Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Metabolic acidosis ABG

7,093 views

Published on

ABG

Published in: Education
  • If you’re struggling with your assignments like me, check out ⇒ www.HelpWriting.net ⇐.
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • Hello! I can recommend a site that has helped me. It's called ⇒ www.WritePaper.info ⇐ They helped me for writing my quality research paper.
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • I’ve personally never heard of companies who can produce a paper for you until word got around among my college groupmates. My professor asked me to write a research paper based on a field I have no idea about. My research skills are also very poor. So, I thought I’d give it a try. I chose a writer who matched my writing style and fulfilled every requirement I proposed. I turned my paper in and I actually got a good grade. I highly recommend ⇒ www.HelpWriting.net ⇐
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • Dating direct: ♥♥♥ http://bit.ly/2u6xbL5 ♥♥♥
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here

Metabolic acidosis ABG

  1. 1. Appraoch to Metabolic Acidosis Dr. Nadia Mohsen Abdu Ibrahim Specialist of Nephrology. NMGH
  2. 2. 1. History taking and physical examination 2. Assess accuracy of data (validity). 3. Identify the primary disturbance 1. Check arterial pH-------- acidosis or alkalosis 2. HCO3 - & pCO2 analysis---primary disorder. 4. Compensatory responses 5. Calculate AG 6. Assess delta ratio 7. Urine anion gab 8. Formulate acid-base diagnosis
  3. 3. • Step 1. History taking and physical examination Comprehensive history taking and physical examination can often give clues as to the underlying acid-base disorder
  4. 4. 1. History taking and physical examination 2. Assess accuracy of data (validity). 3. Identify the primary disturbance 1. Check arterial pH-------- acidosis or alkalosis 2. HCO3 - & pCO2 analysis---primary disorder. 4. Compensatory responses 5. Calculate AG 6. Assess delta ratio 7. Urine anion gab 8. Formulate acid-base diagnosis
  5. 5. Validity
  6. 6. 1. History taking and physical examination 2. Assess accuracy of data (validity). 3. Identify the primary disturbance 1. Check arterial pH-------- acidosis or alkalosis 2. HCO3 - & pCO2 analysis---primary disorder. 4. Compensatory responses 5. Calculate AG 6. Assess delta ratio 7. Urine anion gab 8. Formulate acid-base diagnosis
  7. 7. PCO2HCO3PH           Acidosis Acidosis Alkalosis Alkalosis Metabolic Metabolic Respiratory Respiratory
  8. 8. 1. History taking and physical examination 2. Assess accuracy of data (validity). 3. Identify the primary disturbance 1. Check arterial pH-------- acidosis or alkalosis 2. HCO3 - & pCO2 analysis---primary disorder. 4. Compensatory responses 5. Calculate AG 6. Assess delta ratio 7. Urine anion gab 8. Formulate acid-base diagnosis
  9. 9. Metabolic acidosis Expected pCO2 = 1.5 x [HCO3] + 8 (range: +/- 2) Metabolic alkalosis Expected pCO2 = 0.7 [HCO3] + 20 (range: +/- 5) “If the actual pCO2 or [HCO3 -] is different from the predicted values, You must suspect a 2nd acid-base disorder”
  10. 10. 1. History taking and physical examination 2. Assess accuracy of data (validity). 3. Identify the primary disturbance 1. Check arterial pH-------- acidosis or alkalosis 2. HCO3 - & pCO2 analysis---primary disorder. 4. Compensatory responses 5. Calculate AG 6. Assess delta ratio 7. Urine anion gab 8. Formulate acid-base diagnosis
  11. 11. Basis of Metabolic Acidosis H+ + HCO3-  H2O + CO2 Added acids Loss of NaHCO3 New A- No New A- (rise in plasma AG) (no rise in plasma AG) (Exhaled)
  12. 12. Electrochemical Balance in Blood 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100% CATIONS ANIONS Sulfate Phosphate Mg- OA K - Proteins Ca-HCO3 Na- Cl UAUC Na Cl HCO3
  13. 13. • (Na + K) + UC = (Cl + HCO3) + UA • The anion gap is defined as the quantity of anions not balanced by cations. • Anion Gap= measured cation- measured anion. • AG = [Na + K] – (Cl + HCO3) = 12 ± 4 meq/L • Corrected AG (in Hypoalbuminemia): 4-alb*2.5
  14. 14. High Anion Gap Normal anion gap • 1. Ketoacidosis - Diabetic - Alcoholic - Starvation • 2. Lactic acidosis • 3. Toxicosis - Ethylene glycol - Methanol - Salicylates • 4. Advanced renal failure • 1. GIT HCO3 - loss - Diarrhea - External fistulas • 2. Renal HCO3 - loss - Proximal RTA - Distal RTA - Hyperkalemic RTA metabolic acidosis (MUD PILES) Methanol Uremia Diabetic ketoacidosis Propylene glycol Isoniazid intoxication Lactic acidosis Ethanol ethylene glycol Salicylates
