1. Step by step approach to Arterial
Blood gas analysis

2. What does an ABG look like?
 pH : 7.40 (7.35 – 7.45)
 PCO2 : 40 mm Hg ( 35 – 45 )
 PO2 : 80 – 104 mm Hg
 HCO3 (act) : 24 ± 2 m Eq/L
 HCO3 (std) : 24 ± 2 m Eq/L
 BE : ± 2
 O2 sat : 96% - 98%
 A-a DO2 :

3. What does an ABG look like? (Contd.)
 Na+ : 135 – 148 m mol / L
 K + : 3.5 – 5.5 m mol / L
 Ca + + : 1.13 – 1.32 m mol / L
 Cl– : 98 – 106 m mol / L
 Anion gap : 12(± 4) mMol / L
 Lactate

4. What is pH?
 It is the negative logarithm of H+ ion concentration in
aqueous solution → the extracellular fluid.
 As it is the -ve logarithm → pH↓ as H+ concentration ↑
 Changes in pH are not linearly related to changes in [H+ ]
 pH of 6.8 – 7.8 ( [H+ ] 160-16 nEq/L ) is compatible with life
pH = 6.1 + log (HCO3)
(0.03) × (PCO2)
pH > 7.45 Alkalemia / Alkalosis
pH < 7.35 Acidemia / Acidosis
Henderson-Hasselbach
Equation

5. 100
90
80
70
60
50
40
30
20
H+
(neq/L)
pH
7.0
7.05
7.1
7.3
7.4
7.7
7.5
Relationship between hydrogen ion activity and pH
pH
Normal = 7.35 – 7.45
Acidemia < 7.35
Alkalemia > 7.45

6. Daily acid load & acid-base homeostasis
 Carbohydrate & Lipid metabolism generates volatile
acids (CO2) → 15000mmol/day
 Protein metabolism generates non volatile acids ( H+)
→ 50-100 mmols/day
 Both lungs & kidneys are responsible for maintaining acid-
base homeostasis by excreting these acids
 Alveolar ventilation allows for excretion of CO2
 Kidneys excrete the daily H+ load & reabsorbs filtered HCO3

7. Physiological response to change in acid
base status
 Body regulates pH within normal range with 3 lines
of defence :
– Buffers
– Respiratory regulation
– Renal regulation

8. Buffer systems of the body
 Extracellular
- Bicarbonate- carbonic acid:
quantitatively the largest
H2O + CO2 ↔ H2CO3 ↔ H+ + HCO3
Catalysed by Carbonic Anhydrase
enzyme
Bicarbonate buffer is effective
against metabolic but not
respiratory acid base
disturbances
 Intracellular
– Protein buffer system
Tissues and plasma
– Phosphate buffer system
RBC’s & kidney tubules
– Hemoglobin buffer system
RBC’s
– Bone buffer system

9. Physiological response to change in acid base status
• Respiratory regulation :
– Central chemo-receptors in the medulla → [H+] in CSF
– Peripheral chemo-receptors at carotid & aortic bodies→
[H+], PaCO2, PaO2 & perfusion pressure
– Regulate excretion of CO2 by ↑/↓ the rate & depth of breathing
– Respiratory regulation acts rapidly (30-120 minutes) & has
double the buffering power as compared chemical buffers
 Renal regulation :
– Maintains pH by regulating plasma HCO3 concentration
– Most powerful buffering system → relatively slow → 2-3 days
for peak effect.
-

10. Indicators of extracellular acid-base status
• Base Buffer(BB) = Buffering capacity of blood.
• BB = HCO-
3 + A- (Non-volatile acid buffers)
• Base excess is a quantification of the metabolic acidosis /alkalosis
• Defined as the amount of acid or base that must be added to a
sample of whole blood in vitro to restore the pH of the sample to
7.40 while PaCO2 is at 40mm Hg. Normal range 0 + 2.5 mMol
 Standard Base excess: Copenhagen concept:
- Base excess of whole blood together with interstitial fluid
(ECF) in vivo.
- An ideal metabolic index independent of PaCO2
- SBE = 0.93[ HCO3
-- 24.4] + 13.79 [pH - 7.4]

