The document discusses arterial blood gas (ABG) analysis. It provides information on: 1) What an ABG is and why it is important for evaluating ventilation, oxygenation, and acid-base status. 2) How to properly collect arterial blood, including using heparin as an anticoagulant and analyzing the sample within 10 minutes. 3) A stepwise approach to interpreting ABG results, including determining if acid-base disturbances are primary respiratory or metabolic and if compensations are adequate.

2. What is ABG
• Arterial Blood Gas (ABG) is an
investigation which plays an
important role in therapeutic
decision making
• And requires proper interpretation.
• So a proper understanding of
various components that are
analyzed is vital.

3. Why measuring Blood
Gases?
For evaluation of:
• 1-Adequacy of Ventilation
• 2-Oxygenation
• 3-Acid Base status
• 4-Assess the response to an
intervention

4. Drawing arterial blood for ABG:
• A plastic (15 min) / glass (1 h)
syringe is used.
• 0.1ml of Heparin is used for 1ml of
blood drawn, as an anticoagulant.
(Heparin is withdrawn into the
syringe and pushed back, thus
allowing heparin to just coat the
syringe)

5. • The safest place to draw blood
for ABG is radial artery at the
wrist.
• Allen s test should be done
before arterial sampling to test
the circulation of the hand.
• After the blood is drawn,
pressure applied to the puncture
site for 5-10 minutes to stop the
bleeding.

7. • The syringe should be sealed
immediately with cap (or needle tip
inserted to a cork) to avoid air bubbles.
• Blood drawn should be analyzed
within 10 minutes. Otherwise it should
be cooled to 4 C with ice slush when a
delay of up to one hour is acceptable.
(Usually the syringe is sent in a flask
with ice).
• Routine practice of temperature
correction for blood gas measurements
is not required.

8. • Commonly used in
newborn
• Good in stable babies
• Underestimate PaO2
• Replaced by noninvasive
monitors tcPaO2 and
pulse oximetery
Capillary Sampling

9. •Technique:
–Choose an outer portion of the infant’s
heel, avoiding the antero-medial aspect.
–Consider wrapping the foot in a warm
cloth for five minutes to increase the
blood flow.
–Cleanse the area with alcohol.
–Be sure to allow the area to dry, because
alcohol may alter the reading.
Capillary Sampling

10. –Grasp the heel firmly at the arch and ankle.
–Avoid excessive squeezing of the foot, which
may cause hemolysis.
–Puncture the heel perpendicular to the skin
with one continuous, deliberate motion to a
depth not to exceed 2.5 mm.
–Remove the first drop of blood with a gauze
pad and collect the subsequent large drop of
blood on the capillary tube.
–Once the blood has been obtained, apply
pressure to the puncture site and consider use of
an adhesive bandage if necessary.

11. Unreliable Capillary
Blood Gases
• Seriously ill patients
• Shock, hypotension
• Peripheral vasoconstriction.
• In the first day of life, poor perfusion
to the hands and feet
("acrocyanosis").
=Use arterial blood gases.

12. •Technique:
–Same as routine daily sampling
–Same precautions for air bubbles,
heparin content and timing
Venous Sampling

13. ABG parameters
• Measured values:
• pH
• PaCO2
• PaO2
Calculated values:
• HCO3
• Base Excess
• O2 saturation
• ctO2
• P (A-a) O2

14. Normal Neonatal A B G
Values
• pH 7.4 ± 0.05.
• PaCO2 40 ± 5 mm Hg.
• PaO2 60 ± 10 mm Hg (term infant).
55 ± 10 mm Hg (preterm infant).
• HCO3 24 ± 4 mEq/liter.
• Base Excess 0 ± 4 mEq/liter.
• O2 saturation 92 ± 1%.
• ctO2 15 ± 7 mL / dL.
• P (A-a) O2 < 15 mmHg.

15. Stepwise approach to
ABG Analysis
1-Determine whether patient is
alkalemic or acidemic using the
arterial pH measurement.
2-Determine whether the acid-
base disorder is a primary
respiratory or metabolic
disturbance based on the
PH,pCO2 and serum HCO3
- level.

