ARTERIAL BLOOD GAS ( ABG ) interpretation BY DR RAMI ADEL ALQUDSI

1. ‫الرحيم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬
Arterial Blood Gas
Interpretation
Dr Rami Adel Alqudsi
CONSULTANT OF ANESTHESIOLOGY
(KKGH)
MD
JORDAN BOARD IN ANESTHESIOLOGY

3.  pH 7.35 - 7.45
 PaCO2 35 - 45 mm Hg
 PaO2 70 - 100 mm Hg **
 SaO2 93 – 100%
 HCO3
¯ 22 - 26 mEq/L
 %MetHb < 2.0%
 %COHb < 3.0%
 Base excess -2.0 to 2.0 mEq/L
 CaO2 16 - 22 ml O2/dl
Normal Arterial Blood Gas Values

4. Equations :
 PaCO2 equation
Alveolar gas equation
Oxygen content equation
Henderson-Hasselbalch equation
(Acid-base balance )

7. Hypercapnia

8. Hypercapnia

9. Hyperinflated Lungs : COPD

10. An example of intrapulmonary shunt

11. Diffuse pulmonary infiltrates

12. Why Hypercapnia is dangerous?

13. PCO2 vs. Alveolar Ventilation

14. Alveolar Gas Equation
PAO2 = PIO2 - 1.2 (PaCO2)
Where PAO2 is the average alveolar PO2, and PIO2 is the partial pressure of
inspired oxygen in the trachea
PIO2 = FIO2 (PB – 47 mm Hg)
FIO2 is fraction of inspired oxygen and PB is the
barometric pressure. 47 mm Hg is the water vapor pressure at normal
body temperature.

15. Alveolar Gas Equation
PAO2 = PIO2 - 1.2 (PaCO2)
where PIO2 = FIO2 (PB – 47 mm Hg)
Except in a temporary unsteady state, alveolar PO2 (PAO2) is
always higher than arterial PO2 (PaO2). As a result, whenever
PAO2 decreases, PaO2 also decreases. Thus, from the AG
equation:
 If FIO2 and PB are constant, then as PaCO2 increases both PAO2 and PaO2
will decrease (hypercapnia causes hypoxemia).
 If FIO2 decreases and PB and PaCO2 are constant, both PAO2 and PaO2 will
decrease (suffocation causes hypoxemia).
 If PB decreases (e.g., with altitude), and PaCO2 and FIO2 are constant, both
PAO2 and PaO2 will decrease (mountain climbing leads to hypoxemia).

16. P(A-a)O2
 P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen.
It is commonly called the “A-a gradient,” though it does not actually result
from an O2 pressure gradient in the lungs. Instead, it results from gravity-
related blood flow changes within the lungs (normal ventilation-
perfusion imbalance).
 PAO2 is always calculated based on FIO2, PaCO2, and barometric pressure.
 PaO2 is always measured on an arterial blood sample in a “blood gas
machine.”
 Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg breathing room air (it
increases with age). A higher than normal P(A-a)O2 means the lungs are
not transferring oxygen properly from alveoli into the pulmonary
capillaries. Except for right to left cardiac shunts, an elevated P(A-a)O2
signifies some sort of problem within the lungs.

17. Physiologic Causes of Low PaO2

18. Ventilation-perfusion Imbalance
A normal amount of ventilation-perfusion (V-Q)
imbalance accounts for the normal P(A-a)O2.
By far the most common cause of low PaO2 is an
abnormal degree of ventilation-perfusion imbalance
within the hundreds of millions of alveolar-capillary
units. Virtually all lung disease lowers PaO2 via V-Q
imbalance, e.g., asthma, pneumonia, atelectasis,
pulmonary edema, COPD.
Diffusion barrier is seldom a major cause of low PaO2
(it can lead to a low PaO2 during exercise).

19. SaO2 and Oxygen Content

20. Also shown are CaO2 vs. PaO2 for two different hemoglobin contents: 15 gm% and
10 gm%. CaO2 units are ml O2/dl. P50 is the PaO2 at which SaO2 is 50%.
Oxygen Dissociation Curve: SaO2 vs. PaO2

21.  Normal percentage of COHb in the blood is 1 - 2%, from metabolism and
small amount of ambient CO (higher in traffic-congested areas).
 CO is colorless, odorless gas, a product of combustion; all smokers have
excess CO in their blood, typically 5 -10%.
 CO binds 200x more avidly to hemoglobin than O2, effectively displacing
O2 from the heme binding sites. CO is a major cause of poisoning deaths
world-wide.
 CO has a “double-whammy” effect on oxygenation: 1) decreases SaO2 by
the percentage of COHb present, and 2) shifts the O2-dissociation curve to
the left, retarding unloading of oxygen to the tissues.
 CO does not affect PaO2, only SaO2. To detect CO poisoning, SaO2 and/or
COHb must be measured (requires co-oximeter). In the presence of excess
CO, SaO2 (when measured) will be lower than expected from the PaO2.
Carbon Monoxide – An Important Cause of Hypoxemia

22. .
CO Does Not Affect PaO2 – Be Aware!
Hemoglobin is a tetramer with four oxygen binding sites.
The binding of carbon monoxide at one of these sites
increases the oxygen affinity of the remaining three sites,
which causes the hemoglobin molecule to retain oxygen
that would otherwise be delivered to the tissue. This
situation is described as carbon monoxide shifting the
oxygen dissociation curve to the left. Because of the
increased affinity between hemoglobin and oxygen
during carbon monoxide poisoning, little oxygen will
actually be released in the tissues. This causes hypoxic
tissue injury.

