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ABG interpretation
 Basics
 Analysis of ABG provides essential
information about the over all respiratory and
metabolic function.
 Samples of arterial blood are mainly obtained
by direct puncture of radial artery, why??
 The sample should be immediately immersed
in ice to prevent the metabolic activity of
blood cells from changing the blood gas value.
 Prior to obtaining ABG from the radial artery,
Allen test should be performed.
 Typical ABG report in RA
 Ph 7.4 (7.35-7.45)
 PaO2 95 mmHg ( > 80)
 PaCO2 40 mmHg ( 35-45)
 HCO3 24 meq/L (22-26)
 SaO2 97.5 %
Alv-ventilation Art-oxygenation
Paco2 Pao2

ABG

Hco3

Gas exchange Metabolic aspect of

acid-base balance
 Although partial pressure of O2 in atmosphere
is 159 mmHg. Once it reaches the alveoli, it
decrease to approximately 100 mmHg??
 Once O2 reaches alveoli, it crosses into blood
by the process of diffusion.
 O2 is transported as a gas dissolved in plasma
and is chemically attached to Hb.(98% of O2
is present in chemical combination with Hb &
2% dissolved in plasma).
 The small amount of dissolved O2 is quite
important as it exerts the partial pressure
responsible for the movement of O2 into
tissues.
 As it passes to tissue capillaries, O2 diffuses
from arterial blood to tissue cells.
 After perfusing the tissues, blood is called
mixed venous blood and has PvO2 40 mmHg.
159
air 100
alveoli 95
arteries 40
veins

Oxygen Cascade
 Co2, produced by the cells during the
metabolism, must be removed from the body.
 The normal pressure of co2 in mixed venous
blood is 46 mmHg.
 Co2 is carried in blood as Hco3 attached to
protein and dissolved in plasma.
 As venous blood enters the pulmonary
capillaries,co2 rapidly diffuses into the alveoli
where it is removed through alveolar ventilation.
 Pao2 reported in mmHg reflects the amount of
o2 dissolved in plasma.
 It can be reduced by many factors including
lung diseases and decreased in atm. pr.
 Even with healthy lungs, there are some other
factors reducing Pao2. eg. Breathing air with
low atm. pr. as in high altitude.
 With advancing age, the normal value of Pao2
falls to about 80 mmHg at 60 ys of age
Pao2= 100 – 1/3 age
 As a general guideline, we can subtract 1
mmHg from Pao2 of 80 mmHg for every year
over 60 ys of age.
 An ↑ in altitude → ↓Pao2
 To compensate for lower Pao2, people living in
high altitude increase their level of ventilation &
may develop HB that allow their blood to carry
more o2.
 As the function of o2 in inspired air is increased,
so does Pao2.
 Generally, in healthy lungs, Fio2 is multiplied
by 5 to get rough estimate of the expected Pao2.
 If Pao2 is significantly is less than predicted, it
is often due to exchange problem caused by
lung diseases& this is suggested by ↑ in (A-a)
o2 gradient.
Oxygen dissociation curve
 The proximal portion of the curve indicates
that small drop in Pao2 → large drop in Spo2.
 While in the distal portion, tells us that Pao2
can fall a considerable amount& maintain
adequate Spo2.
 Shift to RT
 This means that HB gives o2 to tissues easily.
 Also means, that the affinity of HB to o2 is
decreased.
 This occurs in:
Exercise, fever, anaemia, acidosis, high
altitude
 Shift to LT
 This means that HB gives O2 hardly& the
affinity of HB to O2 is increased.
 This occurs normally at alveolar level & in
these circumstances:
sleep, co poisoning, polycythemia, hypothermia
 At Pao2 of 60 mmHg → SpO2 90%

