This document discusses acid-base balance and disorders. It defines the anion gap and explains how it is calculated. Causes of increased or decreased anion gap are explained. Acid-base disorders are classified as simple or complex based on whether HCO3- or PCO2 is affected alone or together. The document outlines the primary event, compensation, and correction stages of acid-base disorders. Specific types of disorders discussed include respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Key lab findings and treatments are provided for each disorder type.

1. ACID BASE BALANCE
Dr. Ifat Ara Begum
Assistant Professor
Dept. of Biochemistry
Dhaka Medical College
Dhaka

2. DAY-3
Anion Gap
ABD, their compensation &
correction

3. ANION GAP (AG)
It is the arithmetic approximation of the
difference between routinely measured
cations (Na & K) and anions (Cl & HCO3)
in plasma.
It is based on the principle of the “LAW
OF ELECTRICAL NEUTRALITY”

5. ANION GAP = UA – UC

6. CONTD
Total Anions = Total Cations
Cl- + HCO3
- + UA = Na+ + K+ + UC
UA – UC = (Na+ + K+ ) – (Cl- + HCO3
- )
This (UA – UC) representing the plasma
anion gap here.

7. CONTD
So, we can write:
Anion Gap = (Na+ + K+ ) – (Cl- + HCO3
- )
Normal range: 8 – 16 mEq/L (when K level is
ignored)

8. CONTD
Since plasma K+ concentration doesn’t
vary that much , it can be written as follow
as well:

9. CONTD
Normal range: 8 – 16 mEq/L (when K level is
ignored)

10. CONTD
UA: Plasma protein, phosphate,
sulphate, lactate, keto acid anions, other
organic acid anions
UC: Calcium, magnesium, gamma-
globulin

11. CAUSES OF INCREASED PLASMA ANION GAP
(REMEMBER, AG = UA-UC)
a) Any cause of increased UA:
Ketoacidosis
Lactic acidosis
Renal failure
Poisoning by alcohol, salicylates etc
Alkalosis, etc
b) Any cause of decreased UC:
Hypocalcemia
Hypomagnesaemia
Hypogammaglobulinemia

12. CAUSES OF DECREASED PLASMA ANION GAP
(REMEMBER, AG = UA-UC)
a) Any cause of decreased UA:
Hypoalbuminemia
b) Any cause of increased UC:
Hypercalcemia
Hypermagnesemia
Hyper gamma globulinemia

13. IMPORTANCE OF PLASMA ANION GAP
It helps to differentiate the causes of
metabolic acidosis
It helps to determine the nature of
metabolic acidosis (simple / complex)

14. Acid Base
Disorder
(ABD)

15. CLASSIFICATION OF ABD
1. Simple ABD: Abnormality in either HCO3
-
or PCO2 keeping the other component
normal. It may be metabolic (primary
change in HCO3-) /respiratory (primary
change in blood PCO2) type.
2. Complex / mixed ABD: Abnormality in both
component simultaneously.

16. TYPES OF SIMPLE ABD
Types of
simple
ABD
Primary
event/
defect
Unaffected
component
HCO3
-/PCO2
ratio
pH
Metabolic
Acidosis
↓ ed
HCO3
-
PCO2 ↓ ↓
Metabolic
Alkalosis
↑ ed
HCO3
-
PCO2
↑ ↑

17. CONTD
Types of
simple ABD
Primary
event/
defect
Unaffected
component
HCO3
-
/PCO2
ratio
pH
Respiratory
Acidosis
↑ PCO2 HCO3
- ↓ ↓
Respiratory
Alkalosis
↓ PCO2 HCO3
- ↑ ↑

18. TYPES OF COMPLEX ABD
Type of complex
ABD
Features Example
Double Face
Types
Combination of 2
disorders
M.Acidosis + R.
Acidosis
M. Acidosis + R.
Alkalosis
M. Alkalosis + R.
Acidosis
M. Alkalosis + R.
Alkalosis
Triple Face
Types
Combination of 3
disorders
M.Acidosis + M.
Alkalosis + R. Acidosis

19. EVENTS OF ABD ACCORDING TO TIME
1. Primary Event
2. Buffering by ICF & ECF buffers
3. Compensation / Secondary Event
4. Correction/ repair

20. CONTD
Primary Event: Initiating
process/processes of acid base disorder
which at least transiently alter pH by
altering either PaCO2 or HCO3
concentration.

