1. Interpretation of
the
Arterial Blood Gas
Analysis
DM SEMINAR
Dr. Vishal Golay
2/11/2011

2. Overview of the
discussion
• Basics of acid-base balance.
• Role of kidneys in acid-base homeostasis.
• Step-wise approach in diagnosis of acid-base
disorders.
• Some practical examples.

3. Basic terminology
• pH – signifies free hydrogen ion concentration. pH is inversely
related to H+ ion concentration.
• Acid – a substance that can donate H+ ion, i.e. lowers pH.
• Base – a substance that can accept H+ ion, i.e. raises pH.
• Anion – an ion with negative charge.
• Cation – an ion with positive charge.
• Acidemia – blood pH< 7.35 with increased H+ concentration.
• Alkalemia – blood pH>7.45 with decreased H+ concentration.
• Acidosis – Abnormal process or disease which reduces pH due to
increase in acid or decrease in alkali.
• Alkalosis – Abnormal process or disease which increases pH due
to decrease in acid or increase in alkali.

4. Endogenous sources of acid.
Daily production ~ 1 mEq of H+/kg/day
• Sulfuric acid ( from S containing AA)
• Organic acids (from intermediary metabolism)
• Phosphoric acid ( hydrolysis of PO4 containing
proteins)
• Hydrochloric acid (from metab of cationic AA-
Lysine, Arg, Histidine)

5. pH in humans is tightly regulated between 7.35-
7.45.
Chemical
Buffers
Respiratory
regulatory
responses
Renal regulatory
responses

6. Buffers
• Buffers are chemical systems which either
release or accept H+ and minimize change in
pH induced by an acid or base load.
• First line of defense blunting the changes in
[H+]
A buffer pair consists of:
A base (H+ acceptor) & An acid (H+ donor)

7. Buffers continued……
Extracellular buffers:
Examples:
Intracellular buffers:
• HCO3¯/H2CO3 •Hb
HPO42- + (H+•Proteins 4-
)↔H2 PO
• HPO4²¯/H2PO4
•Organophosphate
H2 O + CO2 ↔H2 CO3 ↔H+ + HCO3-
• Protein buffers compounds
•Bone apatite

8. Respiratory regulation
• 2nd line of defense
• 10-12 mol/day CO2 is accumulated and is
transported to the lungs as Hb-generated HCO3 and
Hb-bound carbamino compounds where it is freely
excreted.
H2 O + CO2 ↔H2 CO3 ↔H+ + HCO3-
• Accumulation/loss of Co2 changes pH within minutes

9. Respiratory regulation contd…..
• Balance affected by neurorespiratory control of
ventilation.
• During Acidosis, chemoreceptors sense ↓pH and
trigger ventilation decreasing pCO2.
• Response to alkalosis is biphasic. Initial
hyperventilation to remove excess pCO2 followed
by suppression to increase pCO2 to return pH to
normal

10. Renal Regulation
• Kidneys are the ultimate defense against the addition
of non-volatile acid/alkali.
HA + NaHCO3↔H2 O + CO2 + NaA
Addition of Acid causes loss of HCO3¯
• Kidneys play a role in the maintenance of this HCO3¯
by:
– Conservation of filtered HCO3 ¯
– Regeneration of HCO3 ¯

11. Net Acid Excretion(NAE)
• Kidneys balance nonvolatile acid generation
during metabolism by excreting acid.
• Each mEq of NAE corresponds to 1 mEq of HCO3 ¯
returned to ECF.
• NAE has three components:
1. NH4⁺ .
2. Titrable acids. (acid excreted that has titrated urinary
buffers)
3. Bicarbonate.
NAE= NH4⁺ + TA-HCO3¯

13. 75-80% HCO3 is absorbed in the proximal tubule.

