Metabolic acidosis ABG

ABG

1. Appraoch to Metabolic Acidosis Dr . Nadia Mohsen Abdu Ibrahim Specialist of Nephrology. NMGH

2. Systematic ABG analysis History taking and physical examination Assess accuracy of data ( validity). Identify the primary disturbance Check arterial pH-------- acidosis or alkalosis HCO 3 - & pCO 2 analysis---primary disorder. Compensatory responses Calculate AG Assess delta ratio Urine anion gab Formulate acid-base diagnosis

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. Systematic ABG analysis History taking and physical examination Assess accuracy of data ( validity). Identify the primary disturbance Check arterial pH-------- acidosis or alkalosis HCO 3 - & pCO 2 analysis---primary disorder. Compensatory responses Calculate AG Assess delta ratio Urine anion gab Formulate acid-base diagnosis

5. Validity H = (PCO2/ HCO3) ×24 =7.8 -PH ×100

6. Systematic ABG analysis History taking and physical examination Assess accuracy of data ( validity). Identify the primary disturbance Check arterial pH-------- acidosis or alkalosis HCO 3 - & pCO 2 analysis---primary disorder. Compensatory responses Calculate AG Assess delta ratio Urine anion gab Formulate acid-base diagnosis

7. Determine whether the patient is : acidemic (pH < 7.35) or alkalemic (pH > 7.45) whether the primary process is : metabolic (initiated by a change in HCO3-) or respiratory (initiated by a change in PaCO2). Step 3. Identify the primary disturbance

8. PCO2 HCO3 PH             Acidosis Acidosis Alkalosis Alkalosis Metabolic Metabolic Respiratory Respiratory

9. Systematic ABG analysis History taking and physical examination Assess accuracy of data ( validity). Identify the primary disturbance Check arterial pH-------- acidosis or alkalosis HCO 3 - & pCO 2 analysis---primary disorder. Compensatory responses Calculate AG Assess delta ratio Urine anion gab Formulate acid-base diagnosis

10. Step 4 . Compensatory responses Metabolic Metabolic acidosis Expected pCO2 = 1.5 x [HCO3] + 8 (range: +/- 2) Metabolic alkalosis Expected pCO2 = 0.7 [HCO3] + 20 (range: +/- 5) “If the actual pCO 2 or [HCO 3 - ] is different from the predicted values, You must suspect a 2 nd acid-base disorder”

11. Metabolic Acidosis

12. Systematic ABG analysis History taking and physical examination Assess accuracy of data ( validity). Identify the primary disturbance Check arterial pH-------- acidosis or alkalosis HCO 3 - & pCO 2 analysis---primary disorder. Compensatory responses Calculate AG Assess delta ratio Urine anion gab Formulate acid-base diagnosis

13. Basis of Metabolic Acidosis H + + HCO3 -  H 2 O + CO 2 Added acids Loss of NaHCO 3 New A- No New A- (rise in plasma AG) (no rise in plasma AG) (Exhaled)

14. Electrochemical Balance in Blood Na Cl HCO 3

15. Step 5: calculating the anion Gap (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

16. 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 HCO 3 - loss - Diarrhea - External fistulas 2. Renal HCO 3 - 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

17. Basis of Metabolic Acidosis H + + HCO3 -  H 2 O + CO 2 Added acids Loss of NaHCO 3 New A- No New A- (rise in plasma AG) (no rise in plasma AG) (Exhaled)

18. Electrochemical Balance in Blood Na Cl HCO 3

19. Systematic ABG analysis History taking and physical examination Assess accuracy of data ( validity). Identify the primary disturbance Check arterial pH-------- acidosis or alkalosis HCO 3 - & pCO 2 analysis---primary disorder. Compensatory responses Calculate AG Assess delta ratio Urine anion gab Formulate acid-base diagnosis

20. Step 6: Calculating the delta ratio Delta ratio= ∆ Anion gap/∆ [HCO3-] ∆ Anion gap = (AG-12) ∆ [HCO3-] = (24 - [HCO3-])

21. 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

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23. 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

24. Treatment of KA Fluids : IVF Insulin infusion Potassium replacement Bicarb replacement: If pH < 7.1 and/or cardiac instability present

25. 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

26. Treatment for Lactic Acidosis Identification of the primary illness and correction of that disturbance. Restoration of tissue oxygen delivery through hemodynamic and/or respiratory support is the key therapeutic goal in type A lactic acidosis. 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 .

27. Actual Bicarbonate Loss Normal Plasma Anion Gap Direct loss of NaHCO 3 Gastrointestinal tract (diarrhea, ileus, fistula or T-tube drainage, villous adenoma) Urinary tract (RTA , use of carbonic anhydrase inhibitors )

28. Renal Tubular Acidosis Inability of the kidney to reabsorb the filtered HCO 3 - Inability of the kidney to excrete NH 4 +

29. Proximal RTA Distal RTA RTA IV cause impairment of HCO3- reabsorption in the proximal tubules Acidification defect Hypoaldosteronism or Pseudohypoaldosteronism Type of Acidosis Hyperchloremic metabolic acidosis Hyperchloremic metabolic acidosis Hyperchloremic metabolic acidosis S.Potassium low low high Urine pH < 5.5 >5.5 < 5.5 Urine HCO3 loss +++ ++ ++

30. Metabolic Acidosis in Renal Failure Normal AG acidosis results from failure of the kidney to generate new HCO 3 - from a reduced rate of synthesis and excretion of NH 4 + Increased AG acidosis results from the reduced GFR, with accumulation of anions: HPO4

31. Management of Metabolic Acidosis Cause

32. 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

33. THANK YOU