1. Acid Base Disorders
Prof. Tahir Shafi

2. Why should we know about acid base disorders
What are acid base disorders
How to interpret acid base disorder
How to establish the cause

3. Why to worry about acid base disorders
Acid base homeostasis fundamental for maintaining life
Extreme acidemia or alkalemia can
alter tertiary protein structure affecting enzyme activities ion transport
alter almost every metabolic pathway

4. Extreme acidemia can
depress cardiac function, impair the vascular response to catecholamines, and cause arteriolar vasodilation and venoconstriction, with resultant systemic hypotension and pulmonary edema.

5. Alkalemia can cause
cardiac arrhythmias, neuromuscular irritability, and contribute to tissue hypoxemia.
fall in cerebral and myocardial blood flow
respiratory depression
potassium abnormalities a common accompaniment of acid-base disorders, also contribute to the morbidity.

6. Identification of mild to moderate disorders can give you important clue to the presence of unsuspected but may be otherwise important medical conditions

7. A patient has the following lab tests:
ABG pH PO mmHg
PCO Bicarb meq/l
Sodium 140 Potassium 4,2
Chloride 80 Bicarb 24
Creatinine Glucose 110
Which one of the following statements is correct
He has normal acid base parameters
He has metabolic acidosis and respiratory alkalosis
He has metabolic alkalosis and respiratory acidosis
He has metabolic acidosis and metabolic alkalosis

8. Regulation of acid base status
Acidity in the ECF measured by [H]+
H+ = nEq/L
Average = mEq/L = 40 nEq/L
pH - negative log of H+ in moles
Maintenance of arterial pH within normal range with average pH 7.4

9. Henderson Hasselbach equation
pH = pk + log
Base
Acid
HCO3
H2CO3 24
apCO2 24
1.2
6.1 + log
1.3
=7.4
a = Log 20

10. Kassirer - Bleich Equation
H+ = 24 x
pCO2
HCO3

11. pH and H+ are inversely related
h H+ results in i pH - Acidemia
i H+ and hpH – Alkalemia
Normal pH or H+ - Euphemia

12. Types of acid base disorders
Acidosis
Alkalosis
Respiratory
pCO2
HCO3
H+ = 24 x
Alkalosis
Acidosis
Metabolic
Stabilization of H+ for every primary disorder there must be physiological compensation by the opposite system

13. Compensations are predictable and can calculated Respiratory compensation
H+ = 24 x
pCO2
HCO3
Primary pH
Initial event
Comp
Resp
Expected Cpmpensation
Met. Acidosis i
iHCO3
ipCO2
For 1 meq iHCO3, pCO2 i by mmHg
PCO2 = HCO3+ 15
PCO2 = last 2 digits of pH
pCO2 = (HCO3) x Winter’s equation
Met. Alkalosis h
hHCO3
hpCO2
For 1 meq h HCO3,PCO2 h by 0.6 mmHg
PCO2 =(HCO3 x 0.9) + 9
PCO2 =(HCO3 x 0.7) + 20

14. Metabolic compensation
H+ = 24 x
pCO2
HCO3
Primary pH
Initial event
Comp
Resp
Expected Cpmpensation
Ac. Resp. Acidosis i
hpCO2
hHCO3
For every 10 mmHg h PCO2 ,HCO3 h by 1
Ch. Resp. Acidosis
hPCO2
For every 10 mmHg h PCO2, HCO3 h by 3.5
Acute Resp Alkalosis h
ipCO2
iHCO3
For every 10 mmHg i PCO2, HCO3 i by 2
Ch. Resp Alkalosis
For every 10 mmHg i PCO2, HCO3 i by 5

15. Rates of correction Buffers function almost instantaneously
Respiratory mechanisms take several minutes to hours
Renal mechanisms may take several hours to days

16. Classification acid base disorders
Simple
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
Primary change in one component
Secondary change in the other component within physiological range
Change in ph in the direction of primary change
Mixed
Double
Primary change with incomplete or over compensation with other component
Triple
Quadruple