 any ↑ in PaO2 will not result in marked ↑ in

SpO2.
 Hypoxaemia:
Decreased Pa02 less than 80mmHg diagnosed only
by ABG.
*Mild hypoxaemia ( 60-80 mmHg)
*Moderate hypoxaemia (40-60mmHg)
*Severe hypoxaemia (< 40mmHg)
 Hypoxaemia may result from:
*V/Q mismatch *LowPaO2(high altitude)
*Diffusion defect( IPF)
*Shunt:
*Intracardiac
*Intrapulm.(Collapse,pulm.oedema)
 PaCO2
Under normal conditions,tissues produce
approximately
200cc/m & utilize 250cc O2/m.
 CO2 is eliminated from the body through
the lungs by alv. vent. By Pressure gradient
bet. art. & ven. Blood.
 PaCO2=40mmHg PvCO2=46
mmHg
 There is an inverse relationship bet.PaCO2 & alv.
Vent.
 A rise in PaCO2 more than 40mmHg lead to
stim.of ventilatory control centre to increase
ventilation.
 The degree & effectiveness of this response will
depend on many factors including:
1-The condition of the lungs.
2- How will the respiratory ms. Response.
 PaCO2 < 35mmHg is defined as Hyperventilation
that may result from:
Pain, Anxiety, Fear, Lung dis eg. P.E
- One may hyperventilate due to metabolic error
causing acidosis eg.DM.
 PaCO2 > 45mmHg is defined as Hypoventilation
that may result from:
Resp. ms. Dis., Emphysema, Morbid obesity
 Acute changes in PaCo2 can have dramatic effect
on PH
 Acute decrease in PaCo2 (Hypocapnia) harmful
effect on the body including cerebral
vasoconstriction leading to decreased blood flow
to the brain.
 Acute increase in PaCo2 (Hypercapnia)
harmful effect& if severe,pose a serious threat to
life for these reasons:
1-Sudden acidaemia can affect heart & brain
function
2-Vasodilatation,oedema & R.C. depression
 GAS EXCHANGE is the passage of O2 from
alveoli to blood&CO2 from blood to alveoli as
a result of partial pressure gradient through
Alv.Cap.membane
 There are 2 sites of gas exchange:

-Tissues (INTERNAL RESPIATION)=RQ

RQ= vol.of CO2 prod. by tissues/m =200

vol. of O2 uptake/m 250

= 0.8
 Lungs (EXTERNAL RESPIRATION)=V/Q ratio
 V/Q=Alv.vent./cardiac output
=4.2L/m/5L/m
=0.84
 The rate at which Co2 is eliminated by the lungs
usually equals the rate at which it is produced by
tissues.
 Similarly ,the rate at which O2 is consumed by
tissues usually equal the amount of O2 uptake by
the lungs.
 ↓Pao2 is not the only indication of a gas
exchanging problem.
 In some cases, Pao2 can be normal & the patient
may still have a gas exchange problem.
 If PAo2 is increased by supplemental O2, Pao2
would be expected to be higher than normal.
 In these cases, evaluation of (A-a)O2 will allow us
to detect the abnormality in gas exchange.
 For RA
 PAo2=0.21(Patm-P H2O) –Paco2/RQ
 P(A-a)=0.21(760-47) -40/0.8] –PaO2
 P(A-a)=0.21x713 -40x1.25 –PaO2
 Normally, P(A-a)O2 =10-12 mmHg
 PH=7.4 PaO2=88mmHg PaCO2=40mmHg
FIO2=40%
 P(A-a)O2=0.4x713 –(40x1.25) -88 =147mmHg
 The increased (A-a)O2 seen with breathing higher
FIO2 does not represent a lung problem unless
the increased gradient is greater than anticipated.
 A B
 PH=7.32 PH=7.33
 PaCo2=57mmHg PaCo2=56mmHg
 PaO2=72mmHg PaO2=61mmHg

 Which patient has a gas exchange problem?