16. Ammonium excretion
2 2

19. Interpreting acid-base
disorders

20. ----- XXXX Diagnostics ------
Blood
248
Pt ID
Gas
05:36
2570 / 00
Report
Jul 22 2000 Normal ABG values
Measured 37.0 C
o pH 7.35 - 7.45
pH 7.463
pCO2 44.4 mm Hg PaCO2 35 - 45 mm Hg
pO2 113.2 mm Hg
o
Corrected 38.6 C PaO2 70 - 100 mm Hg
pH 7.439
pCO2 47.6 mm Hg
pO2 123.5 mm Hg SaO2 93 - 98%
Calculated Data HCO3¯ 22 - 26 mEq/L
TPCO2 49
HCO3 act 31.1 mmol / L
HCO3 std 30.5 mmol / L %MetHb < 2.0%
BE 6.6 mmol / L
O2 CT 14.7 mL / dl
O2 Sat 98.3 % %COHb < 3.0%
ct CO2 32.4 mmol / L
pO2 (A - a) 32.2 mm Hg
pO2 (a / A) 0.79 Base excess -2.0 to 2.0 mEq/L
Entered Data
Temp 38.6 oC
ct Hb 10.5 g/dl
FiO2 30.0 %

21. -----XXXX Diagnostics-----
Blood Gas Report
328 03:44 Feb 5 2006
Pt ID 3245 / 00
Measured 37.0 0C Measured values…
pH 7.452 most important
pCO2 45.1 mm Hg
pO2 112.3 mm Hg
Corrected 38.6 0C Temperature Correction :
pH 7.436
pCO2 47.6 mm Hg Is there any value to it ?
pO2 122.4 mm Hg
Calculated Data
HCO3 act 31.2 mmol / L Calculated Data :
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L Which are useful one?
O2 ct 15.8 mL / dl
O2 Sat 98.4 %
ct CO2 32.5 mmol / L
pO2 (A -a) 30.2 mm Hg 
pO2 (a/A) 0.78 Entered Data :
Entered Data Important
Temp 38.6 0C
FiO2 30.0 %
ct Hb 10.5 gm/dl

22. Measured values should be considered
And
Corrected values should be discarded

23. -----XXXX Diagnostics-----
Blood Gas Report
328 03:44 Feb 5 2006
Pt ID 3245 / 00
Measured 37.0 0C Bicarbonate is calculated on the basis of the
pH 7.452 Henderson equation:
pCO2 45.1 mm Hg
pO2 112.3 mm Hg
[H+] = 24 pCO2 / [HCO3-]
Corrected 38.6 0C
pH 7.436
pCO2 47.6 mm Hg
pO2 122.4 mm Hg
Calculated Data
HCO3 act 31.2 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 ct 15.8 mL / dl
O2 Sat 98.4 %
ct CO2 32.5 mmol / L
pO2 (A -a) 30.2 mm Hg 
pO2 (a/A) 0.78
Entered Data
Temp 38.6 0C
FiO2 30.0 %
ct Hb 10.5 gm/dl

24. -----XXXX Diagnostics----- Standard Bicarbonate:
Blood Gas Report Plasma HCO3 after equilibration
328 03:44 Feb 5 2006 to a PCO2 of 40 mm Hg
Pt ID 3245 / 00
: reflects non-respiratory acid base change
Measured 37.0 0C
: does not quantify the extent of the buffer
pH 7.452
pCO2 45.1 mm Hg base abnormality
pO2 112.3 mm Hg
: does not consider actual buffering capacity of
Corrected 38.6 0C blood
pH 7.436
pCO2 47.6 mm Hg
pO2 122.4 mm Hg
Calculated Data Base Excess:
D base to normalise HCO3 (to 24) with PCO2 at 40
HCO3 act 31.2 mmol / L mm Hg
HCO3 std 30.5 mmol / L (Sigaard-Andersen)
BE 6.6 mmol / L
O2 ct 15.8 mL / dl : reflects metabolic part of acid base D
O2 Sat 98.4 % : no info. over that derived from pH, pCO2
ct CO2 32.5 mmol / L
pO2 (A -a) 30.2 mm Hg  and HCO3
pO2 (a/A) 0.78 : Misinterpreted in chronic or mixed disorders
Entered Data
Temp 38.6 0C
FiO2 30.0 %
ct Hb 10.5 gm/dl

