This document provides a summary of arterial blood gas analysis. It discusses the history of arterial blood sampling dating back to 1912. Key developments include the invention of electrodes that could rapidly measure parameters like PaO2, PaCO2 and pH in the 1950s. By the mid-1960s, several university centers could provide these measurements. The first automated blood gas machine was introduced in 1973. The document reviews normal blood gas values and equations for interpreting PaCO2, PaO2, and oxygen content. It also discusses indications, contraindications, specimen collection and storage, and the physiology required to properly interpret arterial blood gas results.

1. Dr. Md.Toufiqur
Rahman
MBBS, FCPS, MD, FACC, FESC, FRCPE, FSCAI,
FAPSC, FAPSIC, FAHA, FCCP, FRCPG
Associate Professor of Cardiology
National Institute of Cardiovascular Diseases(NICVD),
Sher-e-Bangla Nagar, Dhaka-1207
Consultant, Medinova, Malibagh branch
Honorary Consultant,Apollo Hospitals, Dhaka and
Arterial Blood Gas
Analysis
CRT 2014
Washing
ton DC,
USA

2. HISTORY
 The first arterial puncture was performed in 1912 by
Hurter, a German physician.
 Employing Hurter’s radial artery puncture technique,
W.C.Stadie measured oxygen saturation in patients with
pneumonia and showed that cyanosis of critically ill patients
resulted from incomplete oxygenation of hemoglobin
(Stadie 1919).

3. Over the next 40 years blood gas measurements were more of
a laboratory research tool.
It was not until the 1950s that electrodes were developed that
could rapidly and reproducibly measure PaO2, PaCO2 and pH.
In 1953 Leland Clark invented the platinum oxygen electrode,
a prototype that evolved into the first modern blood gas
electrode(Clark 1953,Clark1957).
HISTORY

4.  Development of commercially viable pH and PCO2 electrodes
soon followed and by the mid -1960s several university centers
were able to provide pH, PaCO2 and PaO2 measurements on
arterial blood.
 In 1973 the first commercially available automated blood gas
machine was introduced (ABLI from Radiometer), and this was
soon followed by machines from other companies (Severinghaus
1986 ).
HISTORY

5. Recent Developments
Non invasive measurements are now available for some of
the results of ABG;
Pulse Oximeter for SpO2
End tidal Gas analysis for PCO2
In Neonates and children skin electrodes for measuring
PO2& PCO2 have found wide application.
Now devices are being developed for continuous blood
gases with fiber optic intra arterial sensors

6. With these improvements the ABG measurements of shifted
from the experimental and developmental stages into clinical
arena.
ABG is probably the single most useful test for pulmonary
function, as arterial levels of O2, CO2, & pH reflect the end
result of ventilation perfusion & gas exchange.
Recent Developments

7. Information Obtained from an ABG:
Acid base status
Oxygenation
Dissolved O2 (pO2)
Saturation of hemoglobin
CO2 elimination
Levels of carboxyhemoglobin and methemoglobin

8. Indications of ABG
1. Routine in all cases of Open-heart surgery
2. Patient under mechanical ventilation
3. In case of thoracic trauma or underlying lung
contusion ABG determines where ventilator is
required or not.

9. 4. Integral part in he management of
premature neonates.
5. To determine acidosis or alkalosis,
whether these are respiratory or
metabolic.
6. In a hypoxaemic patient due to any cause.
Indications of ABG

10. Contraindications:
Bleeding diathesis
AV fistula
Severe peripheral vascular disease, absence of
an arterial pulse
Infection over site

11. Which Artery to Choose?
The radial artery is superficial, has collaterals and
is easily compressed. It should almost always be
the first choice.
Other arteries (femoral, dorsalis pedis, brachial)
can be used in emergencies.

14. Specimen collection
Arterial bloods are obtained from any Arterial sources, (usually
radial, brachial or femoral).
If multiple samples are to be drawn over a period time (as in case
of cardiac surgery) an indwelling arterial line is placed, which is
perfused with heparinised saline to prevent thrombus formation.
Arterial punctures are painful & result hyperventilation. Use of
L/A can result more patient comfort & accurate data.