 A
PAO2=0.21x713-57x1,25=149-71=78mmHg
(A-a)O2=78-72=6 (NORMAL)
 B
PAO2=0.21x713-56x1.25=149-70=79mmHg
(A-a)O2=79-61=18 (ABNORMAL)

 Patient B has a gas exchanging problem rather than

hypoventilation .
 Patient A is on 40%O2 &his ABG is:
PH=7.34 PaCO2=44mmHg PaO2=92mmHg
 Patient B is on 30%O2 &his ABG is
PH=7.41 PaCO2=38mmHg PaO2=146mmHg
 (Patm=742mmHg)
 A (A-a)O2=0.4x695-44x1.25-92=278-55-92=131
 B (A-a)O2=0.3x695-38x1.25-246=161-146=15
 SO, Patient A has a severe gas exchange problem
 IF PaO2(as measured by ABG) is more
than PAO2(as calculated), Then, there is an
error in one of 3 places:
1-The patient is on higher FIO2 than
reported
2- Lab error in measurement
3-Miscommunication bet. Personnel in the
Lab. & persons receiving the data.
 REPIRATORY FAILURE
 Occurs when the resp. system fails to carry out its primary
function which are:
1- Delivery of O2 to Blood.
2-Elimination of O2 from blood.
 This will result in serious ABG abnormalities
 RESP.SYSTEM is composed of :
*A gas exchange unit(alveoli&capillaries)
*A resp. pump unit(resp C.,resp.ms,airways)
 SO,We have
o Type 1 (LUNG FAILURE) hypoxaemic,normo
orhypocapnic RF
o Type 2(PUMP FAILURE) hypoxaemic hypercapnic RF
 In hypoxaemic RF, the basic defect is failure to
oxygenate due to inadequate gas exchange usually
due to shunting or V/Q mismatching.
 NB:
* Sometimes PaO2 may be less than 60mmHg in
absence of RF.
* This situation can occur when there is anatomic
RT to LT shunt or decreased O2 tension in air
(high altitude)
* In type 1 RF. Alv. Vent. Is normal or
high ,so,PaCO2 is normal or low.
 Type 1 RF. Occurs in a wide variety of circumstances:
eg.-ARDS (SHUNT EFFECT)
-Severe pneumonia (INTRAPULM.SHUNT)
-Post. op patient with atelectasis

 PH=7.48 PaCO2=32 PaO2=55 HCO3=24mEq/L

-This is an ABG of 35y female C/O cough,fever&SOB
PaO2…mild hypoxaemia PaCO2 low(hyperventilating)
PH….ALKALOSIS HCO3…. NORMAL
 (A-a)O2=0.21x713-32x1.25-55=55(WIDE)

 Then,we are dealing with a case of hypoxaemic hypocapnic

RF With resp alkalosis(Type 1)
 In hypercapnic RF the pump fails to provide
adequate level of alveolar ventilation → PCO2
> 50 mm Hg.
 E.g. -Narcotic overdose ( R C depression).

-Myasthenia gravis ( N M Ds)

-Flail chest ( chest wall def)
-COPD
 Knowing the site of disturbance contributing
to the hypercapnic RF is essential to diagnosis.
 ?Which part of the pump is failing
 Increased (A-a) O2 gradient means hypercapnic RF
with pulmonary origin.
 Normal (A-a) O2 gradient means hypercapnic RF
with non pulmonary origin.

 E.g. PH 7.2 PaCO2 71 PaO2 38 HCO3 26

this ABG is for a 16 yrs old male with an overdose of
narcotics.
(A-a) O2 gradient = 22
-indicating a pulmonary origin; this pt had
aspiration pneumonia after taking narcotic overdose.
 E.g PH 7.39 PaCO2 52 PaO2 67 HCO3 31
this is an ABG of a Pt with emphysema
admitted to ICU with chest tightness
(A-a)O2 gradient is 17 (increased)
-Acute on top of chronic resp insufficiency 2ry
to pneumonia evidenced by wide (A-a) O2
gradient.
 E.g PH 7.32 PaCO2 78 PaO2 50 HCO3
39
(A-a)O2 gradient = (0.21 x 713)-(78x1.25)-50
=2 “normal”
-so we re dealing with a case of hypercapnic R
F with a 1ry resp acidosis due to a non
pulmonary cause.
Thank you