25. "Step –wise approach"
for ABG analysis 1. Consider the Clinical Setting.
2. Obtain ABG and Electrolyte values
simultaneously.
3. Verify the ABG values.
4. Identify the nature of the disturbance.
5. Calculate the Anion gap in case of MA.
6. Assess ∆AG, ∆ HCO3, ∆Cl & ∆Na
7. Detecting mixed disorders.
8. Clinical correlation

26. Steps 1 & 2
• Basic clinical scenario gives an idea about the
type of the underlying disorder.
• ABG samples should be taken properly.
• Excess of heparin should be avoided during
sampling.

27. Sampling for ABG analysis
 Perform Allen’s test.
Special mention
 Clean the site.
 Use 21 gauze needle with syringe.
1. Specimens held at room temperature must be
analyzed within 10-15 minutes of drawing; iced
 Flush syringe and needle with heparin.
samples should be analyzed within 1 hour.
 Enter skin at 45 angle
2. The PaO2 of samples drawn from subjects with
 Obtain 2-4ml blood without aspiration. Avoid suction of syringe .
elevated white cell counts may decrease very rapidly.
 If sample contains any air bubble, tap it to the surface and push it
out of the syringe. Immediate chilling is necessary. in PaO2 and
Air bubbles can lead to increase
decrease in PaCO2.
 Apply firm pressure at punctured site.

29. Indications for performing an ABG
analysis
• The need to evaluate the adequacy of ventilatory
(PacO2) acid-base (pH and PaCO2), and oxygenation (PaO2
and SaO2) status, and the oxygen-carrying capacity of
blood (PaO2, HbO2, Hbtotal, and dyshemoglobins).
• The need to quantitate the patient's response to
therapeutic intervention and/or diagnostic
evaluation (eg, oxygen therapy, exercise testing)
• The need to monitor severity and progression of
a documented disease process.

30. Steps 2 Verify the ABG
values.
• The values should be checked for internal
consistency.
• In ABG samples, pH and PaCO2 are measured and
HCO3 calculated by the HH equation.
• Simultaneously measured plasma HCO3 should
be within ±2-3 mmol/L of each other.

31. Steps 3 continued…….
• Most ABG reports do not give HCO3. It can be calculated
indirectly from pH an PaCO2 values.
Normal [H+] 40 nmol/L first 2 decimals of
pH value.
For every 0.1 decrease in pH,
[H+] increases by 10nmol/L
• Thus, HCO3 can now be calculated from [H+] and PaCO2
using the Henderson equation.
[H+]=24 (PaCO2/ [HCO3])

32. Step 3 Identify the disorder
• Take a look at the pH, as it directs towards the
principal disorder.
< 7.35• Acidosis
>7.45 • Alkalosis
• Normal
7.35-
• Mixed
7.45
disorder

33. PCO2
HCO3
pH
pH

34. •Metabolic
HCO3 Disorder
•Respiratory
PaCO2 Disorder

35. During compensation HCO3¯ & PaCO2
move in the same direction

36. Compensatory changes (Respiratory disorders).
Primary Primary Compensatory Expected Compensation Limits of
disorder defect response compensation
Respiratory ↑ PCO2 ↑ HCO3 Acute: [HCO3]=38
acidosis + 1 Meq/L ↑ HCO3 for each ↑ Meq/L
PCO2 of 10mmHg
Chronic: [HCO3]=45
+4 Meq/L ↑ HCO3 for each ↑ Meq/L
PCO2 of 10mmHg
Respiratory ↓ PCO2 ↓ HCO3 Acute: [HCO3]=18
Alkalosis -2Meq/l ↓ in HCO3 for each ↓ in Meq/L
PCO2 of 10mmHg
Chronic: [HCO3]=15
-5 Meq/L ↓ in HCO3 for each ↓ in mEq/L
PCO2 of 10mmHg
1 4 2 5

