acid base , abg interpretation

1. ABG INTERPRETATION
MODERATOR: DR A.SUDHAKAR
BY: DR J VIKAS REDDY

2. INTRODUCTION
➤ Arterial blood gas analysis refers to measurement of pH and
partial pressure of oxygen and carbon dioxide in arterial blood.
➤ Chronic, mild derangements in acid–base status may interfere
with normal growth and development, whereas acute, severe
changes in pH can be fatal.
➤ Acid-base homeostasis exerts a major influence on protein
function, thereby critically affecting tissue and organ
performance.

3. TERMINOLOGIES
➤ pH is negative logarithm of h+ ion activity there is inverse
relationship between pH and hydrogen ion concentration
➤ Maintaining a normal pH is necessary because hydrogen ions
are highly reactive and especially likely to combine with
proteins, altering function.
➤ Acidaemia is defined as increase in H+ and decrease in
arterial pH
➤ Acidosis is process that acidifies body fluids , lowers plasma
HCO3 and if unopposed, will lead too fall in pH
➤ Alkalosis is a process than alkalinizes body fluid and if
unopposed lead to rise in pH

4. ➤ Buffers a solution containing a substances that have the
ability to maintain changes in pH when added to it.
➤ 4 major buffers are bicarbonate, plasma protein, hemoglobin,
phosphates.
➤ pKa is negative logarithm of the dissociation constant. If it
describes a buffer system, then it is numerically equal to the
pH of the system when acid and anion are present in equal
concentration.
➤ Base excess is an index of magnitude of the metabolic
contribution to acid base disturbance.
➤ The normal base excess range of +/-2mEq/L

5. ➤ A BE less than -2 signifies the presence of metabolic acidosis,
whereas BE more than +2signifies the presence of metabolic
alkalosis.

6. Under standard conditions
BASE EXCESS
Positive base excess: metabolic
alkalosis
The amount of acid that returns the
pH of blood sample to normal
Negative base excess: metabolic
acidosis
The amount of alkali that returns
the pH of blood sample to normal

7. BUFFERING MECHANISM
➤ Buffers are first line of defense blunting changes in h+
➤ Extracellular buffers are
A buffer pair consists of :
A base {H+ acceptor} & an
acid {H+ donor}
HCO3-
HPO4
Proteins

8. Different buffer systems assume dominant roles
in different parts of the body
Extracelluar fluid
Major buffer
-bicarbonate buffer
system
Minor buffers
-intracellular protein
-phosphate buffer
sytem
Intracellular
fluid
Major buffers
-Proteins
-phosphate
Blood
Major buffers
-bicarbonate
buffer system
-hemoglobin
Minor buffers
-plasma
proteins
-phosphate
Urine
Major buffers
-ammonia
-phosphate

9. Is the carbonic acid system an ideal buffer
system?
Normal blood levels of HCO3 and CO2
HCO3:22-26 mEq/L
CO2 : 40mmHg
i.e.;0.03✕40=1.2mEq/L
(0.03 being the solubility
coefficient of co2)
At the normal body pH of 7.4 the rate of HCO3 : CO2 =24:1.2 =20
An ideal buffer should have a ratio of 1:1.
A HCO3:CO2 ratio of 20:1 would normally make for a poor buffer system if it
were not possible to regulate HCO3 or CO2 concentrations.

10. RESPIRATORY REGULATION
➤ 2nd line of defense
➤ 10-12 mol/day CO2 is accumulated and is transported to
lungs as HB-generated HCO3 and HB-bound carbamino
compounds where it is freely excreted.
➤ accumulation/ loss of co2 changes in pH within minutes
H2O + CO2 = H2CO3
= H+ + HCO3-

11. ➤ Balance affected by neurorespiratory control of ventilation.
➤ During acidosis, chemoreceptors sense decrease in pH and
trigger ventilation decreasing PaCO2.
➤ Response to alkalosis is biphasic. Initial hyperventilation to
remove excess PaCO2 followed by suppression to increase
PaCO2 to return pH to normal

