Acid base balance

1. Disorders of Acid-Base
Balance
S. Kadiri

2. Introduction
• Acids from metabolism
• Fixed or volatile
• Buffered or excreted to maintain pH
Buffer is a substance which limits the change in pH when acid or
base is added
• 70-100 mEq acid eliminated daily
• Kidneys and lungs
• Liver metabolism

3. Buffers
• CO2-HCO3
-quickest
• Haemoglobin
• Protein
-most abundant intracellular
• Phosphate
• Ammonia

4. • pH = - log10[H+]
• pH = base/acid = HCO3/CO2
• Normal 7.35-7.45

5. Introduction (cont)
• H+ = 24 pCO2/HCO3
-pCO2 and HCO3 change in line to stabilize H+
- pCO2 by CNS and lungs
- HCO3 by kidneys
-response never returns H+ to normal in pure ABDs
• 1 ATM = 101.9 kPa
• mmHg/7.5 = kPa

6. • Major approaches to study of AB balance
-Physiologic – most commonly used
-Base excess
• Base excess = 0.93 x [HCO3 -24.4 + 14.8(pH-7.4)]
normal = +/-2

7. Definition
• Buffer base – the sum of HCO3
- and the nonvolatile weak acid buffers (A-)
• Base excess (BE)– 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 the PCO2 is held at
40 mmHg
-negative in acidaemia
-positive in alkalaemia
• Standard base excess
-base excess at reference of Hb 5g/dL
- Hb buffers plasma and much larger extracellular fluid.

8. pH
• Normal
• Acidaemia pH<7.35
• Alkalaemia pH>7.45
• Acidaemia more common
• Metabolic acidosis perhaps most important

9. Compensation
•Kidneys – slow: 1-2 days and full in 3-5 days
•Lungs – can be fast: within mins, full in 1-2 days
•Changes in C02, no change in H+
•With well functioning organs
•pCO2 changes not caused by overproduction

10. Steps to Interpretation
• Note pH : normal, acid, alkaline
• pCO2
• serum HCO3
• Compensation
• Anion gap – may be the only abnormality
• Mixed disorders
• Acute or chronic
• Severity of disorder

11. Interpreting ABG’s (Identifying Imbalances)
1. Look at pH first. Is it normal, acidotic or alkalotic?
2. Look at pCO2 next. Is it normal, high (acidotic) or low
(alkalotic)?
***If pCO2 is inverse with pH, it’s a respiratory problem.
3. Look at HCO3
- next. Is it normal, low (acidotic) or high
(alkalotic).
***If HCO3
- is direct with pH, it’s a metabolic problem.

12. pH CO2 HCO3 2nd ary Responses
RAc < 7.4 > 40 > 24 increased renal acid excretion
(increased HCO3, rarely > 32 mEq/L)
R Alk > 7.4 < 40 < 24 Decreased renal acid excretion
(decreased HCO3, rarely <16 mEq/L)
MAc < 7.4 < 40 < 24 Hyperventilate
M Alk > 7.4 > 40 > 24 Hypoventilate
(pCO2 usually < 55 mmHg)

13. Respiratory acidosis - compensation
• Problem high pCO2
• High H+, low pH
• H+ stimulates kidney to retain HCO3
• Complete in 2-4 days
• Limit of compensation 45
• Expected HCO3
= 0.44 x pCO2 + 7.6 ………+/- 2

14. Respiratory alkalosis - compensation
• Problem low pCO2
• Low H+, high pH
• Stimulates kidneys to excrete HCO3
• Complete in 7-10 days
• Limit is 12 mmol/L

15. Metabolic acidosis - compensation
• Problem low HCO3
• High H+. Low pH
• Stimulates respiration
• Complete in 12-24 hrs
• Expected pCO2
= 1.5 x HCO3 + 8……..+/-2
• Limit 10 mmHg

16. Metabolic alkalosis - compensation
• Problem high HCO3
• Low H+, high pH
• Suppresses respiration which raises pCO2
• Complete in 12-24 hrs
• Expected CO2
= 0.9 x HCO3 + 9 ……..+/- 2
• Limit is 60

17. Mixed acid-base disorders
• Plasma HCO3 and CO2 change in different directions
• Appropriate secondary responses not present
• Secondary responses fully correct or overshoot pH
• Severity and worse outcomes with disorders that enhance pH change

18. pCO2 – respiratory component
• pCO2 inverse to pH – respiratory cause
• If HCO3 also low – combined resp & met acidosis
• If pCO2 direct to pH – not resp
low pCO2 – resp compensation for met acid

19. HCO3/SBE – metabolic component
• pH direct with HCO3/SBE – metabolic
• If pCO2 also high – combined met & resp acid
• If SBE/HCO3 inverse to pH – not metabolic
HCO3/SBE high – compensation

20. additional tips
• Expected pCO2 = last 2 digits of blood pH
• If inadequate, additional respiratory acidosis
• If excessive, additional respiratory alkalosis

21. Acute or chronic ?
• Respiratory compensation fast
• Renal compensation slow
• Ac. R Ac - 10mmHg increase in CO2, HCO3 up by 1
• Ch. R Ac - 10mmHg increase in CO2, HCO3 up by 4
• Ac. R Al – decrease of 10, HCO3 drop by 2
• Ch. R Al – decrease of 10, HCO3 drops by 5

22. severity
Adjective
PCO2
mmHg
SBE
mEq/L
Alkalosis
Severe > 18 > 13
Marked 18 to 25 13 to 9
Moderate 25 to 30 9 to 6
Mild 30 to 34 6 to 4
Minimal 34 to 37 4 to 2
Normal Normal 37 to 43 2 to -2
Acidosis
Minimal 43 to 46 -2 to -4
Mild 46 to 50 -4 to -6
Moderate 50 to 55 -6 to -9
Marked 55 to 62 -9 to -13
Severe > 62 to < -13