37. Compensatory changes (Metabolic disorders).
Primary Primary Compensatory Expected Compensation Limits of
disorder defect response compensation
Metabolic ↓ HCO3 ↓ PCO2 PCO2=1.5[HCO3] + 8 ± 2 PCO2=15mmHg
acidosis PCO2= last 2 digits of pH X 100
PCO2= 15+ [HCO3]
Metabolic ↑ HCO3 ↑ PCO2 PCO2= + 0.6 mmHg for Δ [HCO3] of PCO2=55mmHg
Alkalosis 1 mEq/L
PCO2=15+ [HCO3]

38. Body’s physiologic response to Primary disorder
in order to bring pH towards NORMAL limit
Full compensation
Partial compensation
No compensation…. (uncompensated)
BUT never overshoots,
If a overshoot pH is there,
Take it granted it is a MIXED disorder

39. Step 5 Anion Gap
AG= Na⁺ – (Cl¯ + HCO3¯)
• Normal range is 10 ± 2 mEq /L
• It represents unmeasured anions. These
unmeasured anions can be;
– Anionic proteins
– SO4, PO4, organic anions
– Acid anions (acetoacetate, lactate, uremic anions)

40. • Anion gap can increase either due to:
– Increase in the unmeasured anions.
– Decrease in the unmeasured cations (
hypocal, hypomag)
• Anion gap may decrease due to:
– Increase in unmeasured cations (Ca, Mg, K)
– Addition of abnormal cations (Li)
– Decrease in albumin ( each 1g/dl decrease of alb
decrease AG by 2.5 mEq/L)

41. Step 6 & 7 Detecting mixed
disorders
Clues to the presence of a mixed disorder.
• Clinical history
• pH normal, abnormal PCO2 n HCO3
• PCO2 n HCO3 moving opposite directions
• Acid Base map (Flenley Nomogram)
• Degree of compensation for primary disorder is
inappropriate
• Find Delta Gap

42. Flenley Nomogram

43. • Compensation in excess points towards a mixed
disorder.
• Example: In a case of primary metabolic acidosis,
HCO3=12
Expected compensated PCO3 will be 24-28
(PCO2=1.5XHCO3 + 8 ± 2)
If, PCO2 is < 24, Metabolic acidosis + Respiratory Alkalosis
If, PCO2 is > 28, Metabolic acidosis + Respiratory Acidosis

44. Δs for metabolic acidosis
• Every increase in unmeasured anion (Δ
AG), should be met with similar decrease in
HCO3 (Δ HCO3).
• Thus, Δ AG= Δ HCO3 in a case of simple AG
metabolic acidosis
• However,
If, Δ AG is > Δ HCO3= AG Metabolic acidosis +
Metabolic alkalosis

45. Delta gap
Delta ratio =∆AG/ ∆HCO3
= (observed AG-12)/ (24- obs HCO3)
• <1 =High anion gap & normal AG acidosis
• 1-2= Pure anion gap metabolic acidosis
• >2 = High anion gap acidosis with concurrent
metabolic alkalosis

46. Significance of Δ Cl
• Normally the values of Cl change according to the
hydration stature or Na
• If this proportional change is absent, then it
indicates an acid base disorder.
If there is a disproportionate decrease of Cl=
Metabolic alkalosis or Respiratory acidosis
If there is a disproportionate increase of Cl=
Metabolic acidosis or Respiratory alkalosis

47. "Step –wise approach"
for ABG analysis 1. Consider the Clinical Setting.
2. Obtain ABG and Electrolyte values
simultaneously.
3. Verify the ABG values.
4. Identify the nature of the disturbance.
5. Calculate the Anion gap in case of MA.
6. Assess ∆AG, ∆ HCO3, ∆Cl & ∆Na
7. Detecting mixed disorders.
8. Clinical correlation