12. RENAL REGULATION
➤ Kidneys are the ultimate defense against the addition of non-
volatile acid/alkali.
➤ Kidneys play a role in the maintenance of HCO3 by
-Conservation of filtered HCO3
-Regeneration of HCO3
➤ Net acid excretion {NAE} :
-Kidney balance nonvolatile acid generation during metabolism
by excreting acid.
-Each mEq of NAE corresponds to 1 mEq of HCO3 returned to
ECF

13. ➤ NAE has three components:
1. NH4+
2. TITRABLE ACIDS
3. BICARBONATE

14. RENAL COMPENSATIONS FOR ACID BASE DISTURBANCES
➤ Glutamine metabolism and NH4+ excretion are increased
during acidosis and decreased during alkalosis, the signal is
unknown
➤ Tubular hydrogen ion secretion is
1. Increased by the increased blood Pco2 of respiratory acidosis
and decreased Pco2 of respiratory alkalosis.
2. Increased independently of changes in Pco2 by the local
effects of decreased extracellular pH on the tubules.

15. INDICATIONS & CONTRAINDICATIONS
➤ Indications :
1. Suspected hypercapnia
2. Suspected severe hypoxemia
3. Severe, prolonged and worsening respiratory distress
4. Any severely unwell patient
5. Acute deterioration of consciousness
6. Mechanically ventilated patients
7. Patients with respiratory failure
8. Candidates for long-term oxygen therapy
9. Inborn errors of metabolism

16. ➤ Contraindications:
1. Inadequate collateral circulation at the puncture site
2. Should not be performed through a lesion or a surgical shunt
3. Evidence of peripheral vascular disease distant to the
puncture site
4. A coagulopathy or medium to high dose anticoagulation
therapy

17. TECHNIQUE OF SAMPLING
➤ Sites of puncture: the site chooses for taking arterial blood depends on
factors such as your own preference and skill, access, and patient
clinical condition.
➤ Ideal artery for sampling in newborn is radial or umbilical artery
➤ If sample from umbilical catheter taken, one should assure free flow of
blood and remove three or four times dead space volume before
sample taken
➤ Allen test is performed to ensure collateral blood supply by ulnar
artery

20. ➤ Equipment required for obtaining an arterial sample
1. Skin preparation fluid alcohol or iodine based
2. Syringe size 2ml containing 0.5% or 1% plain lignocaine with
22G needle attached to it
3. Use 0.25ml heparin of lower strength 1000 units per ml
instead of 5000 units per ml
4. Gauze swabs or cotton wool for applying pressure on
puncture site after sample has been taken
5. Slushed ice for transportation

22. ➤ Precautions for collection
1. Heparin is acidic and lowers pH. Use small volume of heparin
just for lubricating syringe and plunger
2. Avoid air bubble and let syringe fill spontaneously. Sluggish
filling of syringe indicates that you have accidentally entered
vein rather than artery.
3. It is desirable to use glass syringe as plastic syringe are
permeable to air
4. Vigorous rotation of syringe between palms of hands for
about 20 sec ensures thorough mixing of blood with heparin
5. Always note whether an ABG was drawn while the patient
was receiving oxygen therapy

23. THE EFFECT OF AN AIR BUBBLE IN THE SYRINGE
The effect of an air bubble on the arterial blood in a syringe can have a variable
effect on the PaO2, and a predictable effect on the pH and the PaCO2. The gases in
the blood sample and in trapped air bubble will, tend to equilibrate with each other
The PaO2 of ambient air at
sea level is approximately
160mmHg, so this PaO2 of air
bubble trapped within syringe
If the PaO2 of
arterial blood
is
<160mmHg it
will rise
If the PaO2 of
the arterial
blood
>160mmHg it
will fall
CO2 is present in
minuscule levels in
ambient air. In other
words the PaCO2 in
trapped air is
virtually zero
The PaCO2 of the
arterial blood will
trend towards zero.
pH
The effect of trapped air
bubble on the pH is
related to its effect on
PaCO2
At the PaCO2 of the
blood falls due to the
effect of the air bubble,
pH will rise i.e, the blood
becomes alkalemic

24. EFFECT OF THE OVER-HEPARINIZATION OF THE SYRINGE
Heparin is a sulfated mucopolysaccharide with acidic properties. An excess of
heparin in syringe can have following effects:
Effect on pH
If the pH is normal
or alkaline to begin
with:
If the pH is very
acidic to begin
with:
Acidemia increases
pH will fall on
contact with acidic
heparin
Acidemia
decreases
pH will rise as the
mildly acidic
heparin reduces
the greater acidity
of blood
Dilutional effect
The PaO2 and PaCO2 can also
be spuriously lowered by
dilution.

