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Srensen (1909)
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
Buffer systems
bicarbonate system HCO3-/H2CO3 - ECF
phosphate - HPO42-/H2PO4- - kidneys, ICF
protein - ICF, ECF
haemoglobin - RBC
Regulatory systems
respiratory
kidneys
liver
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
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
metabolic acidosis
HCO3-
pH < 7,36
HCO3pCO2
pH > 7,44
metabolic alkalosis
respiratory acidosis
HCO3-
pH < 7,36
HCO3pCO2
pH > 7,44
respiratory alkalosis
Metabolic acidosis
1. Increased production of H+
infusion of NH4Cl
toxins (salicylate, ethanol acetate, methanol)
katoacidosis - diabetes mellitus, starvation
lactic acidosis in hypoxia
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
oral/intravenous bicarbonate
antacid therapy
organic acid salts lactate, acetate, citrate
3. K+ depletion
Bartter syndrome
hyperaldosteronism
HCO3-
HCO3HCO3-
Na +
Na +
Na +
Cl -
Cl -
Cl -
K+ depletion
cell
H+
ECF
K+
K+
Respiratory acidosis
1. Central depresion
2. Ventilation disorders
A. Thoracic diseases
trauma
kyfoscoliosis
B. Neuromuscular 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
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
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
pH < 7,36
pH > 7,44
acidaemia
alkalaemia
hypocapnia
hypercapnia
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
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
...