11. The Arterial Blood Gas Report
 Sample should be analysed within 15 minutes of
collection
 Anti-coagulated prior to transport
 Measurement of pH or H+ ,pCO2, pO2 at 37oC with a
glass electrode
 HCO3 & Base excess is derived from the pH & pCO2 →
Siggaard Andersen’s Nomogram

13. Compensatory Responses
 Opposes & limits the effect of the primary change of an acid
base disturbance on the plasma H+ ion conc.
 Are usually not complete.
 Have well defined limits & a characteristic time course.
 Affect the component not involved in the primary change.
 If expected change = actual change, disorder is simple
 If expected change is more or less than actual, disorder is
mixed

14. Relationship between FiO2 And PaO2
 Alveolar Gas Eq: ( PB – PH20 ) FiO2 – PaCO2 / RQ
 (760mmHg -- 47mmHg)0.21 - 40/ 0.8 = 97-105 mm Hg
 PaO2 / FiO2 ratio: 105 / 0.21 = 500 (>500 is normal)
 % of O2 × 5 = Predicted minimum PaO2
( 40 % × 5= 200 mm Hg)
 Normal PO2: 80 – 104 mm Hg on room air
< 80 mm Hg is Hypoxaemia
 Age: For every year of age above 60 yrs acceptable PO2 ↓es
by 1 mm Hg below 80
 New born: Acceptable range :– 40 – 70 mm Hg

15. Respiratory acidosis
 Primary change is ed PaCO2  ed pH
 For each 10 mm Hg ed in PaCO2 – pH es by 0.05
 pH = 0.005 x PaCO2
 Compensation for acute respiratory acidosis:
HCO3es by 1mEq/L for each 10 mm Hg  in PaCO2
Expected pH = 7.40-[0.005x(PaCO2 – 40)]
Expected HCO3 = 24+ [0.1x(PaCO2 - 40)]
 Compensation for chronic respiratory acidosis:
HCO3es by 4–5 mEq/L for each 10 mm Hgin PaCO2.
pH = 0.003x PaCO2
Expected pH = 7.40 - [0.003x(PaCO2-40)]
Expected HCO3 = 24+ [0.4x(PaCO2 - 40)]

16. Causes of Respiratory Acidosis
 SEVERE ACUTE ASTHMA
 COPD
 ALVEOLAR HYPOVENTILATION
 CNS DEPRESSION
 THORACIC CAGE RESTRICTION

17. Respiratory Alkalosis
 Primary change is ed PaCO2  ed pH
 For each 10 mm Hg  PaCO2  pH es by 0.1
 pH = 0.008 x PaCO2
 Compensation for acute respiratory alkalosis:
HCO3 es 2 mmol /L for every 10 mm Hg  PaCO2
Expected pH = 7.40+ [ 0.008x (40-PaCO2) ]
Expected HCO3 = 24 - [0.2x(40 -PaCO2 )]
 Compensation for chronic respiratory alkalosis:
HCO3 es 4-5 mmol/ L for every 10 mm Hg PaCO2
Expected pH = 7.40 +[ 0.003x (40-PaCO2) ]
Expected HCO3 = 24 - [0.4x(40 - PaCO2 )]

18. Causes of Respiratory Alkalosis
 HYPOXAEMIA
 CENTRAL CAUSES
 FEVER
 ANXIETY
 HORMONES –
Catecholamine, progesterone
 DRUGS
Salicylates, analeptics
 SEPSIS
 HYPERTHYROIDISM
 PREGNANCY
 CIRRHOSIS
 PULMONARY OEDEMA
 PULMONARY EMBOLISM
 PNEUMONIA
 VENTILATOR INDUCED

