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Metabolic Acidosis and Alkalosis

Metabolic Acidosis and Alkalosis. Acid/base physiology ​Acid-base equilibrium ​pH = 6.1 + log [HCO3] / (0.3 PCO2) ​simplified (normal conditions): H+ = 24 PCO2 / HCO3 ​Proximal tubule reabsorbs HCO3 ​- Reclamation via Na/H antiport.

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Metabolic Acidosis and Alkalosis

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  1. Metabolic Acidosis and Alkalosis

  2. Acid/base physiology ​Acid-base equilibrium ​pH = 6.1 + log [HCO3] / (0.3 PCO2) ​simplified (normal conditions): H+ = 24 PCO2 / HCO3 ​Proximal tubule reabsorbs HCO3 ​- Reclamation via Na/H antiport

  3. ​- Generation from CO2 (carbonic anhydrase) w/ acid secretion ​- Generation from Gln with NH4+ secretion ​Collecting duct secretes acid ​- Principal cell: Na reabs via ENaC makes lumen negative, promoting acid secretion (aldosterone +ve regulation).

  4. ​- Intercalated A cell: H/K antiport and H+ ATPase pump ​- Exception: intercalated B cell secretes base (like an reverse polarity A cell).

  5. Metabolic alkalosis ​Definition: high pH (> 7.4) due to high HCO3 (> 24) ​Check for respiratory compensation: expect D HCO3 ® 0.5-0.7 D PCO2 ​ Consequences of alkalemia: Increase respiration, increase Hbg O2 affinity, vasoconstriction.

  6. ​Factors that promote acid secretion (alkalosis maintenance) ​¯ ECF​(¯ GFR ® ¯ filtered HCO3) ( Na/H antiport) (aldosterone) ​¯ K​( Na/H antiport) ( NH3 generation) ​¯ Cl​( intercalated A cell activity, ¯ intercalated B cell activity) ​Aldosterone​( Na reabs in collecting duct).

  7. Gastric alkalosis (vomiting, nasogastric suction).

  8. Metabolic acidosis ​Definition: low pH (< 7.4) due to low HCO3 (< 24) ​Check for respiratory compensation: expect D¯ HCO3 ® 1.2 D¯ PCO2.

  9. Metabolic Acidosis is a fall in plasma HCO3, low arterial pH, and compensatory hyperventilation ​to blow off CO2. So in metabolic acidosis, pH, HCO3, and CO2 are all lowered. ​In respiratory acidosis, CO2 and then HCO3 are both elevated.

  10. Two kinds of acids – carbonic and titratable Carbonic acid comes from metabolism of carbohydrates and fats, which releases CO2. This CO2 ​combines with water to form carbonic acid.

  11. Titratable acids come from metabolism of proteins, which releases sulfuric and phosphoric acids. These are what cause metabolic acidosis if kidney funtion is impaired.

  12. HCO3 is the extracellular buffer: Bonesand cells are the intracellular buffer. As H+ moves into cells, K+ moves out. So acidosis ​can also cause hyperkalemia. Acidosis will cause increased tidal volume, rather than respiratory rate (“Kussmaul’s respiration”).

  13. Acid excretion in the kidneys Filtered HCO3 is completely reabsorbed (90% proximal tubule, 10% distal tubule). This requires ​carbonic anhydrase.

  14. H+ is secreted by tubular cells into lumen using a Na+/H+ exchanger, and by intercalated cells using ​an H+ ATPase. H+ in the lumen is buffered by titratable acids HSO4-, HPO4-, or NH3.

  15. Acidosis will stimulate kidneys to generate lots of NH3 to buffer H+ in the lumen. Once it becomes ​NH4+ it cannot diffuse back into cells and is stuck in the lumen and will be excreted.

  16. NH3 is the main acid buffer in the urine.

  17. Solving Acid-Base Problems Always look at the HCO3 levels and compare to pH. If there is acidic pH with low HCO3, it is ​metabolic acidosis. If there is acidic pH with high HCO3, it is respiratory acidosis.

  18. Disorder​​ pH​ H+ ​​Primary​ Compensatory Metabolic acidosis​¯​ ​¯ HCO3- ​¯ PCO2 Metabolic alkalosis​ ​¯​​ HCO3- ​ PCO2 Respiratory acidosis​¯​ ​​ PCO2 ​ HCO3- Respiratory alkalosis​​ ​¯​​¯ PCO2 ​¯ HCO3-

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