25. pH 7.35-7.45
pCO2 35-45mmHg
pO2 80-100mmHg
O2 saturation 95-100%
HCO3 22-26mEq/L
Base Excess + or - 2
Anion gap 10-15mEq/L
Normal values (at sea level) range:

26. 37deg 4deg
pH 0.01 0.001
pCO2 0.1mm Hg 0.01Hg
pO2 0.1mm Hg 0.01Hg
Changes in ABG every 10minutes in vitro

27. STEPS IN ABG
INTERPRETATION

28. STEP ONE: HISTORY AND PHYSICAL EXAMINATION
➤ Clinical conditions associated with specific acid base disorders
Vomiting Metabolic alkaloisis
Diarrhea Metabolic alkaloisis,acidosis
Severe diarrhea Metabolic acidosis
Diuertic therapy Metabolic alkalosis
Sepsis Respiratory alkalosis, metabolic acidosis
Hypotension, low cardiac output states Metabolic acidosis
Dka Metabolic acidosis
Renal failure Metabolic acidosis
Pregnancy Respiratory alkalosis
Pneumonia Respiratory alkalosis
Asthma exacerbation Respiratory alkalosis
Seizures Metabolic acidosis

29. STEP 2: CHECKING THE ACCURACY OF ABG
➤ (H+) = 24 ✕ PaCO2 / HCO3
➤ pH 7.40 = 40 nEq/L (H+)
➤ 0.01 Change in pH within range of 7.20 to 7.50 there is 1nEq/L
inverse change in h+

30. pH (H+) in nm/L
7.00 100
7.10 80
7.20 63
7.30 50
7.40 40
7.50 30
7.60 25
7.70 20
7.80 15
8.00 10
pH is inversely related to (H+). A pH change of
1.00 represents 10 fold change in (H+)

31. STEP 4 : IDENTIFY THE DISORDER
The normal ph is 7.4(7.36-7.45)
Acidosis or alkalosis?
pH<7.36 : acidosis pH>7.44 : alkalosis
What type of acidosis?
If HCO3 low, the
disorder is
metabolic
acidosis
If CO2 is high
the disorder is
respiratory
acidosis
What type of alkalosis?
If the PCO2 low,
the disorder is
respiratory
alkalosis
If the HCO3 is
high, the
disorder is
metabolic
alkalosis

32. TEST NORMAL ↓VALUE ↑ VALUE
pH 7.35-7.45 ACIDOSIS ALKALOSIS
pCO2 35-45 ALKALOSIS ACIDOSIS
HCO3 22-26 ACIDOSIS ALKALOSIS
pO2 80-100 HYPOXEMIA O2 therapy
SaO2 95-100% HYPOXEMIA
Evaluation of abnormal values:

33. pH HCO3 PaCO2
METABOLIC
ACIDOSIS
LOW LOW LOW
METABOLIC
ALKALOSIS
HIGH HIGH HIGH
RESPIRATORY
ALKALOSIS
HIGH LOW LOW
RESPIRATORY
ACIDOSIS
LOW HIGH HIGH
Simple acid base disturbances and pattern of
change

34. ➤ One way to remember this relationship is to use the acronym
ROME
RESPIRATORY OPPOSITE
METABOLIC EQUAL
➤ The CO2 is the respiratory component of the ABG and if it
is low and the pH is high the patient would have a
respiratory alkalosis. They move is opposite direction to
match
➤ The HCO3 is the metabolic component of the ABG. If the
HCO3 is low and the pH is low the patient would have
metabolic acidosis. They move in same direction to match

35. STEP 5 :LOOK FOR COMPENSATION
METABOLIC ACIDOSIS
PaCO2=(1.5✕HCO3)+8 +/- 2
Or
PaCO2 will ↓1.25mmHg per mmol/
L↓ in HCO3
Or
PaCO2=HCO3 + 15
METABOLIC ALKALOSIS
PaCO2 will ↑0.75mmHg per
mmol/L ↑ in HCO3
Or
PaCO2 will ↑6mmHg per 10mmol/L
↑ in HCO3
Or
PaCO2=HCO3+15