16. 3-If a primary respiratory
disorder is present,
determine whether it is acute
or chronic.
4-In respiratory disorders,
determine if there is adequate
compensation of the metabolic
system.

17. 5-In metabolic disorders,
determine if there
is adequate compensation
of the respiratory system.
6-If a metabolic acidosis is
present, determine the
anion gap.

18. 7-In normal (non) anion gap
acidosis, determine the
urinary anion gap - helpful
to distinguish renal from
non renal causes.
8-Determine patient
oxygenation status (PaO2,
ctO2, P (A-a) O2 & SaO2) –
hypoxemic or not.

19. Step one: Are the available
data consistent or not
• You must able to establish that the available
data (PH, pCO2 and HCO3) are consistent.
• Subtract the calculated H+ from 80; this give
the last two digit of a PH beginning with 7.
• PH= 7. (80-H+).
»PH= 7. (80- 24 x pCO2)
HCO 3

20. Step two: Evaluate pH
pH acidemia if ˂ 7.35.
pH alkalemia if ˃7.45.

21. Step three: Evaluate the
Primary Acid-Base Disorder
• In the 2nd stage of the approach, the
measured pH &PaCO2
are used to determine if an acid-base
disturbance is present and, if so, to
identify the primary acid-base disorder.

22. Rule 1
•An acid-base abnormality
is present if either the
PaCO2 or the pH is
outside the normal
range.
A normal pH or PaCO2 does not exclude the
presence of an acid-base abnormality.

23. Rule 2
•If the pH and PaCO2
are both abnormal,
compare the directional
change.

24. Rule 2
•A-If both change in the
same direction (both
increase or decrease),
the primary acid-base
disorder is metabolic.

25. Rule 2
•B-And if both change in
opposite directions,
the primary acid-base
disorder is
respiratory.

26. Example
•Consider a patient with
an arterial pH of 7.23
and a PaCO2 of 23 mm
Hg.

27. Example
• The pH and PaCO2 are both
reduced (indicating a
primary metabolic problem)
and the pH is low (indicating
acidemia), so the problem is
a primary metabolic
acidosis.

28. Rule 3:
• If the pH or PaCO2
one is normal and the
other is abnormal, there
is a mixed metabolic and
respiratory disorder.

29. Rule 3:
• A-If the pH is normal and
PCO2 is abnormal,
the direction of change in PaCO2
identifies the respiratory
disorder. And the
metabolic disorder will be
in the opposite direction.

30. Rule 3:
• B-And if the PaCO2 is
normal and PH is
abnormal, there is double
disorder, acidosis or
alkalosis according to the
direction of PH.

31. Example:
• Consider a patient with an arterial pH of
7.37 and a PaCO2 of 55 mm Hg.
• The pH is normal and PCO2 is abnormal,
so there is a mixed metabolic and
respiratory acid-base disorder.
• The PaCO2 is elevated, so the
respiratory disorder is an acidosis, and
thus the metabolic disorder must be an
alkalosis.

32. Example:
• Therefore, this is a combined
respiratory acidosis and
metabolic alkalosis.
• There is no primary acid-base
disorder in this situation; both
disorders are equivalent in
severity that is why the pH is
normal.

33. •Remember that the
compensatory responses
to a primary acid-base
disturbance are never
strong enough to correct
the pH, but act to reduce
the severity of the change
in pH.

34. • Therefore, a normal pH in the
presence of an acid-base
disorder always signifies a mixed
respiratory and metabolic acid-
base disorder.
• (It is sometimes easier to think of
this situation as a condition of
overcompensation for one of the
acid-base disorders.)

35. Step four: Compensated,
Uncompensated, or Partially
Compensated
• The step four of the approach is for cases
where a primary acid-base disorder has
been identified in Step three.
• The goal in Step four is to determine if the
compensatory responses are adequate and
if there are additional acid-base
derangements.

