.
Control of acid–base balance depends on the kidneys, the lungs, and
intracellular and extracellular buffers.
A normal pH is 7.35-7.45.
There is an inverse relationship between the pH and the hydrogen ion
concentration.

25. Acid Base Disorders
An acid (HA) can dissociate into a
hydrogen ion and a conjugate base (A
− ), as follows:
HA ↔ H+ + A−
H2CO3 <--> H+ + HCO3-

26. Acid base balance
An acid is a
substance that
releases H+ when it
is dissolved in
solution.
Acids therefore
increase the H+
concentration of
the solution (i.e.
lower the pH).
Acidaemia is
blood pH below
the normal
range (<7.35)
Acidosis is
any process
that lowers
blood pH
A base is a
substance that
accepts H + when
dissolved in
solution.
Bases therefore
lower the H+
concentration of
a solution (i.e.
raise the pH).
Alkalaemia is
blood pH above
the normal
range (>7.45)
Alkalosis is
any
process
that raises
blood pH.
A buffer is a substance that
can either accept or release H+
depending on the surrounding
H+ concentration.
Buffers resist big
changes in H+
concentration.

28. Acid base disorders and compensatory
response
pH HCO3- PaCO2
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
Compensatory responses never bring the pH back to normal

29. Metabolic Acidosis
Metabolic acidosis is defined as a
HCO3 level of less than 20 mEq/L
with a pH of less than 7.35.
Metabolic acidosis represents
any process, other than a rise in
PaCO2, that acts to lower blood
pH. It is recognised on an ABG by
a reduction in HCO 3 and a
negative base excess (BE).

30. Anion gap
 The anion gap is the difference in
the measured cation (Sodium and
potassium) and the measured
anions (Bicarbonate and chloride)
in plasma.
 Normal value: 8-16 mmol/L
 It is also the difference between
unmeasured anions and
unmeasured cations.
 Anion gap is increased when there
is increase in unmeasured anions.

32. Causes of metabolic acidosis
Increased anion gap metabolic acidosis (Normal Chloride)
 Lactic acidosis (e.g. hypoxaemia, ischaemia, shock, sepsis)
Ketoacidosis (diabetes, starvation, alcohol excess)
Renal failure (accumulation of sulphate, phosphate, urate)
Poisoning (aspirin, methanol, ethylene glycol)
Massive rhabdomyolysis

33. Causes of metabolic acidosis contd.
Normal or non–anion gap metabolic acidosis
Renal tubular acidosis (types 1, 2 and 4)
Diarrhoea (HCO 3 − loss)
Adrenal insufficiency
Ammonium chloride ingestion
Urinary diversion (e.g. ureterosigmoidostomy)
Drugs (e.g. acetazolamide)

34. Base excess / deficit
Base deficit: Metabolic acidosis.
Base excess: Metabolic alkalosis
Normal: -2 to + 2
BE < −10/HCO 3 < 15: This value is included in several severity
scoring systems and, when due to lactic acidosis, indicates severe
hypoxia at the cellular level.

35. Lactic acidosis
•This is the most common cause of metabolic acidosis in hospitalized
patients. It is defined by a low HCO3
- in association with a plasma
lactate concentration greater than 4 mmol/L.
•When the supply of O2 to tissues is inadequate to support normal
aerobic metabolism, cells become dependent on anaerobic
metabolism – which generates lactic acid as a by-product.
•This can occur due to inadequate local blood supply (e.g. ischaemic
gut or limb) or more commonly due to generalised failure of tissue
oxygenation (e.g. profound hypoxaemia, shock or cardiac arrest).
•The extent of lactic acidosis is an indicator of disease severity.

36. Effects of metabolic acidosis
Hyperventilation (Kussmaul respiration)
Depression of myocardial contractility (PH≤7.2)
Resistance to the effects of catecholamines
Vasoconstriction of pulmonary arteries
Shift of K+ out of cells causing hyperkalaemia

37. Metabolic alkalosis
 A metabolic alkalosis is any
process, other than a fall in
Paco 2 , that acts to increase
blood pH.
 It is characterised on ABG by an
elevated plasma HCO 3 and an
increase in BE.

38. Metabolic alkalosis
•Loss of gastric secretion (vomiting, NG suction)
•Potassium depletion (e.g. diuretics)
•Cushing syndrome
•Conn syndrome (primary hyperaldosteronism)
•Chloride-rich diarrhoea (e.g. villous adenoma)
•Excessive administration of sodium bicarbonate

39. Effects of metabolic alkalosis
•Decreased myocardial contractility
•Decreased cerebral blood flow(cerebral vasoconstriction)
•Pulmonary vasodilation
•Confusion
•Impaired peripheral oxygen unloading (due shift of oxygen
dissociation curve to left).

