1 / 26

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.

holmes-vega
Download Presentation

ACID – BASE DISORDERS

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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

More Related