15. Blood specimen are best collected in the
heparinized glass syringe. Heparine is used
to displace the air form the syringe & no air
should be permitted to enter the syringe
during collection.
Ideally sample should be analysed straight
away. Otherwise it can be capped & stored
in crushed ice.
Specimen collection

16. Storage at room temp. results rise in PCO2
& fall in pH & PO2 due to blood
metabolism.
Capillary samples are used from finger.
Heel, ear lobe. PCO2 & pH results on
capillary blood are close to those of
arterial blood taken at the same time. The
PO2 is less reliable.
Specimen collection

17. Why an ABG instead of Pulse
oximetry?
Pulse oximetry uses light absorption at two
wavelengths to determine hemoglobin saturation.
Pulse oximetry is non-invasive and provides
immediate and continuous data.

18. Collection Problems:
Type of syringe
Plastic vs. glass
Use of heparin
Air bubbles
Specimen handling and transport

19. Type of Syringe
Glass-
Impermeable to gases
Expensive and impractical
Plastic-
Somewhat permeable to gases
Disposable and inexpensive

20. Why an ABG instead of Pulse
oximetry?
Pulse oximetry does not assess ventilation
(pCO2) or acid base status.
Pulse oximetry becomes unreliable when
saturations fall below 70-80%.
Technical sources of error (ambient or
fluorescent light, hypoperfusion, nail polish,
skin pigmentation)
Pulse oximetry cannot interpret
methemoglobin or carboxyhemoglobin.

21. One blood sample & Two sets of tests
One Blood sample
Blood gas refers to any element or compound that is a gas under
ordinary condition and that is also dissolved to some extant in our
blood.
Not all blood gases are routinely measured & not all blood gas
measurements are of true blood gases. CO2 & O2 are routinely
measured as their partial pressure PaCO2 & PaO2.
CO is measured as %COHb,
N2, Helium & others are not measured at all

22. Two sets of tests
All blood gas machine to measure pH, PaCO2 & PaO2 and to
calculate HCO3 value.
A co-oximeter can measure Hb content and values related to
Hb binding; SaO2 %COHb, & %MetHb. From this information
the atrerial O2 content (CaO2) can be calculated
The one vs two machine arrangement is the case in most
laboratories.However newer technology now ncorporates
both machine within a single console so that both sets of
measurements (Blood gas & co-oximetery) can be made
from a single entered sample.

23. Normal ABG Values
 pH 7.35-7.45
PaCO2 35-45 mmHg.
PaO2 70-100 mmHg.
SaO2 93-98%
HCO3
-
22-26 mEq/L
%metHb <2%
%COHb <3%
BE +2 mEq/L
CaO2 16-22 ml O2/dl

24. Electrolyte Measurements
Over the past decade many blood gas labs have taken-on an
additional task; measuring electrolytes in the arterial sample
(Na+
, K+
, Cl-
, HCO3
-
& Ca++
Mg++
)
Electrolytes measurement acts as an aid to understanding
Acid-Base status.

25. What Other information is needed
to interpret blood gas data?
Information about the patients immediate environment
FIO2, PB
Additional Lab data, for example
Previous ABG report, electrolytes, blood sugar, BUN
Hb% or HCT
CXR & pulmonary function test
Clinical information, including history & clinical exam.
Respiratory rate & Other vital signs,
Degree of respiratory effort, mental status & state of tissue perfusion.

26. How much physiology do you need to
know for proper ABG interpretation?
Knowledge of some basic pulmonary physiology is crucial for
understanding ABG data.
There are three physiologic processes and four equations
important in interpretation of ABG.