36. Rule 4:
• If there is a primary metabolic acidosis or
alkalosis, use the measured serum
bicarbonate concentration in Equations;
• Acidosis: Expected pCO2 = (1.5 × HCO3 ) + 8 ±
2.
• Alkalosis: Expected pCO2 = (0.7 × HCO3 ) + 21
± 2.
to identify the expected PaCO2 and
respiratory compensation.

37. Rule 4:
• If the measured and expected PaCO2 are
equivalent, the condition is fully
compensated.
• If the measured PaCO2 is higher than
the expected PaCO2, there is a
superimposed respiratory
acidosis(uncompensated).
• If the measured PCO2 is less than the
expected PCO2, there is a superimposed
respiratory alkalosis.

38. Example:
• Consider a patient with a PaCO2 of
23 mm Hg, an arterial pH of 7.32,
and a serum HCO3 of 15 mEq/L.
• The pH is acidemic and the pH and
PCO2 change in the same direction,
so there is a primary metabolic
acidosis.

39. Example:
• Equation should be used to calculate the
expected PCO2: (1.5 × 15) + (8 ±2) = 30.5 ± 2
mm Hg.
• The measured PaCO2 (23 mm Hg) is lower
than the expected PaCO2, so there is an
additional respiratory alkalosis.
• Therefore, this condition can be described as
a primary metabolic acidosis with a
superimposed respiratory alkalosis.

40. expected
PaCO2 28.5 32.5 40 50
Compensated
metabolic
acidosis.
a primary metabolic acidosis
with a superimposed
respiratory acidosis
a primary metabolic acidosis
with a superimposed
respiratory alkalosis

41. Rule 5:
• If there is a respiratory acidosis or alkalosis, use the
PaCO2 to calculate the expected pH using Equations
for respiratory acidosis:
• Acute: Expected PH = 7.4 - 0.008 × (CO2-40 ).
• Chronic: Expected PH = 7.4 - 0.003 × (CO2-40)
Or Equations for respiratory alkalosis:
• Acute: Expected PH = 7.4 + 0.008 × (40-CO2).
• Chronic: Expected PH = 7.4 + 0.003 × (40-
CO2).

42. • Compare the measured pH to the expected
pH to determine if the condition is acute,
partially compensated, or fully
compensated.
• For respiratory acidosis, if the measured pH
is lower than the expected pH for the acute,
uncompensated condition, there is a
superimposed metabolic acidosis, and if
the measured pH is higher than the
expected pH for the chronic, compensated
condition, there is a superimposed
metabolic alkalosis.

43. pH scale
7.24 7.34 7.4 7.5
partially
Compensated
a primary respiratory acidosis
with a superimposed
Metabolic alkalosis
a primary respiratory acidosis
with a superimposed metabolic
acidosis
acute chronic

44. • For respiratory alkalosis, if the
measured pH is higher than the
expected pH for the acute,
uncompensated condition, there is a
superimposed metabolic alkalosis, and
if the measured pH is below the
expected pH for the chronic,
compensated condition, there is a
superimposed metabolic acidosis.

45. Example
• Consider a patient with a PaCO2 of
23 mm Hg and a pH of 7.54.
• The PaCO2 and pH change in
opposite directions so the primary
problem is respiratory and, since the
pH is alkalemic, this is a primary
respiratory alkalosis.

46. • The expected pH for an acute
respiratory alkalosis is 7.40 + [0.008
× (40 - 23)] = 7.54.
• This is the same as the measured
pH, so this is an acute,
uncompensated respiratory
alkalosis.
• If the measured pH was higher than
7.55, this would be evidence of a
superimposed metabolic alkalosis.