  15. 15. Basis of Metabolic Acidosis H+ + HCO3-  H2O + CO2 Added acids Loss of NaHCO3 New A- No New A- (rise in plasma AG) (no rise in plasma AG) (Exhaled)
  16. 16. Electrochemical Balance in Blood 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100% CATIONS ANIONS Sulfate Phosphate Mg- OA K - Proteins Ca-HCO3 Na- Cl UAUC Na Cl HCO3
  17. 17. 1. History taking and physical examination 2. Assess accuracy of data (validity). 3. Identify the primary disturbance 1. Check arterial pH-------- acidosis or alkalosis 2. HCO3 - & pCO2 analysis---primary disorder. 4. Compensatory responses 5. Calculate AG 6. Assess delta ratio 7. Urine anion gab 8. Formulate acid-base diagnosis
  18. 18. Delta ratio= ∆ Anion gap/∆ [HCO3-] ∆ Anion gap = (AG-12) ∆ [HCO3-] = (24 - [HCO3-])
  19. 19. Delta ratio Assessment Guidelines < 0.4 Hyperchloremic normal anion gap acidosis < 1 High AG & normal AG acidosis = 1 Pure Anion Gap Acidosis Lactic acidosis: average value 1.6 DKA more likely to have a ratio closer to 1 due to urine ketone loss > 1 High AG acidosis and a concurrent metabolic alkalosis
  20. 20. s
  21. 21. Ketoacidosis • In patients with IDDM, alcoholics and pts undergoing fasting or starvation • due to the overproduction of ketone bodies (Ketosis) leading to accumulation of ketones in plasma (Ketonemia) and urine (Ketonuria). • In starvation states where plasma glucose levels are low or in states of low plasma insulin where uptake of glucose by cells is diminished, fatty acids will be mobilized and transported to tissues (brain, skeletal muscle, heart) for fatty acid oxidation and energy production. • acetyl CoA from fatty acid oxidation can not be oxidized and is instead converted to the generation of ketone bodies. (acetoacetate and β- hydroxybutyrate) Which serve as a source of fuel
  22. 22. Treatment of KA • Fluids: IVF • Insulin infusion • Potassium replacement • Bicarb replacement: If pH < 7.1 and/or cardiac instability present
  23. 23. Lactic Acidosis • Dead-end product of glycolysis • Occurs when the body must regenerate ATP without oxygen • Normal lactic level is maintained at 0.7-1.3 mEq/L • Eliminated in liver (50%), kidneys (25%), heart and skeletal muscles • Normal Lactate/Pyruvate ratio suggest that the cause is not related to anaerobic metabolism or anoxia
  24. 24. Treatment for Lactic Acidosis 1. Identification of the primary illness and correction of that disturbance. 2. Restoration of tissue oxygen delivery through hemodynamic and/or respiratory support is the key therapeutic goal in type A lactic acidosis. 3. the use of sodium bicarbonate in lactic acidosis is controversial, particularly in patients with circulatory and respiratory failure. Despite the controversy most physicians support administration of NaHCO3 for very severe acidemia and will give small amounts of NaHCO3 to maintain the arterial pH above 7.10, since a pH beyond this value will promote the development of arrhythmias and cardiac depression.
  25. 25. Actual Bicarbonate Loss Normal Plasma Anion Gap • Direct loss of NaHCO3 • Gastrointestinal tract (diarrhea, ileus, fistula or T-tube drainage, villous adenoma) • Urinary tract (RTA, use of carbonic anhydrase inhibitors)
  26. 26. Renal Tubular Acidosis • Inability of the kidney to reabsorb the filtered HCO3 - • Inability of the kidney to excrete NH4 +
  27. 27. Proximal RTA Distal RTA RTA IV cause impairment of HCO3- reabsorption in the proximal tubules Acidification defect Hypoaldosteronis m or Pseudohypoaldost eronism Type of Acidosis Hyperchloremic metabolic acidosis Hyperchloremic metabolic acidosis Hyperchloremic metabolic acidosis S.Potassiu m low low high Urine pH < 5.5 >5.5 < 5.5 Urine HCO3 loss +++ ++ ++
  28. 28. Metabolic Acidosis in Renal Failure • Normal AG acidosis results from failure of the kidney to generate new HCO3 - from a reduced rate of synthesis and excretion of NH4 + • Increased AG acidosis results from the reduced GFR, with accumulation of anions: HPO4
  29. 29. MANAGEMENT OF METABOLIC ACIDOSIS Cause
  30. 30. • Bicarbonate is probably not useful in most cases of high anion gap acidosis • Bicarbonate therapy may be useful for correction of normal anion gap acidosis
  31. 31. THANK YOU

×