27. Equation Physiologic
Process
1. PaCO2 Alveolar ventilation
2. Alveolar gas equation Oxygenation
3. O2 content equation Oxygenation
4. Henderson-Hasselbach Acid-Base balance equation

28. THE FOUR MOST IMPORTANT EQUATIONS
IN CLINICAL PRACTICE
Equation
Title
Complete Equation
Abbreviation Sufficient for
Most Clinical Applications
PCO 2
equation
PACO2
=VCO2
x 0.863 / VA
where VA=VE-VD
PaCO2
~ VCO2
/ VA
Henderson-
Hasselbalch
equation
pH=pK + log HCO3
-
/
0.03(PaCO2
)
pH ~ HCO3
-
/ PaCO2
Alveolar
gas
equation
PAO2
=FIO2
(PB
-PH2O)
--PACO2
[FIO2
+ (1-FIO2
) / R]
PAO2
=FIO2
(PB
-47)-
1.2(PaCO2
)
Oxygen
content
equation
CaO2
=(SaO2
x Hb x 1.34) + .003(PaO2
)
Where: 1.34=ml O2
/gram Hb
.003=ml O2
/mm Hg PaO2
/dl
Hb=content in grams/dl
CaO2
=SaO2
x 1.34 x Hb

29. PaCO2 and alveolar
ventilation
PaCO2
(mmHg)
Condition in
Blood
State of alveolar
ventilation
>45 Hypercapnia Hypoventilation
35-45 Eucapnia Normal Ventilation
<35 Hypocapnia Hyperventilation

30. The PCO2
equation puts into physiologic perspective one of
the most common of all clinical observations: a patient's
respiratory rate and breathing effort. The equation states
that alveolar PCO2
(PACO2
) is directly proportional to the
amount of CO2
produced by metabolism and delivered to
the lungs (VCO2
) and inversely proportional to the alveolar
ventilation (VA). While the derivation of the equation is for
alveolar PCO2
, its great clinical utility stems from the fact
that alveolar and arterial PCO2
can be assumed to be equal.
Thus:
PCO2
=VCO2
x 0.863 / VA
where VA=VE-VD

31. The constant 0.863 is necessary to equate dissimilar units
for VCO2
(ml/min) and VA (L/min) to PACO2
pressure
units (mm Hg). Alveolar ventilation is the total amount
of air breathed per minute (VE; minute ventilation)
minus that air which goes to dead space per minute
(VD). Dead space includes all airways larger than alveoli
plus air entering alveoli in excess of that which can take
part in gas exchange.
Even when alveolar and arterial PCO2
are not equal (as in
states of severe ventilation-perfusion imbalance), the
relationship expressed by the equation remains valid:
PaCO2
~ VCO2
/ VA

32. PaCO2
vs. alveolar ventilation (VA).
The relationship is shown for carbon
Dioxide production rates of 200 l/min
and 300 ml/min. Changes in PaCO2
Are shown for a one liter decrease
Short Horizontal lines) inVA
starting at two Different PaCO2
values, 30 and 60 mm Hg. A decrease
in alveolar ventilation in the
hypercapnic patient will result in a
Greater rise in PaCO2
than will the
sameVA change when PaCO2
is low
or normal. Also, note that an increase
in carbon dioxide production when
VA is fixed will result in an increase
in PaCO2

33. PaO2 & Alveolar-Arterial PO2
difference
The alveolar gas equation for calculating PAO2
is essential
to understanding any PaO2
value and in assessing if the
lungs are properly transferring oxygen into the blood. Is
a PaO2
of 28 mm Hg abnormal? How about 55 mm Hg?
95 mm Hg? To clinically interpret PaO2
one has to also
know the patient's PaCO2
, FIO2
(fraction of inspired
oxygen) and the PB
(barometric pressure), all
components of the equation for PAO2
:
1-FIO2
PAO2
= FIO2
(PB
-PH20
) - PACO2
[FIO2
+ ------------- ]
R

34. The abbreviated equation below is useful for clinical
purposes; in this version alveolar PO2
equals inspired
PO2
(PIO2
) minus arterial PCO2
x 1.2, assuming the R
value is 0.8 (and assuming identical values for arterial
and alveolar PCO2
). Water vapor pressure in the airways
is dependent only on body temperature and is 47 mm
Hg at normal body temperature (37 degrees C).
PAO2
= FIO2
(PB
-47) - 1.2(PaCO2
)

35. Ambient FIO2
is the same at all altitudes, 0.21.
It is usually not necessary to measure PB
if you
know its approximate average value where the
blood was drawn
If PIO2
is held constant and PaCO2
increases,
PAO2
and PaO2
will always decrease.