47. Step five : Anion gap
• AG is a measure of the relative abundance of
unmeasured anions.
• Used to evaluate patients with metabolic
acidosis.
• Determinants of the Anion Gap:
AG= UA - UC = [Na+]-([Cl-] + [HCO3
-])

48. Unmeasured Anions
Proteins (15 mEq/L)
Organic Acids (5
mEq/L)
Phosphates (2
mEq/L)
Sulfates (1mEq/L)
UA = 23 mEq/L
Unmeasured Cations
Calcium (5 mEq/L)
Potassium (4.5
mEq/L)
Magnesium (1.5
mEq/L)
UC = 11 mEq/L

49. The anion gap
Mg+ 2mEq/L
Ca+ 5 mEq/L
K+ 4 mEq/L
Na+
(135-
145)
mEq/L
Other- 3mEq/L
Proteins –n
16mEq/L
Lactate- 2mEq/L
SO4 2- 2mEq/L
HPO4 2-, 2mEq/L
HCO3-
(22-26)
Cl-
(70-
110)
Normal ABG
Unmeasured Cations
Unmeasured Anions

50. • High AG metabolic acidosis is due to
the accumulation of [H+] plus an
unmeasured anion in the ECF.
–Most likely caused by organic acid
accumulation or renal failure with
impaired [H+] excretion.

51. The anion gap ↑H+
K+ (3.5-4.5)
Na+
(135-
145)
Anion
Gap
HCO3-
(22-26)
Cl-
(70-
110)
Anion
Gap
HCO3-
(<22)
Cl-
(70-110)
K+ (3.5-4.5)
Na+
(135-
145)
Normal ABG Metabolic Acidosis +Wide
Anion Gap

52. • Normal AG metabolic acidosis is
caused by the loss of HCO3
- which is
counterbalanced by the gain of Cl-
(measured cation) to maintain
electrical neutrality.
–Most likely caused by HCO3
- wasting
from diarrhea or urinary losses.

53. The anion gap ↓HCO3
K+ (3.5-4.5)
Na+
(135-
145)
Anion
Gap
HCO3-
(22-26)
Cl-
(70-
110)
Anion
Gap
HCO3-
(<22)
Cl-
(>110)
K+ (3.5-4.5)
Na+
(135-
145)
Normal ABG Metabolic Acidosis
+Normal Anion Gap

54. The anion gap
H ↑ HCO3↓
K+ (3.5-4.5)
Na+
(135-
145)
Anion
Gap
HCO3-
(22-26)
Cl-
(70-
110)
Anion
Gap
HCO3-
(<22)
Cl-
(>110)
Anion
Gap
HCO3-
(<22)
Cl-
(70-110)
K+ (3.5-4.5)
Na+
(135-
145)
K+ (3.5-4.5)
Na+
(135-
145)
Normal ABG Metabolic Acidosis +Wide
Anion Gap
Metabolic Acidosis
+Normal Anion Gap

55. • Normal anion gap: 12± 4 mEq/L
• Increased anion gap:
1. >14 mEq/L in children
2. >16 mEq/L in LBW infants
(<2,500 g)
3. >18 mEq/L in ELBW infants
(<1,000 g)
The anion gap

56. •The cations and anions normally
present in urine are Na+, K+, NH4+,
Ca++,Mg++ and Cl-, HCO3-, sulphate,
phosphate and some organic anions.
•Only Na+, K+ and Cl- are commonly
measured.
•Cl- + UA = Na+ + K+ + UC
•UAG = ( UA - UC ) = [Na+]+ [K+] - [Cl-]
Urinary anion gap

57. •The Urinary Anion gap  differentiate
between GIT and renal causes of a
hyperchloraemic metabolic acidosis.
•Urinary Anion Gap (UAG) provides a
rough index of Urinary ammonium
excretion.
•Ammonium is positively charged so a
rise in its Urinary concentration will
cause a fall in UAG .
Urinary anion gap

58. Urinary anion gap
•If the acidosis is due to loss of base via the
bowel the kidneys can respond by
increasing ammonium excretion
decreased UAG.
•If the acidosis is due to loss of base via the
kidney  not able to increase ammonium
excretion  UAG will not be increased.
•In a patient with a hyperchloraemic
metabolic acidosis:
•Negative UAG  GIT loss of bicarbonate
•Positive UAG  impaired renal distal
acidification.

