1 / 35

(3) Metabolic alkalosis

(3) Metabolic alkalosis. 1) Concept 2) Classification and Pathogenesis 3) Compensation 4) Effects on the body 5) Principle of treatment. 1)Concept Metabolic alkalosis is defined as a primary increase of [HCO 3 ¯ ] in plasma, the pH has a tendency to increase. (means ?).

sani
Télécharger la présentation

(3) Metabolic alkalosis

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. (3) Metabolic alkalosis • 1) Concept • 2) Classification and Pathogenesis • 3) Compensation • 4) Effects on the body • 5) Principle of treatment

  2. 1)Concept • Metabolic alkalosis is defined as a primary increase of [HCO3¯ ] in plasma, the pH has a tendency to increase. (means ?)

  3. 2) Classification and Pathogenesis •  According to the therapeutic effect of 0.9% NaCl, • (a) chloride-sensitive type • (b) chloride-resistant type.

  4. (a) Chloride-sensitive type Pathogenesis a) Increased loss of H+ from stomach • b) Increased loss of H+ from kidney • c) H+ enters into cells • d) Overload of HCO3¯

  5. a) Increased loss of H+ from stomach There is a lot of H+ in the gastric juice. Vomiting and gastric suction will lose gastric fluid . HCO3-is absorbed into blood, then to intestinal juice to neutralizeH+.

  6. b) Increased loss H+ from kidneys: Some diuretics (e.g. furosemide速尿) can inhibit the reabsorption of Cl¯ and Na+ in loop, urine volume is increased (50~60L/24hs). Increased loss H+ from kidneys Concentrated [HCO3¯]

  7. c) H+ enters into cells • Hypokalemia • Unusual aciduria

  8. d) Overload of HCO3¯ Patients with gastric ulcer may be orally given excessive NaHCO3 to neutralize gastric juice. Sharp correction of acidosis by excessive alkali administration can lead to metabolic alkalosis. Lactate and citrate can be catalyzed into HCO3¯ . Transfusion of anticoagulant blood with sodium citrate.

  9. (b) Chloride-resistant type a) Primary hyperaldosteronism Secondary hyperaldosteronism caused by hypovolemia Effect: Stimulate H+-ATPase.

  10. b)Severe hypokalemia(??) K+-Na+ exchange H+ -Na+ exchange c)Cushing Syndrome: more glucocorticoids.

  11. 3) Compensation of metabolic alkalosis The secondary change is the increased [H2CO3] in plasma. The compensation of metabolic alkalosis is the opposite direction of the compensation in metabolic acidosis. (a) Buffering system in ECF (b) Pulmonary compensation (c) Cellular buffering (d) Renal compensation

  12. (a) Buffering system in ECF After the addition of alkali, the buffering system initiates immediately. NaHCO3 Na2HPO4 Hb- ------------- -------------- ------- H2CO3 NaH2PO4 HHb H2CO3 combines the excessive OH¯ (strong) to form HCO3¯ (weak alkaline).

  13. increased pH (b) Respiratory compensation • Via central chemoreceptors inhibit the respiratory center Limitation: High PaCO2 and low PaO2 stimulate the respiratory center. slow shallow respiration more carbon dioxide can be accumulated in blood decrease of pH

  14. (c) Cellular buffering The H+ moves out of cells into ECF, at the same time K+ moves into the cells.

  15. (d) Renal compensation The reabsorption of [HCO3¯ ] is decreased. The acids excretion is decreased.

  16. In metabolic alkalosis, the activity of carbonic anhydrase (CA) decreases, the H+ production is decreased, the H+-Na+ exchange is decreased, the reabsorption of HCO3¯ is decreased.

  17. In metabolic alkalosis, the activity of glutaminase is decreased, less glutamine will be decomposed into HCO3¯ and NH3. Thus less HCO3¯ will be reabsorpted to the blood, more HCO3¯ will be eliminated.

  18. Decreased net acid excretion with urine • Less H2PO4 ¯ and NH4+ are in the end urine. • The pH of urine will elevate due to the decreased net acid excretion with urine .

