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Acid-Base Balance

Acid-Base Balance. Seminar No. 11. Parameters of acid base balance. Measured in arterial blood pH = 7.40 ± 0.04 = 7.36 – 7.44 pCO 2 = 4.8 – 5.8 kPa supporting data: pO 2 , tHb, s O 2 , HbO 2 , COHb, MetHb Calculated [HCO 3 - ] = 24 ± 3 mmol/l (from H.-H. eq.)

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Acid-Base Balance

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  1. Acid-Base Balance Seminar No. 11

  2. Parameters of acid base balance Measured in arterial blood • pH = 7.40 ± 0.04 = 7.36 – 7.44 • pCO2 = 4.8 – 5.8 kPa • supporting data: pO2, tHb, sO2, HbO2, COHb, MetHb Calculated • [HCO3-] = 24 ± 3 mmol/l (from H.-H. eq.) • BE = 0 ± 3 mmol/l (from S.-A. nomogram, see physilogy) • BBs = 42 ± 3 mmol/l • BBb = 48 ± 3 mmol/l

  3. Q. 1

  4. Buffer bases in (arterial) plasma * Molarity of negative charge  binding sites for H+

  5. Q. 2

  6. A. 2 BBs = 42 ± 3 mmol/l BBb = 48 ± 3 mmol/l hemoglobin in erythrocytes increases BBb by 6-8 mmol/l

  7. Q. 3

  8. Oxygen parameters and hemoglobin derivatives

  9. Oxygen parameters and hemoglobin derivatives Tissue hypoxia of any origin leads to lactic acidosis

  10. Q. 4

  11. A. 4 7.4 = 6.1 + log [HCO3-] / 0.22 × 5.3 1.3 = log [HCO3-] / 1.2 101.3 =[HCO3-] / 1.2 20 = [HCO3-] / 1.2 [HCO3-] = 24 mmol/l

  12. Four types of acid-base disorders pH = 6.1 + log Changes in [HCO3-] metabolic acidosis  metabolic alkalosis Changes in pCO2  respiratory alkalosis  respiratory acidosis

  13. Maintanance of constant pH in body

  14. Responses to acute change • compensation • correction

  15. Q. 6

  16. A. 6

  17. Metabolic acidosis is the most common conditionMetabolic alkalosis isthe most dangerous condition

  18. Q. 8

  19. normal status hyperchloremic MAC normochloremic MAC

  20. normal status hyperchloremic MAC normochloremic MAC See Q. 11 NaCl infusions

  21. Q. 9

  22. A. 9 Excessive infusions of NaCl isotonic solution lead to metabolic acidosis Isotonic solution of NaCl has elevated concentration ofCl- compared to plasma Blood plasma is diluted by infusion solution  [HCO3-]decreases pCO2 in alveolar air is the same the ratio [A-] / [HA] in H.-H. equation decreases  pH < 7.40 (acidosis)

  23. Q. 10

  24. Hyperchloremic MAc • excessive infusions of NaCl solution • the loss of HCO3- + Na+ +water (diarrhoea, renal disorders)  relative higher concentration of chlorides in plasma

  25. Q. 11 How is AG calculated?

  26. AG AG calculation = [Na+] + [K+] - [Cl-] - [HCO3-] AG composition = HPO42- + Prot- + SO42- + OA

  27. A. 11 MAc with increased AG • Hypoxia of tissues – insufficient supply of O2 anaerobic glycolysis: glucose  2 lactate • elevated AG – lactoacidosis • Starvation, diabetes • TAG  FA (β-oxidation in liver) acetyl-CoA (excess, over the capacity of CAC)  KB production • elevated AG - ketoacidosis • Renal insufficiency – elevated phosphates, sulfates • Various intoxications

  28. Q. 12

  29. A. 12 • AG – normal values • SID – buffer bases (mainly HCO3-) – decreased • compare Q. 8a)

  30. Q. 13 Metabolic acidosis

  31. Q. 15 Methanol intoxication

  32. Metabolic oxidation of methanol provides a rather strong formic acid • Consequences: • formate in plasma  elevated AG  acidosis • excess of NADH  lactoacidosis

  33. ethanol acetic acid pKA = 4.75 KA = 1.8  10-5 methanol formic acid pKA = 3.75 KA = 1.8  10-4 Compare two acids KA (formic ac.) : KA (acetic ac.) = 10 : 1 formic acid is 10  stronger than acetic acid

  34. ethylene glycol intoxication

  35. Intoxication by ethylene glycol • Consequences: • oxalic acid is rather strong acid (pKA1 = 1.25, pKA2 = 4.29) • oxalate in plasma  elevated AG  acidosis • excess of NADH  lactoacidosis • in urine  calcium oxalate concrements

  36. Calcium oxalate is insoluble chelate Draw formula

  37. Calcium oxalate is insoluble chelate

  38. Why MAc occurs in anemia?

  39. Not enough hemoglobin  insufficient supply of O2  hypoxia  anaerobic glycolysis to lactate elevated AG – lactoacidosis

  40. Q. 16

  41. Metabolic oxidation of ethanol leads to excess of NADH alcohol dehydrogenase (ADH) acetaldehyde acetaldehyde dehydrogenase - NADH+H+ acetic acid acetaldehyde hydrate

  42. Metabolic consequences of EtOH biotransformation Ethanol ADH ADH MEOS the excess of NADH in cytosol is reoxidized by pyruvate to lactate part.soluble in membrane PL acetaldehyde acetate adducts with proteins, NA, biog. amines toxic efects on CNS acetyl-CoA lactoacidosis various products causing hangover FA synthesisliver steatosis

  43. Q. 17

  44. CH3-CO-COOH + CoA-SH + NAD+ CO2 + CH3-CO-S-CoA + NADH+H+ • thiamine is the cofactor of aerobic decarboxylation of pyruvate • thiamine deficit  pyruvate cannot be converted to acetyl-CoA • therefore pyruvate is hydrogenated to lactate • even in aerobic conditions: glucose  lactate • increased plasma lactate  elevated AG  lactoacidosis • Thiamindiphosphate • Lipoate • Coenzym A • FAD • NAD+

  45. Q. 18

  46. A. 18 • calcium cations make electrostatic interactions with carboxylate anions in side chains of glutamate and aspartate (in various proteins) • increased [H+] (= decreased pH) of plasma leads to a partial cation exchange • one calcium ion is liberated and replaced by two protons

  47. Causes of metabolic alkalosis • Repeated vomiting – the loss of chloride (Cl-) anion  hypochloremic alkalosis • Direct administration of buffer base HCO3- per os: baking soda, some mineral waters intravenous infusions of sodium bicarbonate • Hypoalbuminemia severe malnutrition liver damage, kidney damage

  48. What is baking soda?

  49. A. NaHCO3 sodium hydrogen carbonate (sodium bicarbonate) sold in pharmacy

  50. Q. 19 How is SID calculated?

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