59. Interpretation of Anion
Gap
Anion Gap
High anion Gap
Normal or Low
anion Gap
Lactic acidosis
Ketoacidosis
•Diabetes
•Alcohol
•Starvation
Toxins
•Salicylate,
•Methanol
•Ethylglycol
Renal failure
Urinary Anion Gap
Positive Negative
Renal (RTA) GIT (Diarrheal)
Fistula

60. PIO2 ( Pressure of Inspired Oxygen) = (Bp – H2O p) X FIO2
= (760 – 48) X 0.21
= 150 mmgh
PAO2 ( Pressure of alveolar Oxygen) = PIO2 – (PaCO2/R)
= 150 – ( 45/0.8)
= 100 mmgh
PaO2 ( Pressure of arterial Oxygen) = 60 – 90 mmgh
Step six : Oxygenation

61. Arterial oxygen
content is the sum of
hemoglobin
bound
oxygen in
100 ml
blood
oxygen
dissolved
in
plasma

62. Oxygen content (ml/100 ml of blood)
= (1.37 x Hb )x SaO2) + (0.003 x PaO2)
Where:
1.37 = Milliliters of oxygen bound to 1
g of hemoglobin at 100 percent
saturation(%)
0.03 = Solubility factor of oxygen in
plasma (ml/mm Hg)

63. Ratio between the concentrations of O2Hb
and HHb+ O2Hb
sO2(a) is the percentage of oxygenated Hb
in relation to the amount of Hb capable of
carrying oxygen.
Reference ranges: 90 –95 %
Arterial oxygen saturation

65. Clinical interpretation of
sO2
•Normal sO2  Sufficient
utilization of actual oxygen
transport capacity.
•Low sO2 
Impaired oxygen uptake
Right shift of ODC

66. The situation in
tissues
The
situation
in lung

67. Several factors can affect the
affinity of hemoglobin for oxygen
• Alkalosis,
hypothermia,
hypocapnia, and
decreased levels of 2,
3-diphosphoglycerate
(2, 3 DPG)
• increase the affinity
of hemoglobin for
oxygen.
• Shift to left
• Acidosis, hyperthermia,
hypercapnia and increased
2, 3 DPG have the
opposite effect.
• decreasing the affinity of
hemoglobin for oxygen.
• shifting to the right.

69. • This characteristic of hemoglobin
facilitates oxygen loading in the lung
and unloading in the tissue where the
pH is lower and the PaCO2 is higher
• Fetal hemoglobin, which has a higher
affinity for oxygen than adult
hemoglobin, is more fully oxygenated
at lower PaO2 values, This is important
in utero.

70. ctO2 Arterial concentration of
total oxygen tO2
ctO2 = sO2 × 1.37 × ctHb + 0.003 × pO2
ml / dl.
Reference ranges : 8.8-22.3 mL / dL
Normal ctO2  adequate oxygen
content of the arterial blood.

71. Clinical interpretation of
ctO2
High ctO2:
•High pO2  Over oxygenation
•Normal pO2  high ctHb (i.e.
hemoconcentration, polycytemia).
Low ctO2:
•low pO2  hypoxemia
•Normal pO2 low ctHb and/or
dyshemoglobinemia

72. • Cao2= (1.37 x 14gdl )x 92%) + (0.003 x 60mmhg)
•Cao2= (17.6 ml) + (0.1 ml)
•Cao2= (99%) + (1%)
In premature
In the same infant with IVH & Hb content. Drops to 10.5 g/dl
• Cao2= (1.37 x 10.5gdl )x 92%) + (0.003 x 60mmhg)
•Cao2= (13.3 ml) + (0.1 ml) =13.4
•Thus without change in PaO2 & SaO2 a 25% drop in
Hb concent. reduces the O2 content by 24%

73. • This concept is important to
remember when taking care of
infant with respiratory disease.
• Hb level should be monitored & if
low rapid correction to keep
adequate level of oxygenation.

74. Hb type& quantity,
Hb%,Meth,Oxy,
Cardiac output&
tissue perfusion
Lung function&
Breathing
O2 delivery to tissue
O2 content in
blood

75. The key concept is that when
assessing a patient’s oxygenation,
more information than just PaO2 and
SaO2 should be considered.
PaO2 and SaO2 may be normal,
but if hemoglobin concentration is
low or cardiac output is decreased,
oxygen delivery to the tissue is
decreased.