36. The alveolar-arterial PO2
difference, notated
P(A-a)O2
, varies normally with age and FIO2
.
Up to middle age, breathing ambient air,
normal P(A-a)O2
ranges between 5 and 20
mm Hg. Breathing an FIO2
of 1.0 the normal
P(A-a)O2
ranges up to about 110 mm Hg
If P(A-a)O2
is increased above normal there is
a defect of gas transfer within the lungs; this
defect is almost always due to V-Q imbalance.

37. Because of several assumptions in clinical use
of the alveolar gas equation, precision in
calculating PAO2
is not achievable.
Fortunately an estimate of P(A-a) O2
is usually
sufficient for clinical purposes.
Since oxygen enters the pulmonary capillary
blood by passive diffusion, it follows that in a
steady state the alveolar PO2
must always be
higher than the arterial PO2

38. Physiologic causes of Low PaO2
Respiratory cause Effects on
P(A-a)O2 PaO2/FIO2
Pulmonary R-L shunt; Increased Decreased
Vent-perfusion imbalance Increased Decreased
Diffusion barrier Increased Decreased
Hypoventilation ( PaCO2) Normal Decreased

39. Physiologic causes of Low PaO2
Non-Respiratory cause Effects on
P(A-a)O2 PaO2/FIO2
Cardiac R-L shunt Increased Decreased
Decreased PIO2 Normal Normal
Low mixed venous O2 content Increased Decreased

40. PaO2, SaO2 & Oxygen content
(Oxygen Content Equation )
All physicians know that hemoglobin carries
oxygen and that anemia can lead to severe
hypoxemia. Making the necessary
connection between PaO2
and O2
content
requires knowledge of the oxygen content
equation.
CaO2
= (SaO2
x Hb x 1.34) + .003(PaO2
)

41. The oxygen carrying capacity of one gram of
hemoglobin is 1.34 ml. With a hemoglobin
content of 15 grams/dl blood and a normal
hemoglobin oxygen saturation (SaO2
) of 98%,
arterial blood has a hemoglobin-bound oxygen
content of 15 x .98 x 1.34 = 19.7 ml O2
/dl
blood.

42. An additional small quantity of O2
is carried
dissolved in plasma: .003 ml O2
/dl
plasma/mm Hg PaO2
, or .3 ml O2
/dl plasma
when PaO2
is 100 mm Hg. Since normal CaO2
is 16-22 ml O2
/dl blood, the amount
contributed by dissolved (unbound) oxygen is
very small, only about 1.4% to 1.9% of the
total

43. Given normal pulmonary gas exchange (i.e., a
normal respiratory system), factors that lower
oxygen content - such as anemia, carbon
monoxide poisoning, methemoglobinemia,
shifts of the oxygen dissociation curve - do not
affect PaO2
. PaO2
is a measurement of pressure
exerted by uncombined oxygen molecules
dissolved in plasma; once oxygen molecules
chemically bind to hemoglobin they no longer
exert any pressure.

44. PaO2
affects oxygen content by determining,
along with other factors such as pH and
temperature, the oxygen saturation of
hemoglobin (SaO2
). The familiar O2
-
dissociation curve can be plotted as SaO2
vs.
PaO2
and as PaO2
vs. oxygen content

45. Oxyhemoglobin dissociation curve

47. When hemoglobin content is adequate, patients can have a
reduced PaO2
(defect in gas transfer) and still have sufficient
oxygen content for the tissues (e.g., hemoglobin 15 grams%,
PaO2
55 mm Hg, SaO2
88%, CaO2
17.8 ml O2
/dl blood).
Conversely, patients can have a normal PaO2
and be profoundly
hypoxemic by virtue of a reduced CaO2
. This paradox - normal
PaO2
and hypoxemia - generally occurs one of two ways: 1)
anemia, or 2) altered affinity of hemoglobin for binding
oxygen.

