Acid-Base Balance Disorders

H+ concentration (activity) in arterial blood

40 4 nmol/l (or 4*10-8 mol/l, or 0,00000004 mol/l)

Srensen (1909)

pH = -log [H+] (pH negative logarithm of [H+] )

[H+] = 40 nmol/l = 40.10-9 mol/l = 4.10-8 mol/l
pH = - log [H+]
pH = - log 4.10-8
pH = - (log 4 + log 10-8)
pH = - (0,6 + [-8])
pH = - (-7,4)
pH = 7,4

pH in some cells and body fluids

arterial blood
urine
erythrocytes
muscle cells
bile
gastric juice

pH
7,36 - 7,44
4,50 - 8,00
7,28
6,90
6,2 - 8,5
1,2 - 3,0

aH+ nmol/l
44 - 36
32000 - 10
53
126
631 - 3
1000 - 63

Daily production of acids

Daily H2CO3 production: 20 mol (300 360 l)

complete oxidation of fats, carbohydrates and proteins

Non-volatile (fixed) acids: 60 70 milimol/day

oxidation of SH groups (amino acids) - H 2SO4

hydrolysis of phosphoproteins, phospholipids... H 3PO4
keto acids
lactic acid

Buffering and regulatory systems

Buffer systems
bicarbonate system HCO3-/H2CO3 - ECF
phosphate - HPO42-/H2PO4- - kidneys, ICF
protein - ICF, ECF
haemoglobin - RBC

Regulatory systems
respiratory
kidneys
liver

Bicarbonate buffer system

Henderson-Hasselbalch equation

pH = pK + log [HCO3-]/[H2CO3]
pK = 6,1
HCO3- = 24 mmol/l
H2CO3 = 1,2 mmol/l
pH = 6,1 + log (24/1,2) = 6,1 + 1,3
pH = 7,4

simplyfied

pH ~ [HCO3-]/pCO2
pCO2 [torr] . 0,03 = H2CO3 [mmol/l]
40 . 0,03 = 1,2

Role of the lungs in acid-base homeostasis

CO2 excretion
Hyperventilation - pCO2
Hypoventilation - pCO2

Role of the kidney in acid-base homeostasis

excretion of H+ ions
phosphate buffer
ammonia
excretion of fixed acids
reabsorption of filtered HCO 3

Bicarbonate reabsorption in kidneys

blood

tubular cell

HCO3 + H
-

HCO3-

glomerular filtrate

H+ + HCO3-

HCO3- + H+
H2CO3
H2CO3

carbonic anhydrase

carbonic anhydrase

H2O + CO2

CO2 + H2O

Disturbances of ABB
metabolic component

respiratory component

pH ~ [HCO3-]/pCO2
metabolic component

respiratory component

HCO3-

pCO2

pH = 7,4

Simple disturbances of ABB

pCO2

metabolic acidosis

HCO3-

pH < 7,36

HCO3pCO2

pH > 7,44

metabolic alkalosis

Simple disturbances of ABB

pCO2

respiratory acidosis

HCO3-

pH < 7,36

HCO3pCO2

pH > 7,44

respiratory alkalosis

Simple disturbances of ABB

acute
chronic
uncompensated
partly compensated
compensated

Metabolic acidosis
1. Increased production of H+

infusion of NH4Cl
toxins (salicylate, ethanol acetate, methanol)
katoacidosis - diabetes mellitus, starvation
lactic acidosis in hypoxia

high anion gap

2. Decreased renal excretion of H+

renal failure
renal tubular acidosis (RTA) type I distal (disorder of H + excretion)

3. Loss of HCO3

acute diarhoea
RTA type II proximal (disorder of HCO3- reabsorption)
diuretics acetazolamide, tiazide (inhibitors of carbonic anhydrase)

Metabolic alkalosis
1. Deficiency of Cl

vomiting
chloride diarhoea

2. Increased exogenous bicarbonte

oral/intravenous bicarbonate
antacid therapy
organic acid salts lactate, acetate, citrate