19. Metabolic Acidosis
 Primary change is ed HCO3/ ed H+  ed pH
 For each  in HCO3 of 7 – 7.5 m mol/ L pH es by 0.1
COMPENSATORY CHANGE IS ed PaCO2
 Expected PaCO2 = 1.5  HCO3 + 8 ( 2)
(Winter’s formula)

20. Anion Gap
 It is an acid base parameter that is used to evaluate patients
with metabolic acidosis to determine whether the problem is
due to accumulation of H+ ions -- High Anion Gap (eg. Lactic
acidosis)
 or due to loss of HCO3 ions -- Normal Anion Gap (eg.
Diarrhea)

21. Concept of Anion Gap
 To achieve electrochemical balance, ionic elements in
ECF must have a net zero charge
 So Anions must balance Cations -
(Na+) + (U Cations) = (Cl + HCO3) + (U Anions)
(Na+) – (Cl + HCO3) = (U Anions – U Cations )
= Anion Gap

22. Concept of Anion Gap ( contd)
 Unmeasured Anions (UA): Proteins (15)+ organic acids (5)
+ Phosphates(2) + Sulphates(1)  23 mEq / L
 Unmeasured Cations (UC): Calcium(5) + Potassium (4.5) +
Magnesium(1.5)  11 mEq / L
 Normal Anion Gap (AG) = 12 ± 4 mEq/L
 When organic acids like Lactic acids , Ketoacids, Ethanol
, they cause ed anion gap ( AG > 20 mEq / L)

23. Anion gap- influence of albumin
 Albumin is the major source of unmeasured anion
 With hypoalbuminemia, 50% reduction in albumin es
anion gap by 75%.
 Adjusted anion gap = Observed anion gap + 2.5 [4.5-
measured albumin]
 For eg. If Albumin is 2.5, and the observed AG is 10, then
the adjusted AG = 10 + 2.5 (4.5-2.5) = 15
 Normal AG = 2(Albumin gm/dL)+ 0.5(Phos mg/dL)

24. Causes of High Anion Gap Acidosis
( H+ accumulation)

25. Causes of Normal Anion Gap Acidosis
 G.I. LOSS OF BICARB
1. Diarrhea
2. Uretero sigmoidostomy
 RENAL BICARB LOSS
Proximal Type II RTA
[Urine pH < 5.5, Urine AG –ve, serum K+ ,SBE -6 to -15mEq/L,]
1. Fanconi’s syndrome
2. Carbonic Anhydrase inhibitors
3. Ileal bladder

26. Causes of Normal Anion Gap Acidosis
 REDUCED RENAL H+ SECRETION
1 ─ DISTAL RTA Type I
[ Urine pH > 5.5,UAG +ve ,↓Serum K+, SBE< - 15 mEq/L]
Familial, Sjogren’s syndrome, Autoimmune diseases,
Amphotericin, Renal Transplant
2 – TYPE IV RTA
[Urine pH < 5.5, UAG +ve /Serum K+ ,SBE= -6 to -8 mEq/L]
Hyporeninemic–Hypoaldosteronism, DM, NSAIDS
Addison’s Disease, chronic heparin therapy

27. Causes of Normal Anion Gap Acidosis
3 – Inadequate renal response to mineralocorticoids –
SLE, K+ sparing diuretics
4 – Early Uremia
HCL/HCL PRECURSOR INGESTION:
HCl, NH4Cl, NaCl, Arginine HCl
OTHERS:
- Post Chronic hyperventilation
- Recovery from DKA
- Toluene Inhalation

28. Metabolic Alkalosis
 Primary change is ed HCO3 / or ed H+ → ed pH
 For each  in HCO3 of 7-7.5 mEq/L - pH es by 0.1
Respiratory compensation- ed PaCO2
(Not very common)
 Expected PaCO2 in Metabolic Alkalosis:
 0.7 × HCO3 + 21 ( ±2)

29. Classification of Metabolic Alkalosis
 Chloride Responsive:
Urinary chloride < 15m Eq/L
1 – Loss of gastric acid – vomiting/NG Tube
2 – Diuretics (long term use)
3 – Volume depletion
4 – Chloride losing diarrhea
5 – Post - hypercapnia