48. A common misconception is that anemia affects PaO2
and/or
SaO2
; if the respiratory system is normal, anemia affects neither
value. (In the presence of a right to left intrapulmonary shunt
anemia can lower PaO2
by lowering the mixed venous oxygen
content; when mixed venous blood shunted past the lungs mixes
with oxygenated blood leaving the pulmonary capillaries,
lowering the resulting PaO2
.

49. With a normal respiratory system mixed venous blood is
fully oxygenated - as much as allowed by the alveolar PO2
-
as it passes through the pulmonary capillaries.)

50. Causes of hypoxia
1. Hypoxemia
1. Reduced PaO2
2. Reduced SaO2
3. Reduced Hb content (anemia)
2. Reduced O2 delivery to the tissue
1. Reduced Cardiac Output
2. Left-right systemic shunt
3. Decreased O2 uptake
1. Mitochondrial poisoning (cyanide)
2. Left shifted Oxyhemoglobin dissociation curve

51. The Henderson-Hasselbalch
Equation
Of the four equations in this paper, the
Henderson-Hasselbalch is the one with which
physicians are most familiar. The H-H equation
is repeatedly emphasized in basic science
courses and in renal and pulmonary
pathophysiology lectures; students hear about
it on many occasions.

52. The bicarbonate buffer system, quantitatively
the largest in the extracellular fluid,
instantaneously reflects any blood acid-base
disturbance in one or both of its buffer
components (HCO3
-
and PACO2
). The ratio of
HCO3
-
to PACO2
determines pH and
therefore the acidity of the blood:

53. pH=pK + log HCO3
-
/ 0.03(PaCO2
)
pH is the negative logarithm of the hydrogen ion
concentration, [H+
], in nM/L (nM = nanomole = 1
x 10-9
moles; pH 7.40 = 40 nM/L [H+
]). Because of
the negative logarithm, small numerical changes of
pH in one direction represent large changes of [H+
]
in the other direction . An 0.1 unit fall in pH from
7.4 to 7.3 represents a 25% increase in [H+
]; a
similar percentage change in serum sodium would
increase its value from a normal 140 mEq/L to 175
mEq/L!

54. pH and Hydrogen Ion Concentration
Blood pH [H+
] (nM/L) % Change from normal
Acidemia
7.00 100 + 150
7.10 80 + 100
7.30 50 + 25
Normal
7.40 40
Alkalemia
7.52 30 - 25
7.70 20 - 50
8.00 10 - 75

55. Unfortunately, the logarithmic nature of pH and the fact
that acid-base disorders involve simultaneous changes in
three biochemical variables and in the function of two organ
systems (renal and respiratory), have all combined to made
acid-base a difficult subject for many clinicians.
If any of the three H-H variables is truly abnormal the
patient has an acid-base disturbance without exception. Thus
any patient with an abnormal HCO3
-
or PaCO2
, not just
abnormal pH, has an acid-base disorder. Most hospitalized
patients have at least one bicarbonate measurement as part
of routine serum electrolytes; this is usually called the 'CO2
'
or 'total CO2
' when measured in venous blood.

56. The simplified version of the H-H equation eliminates
the log and the pK, and expresses the relationships
among the three key values
pH ~ HCO3
-
/ PaCO2
This version is sufficient for describing the four primary
acid-base disturbances and their compensatory changes
If the numerator is first to change the problem is either
metabolic acidosis (reduced HCO3
-
) or metabolic
alkalosis (elevated HCO3
-
); if the denominator is first to
change the problem is either respiratory alkalosis
(reduced PaCO2
) or respiratory acidosis (elevated
PaCO2
).