23. 1. Hypoxemia (= low PaO2 and/or low CaO2)
a. reduced PaO2 – usually from lung disease (most common physiologic
mechanism: V-Q imbalance)
b. reduced SaO2 – most commonly from reduced PaO2; other causes
include carbon monoxide poisoning, methemoglobinemia, c. reduced
hemoglobin content – anemia
2. Reduced oxygen delivery to the tissues
a. reduced cardiac output – shock, congestive heart failure
b. right to left systemic shunt (as may be seen in septic shock)
3. Decreased tissue oxygen uptake
a. mitochondrial poisoning (e.g., cyanide poisoning)
b. left-shifted hemoglobin dissociation curve (e.g., from acute alkalosis,
excess CO, or abnormal hemoglobin structure)
Causes of Hypoxia
A General Classification

24. The answer must be based on some oxygen value, but
which one? Blood gases give us three different oxygen
values: PaO2, SaO2, and CaO2 (oxygen content).
Of these three values, PaO2, or oxygen pressure, is the
least helpful to answer the question about oxygen
adequacy in the blood. The other two values - SaO2 and
CaO2 - are more useful for this purpose.
How much oxygen is in the blood, and is it
adequate for the patient?
PaO2 vs. SaO2 vs. CaO2

25. OXYGEN PRESSURE: PaO2
Since PaO2 reflects only free oxygen molecules dissolved in plasma and not those bound to
hemoglobin, PaO2 cannot tell us “how much” oxygen is in the blood; for that you need to know how
much oxygen is also bound to hemoglobin, information given by the SaO2 and hemoglobin content.
OXYGEN SATURATION: SaO2
The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen
saturation (in arterial blood, the SaO2). Note that SaO2 alone doesn’t reveal how much oxygen is in the
blood; for that we also need to know the hemoglobin content.
OXYGEN CONTENT: CaO2
Tissues need a requisite amount of O2 molecules for metabolism. Neither the PaO2 nor the SaO2
provide information on the number of oxygen molecules, i.e., how much oxygen is in the blood.
(Neither PaO2 nor SaO2 have units that denote any quantity.) Only CaO2 (units ml O2/dl) tells us
how much oxygen is in the blood; this is because CaO2 is the only value that incorporates the
hemoglobin content. Oxygen content can be measured directly or calculated by the oxygen
content equation:
CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
How much oxygen is in the blood?
PaO2 vs. SaO2 vs. CaO2

26. Acid-base Balance
Henderson-Hasselbalch Equation
[HCO3
-]
pH = pK + log ----------------
.03 [PaCO2]
For teaching purposes, the H-H equation can be shortened to its basic
relationships:
HCO3
-
pH ~ ---------
PaCO2
PHa = negative logarithm of arterial concentration of H+
PK = 6.1 at 37 ˚C
HCO3 = concentration of bicarbonate
0.03 = solubility coefficient for Co2 in the plasma
PaCo2 =arterial partial pressure of Co2

27. Maintenance of the H+concentration
is necessary to:
Ensure the optimal functions of
enzymes
Maintain proper distribution of
electrolytes
Optimize myocardial contractility
Maintain optimal saturation of
hemoglobin with oxygen

28. Normal values :
PHa = 7.4
PaCO2 = 40 mmHg
HCO3 = 24mEq/L

29. Acid-base Terminology
Acidemia: blood pH < 7.35
Alkalemia: blood pH > 7.45

30. Maintenance of the H+concentration
is necessary to:
Ensure the optimal functions of
enzymes
Maintain proper distribution of
electrolytes
Optimize myocardial contractility
Maintain optimal saturation of
hemoglobin with oxygen

31. Compensatory responses
in acid–base disturbances

32. DIAGNOSIS OF ACID-BASE
DISORDERS
1. Examine Arterial pH: Is acidemia or alkalemia?
2. Examine Pa co 2 : Is the change in Pa co 2 ?
3. Examine [HCO 3 − ] : Is the change in [HCO 3 − ]
4. Compare the change in [HCO 3 − ] with the change in
Paco 2
5. If the compensatory response is more or less
than expected, by definition, a mixed acid–base disorder
exists.
6. Calculate the plasma anion gap in the case of
metabolic acidosis.
7. Measure urinary chloride concentration in the case of
metabolic alkalosis

33. DIAGNOSIS OF ACID-BASE
DISORDERS
Is to correlate changes in pH with changes in
CO 2 or HCO 3 . For a respiratory disturbance,
every 10 mm Hg change in CO 2 should change
arterial pH by approximately 0.08 U in the
opposite direction.
During metabolic disturbances, every 6 mEq
change in HCO 3 also changes arterial pH by 0.1
in the same direction. If the change in pH
exceeds or is less than predicated, a mixed
acid–base disorder is likely to be present.