30.  Chloride Unresponsive:
Urinary chloride > 25m Eq/L
1 – Potassium depletion
2 – Diuretics (Recent use)
3 – Mineralocorticoid Excess
4 – Primary hyper aldosteronism
5 – Cushing’s disease
6 – Ectopic ACTH
Classification of Metabolic Alkalosis

31. Correction of Alkalosis
 Saline infusion for Cl- responsive alkalosis
 Chloride deficit (mEq) = 0.3 X WT. (kg) x (100 –
Plasma Cl-)
 Volume of Isotonic Saline (L): Chloride deficit / 154
• For Chloride Unresponsive--
Correct Hypokalemia, Mineralocorticoid &
glucocorticoid excess.

32. Identifying the Obvious Disorder
Disorder pH pCO2 HCO3
-
Metabolic
Acidosis
Decreased Decreased Decreased
Metabolic
Alkalosis
Increased Increased Increased
Respiratory
Acidosis
Decreased Increased Increased
Respiratory
Alkalosis
Increased Decreased Decreased

33. How to read an ABG?
 STEP – 1 : First look at the pH
* Acidemia - ed pH
* Alkalemia - ed pH
* Normal -  pH
 STEP – 2 : If acidemia is there – Check PaCO2
* Normal – Metabolic acidosis
* Low – Metabolic acidosis
* High - Respiratory acidosis

34.  If pH is Acidemic and PaCO2 is Normal OR Low :
* Then calculate the difference between measured
and expected PaCO2
Expected PaCO2 = 1.5 x HCO3 + 8 (±2)
* If pH is Acidemic and PaCO2 is High:
* Then determine the change in pH & HCO3- to decide
whether Chronic or Acute , and if there is any other
superimposed problem
How to read an ABG?

35. How to read an ABG?
 Acute Respiratory Acidosis
– Expected pH= 7.4 – [0.005x(PaCO2 - 40)]
– Expected HCO3 = 24+ [0.1x(PaCO2 - 40)]
 Chronic Respiratory Acidosis
– Expected pH= 7.4 – [0.003x(PaCO2 - 40)]
– Expected HCO3 = 24+ [0.4x(PaCO2 - 40)]

36.  STEP – 3 : If Alkalemia is there – Check PaCO2
* If pH is Alkalemic and PaCO2 is Normal or High
It indicates Primary Metabolic Alkalosis
 Then compare measured and expected PaCO2 to
identify any associated Respiratory disorder
 Expected PaCO2 in Metabolic Alkalosis:
 0.7 × HCO3 + 21 ( ±2)
How to read an ABG?

37.  STEP – 3 (contd)
* If pH is Alkalemic and PaCO2 is Low
It indicates Primary Respiratory Alkalosis
Then we determine the change in pH & HCO3- to decide
whether Acute or Chronic, and for any other
superimposed problem
How to read an ABG?

38. How to read an ABG?
 Acute Respiratory Alkalosis
– Expected pH= 7.4 + [0.008x(40 - PaCO2)]
– Expected HCO3 = 24 - [0.2x(40 -PaCO2 )]
 Chronic Respiratory Alkalosis
– Expected pH= 7.4 + [0.003x(40 - PaCO2 )]
– Expected HCO3 = 24 - [0.4x(40 - PaCO2 )]

39.  STEP – 4 :
If Normal pH – Check PaCO2, can be High or Low
* High PaCO2 indicates a Mixed Respiratory Acidosis
– Metabolic Alkalosis
* Low PaCO2 indicates a Mixed Respiratory Alkalosis
– Metabolic Acidosis
How to read an ABG?

