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酸碱平衡及紊乱 Acid – Base Balance and Disturbances

酸碱平衡及紊乱 Acid – Base Balance and Disturbances. Acid-Base Balance Maintenance of the H + concentration in body fluid in a normal range. H + mol/L pH Extracellular fluid Arterial blood 4.0 x 10 -8 7.40 ± 0.05 Venous blood 4.5 x 10 -8 7.35

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酸碱平衡及紊乱 Acid – Base Balance and Disturbances

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  1. 酸碱平衡及紊乱Acid – Base Balance and Disturbances

  2. Acid-Base BalanceMaintenance of the H+ concentration in body fluid in anormal range H+ mol/LpH Extracellular fluid Arterial blood4.0 x 10-87.40 ± 0.05 Venous blood 4.5 x 10-8 7.35 Interstitial fluid 4.5 x 10-8 7.35 Intracellular fluid 1.0 x 10-6 6.0 to 4.0 x 10-8 7.4 pH = - lg H+

  3. Why is the acid - base balance important for life ?

  4. Acid generation • Volatile acid CO2 + H2O  H2CO3  H+ + HCO3- H+ 15 –20 mol /d •Fixed acids phosphoric, sulfuric, lactic, ketone bodies etc. H+ < 0.05 –0.10 mol /d

  5. Regulation of acid – base balance • Buffering Buffer system can bind and release H+ Dissociated buffer + H+ H undissociated buffer Principal buffers in blood: in Plasma in RBC H2CO3 / HCO3- 35% 18% HHb / Hb- 35% HProt / Prot- 7% H2PO4- / HPO42- 5%

  6. Bicarbonate buffer system determines the pH of blood plasma CO2 + H2O  H2CO3 H+ + HCO3- Handerson-Hasselbalch Equation + pH = pK + lg HCO3- / H2CO3 Na+ = 6.1 + lg HCO3- / 0.03 x PCO2 = 6.1 + lg 24 / 1.2 = 7.4 • Bicarbonate-carbonic acid system is the major extracellular buffer 53% • H2CO3 can be regulated by lung • HCO3- can be regulated by kidney

  7. Respiratory regulation PaCO2, pH  Chemorecertor   Pulmonary ventilation  PaCO2 pH 7.0  VA increases by 4-5 times pH  VA decreases less

  8. Renal regulation Plasma pH HCO3-  H+ Reabsorption & Excretion Regeneration Plasma pH Renal H+ excretion = fixed acid production = 1mmol/kg/d

  9. Reabsorption of HCO3- in different segments of renal tubule

  10. Reabsorption of HCO3- coupled with H+ excretion in proximal tubules Na+ CA

  11. Regeneration Regeneration of HCO3- coupled with the buffering of secreted H+ by filtered Na2HPO4 in distal tubules ATP Cl-

  12. Regeneration of HCO3- coupled with buffering ofH+ by NH3 in proximaltubular cells Glutamine Tubular lumen glutaminase NH3 NH3 -keto glutaric acid NH4+ NH4+ H2CO3 Na+ Na+ HCO3- H+ H+ ATP

  13. Regeneration of HCO3- coupled with buffering of H+ by NH3 in collecting tubular cells Cl-

  14. Net acid excretion by kidney = NH4+ excretion + urinary titratable acid – bicarbonate excretion = nonvolatile acid production In acidosis, a net addition of HCO3- back to blood as more NH4+ and urinary titratable acid are excreted In alkalosis, titratable acid and NH4+ excretion drop to 0, whereas HCO3- excretion increases (No new bicarbonate is generated)

  15. Parameters of acid – base balance • pH = 6.1 + lg HCO3-/ H2CO3 Normal value of pH in arterial blood 7.4±0.05 pH normal, may be 1) acid-base balance 2) compensatory acid-base disorder 3) mixed acid-base disorder

  16. 2. PaCO2 x 0.03 = H2CO3 Normal PaCO2 40 ± 6 mmHg determined by the rate of CO2 elimination (alveolar ventilation), not by its production. --- Respiratory parameter 3. Bicarbonate ( HCO3- ) Normal value of HCO3- in plasma under actual condition is 24 ± 2 mmol/L HA + NaHCO3 NaA + H2CO3 determined by the amount of nonvolatile acid produced in metabolism --- Metabolic parameter

  17. Cl- (104) Na+ (140) HCO3- (24) UA (23) UC (11) mEq/L 4. Anion gap (AG) = UA - UC = Na+ - ( HCO3-+Cl- ) = 140 - ( 24+104 ) = 12±2mEq/L dAG =dUA = dHCO3-

  18. Summary • The maintenance of H+ concentration of body fluid in a normal range is very important for life. • Normal value of arterial pH is 7.35 – 7.45, which is determined by the HCO3-/H2CO3 ratio, and regulated by buffering, lung and renal regulation. • Buffers act to minimize changes in pH induced by acid or base load; PaCO2 is controlled by alteration of pulmonary ventilation; HCO3- in plasma is regulated by renal reabsorption and regeneration of HCO3- coupled with equivalent H+ excretion.

  19. Simple acid-base disorders Metabolic acidosis Primary decrease in plasma HCO3- Causes of metabolic acidosis: • High AG type ---- Fixed acid  HCO3- 1.  Production of fixed acids 2. Retention of fixed acids ---  GFR 3. Acid intake – salicylate etc.