40. Management of metabolic alkalosis
•Mild or even moderate alkalosis may not require correction.
•Because volume depletion is common so, infusion of isotonic saline
(0.9% sodium chloride) is the most common method of chloride
replacement in this condition.
•Treatment of cause.

41. Respiratory Acidosis
A respiratory acidosis is, simply,
an increase in Paco 2 .
Because CO 2 dissolves in blood
to form carbonic acid, this has
the effect of lowering pH (↑H +
ions)

42. Respiratory acidosis
•Normally, lungs are able to increase ventilation to maintain a normal
Paco 2 – even in conditions of increased CO 2 production (e.g.
sepsis).
•Thus, respiratory acidosis always implies a degree of reduced
alveolar ventilation.
•This may occur from any cause of type2 respiratory impairment
• or to counteract a metabolic alkalosis.

43. Effects of respiratory acidosis
Acidemia, no matter the etiology, affects the cardiovascular system.
An arterial pH <7.2 impairs cardiac contractility.
Hypercapnia causes cerebral vasculature vasodilation.
Hypercapnia produces vasoconstriction of the pulmonary circulation
Central depression at very high levels of pCO2

44. Treatment of Respiratory Acidosis
Improve Ventilation:
Intubate patient and place on ventilator, increase ventilator rate,
reverse narcotic sedation with naloxone (Narcan), etc
Causes can be treated rapidly include pneumothorax, pain and
CNS depression r/t medication.

45. RESPIRATORY ALKALOSIS:
A respiratory alkalosis is a decrease in Paco 2 and is caused by alveolar
hyperventilation.
Primary causes are
•Pain,
•Anxiety (hyperventilation syndrome),
•Fever,
•Breathlessness and
•Hypoxaemia.
•It may also occur to counteract a metabolic acidosis

46. Effects of respiratory alkalosis
•Decreased intracranial pressure (secondary to cerebral
vasoconstriction)
•Inhibition of respiratory drive via the central & peripheral
chemoreceptors
•Decreased myocardial contractility
•Shift of the haemoglobin oxygen dissociation curve to the left
(impairing peripheral oxygen unloading)
•Slight fall in plasma [K+]

47. Treatment of Respiratory Alkalosis
Correct the underlying disorder.

48. Mixed respiratory and metabolic acidosis
This is the most dangerous pattern of
acid–base abnormality.
It leads to profound acidaemia as there
are two simultaneous acidotic processes
with no compensation.
It is often due to severe ventilatory
failure, in which the rising Paco 2
(respiratory acidosis) is accompanied by
a low Pao 2 , resulting in tissue hypoxia
and consequent lactic acidosis

49. Stepwise approach to
ABG Analysis

50. Step 1: Look at the PO2
PO2 (<80 mm Hg):
hypoxemia
SaO2 saturation (<90%):

51. Step 2: Look at the pH
< 7.35 : Acidosis
> 7.45 : Alkalosis
7.35 – 7.45 : Normal/Mixed Disorder
pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L.
• ACIDOSIS

52. Step 3: Look at the PCO2
> 45 mm Hg : Increased (respiratory acidosis)
< 35 mm Hg : Decreased (respiratory alkalosis)
pH of 7.30, PaCO2 of 80 mm Hg, and HCO3
- of 27 mEq/L.
• INCREASED

53. Step 4: Look at the HCO3
-
> 26 mEq/L : Increased (metabolic alkalosis)
< 22 mEq/L : Decreased (metabolic acidosis)
pH of 7.30, PaCO2 of 80 mm Hg, and HCO3
- of 27 mEq/L.
• INCREASED

54. Step 5: match either the pCO2 or the
HCO3 with the pH to determine the acid-base
disorder
•The CO2 is the respiratory component of the ABG. It move in opposite directions to match with pH
↓pCO2 ↑ pH
↑ pCO2 ↓ pH
•The HCO3 is the metabolic component of the ABG. It move in the same direction to match with pH
↓ HCO3 ↓ pH
↑ HCO3 ↑ pH
pH of 7.30, PaCO2 of 80 mm Hg, and HCO3
- of 27 mEq/L.
•pH acidotic, PCO2 increased
RESPIRATORY ACIDOSIS

55. Step 6: does either the CO2 or HCO3
go in the opposite direction of the pH?
To find what is the primary acid base disorder and
what is compensatory
pH of 7.30, PaCO2 of 80 mm Hg, and HCO3
- of 27 mEq/L.
•HCO3 is going in opposite direction of pH.
So it is METABOLIC COMPENSATION.