  19. Changes of laboratory parameters • Primary increase of [HCO3¯]: • AB,SB,BB ??? • AB ?? SB • BE ? • Secondary compensation: • PaCO2 ? • pH ?

  20. Changes of laboratory parameters • Primary increase of [HCO3¯]: • AB,SB,BB increase • AB > SB • BE positive increase • Secondary compensation: • PaCO2 increase • pH tends to increase.

  21. Predicted compensatory formula ΔPaCO2(mmHg) = 0.7 x ΔHCO3-±5 Secondary compensation primary change Or: PaCO2=40+0.7xHCO3-±5 PaCO2 can increase maximal to 55 mmHg. Value measured > value predicted: with respiratory acidosis Value measured < value predicted: with respiratory alkalosis

  22. 4) Effects on the body  (a) The left-shift of oxygen-hemoglobin dissociation curve (b) Effects on the central nervous system. (c) Decrease of ionized calcium (Ca2+) in plasma (d)Hypokalemia

  23. (a)The left-shift of oxygen-hemoglobin dissociation curve leads to hypoxia. This “left –shift” means the Hb combines more oxygen under the same PaO2 and the O2 is more difficult to dissociate from Hb. (hypoxia)

  24. (b) Effects on the central nervous system • a) Manifestations: • Excitability is increased. • dysphoria (agitation), • malaise (discomfort), • delirium ( mental disturbance with wild talk and wild excitement), • confusion,

  25. b)The reasons : • The left-shift of oxygen-hemoglobin dissociation curve leads to brain hypoxia.

  26. Glutamate decarboxylase r-GABA, r-aminobutyric acid Glutamic acid r-GABA transaminase Succinic acid Kreb’s cycle The production of GABA (gama aminobutyric acid, a inhibitory transmitter) is decreased due to the activity of enzyme for the production is reduced in alkalosis.

  27. (c) Decrease of Ca2+ in plasma More calcium combines to the plasma proteins in alkalosis. • OH- • Ca2+ protein-bound calcium •  Ca2+ protein-bound calcium • H+

  28. Manifestation: • The main character is the increased neuromuscular excitability. • The symptoms include : • a) twitching 颤搐(quick uncontrollable muscle movement) • b)tetany手足搐搦 • c) cramping (convulsions)

  29. (d) Hypokalemia • Causes: • a)H+ shifts out of the cells as the compensation of alkalosis. Therefore the K+ moves into the cells as an exchange for electro-equilibrium. b) Less H+ -Na+ exchange and more K+-Na+ exchange leads more K+ excretion with urine. Manifestations: arrhythmias

  30. (4) Principle of treatment. • 1) For chloride-sensitive type • (A) Replenish 0.9% NaCl • [Na+] [Cl-]( mmol/L) • --------------------------------------------------------- • 0.9%NaCl 154 154 • Plasma 140 104 • --------------------------------------------------------- • A) Dilute the [HCO3-] • B) Increase the blood volume, reduce the reabsorption of HCO3-. • C) Increased Cl- in distal tubule leads to increased excretion of HCO3-in collecting duct.

  31. (B) Replenish KCl for the patients with potassium deficiency.

  32. 2) For chloride-resistant type Treating of underlying disorders Antagonists of aldosterone Replenish KCl Acetazolamide乙酰唑胺( inhabit the CA activity) for the patients with edema with alkalosis.

  33. A 25-year-old woman was brought to the emergency room by her husband. The patient had one-week history of weakness. She denied vomiting, diarrhea, or diuretic use (but a urine test for diuretics is positive). There was no history of fever or chills.

  34. Physical examination: • BP=110/80 mmHg, • Pulse=84/min, Temperature=37.C. • The neurological examination found weakness in both lower extremities. • Laboratory results: • [Na+] = 138 mmol/L, [K+] = 2.1 mmol/L, • [Cl-] = 85 mmol/L, [HCO3-] = 41 mmol/L, • pH = 7.45, PaCO2=50 mmHg, • EKG: Sinus rhythm, flattened T-wave

  35. Hypokalemia, • metabolic alkalosis. ΔPaCO2(mmHg) = 0.7 x ΔHCO3-±5 Secondary compensation primary change • (12) (41-24) • 40+12=52 ±5

More Related