17. Normal acid base homeostasis

18. Metabolic acidosis
Exogenous
load
HCl
Other acids

19. Types of metabolic acidosis
Addition of acid other than HCl
Serum chloride normal, bicarbonate low
High anion metabolic acidosis
Addition of HCl
Serum chloride high, bicarbonate low
Normal anion or hyperchloremic metabolic acidosis

20. Anion gap

21. Albumin is a major source of unmeasured anions!
Corrected AG = Observed AG x (4.5 – measured albumin)
If serum albumin is high, corrected anion gap will be lower

22. Metabolic Acidosis K Diabetic Ketoacidosis
Causes of high Anion Gap metabolic acidosis
K Diabetic Ketoacidosis
U Uremia
S Salicylate intoxication
S Starvation ketosis
M Methanol ingestion
A Alcohol ketoacidosis
U Unmeasured Osmoles, Ethylene Glycol, Paraldehyde
L Lactic acidosis
MUDPILES Methanol, Uremia, DKA, Paraldehyde, INH/Iron toxicity, Lactic acidodis, Ethanol/Ethlene glycol, Salicylate toxicity

23. Metabolic Acidosis Causes of normal Anion Gap metabolic acidosis
H Hyperalimentation
A Acetazolamide
R Renal tubular acidosis
D Diarrhoea
U Uretero sigmoidostomy
P Pancreatic fistula

24. D – Diarrhea
U – Ureteral diversion
R – Renal tubular acidosis
H – Hyperalimentation
A – Acetazolamide
M - Miscellaneous (toluene, amphotericin B

25. Hyperchloremic metabolic acidosis
Normal or high ammonia excretion
Decreased ammonia excretion

26. Urine anion gap
Negative urine anion gap positive urine anion gap

27. Urine osmolal gap
Measured urine osmolality – calculated urine osmolality
Calculated urine osmolality
= 2 (UNa + UK )+
< 150 mosm /l= impaired NH4 excretion
>150 mosm/l = increased NH4 excretion
Urine ammonia level = half urine osmolal gap
Urea 6

28. Metabolic acidosis & osmolal gap
Ethyl Alcohol Acetaldehyde Acetic Acid
Methyl Alcohol Formaldhyde Formic Acid
Ethylene Alcohol Glycoaldehyde Glycolic acid Glycooxalic acid Oxalic acid
OSMOLAL GAP = Measured osmolality- calculated osmolality
Normal = < mOsmol/Kg of H2O
Urea 6 BS 18
Calculated serum osmolaliy = 2(Na)

29. Metabolic alkalosis Addition of base or loss of acid from body
High pH, high bicarbonate, high pCO2

30. Metabolic alkalosis Saline responsive alkalosis
Low urinary Cl- (<10 mmol/l)
Normal or low BP
vomiting
Post diuretics
After hypercapnia
K+ depletion
Refeeding alkalosis
Saline resistant alkalosis
High Urinary Cl- (>10 mmol/l)
Normal BP High BP
Bartter’s syndrome Reno vascular
Diuretics disease
Mg++ depletion Conn’s syndrome
Severe K+ depletion Cushing’s syndrome

31. More then one problem? The “gap-gap” or “delta-delta” ratio
In the presence of a high AG metabolic acidosis, ? another metabolic acid base disorder
Comparing the AG excess to the HCO3 deficit - D AG =D HCO3
D AG = (Observed AG – 12)
D HCO3 = (Observed – Normal HCO3)

32. Mixed metabolic acid base disorders
Coexistent
Metabolic alkalosis
delta/delta > 1 hh
D AG
D HCO hh
Coexistent
Hypercholemic acidosis
delta/ delta <1

33. Mixed metabolic acid base disorders
Corrected bicarbonate = observed biacrbonate +
> 24 meq/l g Metabolic Alkalosis
< 24 meq/l g Metabolic Acidosis
D AG

