1. ACID – BASE DISORDERS
M. Tatár

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

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

4. H+ balance per day H+ poduction Volatile acid 20 000 mmol
Fixed and volatile acids
30-80 mmol
H+ elimination
Lungs (CO2)
Kidneys

5. Hydrogen ion pH = - log [ H+] mol . l-1
[ H+ ] = from ,44 to ,36
= 0, , mol . l-1
= nmol . l-1
pH = - log [ H+] mol . l-1
pH = 7,4  0,04
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 = log
( log 20 )
30/1.5
18/0.9
1.2 mmol
pH = = 7,4

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

10. CO2 transport

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

12. Proximal tubule
„reabsorbed“ HCO3-
Na,K,ATP-ase

13. Distal nephron
„new“ HCO3-

14. 13.3
10.6
hypoventilation
8.0
(kPa)
6.7
Pco2
5.3
4.0
hyperventilation
2.7
7.0
7.2
7.4
7.6 pH

15. 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

16. [ Na+ ] - ( [Cl-] + [ HCO3-] ) = 10 - 12 mmol.l-1
Anion gap
[ Na+ ] - ( [Cl-] + [ HCO3-] ) = mmol.l-1
( ) = 12 mmol.l-1 
>
organic or fixed acids

17. Causes of metabolic acidosis (MAC)
I. Normal anion gap MAC
bicarbonate loss  hyperchloremic MAC
a) via the GIT: diarrhea, small bowel fistula
b) renal tubular acidosis (reduced H+ excretion)
[ Na+ ] - ( [Cl-] + [ HCO3-] ) = 12 mmol.l-1
II. High anion gap MAC
gains of noncarbonic acids
a)  lactic acid: hypoxia, liver insufficiency
b) ketoacidosis: diabetes mellitus, starvation
c) retention of fixed acids: renal failure
[ Na+ ] - ( [Cl-] + [ HCO3-] ) > 12 mmol.l-1
acids

18. 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

19. Causes of metabolic alkalosis (MAL)
Primary Cl- lost (hypochloremic alkalosis)
b) kidneys: diuretics (furosemid)
a) GIT: prolonged vomiting
Cl- and HCO3- have a reciprocal relationships to maintaine electroneutrality of ECF
[ Na+ ] - ( [Cl-] + [ HCO3-] ) = 12 mmol.l-1

20. 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

21. 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

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