40.  STEP – 5 :
If Metabolic Acidosis is diagnosed –
Check Anion Gap
How to read an ABG?

41. Some examples
 pH = 7.52 PCO2 = 26 mm Hg
 PO2 = 105 mm Hg HCO3 = 21 m mol / L
 BE = - 3 SaO2 = 99%
 Na+ = 138 m mol / L K+ = 3.8 m mol / L
 Cl- = 104 m mol / L Anion Gap = 13
Acute Respiratory Alkalosis

42. Examples
 pH = 7.3 PCO2 = 60 mm Hg
 PO2 = 60 mm Hg HCO3 = 26 m mol / L
 BE = + 2 SaO2 = 89 %
 Na+ = 140 m mol / L K+ = 4 m mol / L
 Cl- = 100 m mol / L
Acute Respiratory Acidosis

43. Examples
 pH = 7.44 PCO2 = 29 mm Hg
 PO2 = 100 mm Hg HCO3 = 19 m mol / L
 BE = - 5 SaO2 = 98 %
 Na+ = 137 m mol / L K+ = 3.7 m mol / L
 Cl- = 108 m mol / L
Chronic Respiratory Alkalosis

44. Examples
 pH = 7.32 PCO2 = 70 mm Hg
 PO2 = 62 mm Hg HCO3 = 32 m mol / L
 BE = + 8 SaO2 = 90 %
 Na+ = 136 m mol / L K+ = 3.5 m mol / L
 Cl - = 96 m mol / L
Chronic Respiratory Acidosis

45. Examples
 pH = 7.30 PCO2 = 30 mm Hg
 PO2 = 80 mm Hg HCO3 = 10 mmol / L
 BE = - 14 SaO2 = 95 %
 Na+ = 139 m mol / L K+ = 4.1 m mol / L
 Cl- = 100 m mol / L Anion Gap = 29
High Anion Gap Metabolic Acidosis with Respiratory
Acidosis
Expected PaCO2:
(HCO3)  1.5 + 8 (±2) = 10  1.5 + 8 (±2)
= 21 – 25 mm Hg

46. Examples
 pH = 7.50 PCO2 = 50 mm Hg
 PO2 = 75 mm Hg HCO3 = 40 mmol / L
 BE = + 16 SaO2 = 95 %
 Na+ = 132 m mol / L K+ = 3.1 m mol / L
 Cl- = 88 m mol / L Anion Gap = 4
Compensated Metabolic Alkalosis
Expected PaCO2:
(HCO3)  0.7 + 21 (±2) = 40  0.7 + 21 (±2)
= 47 – 51 mm Hg

47. Mixed acid-base disorders
 Mixed Metabolic acidosis and Metabolic alkalosis:
 Essential clue to mixed disorders is the Anion gap ─ HCO3
Relationship
 AG/  HCO3 ---- Called gap-gap
 AG excess/ HCO3 deficit
 (AG - 12/24 - HCO3)
 For high Anion Gap acidosis --- AG/HCO3 1
 For Hyperchloremic (normal) AG acidosis --AG/HCO3  0

48.  For metabolic acidosis with metabolic alkalosis ---
AG/HCO3 1.5
 i.e. Change in AG excess is greater than change in
HCO3 deficit
 TRIPLE DISORDERS:
Combination of metabolic acidosis and metabolic
alkalosis combined with either respiratory acidosis or
respiratory alkalosis

49. Examples of mixed disorders
 pH : 7.55
 PCO2 : 30 mm Hg
 PO2 : 104 mm Hg
 HCO3 : 29mmol/L
 BE : +5
 Sats : 99%
 Na+ : 135mmol/L
 K+ : 3.5mmol/L
 Cl- : 95mmol/L
 Anion Gap: 11
Respiratory
Alkalosis with
Metabolic
Alkalosis

50.  pH : 7.36
 PCO2 : 34 mm Hg
 PO2 : 100 mm Hg
 HCO3 : 16mmol/L
 BE : -8
 Sats : 98%
 Na+ : 140mmol/L
 K+ : 3.5mmol/L
 Cl- : 98mmol/L
 Anion Gap : 26
High Anion Gap
Metabolic Acidosis with
Metabolic Alkalosis with
Respiratory
compensation
ΔAG / Δ HCO-
3 =
(26-12) / (24-16) = 1.75