34. Diagnosis of acid–base disorders

35. Compensatory Mechanisms
Immediate chemical buffering
Respiratory compensation
Renal compensation

36. Immediate chemical buffering
Bicarbonate is the most important buffer
in the extracellular fluid compartment

37. Respiratory compensation
Metabolic acidosis
PCo2 = 1.5 x HCO3 + 8
Metabolic alkalosis
PCo2 = .7 x HCO3 + 21

38. Metabolic compensation
Acute respiratory acidosis
∆PH= .008 x(PCO2-40)
Chronic respiratory acidosis
∆PH= .003 x(PCO2-40)
Acute respiratory alkalosis
∆PH= .008 x(40-PCO2)
Chronic respiratory alkalosis
∆PH= .017 x(40-PCO2)

39. Immediate chemical buffering
Bicarbonate is the most important buffer
in the extracellular fluid compartment

40. Hemoglobin as a Buffer
Is the most important noncarbonic buffer
in extracellular fluid

41. Respiratory Compensation
During Metabolic Acidosis
Decreases in arterial blood pH stimulate medullary
respiratory centers. The resulting increase in
alveolar ventilation lowers Pa co 2 and tends to
restore arterial pH toward normal.
During Metabolic Alkalosis
Increases in arterial blood pH depress respiratory
centers. The resulting alveolar hypoventilation tends
to elevate Pa co 2 and restore arterial pH toward
normal.

42. Renal Compensation During Acidosis
The renal response to acidemia is 3-fold:
(1) increased reabsorption of the filtered HCO 3 −
(2) increased excretion of titratable acids
(3) increased production of ammonia
Renal Compensation During Alkalosis
The tremendous amount of HCO 3 − normally filtered
and subsequently reabsorbed allows the kidneys
to rapidly excrete large amounts of bicarbonate, if
necessary

43. Compensatory responses
in acid–base disturbances

44. Causes of respiratory acidosis
(increase co2)
•Alveolar hypoventilation
•Central nervous system depression
• Drug-induced , Sleep disorders , Obesity hypoventilation
(Pickwickian) syndrome , Cerebral ischemia ,Cerebral
trauma
•Neuromuscular disorders : Myopathies , Neuropathies
•Chest wall abnormalities
•Pleural abnormalities : Pneumothorax , Pleural effusion

45. Causes of respiratory acidosis
(increase co2)
Airway obstruction :
 Upper airway : eg. Foreign body ,Tumor
Lower airway : eg. Severe asthma ,Chronic
obstructive pulmonary disease
Parenchymal lung disease :
 Pulmonary edema : Cardiogenic , Noncardiogenic
 Pulmonary emboli
 Pneumonia
 Aspiration
 Interstitial lung disease
Ventilator malfunction

46. Causes of respiratory acidosis
(increase co2)
Increased CO 2 production
 Large caloric loads
 Malignant hyperthermia
 Intensive shivering
 Prolonged seizure activity
 Thyroid storm
 Extensive thermal injury (burns)

47. Treatment of Respiratory
Acidosis
 By increasing alveolar ventilation.
 Treatment the causes :
(eg. dantrolene for malignant hyperthermia,
muscle paralysis for tetanus, antithyroid medication
for thyroid storm, and reduced caloric intake
in patients receiving enteral or parenteral nutrition).
Improving alveolar ventilation include bronchodilation,
reversal of narcosis, or improving lung compliance
(diuresis). Severe acidosis (pH <7.20), CO 2 narcosis,
and respiratory muscle fatigue are indications for
mechanical ventilation.

48. Causes of metabolic acidosis

49. Anion gap = 140 − (104 + 24) = 12 mEq/L
normal range = 7 − 14 mEq/L)

50. Treatment of Metabolic Acidosis
1- Respiration should be controlled
2-Treatment the causes of metabolic
acidosis : eg. Renal failure , DKA

51. Causes of respiratory alkalosis

52. Treatment of Respiratory Alkalosis
Correction of the underlying process is the
only treatment for respiratory alkalosis.
For severe alkalemia (arterial pH >7.60),
intravenous hydrochloric acid, arginine
chloride, or ammonium chloride may
be indicated

53. Causes of metabolic alkalosis.

54. Treatment of Metabolic Alkalosis
1- Respiration should be controlled
2- Treatment the causes of Metabolic
Alkalosis

55. THANK YOU