48. Interpretation with examples

49. Clinical examples

50. Example 1
• A 19 year old pregnant insulin dependent
diabetic patient was admitted with a history of
polyuria and thirst. She now felt ill and presented
to hospital. There was a history of poor
compliance with medical therapy.
• She was afebrile. Chest was clear. Circulation was
adequate. Urinalysis: 2+ ketones, 4+ glucose.
• Na+ 136, K+ 4.8, Cl- 101, pH 7.26, pCO2 16 mmHg,
pO2 128 mmHg, HCO3 7.1 mmol/l

51. • Clinical possibilities:
– Diabetic ketoacidosis
– Lactic acidosis
– Hyperchloremic metabolic acidosis
– Respiratory acid-base disturbances
• Check the internal validity of the report. Observed
HCO3 report= 7.1, calculated HCO3= 7 CORRECT
• Look at the pH: 7.26 ACIDOSIS
• Then find the primary disorder: Low HCO3 along
with low pCO2 suggests a METABOLIC disorder.

52. • Check for compensation: compensation for
metabolic acidosis brings pCO2 to 16.5-20.6
mmHg. Thus the acidosis is FULLY COMPENSATED
by respiratory regulation and there is
NO MIXED disorder.
HIGH ANION
• Anion Gap= 136-(101+7.1)=28.1 GAP acidosis
• ∆AG=27.9-12=15.9, ∆HCO3=24-7.1=14.9
• Delta ratio=15.9/14.9=1.07 PURE ANION GAP
ACIDOSIS
• Na is normal with low Cl (NO HYPERCHLOREMIA)
PURE ANION GAP
FINAL ABG DIAGNOSIS
METABOLIC ACIDOSIS
(Etiology, DKA)

53. Example 2
• A 60 year old woman was admitted with lobar
pneumonia. She was on a thiazide diuretic for 9
months following a previous admission with
congestive cardiac failure. The admission arterial
blood results were:
• pH 7.64
• pCO2 32 mmHg
• pO2 75 mmHg
• HCO3 33 mmol/l
• K+ 2.1 mmol/l

54. • Clinical possibilities:
– Severe hypokalemis to be corrected immediately
– Respiratory acidosis (respiratory failure)
– Respiratory alkalosis (dyspnea)
– Metabolic alkalosis (diuretics)
• Look at the pH: 7.64 ALKALOSIS
• Then find the primary disorder: Low pCO2 along
with high HCO3 suggests a
MIXED ALKALOSIS.

55. Check for compensation:
• Considering Chronic respiratory alkalosis, expected
HCO3 is 20mEq/l on maximal compensation.
Observed value is much higher so a Metabolic
alkalosis should be present.
• Considering Metabolic alkalosis, predicted pCo2
after compensation is 43mmHg. The observed value
is much lower so a respiratory alkalosis should be
present.
FINAL ABG DIAGNOSIS
MIXED METABOLIC &
RESPIRATORY ALKALOSIS

56. For the audience
Ph 6.99
PCo2 10.5 mmHg
P02 111 mmHg Expected fall in PCO2
BE -29 mmol/L =(1.5 x HCO3)+8
HCo3 2.6 = (1.5 x 2.6) +8 2
= 9.9 to 13.9
Tco2 45
Thus the compensation is
SO2 95 within limits and the
Na+ 138 mmol/L diagnosis is
K+ 4.2 mmol/L COMPENSATED
iCa+ 1.06 mmol/L METABOLIC ACIDOSIS
Hb 12.6 g/dl

57. For the audience
Primary dis- Respiratory alkalosis.
For acute Resp. alkalosis---
Expected HCO3
= 24- 2(40-19)/10
= 19.8
but actual HCO3=13.5 which is
less then the expected.
So it is mixed disorder with
Respiratory alkalosis with
Metabolic acidosis

58. “Understanding ABG is not
magic but an art learned by
continued practice”

59. THANK YOU