24. Origin of acidosis
• Addition of acid
endogenous
exogenous
• Reduced excretion of acid
• Loss of bicarbonate

25. Renal excretion of acid
• Secretion of ammonia
• Titratable acidity
• Secretion of H+
• Reabsorption of bicarbonate

26. Excretion of ammonia
• Produced in tubular cells
• Captures H+ in lumen
• Excretion of NH4
- salts
• Facilitated by acidaemia and hypokalaemia
• Inhibited by alkalaemia and hyperkalaemia

27. Titratable acidity
• Definition
• Mainly P04
- and SO4
-
• Capture H+ in lumen

28. Bicarbonate reabsorption
• 80-90% in PCT
• Brush border carbonic anhydrase
• 10-20% in distal segments
• Daily filtered about 4500 mEq

29. Metabolic acidosis

30. Classification
• High and Normal anion gap MA
• [Na] – [HCO3
- - Cl-}
• Owing to serum albumin, unmeasured anions
• Normal 4-12
• Correction for low albumin
- AG + 0.25( 4.4 – measured se-albumin)

31. Low anion gap - causes
• Hypoalbuminaemia
• Hyperlipidaemia
• Hyperviscosity
• Paraproteinaemia
• Increased cations

32. Causes of metabolic acidosis
Normal AG
Renal acidification defects
• Proximal renal tubular acidosis
• Classic distal tubular acidosis
• Hyperkalemic distal tubular acidosis
• Early renal failure
Gastrointestinal loss of bicarbonate
• Diarrhea
• Small bowel losses
• Ureteral diversions
• Anion exchange resins
• Ingestion of CaCl2
Acid infusion
• HCl
• Arginine HCl
• Lysine HCl
Increased AG
Endogenous acid load
• Ketoacidosis
-Diabetes mellitus
-Alcoholism
-Starvation
• Uremia
• Lactic acidosis
Exogenous toxins
• Osmolar gap present
-Methanol
-Ethylene glycol
• Osmolar gap absent
-Salicylates
-Paraldehyde

33. Renal failure
• Impaired secretion of NH3
-maybe NAG at this stage
• Retention of PO4
- and SO4
-
• Bicarbonate wastage
-HAG at this stage

34. Acid and Cl- administration
• HCl from parenteral nutrition
• NaCl infusion and expansion acidosis
• Fall in blood pH
• Cl- keeps anion gap

35. Bicarbonate losses - GIT
• Severe diarrhoea
• Pancreatic fistula
• Biliary drainage
• Pancreas-bladder anastomosis
• Urine diversion to colon or ileum
• HCO3
- exchanged for Cl- in ileum and colon

36. Bicarbonate losses - kidneys
• Proximal tubular disorder
• Hypocapnia
• Reduced bicarbonate reabsorption

37. Reduced H+ excretion
• Type-1 renal tubular acidosis
• Type-4 renal tubular acidosis
-hypoaldosteronism

38. Type-1 RTA
• Impaired H+ extrusion from α-intercalated cells
• Urine pH > 5.3
• K+ excretion for Na+ reabsorption
• Hypokalaemia
• Hyperkalaemic form may occur with obstruction
• Ca phosphate stones and nephrocalcinosis

39. Calcium phosphate stones
• Calcium citrate more soluble than calcium phosphate
• Increased PT reabsorption of citrate
• Hypokalaemia promotes hypocitraturia
• Hypocitraturia promotes phosphate stones
• Ca phosphate stones less soluble than citrate stones

40. Type-4 RTA - causes
• Diabetes mellitus
• NSAID
• Cyclosporin
• ACEI, ARB
• Heparin

41. Type-4 RTA
• Impaired Na+ reabsorption
• Impaired K+ secretion
• Hyperkalaemia inhibits NH3 production
• Acidosis, urine pH < 5.3

42. Acidosis – clinical features
Blood pH > 7.20
Counter regulatory hormones actives
• Kussmaul’s respiration
• Nausea, vomiting
• Change in mental status

43. Blood pH < 7.20 -- Counter regulatory
hormones ineffective
• Hypotension
• Depressed myocardial
contractility, vasodilatation
• Reentrant arrhythmias
• Ventricular fibrillation
• reduced albumin synthesis
• Activation of complement
• Enhanced muscle breakdown
• Bone buffering and resorption

44. Investigations
• pH
• HCO3
-
• pCO2
• H+
• Anion gap
• Serum K+

45. Increased anion gap
• Due to unmeasured anions
-Deplete bicarbonate
• Corrected HCO3
= measured HCO3 + (anion gap – 12)
Normal = 22-26
• If reduced, additional metabolic acidosis
• If elevated, additional metabolic alkalosis

46. Normal anion gap MAc
• 2 large groups – renal/GI
• Clinical differentiation
• Urine anion gap
• Positive UAG, renal cause
• Negative UAG, GI cause

47. Urine anion gap
• UAG= [Na+ + K+] – [Cl-]
• <0 in diarrhoea
• >0 in type-1 RTA

48. Treatment
• Of acidaemia
• Of underlying disorder
• Alkali
• Dialysis

49. Alkali therapy
• Serum HCO3
- < 12 mEq/L
• Newer recommendations to keep level 20-25
• 0.5-1 mEq/Kg/day
• 0.3 x weight x BE
• NaHCO3
• K citrate in type-1 RTA

51. Thank you.