3. K+ depletion

Bartter syndrome
hyperaldosteronism

Hypochloremic metabolic alkalosis

HCO3-

HCO3HCO3-

Na +

Na +

Na +
Cl -

Cl -

Cl -

K+ depletion

cell

H+

ECF

K+
K+

Respiratory acidosis
1. Central depresion

trauma, cerebrovacular accidents, CNS infection, tumors, ischaemia,

Pickwick sy.
drugs sedative, narcotics

2. Ventilation disorders
A. Thoracic diseases

trauma

kyfoscoliosis
B. Neuromuscular diseases

myopathies, multiple sclerosis, poliomyelitis

C. Lung diseases

obstructive disease

empysema

pneumonia...

Respiratory alkalosis
1. Central stimulation

anxiety/hysteria
pregnancy (stimulation by progesterone)
gram-negative septicaemia
hepatic encephalophaty
salicylate overdose
infection, trauma
tumour

2. Pulmonary pathology

embolism
congestive heart failure (lung oedema)
asthma, pneumonia

Clinical signs
Metabolic acidosis
hyperventilation (Kussmaul breathing)

Metabolic alkalosis
Ca2+ (binding on proteins neuromuscular activity tetanic
cramps,
dysrhytmias

Respiratory acidosis
cerebral vasodilatation headache, stupor, coma

Respiratory alkalosis
cerebral vasoconstriction headache
tetany

Mixed acid-base disturbances

MAC and MAC

Lactate acidosis and ketoacidosis diabetes mellitus

MAC and RAC

RAC + lactate MAC - CHBPD

MAC and MAL

diarhea and vomiting

alcohol intoxication and vomiting

MAC and RAL

lung oedema in early stage lactate MAC + hyperventiltion (RAL)

MAL and RAL

MAC compensation + alcalisation

never
RAC and RAL

Compensation
- the body homeostatic mechanisms try to keep the pH of the body
fluids as near normal as possible
-if the pH change is caused by metabolic component (HCO3-)
- compensation respiratory component (lungs)
-if the pH change is caused by respiratory component (pCO2)
- compensation metabolic component (kidneys)

Compensation
metabolic acidosis

compensation

HCO
lungs~
pH
pCO2
(hyperventilation)
3

respiratory acidosis

pH ~

HCO3pCO2

compensation

HCO3pH ~
kidneys pCO2
(higher HCO3- reabsorption)

HCO3pH ~
pCO2

Compensation
metabolic alkalosis

HCO
pH ~
pCO2

respiratory alkalosis

HCO3pH ~
pCO2

compensation

pH ~

HCO3pCO2

lungs
(hypoventilation)

compensation

HCO3pH ~
pCO2

kidneys

(lower HCO3- reabsorption)

Acid-base parameters

pH
pCO2

7,4 0,04
5,3 - 0,5 kPa (40 mmHg)

BE
HCO3-

0 2 mmol/l
24 2 mmol/l

AG
pO2

15,2 1,6 mmol/l

10,0 - 13,3 kPa

pH < 7,36
pH > 7,44

acidaemia
alkalaemia

pCO2 < 4,8 kPa

pCO2 > 5,9 kPa

hypocapnia
hypercapnia

HCO3- < 22 mmol/l

HCO3- > 26 mmol/l

hypobasemia
hyperbasemia

Base excess/deficit
BE = 0 2,0 mmol/l

Buffer base
BB = HCO3- + proteins
or BB = (Na+ + K+) - ClBB = 48,0 2,0 mmol/l

SID = strong ion difference

SID = HCO3- + proteins + phosphate

Anion gap
AG = (Na+ + K+) - (Cl- + HCO3-)
AG = 15,2 1,6 mmol/l

Anion gap
15
25

Na+

AG
HCO3-

15

25

15
15

140
100

110

Cl

100

ketoacids
lactate
...