36. RESPIRATORY ALKALOSIS
ACUTE: HCO3 will ↓0.2mmol/L
per mmHg ↓ in PaCO2
CHRONIC: HCO3 will ↓ 0.4mmol/L
per mmHg ↓ in PaCO2
RESPIRATORY ACIDOSIS
ACUTE: HCO3 will ↑ 0.1mmol/L
per mmHg ↑ in PaCO2
CHRONIC: HCO3 will ↑ 0.4 mmol/L
per mmHg ↑ in PaCO2

37. RESPIRATORY COMPENSATION IS
ALWAYS FAST …12-24 hrs
METABOLIC COMPENSATION IS ALWAYS
SLOW ….5-7 DAYS
➤ Body’s physiologic response to primary disorder in order to
bring pH towards normal limit
➤ There can be full compensation, partial compensation, no
compensation( uncompensated )
➤ But never overshoot , if overshoot pH is there it is a mixed
disorder

38. STEP 6 :ANION GAP
➤ Anion gap= Na - (Cl + HCO3)
➤ Normal range is 10+/-2 mEq/L
➤ It represents unmeasured anions. These unmeasured anions
can be;
1. Anionic proteins
2. SO4, PO4, Organic anions
3. Acid anions(acetoacetate, lactate, uremic anions)

39. ➤ Anion gap can increase either due to:
1. Increase in the unmeasured anions.
2. Decrease in the unmeasured cations(hypocalcemia,
hypomagnesemia)
➤ Anion gap may decrease due to
A. Increase in unmeasured cations( Ca, Mg, K)
B. Addition of abnormal cations (Li)
C. Decrease in albumin (each 1g/dl decrease of albumin AG by
2.5 mEq/L

40. Bicarbonate gap(the delta gap/ratio)
➤ The difference between the increase in the anion gap and decrease in
bicarbonate is termed the bicarbonate gap
Normally, increase in anion gap=decrease in the serum bicarbonate
For ex if the anion gap has increased by 8mEq/L the serum bicarbonate is also
expected to fall by 8mEq/L
The increase in the anion gap
significantly exceeds decrease in the
bicarbonate
If the bicarbonate has not fallen
proportionately ,a process that is
contributing to a relative increase in
bicarbonate anticipated
Positve bicarbonate gap >6mEq/L
An associated metabolic alkalosis is
present
The decrease in the bicarbonate
significantly exceeds the increase in
the anion gap
Negative bicarbonate ion gap
<6mEq/L
An associated narrow anion gap
metabolic acidosis is present

41. STEP 7: DETECTING MIXED DISORDERS
➤ Clues to the presence of a mixed disorder
1. Clinical history
2. pH normal, abnormal PCO2 and HCO3
3. PCO2 and HCO3 moving opposite directions
4. Acid base map (flenley nomogram)
5. Degree of compensation for primary disorder is inappropriate
6. Delta gap

42. ➤ Example : in a case of primary metabolic acidosis, HCO3=12
Expected compensated PCO3 will be 24-28
(PCO2=1.5HCO3+8 +/-2) (winter’s formula)
If PCO2 is <24, metabolic acidosis +respiratory alkalosis
If PCO2 is >28, metabolic acidosis + respiratory acidosis

43. Coexistence of acid-base disorders
➤ Frequently two(sometimes three) acid-base disorders occur simultaneously
Two respiratory
disorders cannot
coexist
The lungs cannot
simultaneously
retain and excrete
CO2
Other combinations four acid base disorders are
possible
One metabolic can
occur together
with a respiratory
disturbance
Two metabolic
disorders can
occur together
Two metabolic
disorders can
occur with single
respiratory
disturbance

44. REFERENCES :
1. Handbook of blood gas/ acid-base interpretation, springer
monograph by ashfaq hasan
2. Blood gas analysis by t.shyam sunder
3. newbornwhocc.org
4. Harrison’s internal medicine 19th edition
5. Arterial blood gases made easy 2edition
Thank you