76. •The force that loads hemoglobin with
oxygen in the lungs and unloads it in
the tissues is the difference in partial
pressure of oxygen.
•In the lungs alveolar oxygen partial
pressure is higher than capillary oxygen
partial pressure so that oxygen moves
to the capillaries and binds to the
hemoglobin.
•In tissue partial pressure of oxygen is
lower than that of the blood, so oxygen
moves from hemoglobin to the tissue.

77. Oxygen Parameters
definitions
• Hypoxemia refers to a
lower than normal arterial
PO2.
• hypoxia refers to
inadequate oxygen supply
to the body tissue.

78. P (A-a) O2
Difference between the measured
pressure of oxygen in the blood stream
and the calculated oxygen in the
alveolus.
N < 15 mmHg
Indicates whether hypoxia is a
reflection of hypoventilation or due to
deficiency in oxygenation
P (A- a) O2 = 150 - (1.25 x PaCO2) -
PaO2 mm Hg

79. Alveolar-arterial Difference
Inspired O2 = 21 %
piO2 = (760-45) x . 21 = 150 mmHg
O2
CO2
palvO2 = piO2 – pCO2 / RQ
= 150 – 40 / 0.8
= 150 – 50 = 100 mm Hg
PaO2 = 90 mmHg
palvO2 – partO2 = 10 mmHg

80. P (A-a) O2
A normal A-a gradient in the face of
hypoxemia suggests the hypoxemia is
due to hypoventilation and not due to
underlying lung disorders.
An increased A-a gradient identifies
decreased oxygen in the arterial blood
compared to the oxygen in the alveolus.

81. Alveolar- arterial Difference
O2
CO2
Oxygenation Failure
WIDE GAP
piO2 = 150
pCO2 = 40
palvO2= 150 – 40/.8
=150-50
=100
PaO2 = 45
D = 100 - 45 = 55
Ventilation Failure
NORMAL GAP
piO2 = 150
pCO2 = 80
palvO2= 150-80/.8
=150-100
= 50
PaO2 = 45
D = 50 - 45 = 5
PAO2 (partial pres. of O2. in the alveolus.)
= 150 - ( PaCO2 / .8 )
760 – 45 = 715 : 21 % of 715 = 150
No click

82. Other Oxygen parameters
• p50a - oxygen tension at 50% saturation on
Oxygen Dissociation Curve. This is used to reflect
affinity of Hb for oxygen. 25-29mmhg
• FMetHb - This is the fraction of
methaemoglobin. Think of methaemoglobin like
haemoglobin, but we carry less than 1% of it in
our blood. As it is unable to combine with oxygen
and it also decreases the oxygen carrying capacity
of blood. Exposure to certain drugs and chemicals
can dangerously elevate levels(iNO).
• 0.2-0.6%

83. •FCOHb- Fraction of
carboxyhaemoglobin. Much similar to
FMetHb in its actions. Affinity of Hb for
carbon monoxide is 200 times greater
than that of oxygen and impairs oxygen
transport and release (ODC shift to left,
alkolosis). This level can be high in
heavy smokers.
• 0.0-8.0%

84. • Fshunte - Relative physiological shunt.
Basically the amount of venous (de-
oxygenated) blood that did not receive
oxygen whilst travelling through the
lungs. This can be caused by atelectasis,
a pulmonary embolism (PE), mucous
plugs and pulmonary oedema, all of
which reduces oxygen transport into the
blood.
• 1.0-10%

85. Blood Gas Arterial Sample Venous Sample
Capillary sample
(Arterialized)
PaCO2 36-44 mmHg 42-50 mmHg 35-45 mmHg
pH 7.37-7.43 7.32- 7.38 7.35-7.45
PaO2 60-110 mmHg 37-42 mmHg 50-70 mmHg
HCO3 22-26 mEq/liter 23-27 mEq/liter 22-26 mEq/liter
Normal Ranges for Blood
Gases in Healthy Newborns

86. Errors in Blood Gas
Measurement
• During collection and analysis of blood
gases, the clinician should be aware of the
following potential sources of error:
• 1- Temperature – blood gas machines
report results for 37° C. Hypo or
hyperthermia can alter true arterial gas
values.
• 2- Hemoglobin – calculated oxygen
saturations are based on adult
hemoglobin, not on fetal or mixed
hemoglobins.

