1. Prof. M. Tatár Dept. of Pathophysiology JLF UK
ACID – BASE DISORDERS
Prof. M. Tatár
Dept. of Pathophysiology JLF UK

2.   H+ affects structure and function of proteins
changes of cellular enzymes activity 
cellular and organ functions changes

3. HCO3-  H+ + CO32- HCO3- + H+  H2 CO3
acid – substance containing (H+) that can be liberated in solution (proton donor)
base – substance that can combine with (H+) from
a solution (proton acceptor)
HCO3-  H+ + CO32-
HCO H+  H2 CO3

4. Sources of H+ in organism
a) Volatile acid
CO2 + H2O  H2CO3  H+ + HCO3-
b) fixed acids
H2SO4, H3PO4
c) organic acids
lactic acid, ketoacids

5. Hydrogen ion [ H+ ] = 10 - 7,44 až 10 - 7,36
= 0, , mol . l-1
= nmol . l-1
pH = - log [ H+] mol . l-1
pH = 7,4  0, μm3 …… activity of 40 H+
mitochondria : active H+

6. pH H+ (nmol.l-1) 160 140 120 100 80 acidaemia 60 norm 40 basaemia 20
6,8
7,1
7,4
7,7
acidaemia
norm
basaemia

7. acidemia acidosis
alkalemia alkalosis

8. HENDERSON - HASSELBALCH
equation
[ H+ ] . [ HCO3-]
K =
[ H2CO3]
[ H2CO3]
[ H+ ] = K
[ HCO3-]
[ HCO3-]
log = log log
[ H+ ] K [ H2CO3]
[ HCO3-]
pH = pK + log
[ H2CO3]
24 mmol
pH = 6,1 + log
( log 20 )
1,2 mmol
pH = 6,1 + 1,3 = 7,4

9. NL Alkalosis Acidosis Death One part of 20 parts of H2CO3 HCO3-
7,38
7,42
7,25
7,55 NL
pH 6,80
Acidosis
Alkalosis
7,8
7,36
7,44
Death
Death
One part of
H2CO3
(1.2 mmol/l)
PCO2 = 5.3 kPa
20 parts of
HCO3-
(24 mmol/l)
Blood pH

10. NL Alkalosis Acidosis Death 1.5 part of H2CO3 (1.8 mmol/l)
7,38
7,42
7,25
7,55 NL
pH 6,80
Acidosis
Alkalosis
7,8
7,36
7,44
Death
Death
1.5 part of
H2CO3
(1.8 mmol/l)
PCO2=8.0 kPa
20 parts of
HCO3-
(24 mmol/l)
Blood pH

11. NL Alkalosis Acidosis Death 24 parts of HCO3- (29 mmol/l) One part of
7,38
7,42
7,25
7,55 NL
pH 6,80
Acidosis
Alkalosis
7,8
7,36
7,44
Death
Death
24 parts of
HCO3-
(29 mmol/l)
One part of
H2CO3
(1.2 mmol/l)
Blood pH

12. Buffers 1 [ HCO3- ] 1. Bicarbonate system ------------ [ H2 CO3 ]
HCl + NaHCO3  H2 CO3 + NaCl
NaOH + H2 CO3  NaHCO3 + H2O Hb
2. Hemoglobin system
HbO2

13. CO2 transport

14. Buffers 2 proteinate- 3. Plasma proteins --------------- H - protein
HPO42-
4. Phosphate system
H2PO4-
HCO % (plasma 35%, RBC- 18%)
buffers Hb - HbO %
in blood Phosphates %
Plasm. prot %

15. Proximal tubule
„reabsorbed“ HCO3-
Na,K-ATPase

16. Distal nephron
„new“ HCO3-

17. 13,3
10,6
8,0
(kPa)
6,7
Pco2
5,3
4,0
2,7
7,0
7,2
7,4
7,6 pH

18. Mechanisms of acid – base disorders
metabolic
metabolic
1. acidosis
2. alkalosis
3. acidosis
4. alkalosis
HCO3- pH
= pK + log
PCO2
respiratory
5. acidosis
6. alkalosis

19. Anion gap
[ Na+ ] - ( [Cl-] + [ HCO3-] ) = mmol.l-1
( ) = 12 mmol.l-1

20. Causes of metabolic acidosis (MAC)
I. Normal anion gap MAC
bicarbonate loss  hyperchloremic MAC
a) via the GIT: diarrhea, small bowel fistula
b) kidneys: renal tubular acidosis
II. High anion gap MAC
gains of noncarbonic acids
a)  lactic acid: hypoxia, liver insufficiency
b) ketoacidosis: diabetes mellitus, starvation, etanol
c) retention of fixed acids: renal failure

21. Compensatory response in MAC
1.  ventilation
M M
----- 
R R
2. HCO3- retention in kidneys
Clinical features
- Kusmaul breathing
-  cardiac contractility
- lethargy
- renal osteodystrophy
- hyperkalemia
- vomiting

22. Causes of metabolic alkalosis (MAL)
Cl- lost (hypochloremic alkalosis)
a) GIT: prolonged vomiting
b) urine: diuretics (furosemid)
Cl- and HCO3- have a reciprocal relationships to maintaine electroneutrality

23. Compensatory response in MAL
1. Alveolar hypoventilation
M M 
R R
2. Renal excretion of the excess HCO3-
Clinical features
- occasionally tetany
-  risk of cardiac dysrhythmias
-  afinity of Hb to O2
- hypokalemia

24. Causes of respiratory acidosis (RAC)
Respiratory disorders  CO2 accumulation
- alveolar hypoventilation
Compensatory response
HCO3- retention in kidneys
M M 
R  R
Clinical features
- CNS dysfunction: confusion, somnolence
- cerebral vasodilation:  intracranial pressure,

25. Causes of respiratory alcalosis (RAL)
Alveolar hyperventilation as a result of respiratory centre stimulation
a) the most common: anxiety and emotional stress
b) hypermetabolic conditions: fever, CNS lesions, thyreotoxicosis
c) hypoxia: pneumonia, pulmonary edema, high alitude
Compensatory response
Clinical features
 renal excretion of HCO3-
M M  
R  R 
tetany
- vomiting

26. Mixed acid – base disorders
- cardiopulmonary arrest
- sepsis
- pulmonary diseases and diabetes mellitus
- vomiting in renal failure