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ACID – BASE DISORDERS

ACID – BASE DISORDERS. Prof. M. Tatár Dept. of Pathophysiology JLF UK. H + affects structure and function of proteins. . changes of cellular enzymes activity. . cellular and organ functions changes.

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ACID – BASE DISORDERS

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  1. 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. 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- HCO3- + 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 = 0,000000036 - 0,000000044 mol . l-1 = 36 - 44 nmol . l-1 pH = - log [ H+] mol . l-1 pH = 7,4  0,04 1.6 μm3 …… activity of 40 H+ mitochondria : 2 - 5 active H+

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

  7. acidemia - acidosis alkalemia - alkalosis

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

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

  10. 7,42 7,38 7,25 7,55 NL Acidosis Alkalosis pH 6,80 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. 7,42 7,38 7,25 7,55 NL Acidosis Alkalosis pH 6,80 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- HCO3- - 53% (plasma 35%, RBC- 18%) buffers Hb - HbO2 - 35% in blood Phosphates - 5% Plasm. prot. - 7%

  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 7,4 7,6 7,0 7,2 pH

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

  19. Anion gap [ Na+ ] - ( [Cl-] + [ HCO3-] ) = 10 - 12 mmol.l-1 140 - ( 104 + 24 ) = 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- retentionin 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- retentionin kidneys M M -------  ------- R  R Clinical features - CNS dysfunction:confusion, somnolence - cerebralvasodilation:  intracranialpressure,

  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 • tetany • - vomiting  renal excretion of HCO3- M M  ------  ------- R  R 

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

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