57. By convention 'acidosis' and 'alkalosis' refer to in-vivo physiologic
derangements and not to any change in pH. Each primary acid-base
disorder arises from one or more specific clinical conditions, e.g.,
metabolic acidosis from diabetic ketoacidosis or hypoperfusion lactic
acidosis; metabolic alkalosis from diuretics or nasogastric
suctioning; etc. Thus the diagnosis of any primary acid-base disorder
is analogous to diagnoses like "anemia" or "fever"; a specific cause
must be sought in order to provide proper treatment.

58. Because of the presence of more than one acid-base disorder
('mixed disorders') a patient with any acidosis or alkalosis may
end up with a high, low or normal pH. For example, a patient
with obvious metabolic acidosis from uremia could present
with a high pH due to a concomitant metabolic alkalosis (which
may not be as clinically obvious). Acidemia (low pH) and
alkalemia (high pH) are terms reserved for derangements in
blood pH only.

59. Compensation for a primary disorder takes place when the other
component in the H-H ratio changes as a result of the primary
event; these compensatory changes are not classified by the terms
used for the four primary acid-base disturbances. For example, a
patient who hyperventilates (lowers PaCO2
) solely as compensation
for metabolic acidosis does not have a primary respiratory alkalosis
but simply compensatory hyperventilation.

60. This terminology helps separate diagnosable and treatable
clinical disorders from derangements in acid-base that exist only
because of the primary disorder.
Compensatory changes for acute respiratory acidosis and
alkalosis, and metabolic acidosis and alkalosis,occur in a
predictable fashion, making it relatively easy to spot the
presence of a mixed disorder in many situations. For example,
single acid-base disorders do not lead to normal pH.

61. Two or more disorders can be manifested by normal pH when
they are opposing, e.g., respiratory alkalosis and metabolic acidosis
in a septic patient. Although pH can end up in the normal range
(7.35-7.45) in single disorders of a mild degree when fully
compensated, a truly normal pH with abnormal HCO3
-
and PaCO2
should make one think of two or more primary acid-base
disorders. Similarly, a high pH in a case of acidosis or a low pH in a
case of alkalosis signifies two or more primary disorders.

62. Maximal respiratory compensation for a metabolic disorder takes
about 12-24 hours and maximal renal compensation for a
respiratory disorder takes up to several days. As a rule of thumb, in
maximally compensated metabolic acidosis the last two digits of the
pH approximate the PaCO2
. For example, a patient with a disease
causing uncomplicated metabolic acidosis over 24 hours' duration,
whose pH is 7.25, should have a PaCO2
equal or close to 25 mm
Hg. In metabolic alkalosis respiratory compensation is more
variable and there is no simple relationship by which to predict the
final PaCO2

64. How to calculate the degree of
compensation
Scale of compensation
Primary change
(for 1unit change)
Compensation
(scale of change)
M Acidosis pH HCO3 mEq/L 1.2 PCO2mmHg
M Alkalosis pH HCO3 mEq/L 0.5 PCO2 mmHg
R Acidosis pH PCO2 mmHg 0.35 HCO3 mEq/L
R alkalosis pH PCO2 mmHg 0.5 HCO3 mEq/L

65. Summary of Acid-Base balance
pH PCO2 HCO3 BE
Met.
Acidosis
Uncompensated N
Compensated N
Met.
Alkalosis
Uncompensated N
Compensated N
Resp.
Acidosis
Uncompensated N N
Compensated N
Resp.
Alkalosis
Uncompensated N N
Compensated N

66. Conclusion
It should be remembered that there is always more
than a single explanation for any given set of blood
gas results. So it is not possible to make a diagnosis
on the basis of these result alone, which must
always be considered together with the pt.’s
history, heamodynamic parameters & other
investigations.

67. Thank You
drtoufiq19711@yahoo.com
Asia Pacific Congress of
Hypertension, 2014, February
Cebu city, Phillipines
Seminar on
Management of
Hypertension,
Gulshan, Dhaka