21. CONTD
Secondary Event/ Compensation:
It follows primary event and
affects the unaffected component
between PaCO2 and HCO3 in line with the
affected component in primary event
with the objective to minimize the
alteration of pH.
May be complete (brought back to normal
limit)/ incomplete (if range is still outside
normal)

22. CONTD
If underlying problem is metabolic,
hyper/hypo ventilation may help :
respiratory compensation
If problem is respiratory, renal
mechanisms can bring about metabolic
compensation

24. CONTD
ABD Primary
event/defect
Unaffected
component
Secondary
event/
compensation
Metabolic
Acidosis
↓ HCO3
- PCO2 ↓ in PCO2
Metabolic
Alkalosis
↑ HCO3
- PCO2 ↑ in PCO2
Respiratory
Acidosis
↑ PCO2 HCO3
- ↑ in HCO3
-
Respiratory
Alkalosis
↓ PCO2 HCO3
- ↓ in HCO3
-

25. CORRECTION
Removal of the cause of ABD
Renal activity to normalize plasma
bicarbonate concentration:
In metabolic acidosis: Kidney excretes
acidic urine and generates HCO3
- in CD
In metabolic alkalosis: HCO3
-
reabsorption from PCT is inhibited to
excrete alkaline

26. CONTD
In respiratory acidosis: Inhibition of
HCO3
-reabsorption from PCT with
increased renal HCO3
- excretion
In respiratory alkalosis: Increased renal
HCO3
-reabsorption from PCT

27. Specific Acid
Base Disorder
(ABD)

29. I) RESPIRATORY
ACIDOSIS

30. WHAT HAPPENS?
Respiratory system fails to eliminate
CO2 as fast as it is produced.
Hallmark: elevation of arterial PCO2
(Hypercapnia) & decreased pH

31. CAUSES
Failure of CO2 transport from tissue
to alveoli : Severe
pneumonia/pulmonary edema,
massive pulmonary embolism, RDS,
Interstitial lung disease, cardiac
arrest, cardiogenic shock
&/Or
From alveoli to atmosphere : airway
obstruction like asthma/COPD,
neuromuscular defect like GBS/
Poliomyelitis, restrictive defects like
pneumothorax/ hydrothorax)

32. CAUSES
Respiratory centre depression :
effects of sedative/anesthetics , in
CVD
Mechanical hypoventilation

33. RENAL COMPENSATION TO RAISE
PLASMA HCO3- DONE BY
Complete HCO3- reabsorption from
PCT
Activation of HCO3- generation
mechanism in CD
Net effects:
Renal acid excretion
Raised plasma HCO3- concentration.

34. CORRECTION
Following treatment of initial cause of
acidosis, body gives up compensatory
activity
Kidney decreases plasma HCO3- back
to normal by increasing renal HCO3-
excretion through inhibition of HCO3
reabsorption from PCT.

36. LAB FINDINGS
pH: Low
PCO2: High
Plasma HCO3- : High
Plasma AG: Normal
Plasma Cl- : Low usually
BE : Positive
Serum K+ : High usually
Net urinary acid excretion : Increased

37. TREATMENT
Restore & improve alveolar ventilation
I /V lactate solution (converted to
bicarbonate ions in liver)
Treatment of underlying dysfunction/
disease

38. II) RESPIRATORY
ALKALOSIS

39. WHAT HAPPENS?
Respiratory system eliminates CO2
faster than it is produced.
Hallmark: Decreased PCO2 &
increased pH

40. CAUSES
CNS mediated stimulation of
respiratory center:
Neurological diseases like
encephalitis
Drugs (nicotine, salicylates etc)
Hysteria, anxiety
High fever, septicemia, hepatic
encephalopathy