87. • 3- Dilution – heparin in a gas sample will
lower the PCO2 and increase the base
deficit without altering the pH.
• 4- Air bubbles – room air has a PCO2
close to 0 and a partial pressure of oxygen
of 150. Therefore, air bubbles in the
sample will decrease the PCO2 and
increase the PO2 unless the PO2 is greater
than 150.

88. • Steady state. Ideally, blood gases
should measure the infant’s
condition in a state of equilibrium.
• After changing ventilator settings or
disturbing the infant, a period of 20
to 30 minutes should be allowed for
arterial blood chemistry to reach a
steady state. This period will vary
from infant to infant.

89. • 5-DELAYED ANALYSIS
Consumptiom of O2 & Production of CO2
continues after blood drawn into syringe.
Iced Sample maintains values for 1 hour
Uniced sample quickly becomes invalid
PaCO2  3-10 mmHg/hour
PaO2  at a rate related to initial value &
dependant on Hb Saturation.

90. • 6-TYPE OF SYRINGE
pH & PCO2 values unaffected
PO2 values drop more rapidly in plastic syringes
(ONLY if PO2 > 400 mm Hg)
Other advantage of glass syringes:
Minimal friction of barrel with syringe wall
Usually no need to ‘pull back’ barrel – less
chance of air bubbles entering syringe
Small air bubbles adhere to sides of plastic
syringes – difficult to expel
Though glass syringes preferred, differences
usually not of clinical significance  plastic
syringes can be and continue to be used

91. Example
3ds ♂ old is admitted to the hospital. He was
diagnosed as severe anoxia. His arterial blood
gas values are reported as follows:
pH 7.32
PaCO2 32
HCO3- 18

92. • pH 7.32 PaCO2 32 HCO3- 18
• 1. Assess the pH. It is low (normal 7.35-7.45);
therefore we have acidemia.
• 2. Assess the PaCO2. It is low. Normally we
would expect the pH and PaCO2 to move in
opposite directions, but this is not the case.

93. • pH 7.32 PaCO2 32 HCO3- 18
• Because the pH and PaCO2 are moving in the
same direction, it indicates that the acid-base
disorder is primarily metabolic.
• In this case, the lungs, acting as the primary acid-
base buffer, are now attempting to compensate by
“blowing off excessive C02”, and therefore
increasing the pH.

94. • pH 7.32 PaCO2 32 HCO3- 18
• 3. Assess the HCO3. It is low (normal 22-
26). We would expect the pH and the
HCO3 - to move in the same direction,
confirming that the primary problem is
metabolic.

95. • pH 7.32 PaCO2 32 HCO3- 18
• What is your interpretation? Because
there is evidence of compensation (pH
and PaCO2 moving in the same
direction) and because the pH remains
below the normal range, we would

96. interpret this ABG result as a
• partially compensated
metabolic acidosis.
-
•pH ↓ PaCO2 ↓ HCO3 ↓

97. Assessment of Acid–Base Status

98. http://www.medcalc.com/acidbase.html

99. Take home message:
• Do not take decision on single ABG
result especially if there is major
change than the previous ABG.
• Correlate the ABG result with the
clinical condition of the case.
• PH &PCo2 both normal = normal
ABG.

100. Take home message:
• PH& PCo2 both change in same direction=
the 1ry disorder is metabolic.
• PH& PCo2 both change in opposite
direction= the 1ry disorder is respiratory.
• PH normal & PCo2 abnormal = mixed
disorder respiratory disorder according to
the direction of PCo2 and metabolic in the
opposite direction.

101. Take home message:
• PH abnormal & PCO2 normal=
Double acidosis or double alkalosis
according to the direction of PH.
• In metabolic acidosis you must
calculate anion gap.
• Do not forget to comment on
oxygenation.