58. Example-1
pH = 7.30 (7.35) ACIDOSIS
PaCO2 = 56 (35-45) ACIDOSIS = Lungs
HCO3 = 24 (20-28) NORMAL
Respiratory Acidosis (Uncompensated)

59. Example-2
pH = 7.33(7.35-7.45) ACIDOSIS
pCO2 = 62 (35-45) ACIDOSIS
HCO3 = 35 (20-28) ALKALOSIS
Respiratory Acidosis (compensated )

60. Example-3
pH =7.31 (7.35-7.45) ACIDOSIS
PaCO2 = 39 (35-45) NORMAL = lungs
HCO3 = 17 (22-26) ACIDOSIS = kidneys
Metabolic Acidosis (Uncompensated)

61. Example-4
pH = 7.29 (7.35-7.45) ACIDOSIS
HCO3 = 18 (22-26) ACIDOSIS
pCO2 = 30 (35-45) ALKALOSIS
Metabolic Acidosis (compensated)

62. Step 6: Determine whether the patient’s
compensation is appropriate?
Appropriate compensation Simple acid-base disorder
Inappropriate compensation Mixed acid-base disorder

63. Metabolic Acidosis:
Expected PaCO2=1.5HCO3+8±2
(Winter’s formula)
Expected PCO2 in metabolic acidosis
= 1.5 x HCO3 + 8 (range: +/- 2)
= 1.5 x 7 + 8 = 18.5
pH 7.28
PCO2 20 mm Hg
HOC3 7 mEq / L

64. Appropriate Compensation

65. Example-5
pH =7.21 (7.35-7.45) ACIDOSIS
pCO2 = 33 (35-45) ALKALOSIS
HCO3 = 16 (22-26) ACIDOSIS
Expected Compensation(Pco2) = 1.5 X 16 + 8± 2
= 32 ± 2
= 30-34
So, compensation is appropriate
Simple Metabolic Acidosis (compensated )

66. Example-6
pH =7.14 (7.35-7.45) ACIDOSIS
pCO2 = 45 (35-45) NORMAL
HCO3 = 17 (22-26) ACIDOSIS
Expected Compensation(Pco2) = 1.5 X 17 + 8± 2
= 33.5 ± 2
= 31.5-35.5
So, compensation is inappropriate, PCO2 > Expected
Mixed Metabolic and Respiratory Acidosis

67. Arterial vs. venous blood: normal values
VALUE ARTERIAL MIXED
VENOUS
TYPICAL A-V
DIFFERENCE
PO2( mm Hg) 70-100 35-40 PaO2 - 60
SO2 (%) 93-98 65-75 SaO2 - 25
PCO2(mm Hg) 33-35 42-52 6-8
pH 7.35- 7.45 7.32-7.41 0.03-0.04
HCO3 22-26 24-28 2-4

68. Quiz 1
Baby boy, 28 wks GA, admitted 3 hrs ago, intubated initially, given surfactant, then extubated
immediately to nasal CPAP, pressure 5 cm H2O, FiO2 0.5.
ABG now: pH=7.20, PCO2=68, PO2=40, HCO3=22, SaO2=85%
Interpret above blood gas
Acidosis
Respiratory
Exp Hco3: 29
Metabolic Acidosis
Hypoxemia

69. Quiz 2
Baby girl, born at term by emergency CS, because of cord prolapse and
severe fetal distress. She was flat, needed thorough resuscitation
(intubation, UVC, 2 doses of epinephrine)
Now she is 6 hrs old, ventilated, FiO2 0.3, and had focal seizure.
ABG: pH=7.15, PCO2=30, PO2=60, HCO3=6, SaO2=92%
Interpret above blood gas
Acidosis
Metabolic
Exp Pco2 15-18
Respiratory acidosis

70. Quiz 3
pH 6.99
PaO2 112
PaCO2 21
HCO3 6
BE -20.6
SaO2 96
Known case of type1 diabetes with
history of
severe abdominal pain, polyuria,
polydipsia and acidotic breathing.
Interpretation
Metabolic acidosis

71. Same patient after treatment initiation with
rehydration and insulin infusion.
pH 7.34
PaO2 123
PaCO2 31
HCO3 15.6
BE -6.8
SaO2 98

72. Quiz 4
5 yr old child with acute onset fever, seizures
and altered sensorium presented to the
emergency with increased ICP and neurogenic
breathing.
pH 7.47
PaO2 154
PaCO2 22
HCO3 15.4
BE -5.8
SaO2 99.4%
Interpretation :
Respiratory alkalosis with metabolic acidosis

73. Quiz 5
Child presented with fever, loose stools,
respiratory distress.
Dx. pneumonia with septic shock.
pH 7.012
PaO2 72
PaCO2 74
HCO3 18
BE -12.6
SaO2 92
Interpretation
Metabolic plus respiratory acidosis

74. Quiz
Child with sepsis and on mechanical
ventilation..on
day 12 of hospital stay,on weaning, started on
furosemide for fluid overload.
pH 7.521
PaO2 124
PaCO2 44
HCO3 39.4
BE 14.3
SaO2 99.4%
Interpretation
Metabolic alkalosis

75. Thank you all