ABG - Introduction
Blood gas and pH analysis has more immediacy
and potential impact on patient care than any other
laboratory determination.(National committee for Laboratory
Cornerstone in the diagnosis & management of
clinical oxygenation and acid-base disturbances.
Of all the concepts employed in the diagnosis and
treatment of respiratory disorders, few are more
important or less well understood than those of
blood gas interpretation.
Information from ABGs
VENTILATION & ACID BASE
(0.21 – 1.0)
2. VENTILATION & ACID
CO2 +H2O H2CO3 H+ + HCO3-
Expired CO2 H+
PaO2 >80mm Hg
– In supine posture PaO2=109-(0.43 Х age)
– PaO2=100mmHg in 10 year old child, PaO2
falls approximately 5mmHG for every 10 years
upto 90 years.
– 5 mmHg higher in the sitting position that
Blood samples must be drawn only when the patient
is in steady state.
20 to 30 min waiting period is recommended before
taking ABG after a change in oxygen therapy or
ventilation in those with pulmonary disease.
Sampling errors -Air contamination
Most important change: PaO2 tends to
increase towards 158mm Hg,
Less significant change: PaCO2 falls, pH
All air bubbles should be expelled
All samples with visually apparent froth
should be discarded.
Mixed venous blood – pH 7.38, pCO2 48mmHg,
PaO2 40mmHg, SaO2 75%
Flash of blood on entering artery, pulsations during
syringe filling, auto-filling of syringe, correlate
with pulse oximetry.
Addition of one-tenth of venous blood to an
arterial sample could produce 25% drop in
measure PaO2. Blood Volume (ml) PaO2
Arterial 4.5 86
Venous 0.5 31
Mixed 5.0 56
0.05ml of heparin(1,000units/ml) is required to
anticoagulate 1 ml of blood.
Dead space of a standard 5ml syringe with 22G
needle is 0.2ml; i.e. filling the syringe dead space
with heparin provides sufficient volume to
anticoagulate a 4ml blood sample.
Heparin – weak acid equilibrated with room air
Initially PaCO2 falls,
In extreme dilution pH and bicarbonate falls
PaO2 usually unchanged.
Time delay - metabolism
Samples should be analyzed within 20 min
to avoid error.
Measurement Direction Magnitude/Hour
pH ↓ 0.05
PCO2 ↑ 5
PaO2 ↓ 20
Placing the sample in iced water slows metabolism to
Leukocyte Larceny – Rapid fall in PaO2 in
blood samples with high leukocyte counts –
due to metabolism by leukocytes.
Approach to Hypoxia
Six basic mechanisms of hypoxia
1. Decrease in inspired PO2
4. V/Q mismatching
5. Diffusion barrier – least common cause
6. Increased tissue consumption – not
significant if lungs are normal
Driving force for oxygen to enter blood
Indicator of the extent of parenchymal
dysfunction in the lung
PAO2=[FiO2 Х (PB-PH20)] – PaCO2/R
PAO2=150-[1.25 Х PaCO2]
Normal= <15mmHg in <30yr old
Increases by ~3mmHg per decade
PaCO2=60; PaO2=35; pH=7.36.
Mechanism of Hypoxia?
AO2=150 – 1.25 Х 60 = 75
Ans: hypoventilation with another
P/F ratio (PaO2/FiO2)
Easy to calculate index of pulmonary
Does not consider PaCO2.
Moderate pulmonary dysfunction 200-400
Substantial pulmo. Dysfunction <200.
Helps to decide the safe limits of reduction of
FiO2 during weaning from oxygen.
E.g: PaO2-160 on FiO2 of 0.8. If we want
PaO2 of 80 reduce FiO2 to 0.4.
Steps in Acid-base classification
1. pH classification
2. PaCO2 classification
3. Metabolic classification
4. Compensation evaluation
5. Complete acid-base classification
Verification of internal
pH=6.1 + HCO3 / ( 0.031 Х PCO2)
7.35-7.45 – Normal
<7.35 – acidosis
>7.45 - alkalosis
Respiratory acidosis >45
Normal 0 ±2 24 ±2
Met.acidosis <-2 <22
Met.alkalosis >+2 >26
Anion gap: Plasma anions not measured by routine laboratory.
AG= (Na+K) – (Cl+HCO3). Normal = 12 + 4 mEq/L
In Respiratory Failure
Causes – from cerebral cortex to the
peripheral nerve innervating respiratory
muscle; from large airway to pleura..
Treatment – mechanical ventilation,
As in Hyperventilation
Results in Hypocarbia
Causes- Anxiety, cerebral stimulation,
sepsis, drugs, hypoxia.
Treatment - Cause, rebreathing
Check too much Heparin ??
Increased Anion gap – Sepsis, renal Failure,
Ketoacidosis, Drugs and Poisons
Normal Anion Gap – GI-loss, Renal tubular
acidosis, Endocrine (steroid def, renin def) Drugs
( Spironolactone, Amiloride, Triamterene )
Treatment – Cause, Bicarb to replace buffer.
- Vomiting as in Gastric outlet obstruction;
loss of HCl acid,
- Renal with increased steroids,
- K+ depletion as with loop diuretics,
- Iatrogenic as with bicarbonate therapy.
Treatment – correct perpetuating cause(s):
volume depletion, potassium correction
Return of an abnormal pH towards normal
by the component that was not primarily
Body does not over compensate for a
primary acid-base disturbance. In other
words, when the pH reaches the normal
range, compensatory mechanisms are no
Disorder Initial change Compensation
Met. Acidosis ↓ in HCO3 1.2 mmHg ↓in PCO2
for every 1 ↓ in
Met. Alkalosis ↑ in HCO3 0.6 ↑ in PCO2 for
every 1 ↑ in HCO3
Resp.acidosis – Acute ↑ in PCO2 1 ↑ in HCO3 for every
10 ↑ in PCO2
Resp.acidosis – 3.3 ↑ in HCO3 for
Chronic every 10 ↑in PCO2
Resp.alkalosis – Acute ↓ in PCO2 2.2 ↓ in HCO3 for
every 10 ↓ PCO2
Resp.alkalosis – 4.4 ↓ in HCO3 for
Chronic every 10 ↓ in PCO2.
pH PaCO2 HCO3 Diagnosis
7.6 30 31 MAlk+RAlk
7.1 70 14 MAci+RAci
7.5 25 21 RespAlk
7.4 20 12 MAc+Ralk
7.5 47 36 MAlk