34. Respiratory acid base disorders
Respiratory acidosis Respiratory alkalosis
Hypoventilation Hyperventilation
Primary event
Change in pCO2
H+ = 24 x
pCO2
HCO3

35. Respiratory Alkalosis or Acidosis
Neuro respiratory control
Central hypo or hyperventilation
Intrinsic lung disease
A-a gradient (Alveolar arterial gradient)
Alveolar O2 =(760 – 47) * 0.21* PCO2/0.8 =100
Atmospheric pressure – water vapor pressure * FiO2* PaCO2
Arterial (a) =100
A-a gradient normal is < 10 in adults and < 20 in elderly

36. Respiratory Alkalosis
Low pCO2, low bicarbonate, high pH
A–a difference >10 mm Hg (>20 mm Hg in elderly) - Hyperventilation with intrinsic lung disease, ventilation–perfusion mismatch, or both (e.g., pneumonia, pulmonary embolism)
A–a difference <10 mm Hg (<20 mm Hg in elderly) Hyperventilation without intrinsic lung disease (e.g., fever, pregnancy)

37. Respiratory Acidosis High pCO2, high bicarbonate, low pH
A–a difference >10 mm Hg (>20 mm Hg in elderly) Hypoventilation with intrinsic lung disease, ventilation–perfusion mismatch, or both (e.g., pneumonia, pulmonary embolism)
A–a difference <10 mm Hg (<20 mm Hg in elderly) - Hypoventilation without intrinsic lung disease (CNS suppression)

38. Approach to Acid Base Disorders

39. Urinary electrolytes – Urinary anion gap urine osmolal gap
History
Physical examination
Serum electrolytes
Anion gap
Delta/delta ratio
Arterial blood gases
Urinary electrolytes – Urinary anion gap urine osmolal gap
Serum osmolal gap

40. Acid Base Analysis Step 1 : Look at pH. acidemic or alkalemic?
Step 2 : Look at pCO2
High – respiratory acidosis
Low – respiratory alkalosis
Step 3: Look at HCO3
High – metabolic alkalosis
Low – metabolic acidosis
Step 4: Determine primary event direction of pH

41. Step 5: Is it simple or mixed disorder. compensatory response within
Step 5: Is it simple or mixed disorder. compensatory response within physiological range ?
Golden rules: 1- Mixed problem present if
only one component abnormal
2- Normal pH – both components
abnormal
3-Both components in same direction
Step 6 : Look at base excess if available
Step 7: If the respiratory disturbance is present, is it acute or chronic?

42. Step 8 : Is there increased anion gap?
Step 9 : If anion gap increased, calculate corrected HCO3 or delta/delta
Step 10 : Calculate osmolal gap if ingestion of alcohols suspected
Step 11: Calculate urine anion gap or osmolol gap

43. Acid Base Disorders pH 7.54 PCO2 30 mmHg HCO3 25 meq/l Na+ 140 meq/l
Cl- 92 meq/l
K meq/l

44. Acid Base Disorders pH 7.25 pO2 70 mmHg PCO2 40 mmHg HCO3 17 meq/l
A 55 years old man with renal failure presented with vomiting altered consciousness and fever
pH 7.25
pO2 70 mmHg
PCO2 40 mmHg
HCO3 17 meq/l
Na meq/l
Cl- 89 meq/l
K meq/l
A. Respiratory acidosis
Metabolic Acidosis
Metabolic alkalosis + respiratory acidosis
D. Metabolic acidosis +
Respiratory acidosis
E. D + Metabolic alkalosis

45. Acid Base Disorders pH 7.25 pO2 70 mmHg PCO2 40 mmHg HCO3 17 meq/l
A ss years old man with renal failure presented with vomiting and pleuritic chest pain
pH 7.25
pO2 70 mmHg
PCO2 40 mmHg
HCO3 17 meq/l
Na meq/l
Cl- 89 meq/l
K meq/l
AG (89+17) =34
D AG = 34-10=24
HCO3 = 24-17=7
High A-a gradient