  20. • Normal AG type ---- hyperchloremic 1. HCO3- reabsorption or regeneration in renal tubules: Renal tubular acidosis ( RTA ) Renal failure Carbonic anhydrase inhibitor 2. HCO3- losses in alimentary tract: Diarrhea 3. HCl, NH4Cl intake 4. Hyperkalemia

  21. § Hyperchloremia in normal AG type due to reabsorption of Cl- RTA  HCO3- reabsorption Cl-reabsorption Diarrhea  Ald NaCl reabsorption § Paradoxical alkaluria in acidosis Renal tubular acidosis --- HCO3- reabsorption or  H+ excretion Hyperkalemia  renal H+ excretion

  22. Compensation of metabolic acidosis: 1) Extracellular buffering --- immediately HA + NaHCO3  NaA + H2CO3 2) Respiratory compensation Ventilation in few min, maximal in 12-24 h d PaCO2 = 1.2 d HCO3- ± 2 3) Intracellular buffering --- in 2-4h 4) Renal compensation begin in several h, maximal in 3-5d

  23. Respiratory acidosis Primary increase of PaCO2 Causes: 1) External respiratory dysfunction 2) PCO2 in inspired air

  24. KHb K+ HHb Compensation of respiratory acidosis 1. Buffering ---- immediately CO2 H2O H2CO3 H2CO3 K+ HCO3- H+ HCO3- HCO3- Cl-

  25. 2. Renal compensation Acute --- d [ HCO3-] = 0.1 d PaCO2 ± 1.5 Chronic ---d [HCO3-] = 0.4 d PaCO2 ± 3

  26. Ca2+influx H+ SR [Ca2+]i↑ Contraction Binding to Troponin Pathophysiological changes caused by acidosis • Cardiovascular system 1) Decrease of myocardial contractility – pH<7.2Responsiveness of -adrenoceptor

  27. 2) Cardiac arrhythmia Acidosis  hyperkalemia  arrhythmia 3) Vasodilation  Responsiveness of -adrenoreceptor

  28. Central nervous system depression, coma ( pH < 6.9 ) 1) GABA ---- glutamate decarboxylase activity 2) Oxidase activity   ATP 3) Cerebral vasodilation  intracranial pressure What kind of acidosis has more effect on CNS, metabolic or respiratory?

  29. Hyperkalemia --- 1) [H+]e exchange for [K+]i • 2) Decreased excretion of K+ by distal renal tubules H+ (-) Na+ Na+ Ald Ald ATPase [K+]e K+channel K+ K+[K+]e H+ (-) Mg2+(-) Urine flow K+ Tubular l Principal cell Interstitial fluid

  30. Metabolic alkalosis Primary increase of HCO3- Causes: 1) Excess bicarbonate load ---- intake 2) Gastric H+ loss ---- vomiting Why HCO3- in plasma is increased? 3) Renal H+ loss Diuretics --- distal urine flow Hyperaldosteronism --- activation of H+ pump and Na+-K+ pump 4) Hypokalemia

  31. Compensation of metabolic alkalosis 1) Buffering --- in cells 2) Respiratory compensation ---incomplete 3) Renal compensation --- tremendous

  32. The causes of paradoxical aciduria? • What kind of metabolic alkalosis is saline responsive? or saline resistant? vomiting? diuretics? primary hyperaldosteronism?

  33. Respiratory alkalosis Primary decrease of PaCO2 • Cause ---- alveolar hyperventilation Hypoxia, psychoneurosis, fever etc. • Compensation Buffering Renal compensation Acute -----dHCO3 = 0.2 d PaCO2 2.5 Chronic ---dHCO3 = 0.5 d PaCO2 2.5

  34. Functional and Metabolic Changescaused by alkalosis • Central nervous system Dysphoria, confusion, seizure, coma etc. 1)  GABA 2) Hypoxia from: hypoventilation, cerebral vasoconstriction left-shift of oxyhemoglobin dissociation curve • Neuromuscular excitability ---- cramping  ionic calcium in plasma •Hypokalemia --- paresis, arryhthmia

  35. Analysis of simple acid-base disorder

  36. Mixed acid-base disorders • Double acid base disorders Metabolic Metabolic acidosis alkalosis Respiratory Respiratory acidosis alkalosis

  37. COPDO2HCO3-  PaCO2 pH CO2PaCO2 HCO3- pH  HCO3-/  PaCO2   pH • COPD + O2 PaCO2 HCO3- pH + Diuretics  HCO3- PaCO2 pH   HCO3- /  PaCO2  pH normal

  38. Renal failure HCO3-  PaCO2 pH Vomiting  HCO3-   PaCO2 pH N HCO3- / N PaCO2  pH normal All these parameters are normal, how to find out the acid-base disorder?

  39. Triple acid-base disorders Metabolic Metabolic acidosis alkalosis Respiratory Respiratory acidosis alkalosis

  40. Exp: COPD  O2 HCO3-  PaCO2  pH CO2 PaCO2  HCO3  pH Diuretics   HCO3-  PaCO2  pH HCO3-PaCO2   pH

  41. Summery • Metabolic acidosis is induced by primary decrease of HCO-3 owing to increased production or retention of fixed acides or HCO-3 loss. • Metabolic alkalosis is induced by primary increase of HCO-3 due to H+ loss. • Respiratory acidosis or alkalosis is induced by primary increase or decrease of CO2 caused by hypoventilation or hyperventilation.

  42. Acidosis depresses activity of CNS and myocardial contractility, and induces cardiac arrhythmia and vasodilation. • Alkalosis results in dysfunction of CNS and cramping. • Different kinds of acid-base disorders may coexist in patients.

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