41. CONTD
Tissue hypoxia mediated stimulation
of respiratory center:
CCF, Congenital cyanotic heart
disease
Severe anemia
Pulmonary diseases like pneumonia,
pulmonary edema, pulmonary
embolism, interstitial lung diseases

42. RENAL COMPENSATION TO REDUCE
PLASMA HCO3- DONE BY
Inhibition of HCO3- reabsorption from
PCT
Renal HCO3- excretion

43. CORRECTION
Following treatment of initial cause of
acidosis, body gives up compensatory
activity
Kidney increases plasma HCO3 back
to normal by reducing renal HCO3
excretion.

45. LAB FINDINGS
pH: High
PCO2: Low
Plasma HCO3- : Low
Plasma AG: Normal usually
Plasma Cl- : High usually
BE : Negative
Serum K+ : Low usually
Net urinary acid excretion : Reduced

47. III)
METABOLIC
ACIDOSIS

48. WHAT HAPPENS?
Blood concentration of HCO3- drops
below 22 mEq/L
Hallmark: Decreased plasma HCO3 &
decreased pH

49. TYPES BASED ON ANION GAP & THEIR CAUSES
Types of metabolic
acidosis based on
AG
Causes Comments
High AG type/
Normochloremic
type
RF, Lactic
acidosis,
Ketoacidosis,
Poisoning/
Intoxication
Here serum Cl-
remains normal. AG
increases in same
proportion as to the
fall of HCO3-
Normal AG type/
hyperchloremic
type
GIT causes
(diarrhoea),
RTA
Here serum Cl-
increases in same
proportion as to the
fall of HCO3-

50. COMPENSATION
Increased ventilation to reduce PCO2
proportionately

51. CORRECTION BY ACIDIC URINE
EXCRETION
Following treatment of initial cause of
acidosis, body gives up compensatory
activity
kidney comes forward to raise serum
HCO3- back to normal with
simultaneous excretion of acid by renal
HCO3 generation mechanism.

53. LAB FINDINGS
pH: Low
PCO2: Low
Plasma HCO3- : Low
Plasma AG: High (if normochloremic
type)or normal (if hyperchloremic type)
Plasma Cl- : High /normal
BE : Negative
Serum K+ : High usually
Findings specific for etiology: High serum
creatinine (RF) / ketone bodies
(ketoacidosis) etc

55. IV) METABOLIC
ALKALOSIS

56. WHAT HAPPENS?
Blood concentration of HCO3- rises
above 28 mEq/L
Hallmark: Increased plasma HCO3- &
increased pH

57. TYPES (ACCORDING TO URINARY
CHLORIDE <10 OR >10 MMOL/L)
Chloride / saline responsive: GIT
cause (vomiting, NG suction), diuretic
abuse, exogenous alkali
administration, etc
Chloride / saline resistant:
Hyperaldosteronism, Chronic
hypokalemia, Cushing syndrome, etc

58. COMPENSATION
Hypoventilation to increase PCO2
proportionately

59. CORRECTION
Following treatment of initial cause of
alkalosis, body gives up compensatory
activity
Kidney comes forward to reduce
serum HCO3- back to normal by
increasing renal HCO3 excretion
through decreased HCO3- reabsorption
in PCT

61. LAB FINDINGS
pH: High
PCO2: High
Plasma HCO3- : High
Plasma AG: Modestly raised
Plasma Cl- : Low usually
BE : Positive
Serum K+ : Low usually

63. SUMMARY

67. NICE TO REMEMBER

68. PROBLEMS

69. INTERESTING FACTS ABUT ABG
Primary change and compensatory change
always occur in same direction
pH and primary change in same direction
suggests a metabolic problem
pH and primary change in opposite
direction suggests a respiratory problem

70. INTERESTING FACTS ABUT ABG
Renal & pulmonary compensatory
mechanisms return pH towards but
rarely to normal
A normal pH in presence of changes in
PCO2 or HCO3 suggests a mixed ABD