51.  pH : 7.40
 PCO2 : 28 mm Hg
 PO2 : 60 mm Hg
 HCO3 : 15mmol/L
 BE : -9mmol/L
 Sats : 90%
 Na+ : 140mmol/L
 K+ : 3.5mmol/L
 Cl- : 98mmol/L
 Anion Gap : 27
High Anion Gap
Metabolic Acidosis with
Metabolic Alkalosis with
Respiratory Alkalosis –
“Triple disorder”
ΔAG / Δ HCO-
3 = 15/9
= 1.66

52.  pH : 7.16
 PCO2 : 44 mm Hg
 PO2 : 96 mm Hg
 HCO3 : 13 mmol/L
 BE : -12mmol/L
 Sats : 96%
 Na+ : 145mmol/L
 K+ : 5.5mmol/L
 Cl- : 115mmol/L
 Anion Gap : 17
 Albumin : 2gm/dL
 Lactate : 3.8 mmol/L
Respiratory Acidosis with
Metabolic Acidosis
Adjusted Anion Gap =
17 +[2.5x(4.5-2)] = 23
ΔAG / Δ HCO-
3= 11/11=1
High Anion Gap
Expected PaCO2 = 29-30 mmHg
1.5 X (HCO3=13)+8 ± 2
Severe Pancreatitis + Septic
Shock + AKI + ARDS

53. Examples
 pH = 7.30 PCO2 = 30 mm Hg
 PO2 = 80 mm Hg HCO3 = 10 mmol / L
 BE = - 14 SaO2 = 95 %
 Na+ = 139 m mol / L K+ = 4.1 mmol / L
 Cl- = 100 m mol / L Anion Gap = 29
 Lactate = 5.8 Albumin = 2.5
High Anion Gap Metabolic Acidosis with Respiratory Acidosis
Adjusted Anion Gap= 29+[2.5(4.5-2.5)]= 35
∆AG/ ∆HCO3 = 23/14 = 1.65
+ Metabolic Alkalosis → “Triple disorder”
Expected PaCO2:
(HCO3)  1.5 + 8 (±2) = 10  1.5 + 8 (±2) = 21 – 25 mm Hg

54.  pH : 7.45
 PCO2 : 15 mm Hg
 PO2 : 101 mm Hg
 HCO3 : 10mmol/L
 BE : -14mmol/L
 Sats : 90%
 Na+ : 140mmol/L
 K+ : 3.5mmol/L
 Cl- : 100mmol/L
 Anion Gap : 30
 Albumin : 2.5
 Lactate : 1.5
High Anion Gap Metabolic
Acidosis with Respiratory
Alkalosis
Adjusted AG = 30+ 5= 35
ΔAG / Δ HCO-
3 = 23/14 = 1.65
+ Metabolic Alkalosis →
“Triple disorder”
Acute posterior circulation
stroke + Sepsis + Acute on
CKD → Given mannitol

55. Thank you!

56. Concept of Urinary Anion Gap
 UAG = (Urinary [Na] + Urinary [K]) – (Urinary [Cl])
 UAG is normally zero or slightly positive
 Helps to identify the source of HCO3 loss in non-anion
gap acidosis when the cause is not clinically evident
 With GI losses the UAG becomes negative (-20 to -50
mEq/L)
 No utility in the setting of hypovolemia, oliguria,
hyponatremia

57. How to read an ABG
 Checking the Reports Validity.
 Calculate H+ ion concentration from the formula.
 H+ = 24 X pCO2/HCO3
-
 This should correspond to the H+ ion
concentration of the pH in the ABG report.