46. Acid Base Disorders 16 years old boy , a case of FSGS on diuretics and
Steroids presented with BP 70/40 mmHg
pH 7.4
PCO mmHg
HCO meq/l
Na meq/l
Cl meq/l
K meq/l
S. Albumin 1 gram/dl
no acid base disorder
Respiratory acidosis
Metabolic alkalosis + resp acidosis
Metabolic acidosis +
resp alkalosis
E, None of the above

47. Acid Base Disorders 16 years old boy , a case of FSGS on diuretics and
Steroids presented with BP 70/40 mmHg
pH 7.4
PCO mmHg
HCO meq/l
Na meq/l
Cl meq/l
K meq/l
S. Albumin 1 gram/dl
no acid base disorder
Respiratory acidosis
Metabolic alkalosis + resp acidosis
Metabolic acidosis +
resp alkalosis
E, None of the above
AG =143-(95+24) = 24
Corrected AG=
24+(4- Alb) * 2.5 = 31.5
Delta AG = 21.5
Delta bicarb = 0
Mixed high anion gap metabolic acidosis + Alkalosis

48. Glucose mg/dl
Urea mg/dl
Serum Sodium 136 meq/l
Serum potassium 4 meq/l
Calc osm mosm/l
Serum osm mosm/l
Osmolar gap =20 delta OG=10
460 mg/l of ethanol or
320 mg/l of methanol

49. Acid Base Disorders HCO3 17 meq/l Na+ 140 meq/l Cl- 89 meq/l
K meq/l

52. Figure 1 Assessment of Acidosis
Figure 1 Assessment of Acidosis. Reference values for the alveolar–arterial (A–a) oxygen tension difference are less than 10 mm Hg in young persons and less than 20 mm Hg in the elderly. ΔAG denotes delta anion gap, PaCO2 partial pressure of arterial carbon dioxide (mm Hg), PaO2 partial pressure of arterial oxygen (mm Hg), and RTA renal tubular acidosis. To convert the values for PaCO2, PaO2, and the alveolar–arterial difference to kilopascals, multiply by
If delta delta ratio
=1 only high AG
Met Acidosis
Berend K et al. N Engl J Med 2014;371:

53. Figure 2 Assessment of Alkalosis
Figure 2 Assessment of Alkalosis. Reference values for the alveolar–arterial (A–a) oxygen tension difference are less than 10 mm Hg in young persons and less than 20 mm Hg in the elderly. PaCO2 denotes partial pressure of arterial carbon dioxide (mm Hg), and PaO2 partial pressure of arterial oxygen (mm Hg). To convert the values for PaCO2, PaO2, and the alveolar–arterial difference to kilopascals, multiply by
Berend K et al. N Engl J Med 2014;371:

54. Base Excess = 0.9287 (HCO3 - 24.4 + 14.83 (pH - 7.4))
Predicted pH = pCO2 * 0.08
pH = Actual pH – predicted pH
Base Excess = pH *10/0.15
For each 0.15 unit difference in pH
Base excess or deficit will be =10

55. Approach to Acid Base Disorders
Traditional or Boston approach
Copen Hagen approach
Base excess
Stewart / Physiochemical approach
PCO2
Non-volatile weak ion acid buffer A Total
Atotal = A- + AH (Albumin, Pi, SO4, Hb)
Strong ion difference (SID)
(Na+K+Ca+Mg) – (Cl+Lac)
= A- + HCO3
= 40-42

56. The physiologic or “Boston” method
uses measurements of arterial pH, pCO2, and [HCO3−] together with an analysis of the anion gap (AG) and a set of compensation rules.
2. The Base Excess (BE) or “Copenhagen” method uses
measurements of arterial pH and pCO2, and calculation of the BE and the AG.
3. The physicochemical or “Stewart” method uses
Measurements of arterial pH and pCO2 together with the calculated apparent (SIDa) and effective (SIDe) “Strong Ion Difference,” the “Strong Ion Gap” (SIG = SIDa-SIDe), and the total concentration of plasma weak acids (Atot).