58. Estimating H ion conc from pH
pH 6.70 6.75 6.80 6.85 6.90 6.95 7.00 7.05 7.10 7.20 7.25
H+
ion
200 178 158 141 126 112 100 89 79 63 56

59. Estimating H ion conc from pH
pH 7.30 7.35 7.40 7.45 7.50 7.55 7.60 7.6
5
7.70 7.75 7.80
H+
ion
50 45 40 35 32 28 25 22 20 18 16

60. Stewart’s approach – The strong ion
difference
 “Strong ion” is one that completely or near completely
dissociates in water ( Na+, K+, Ca++, Mg++ & Cl- )
 In blood plasma strong cations outnumber strong anions
 (Na+K+Mg+Ca) – (Cl+Lactate) = apparent SID (40 to 42
meq/L)
 SID normally regulated by the kidneys through excretion of Cl-
 Metabolic acidosis  SID decreases
 Metabolic alkalosis  SID increases

61. Stewart’s approach – The strong ion difference
 SIDa – SIDe = SIG ( strong ion gap)[ N = 0]
 +ve SIG – umeasured anions > cations
 -ve SIG – unmeasured cations > anions
 Anion gap AG = SIG + A-
 A- = 2(albumin gm/dL) +0.5(PO4 mg/dL)
 SID – (CO2 + A- ) = 0.
 Remaining negative charge on a blood sample = effective
SID (SIDe)
 SIDe = SID = buffer base(BB) = CO2+ A-
 Standard base excess (SBE) = change in SID, where pH =
7.4 and pCO2 = 40 mm of Hg.

63. Plots of pH and H+ conc against
Strong Ion Difference
1
2
3
4
5
6
7
8
9
10
-10 0 10 20 30 40 50 60 70 80
10
20
30
40
50
60
70
80
90
100
H+
nmol/L
SID meq/L
pH

64. Strong Ion difference in critical care
 Critically ill patients have increased SIG values.
 Increased SIG correlates with mortality.
 Causes:
 Saline loading
 Unmeasured anions in resuscitation fluids.
 Sepsis
 Hypoalbuminemia
 Endogenous ketones and sulfate
 Acute phase proteins
 Cytokines and chemokines.

67. Stewart approach
Gilfix et al. [13] and then Kellum et al. [14] used this approach to
determine the cause of metabolic acidosis in critically ill patients.
the Stewart approach
could detect unmeasured ions in the plasma of critically
ill patients far more readily than the more traditional
methods of base excess or anion gap. Unidentified
anions or cations have been identified in the plasma of
patients with sepsis [17] and liver dysfunction [18]. The
cause of this unexplained ion load in liver dysfunction
has been shown to be an increased release of anions
from the liver during endotoxemia [11]. This increase in
anion load causes a decrease in the SID, resulting in an
increase in the dissociation of water to H+ to compensate
for the charge imbalance and thus an acidosis

69. Basic terminologies
 Normal pH = 7.4 ± 0.05 (7.35 – 7.45)
– Acidosis if pH <7.35
– Alkalosis if pH >7.45
 Normal PaCO2 = 40 ± 5 (35 – 45)
– Respiratory disorder refers to disorder that results from
a primary alteration in PaCO2 due to altered CO2
elimination.
 Normal HCO3 = 24 ± 2 (22 – 26)
– Metabolic disorder refers to disorder that results from a
primary alteration in HCO3.

70. Copenhagen Approach: Concept of Base
Excess
Base Buffer(BB) = Buffering capacity of blood.
= HCO-
3 + A- (Non-volatile acid buffers)
Base excess is a quantification of the metabolic acidosis/alkalosis
The amount of acid (H+) or base (HCO3-) that must be added to a
sample of whole blood in vitro to restore the pH of the sample to
7.40 while PaCO2 is at 40mm Hg at full O2 saturation & at 37C
Normal range 0 + 2.5 mM
 It is usually derived from a monogram
 A negative value indicates Metabolic Acidosis and a positive value
indicates Metabolic Alkalosis

71. Copenhagen Approach
 Standard Base Excess(SBE) – Base excess
of whole blood together with interstitial fluid
in vivo
 Copenhagen concept: An ideal metabolic
index independent of PaCO2
 SBE = 0.93[ HCO3
-- 24.4] + 13.79 [pH - 7.4]
 Ref Range: -3 to +3 mEq/L

72. Primary Acid Base Disorders
 Normal ranges for pH, PCO2 and HCO3 concentration in
extracellular fluid as reference points are –
• pH = 7.36 to 7.44
• PCO2 = 36 to 44 mm Hg
• HCO3 = 22 to 26 mEq/L
 A change in either the PCO2 or HCO3 will cause a change
in the pH of extracellular fluid.
[H+] = 24 X ( PCO2/HCO3)

73. Primary Acid Base Disorders
 Respiratory Acid Base Disorder involves change in
PCO2
 Increase in PCO2 is respiratory acidosis
 Decrease in PCO2 is respiratory alkalosis
 Metabolic Acid Base Disorder involves change in
HCO3
 Decrease in HCO3 is metabolic acidosis
 Increase in HCO3 is metabolic alkalosis
 Suffix emia is used to describe the acid–base
derangement in blood
 Acidemia is the condition where pH falls below 7.36
 Alkalemia is the condition where the pH rises above 7.44

74. Secondary/”Compensatory” Changes
Primary Disorder Primary Change Secondary Change
Respiratory acidosis Increased PCO2 Increased HCO3
Respiratory alkalosis Decreased PCO2 Decreased HCO3
Metabolic acidosis Decreased HCO3 Decreased PCO2
Metabolic alkalosis Increased HCO3 Increased PCO2

75. Why to calculate the “compensation”
 Importance of calculating the “compensation” lies
in differentiating simple disorders from mixed
disorders
– If expected change = actual change, disorder is simple
– If expected change is more or less than actual,
disorder is mixed
– “Compensation” follows “rule of same direction”-if
changes are in opposite direction, think of mixed
disorder
– “Compensation” never overcorrects, so if more than
predicted, think of mixed disorder

76. Concept of pH
• [H+ ] in aqueous solution is traditionally expressed by pH
 It is the negative logarithm of H+ ion concentration in the
extracellular fluid
pH = log(1/ [H+ ]) = - log[H+ ]
 It varies in opposite direction to changes in [H+ ], ie. pH
decreases as H+ increases
 Changes in pH are not linearly related to changes in [H+ ]
• pH of 6.8 – 7.8 ( [H+ ] 150-50 nEq/L ) is compatible with
life

78. Henderson-Hasselbalch Equation
pH = 6.1 + log (HCO3)
(0.03) × (PCO2)

79. Hydrogen Ion concentration
 Hydrogen ion concentration [H+] in extracellular fluid is determined
by the balance between the partial pressure of CO2 and the
concentration of HCO3- in the fluid
 [H+](nEq/L)= 24x(PCO2/HCO3-)
 Using Normal arterial PCO2 of 40mm Hg and normal HCO3-
concentration of 24 mEq/L, the normal [H+] in arterial blood is
24 X ( 40/24 )= 40nEq/L [H+] = pH= 7.40
Is Necessary For Cellular Enzymes To Work
• A stable [H+] concentration of 40 mEq/L is required for all cellular
enzymes to work

80. How to read an ABG?
 Acute Respiratory Acidosis
– Expected pH= 7.4 – [0.008x(PaCO2 - 40)]
– Expected HCO3 = 24+ [0.1x(PaCO2 - 40)]
 Chronic Respiratory Acidosis
– Expected pH= 7.4 – [0.003x(PaCO2 - 40)]
– Expected HCO3 = 24+ [0.4x(PaCO2 - 40)]

81. Response of the body
 Extracellular buffering : Immediately
 Respiratory compensation: Minutes
 Intracellular and bone buffering: Hours
 Renal excretion of the H+ ion load: Hours to days

82. Oxygenation
 Normal PO2: 80 – 104 mm Hg on room air
< 80 mm Hg is Hypoxaemia
 Age: For every year of age above 60 yrs
acceptable PO2 ↓es by 1 mm Hg below 80
 New born: Acceptable range :– 40 – 70 mm Hg