1. Approach to Acid Base Disorder Dr.M.Nazrul Islam Associate Professor Department of Biochemistry Dinajpur Medical College Bangladesh

2. Slide 2 Acid Base Balance Homeostasis of H + concentration

3. Slide 3 Acid Base Disorder Disorder or abnormalities in H + concentration

4. Slide 4 Acid-Base load in the body(Sources) Exogenous: Dietary/others Endogenous: Metabolic

5. Slide 5 Acid-base load in the body Volatile acid(15-20 mol) Nonvolatile acid(230 mmol) Nonvolatile base(160 mmol)

6. Slide 6 Neutralization of acid-base load in the body Volatile acid(15-20 mol)-Excreted by lungs Nonvolatile acid (230 mmol) and Nonvolatile base(160m mmol) neutralize each other as one to one ratio Retained Nonvolatile acid=(230-160 mmol)=70 mmol

7. Slide 7 Neutralization of acid-base load in the body Our body is net acid producer

8. Slide 8 Mechanism of Neutralization Buffer system: Ist line defense Respiratory buffering: 2 nd line defense Renal buffering:3 rd line defense

9. Slide 9 Why body need this balance of H+ ion (pH)? Why body need this balance of H+ ion (pH)? Optimum enzyme & hormone activity Structural conformation of biomolecules specially protein Electrolyte balance Optimum vascular resistance Oxyhaemoglobin association and dissociation Chemical control of respiration

10. Slide 10 What imbalance /disorder of H+ ion /pH may occur ? Acidemia: Blood pH <7.35 Alkalemia: Blood pH >7.45

11. Slide 11 What may happen with these abnormalitie s? Acidosis: Physiological state resulting from abnormally low pH & Alkalosis: Physiological state resulting from abnormally low pH

12. Slide 12 Biochemical basis of ABD Three important biochemical components are related. H+ ion / pH CO2 (Volatile acid) HCO3 (Base) Their relationship deducted by Henderson-Hasselbalch equation of bicarbonate buffer.

13. H-H equation for Bicarbonate buffer system Slide 13

14. H-H equation for Bicarbonate buffer system Slide 14

15. Slide 15 Biochemical basis of abnormalitie s H-H equation clearly spells out that pH depends on the ratio of HCO3- and pCO2 Thus pH will be abnormal if If HCO3- concentration is abnormal (with normal pCO2) If pCO2 abnormal with (normal HCO3) If both HCO3- and pCO2 become abnormal simultaneously

16. Biochemical basis of abnormalities pH ∞ HCO3 pCO2 HCO3 is a metabolic component pCO2 is a respiratory component Slide 16

17. Mosby items and derived items © 2006 by Mosby, Inc. Slide 17

18. pH Acidosis Alkalosis HCO3 pCO2 decrease inecrease Metabolic Respiratory

19. Slide 19 Simple AB disorder

20. Slide 20 Types of ABD Simple ABD Mixed/complex ABD

21. Slide 21 Simple ABD Caused by the abnormalities of either HCO3- or pCO2 keeping the other component normal (One parameter changes)

22. Simple acid –base disorder Mosby items and derived items © 2006 by Mosby, Inc. Slide 22

23. Slide 23 Mixed of ABD Caused by the abnormalities of both HCO3- and pCO2 simultaneously. Clinically represents the co-existence of different simple ABD

24. Rules of Mixed ABD Respiratory acidosis and alkalosis never coexist. Metabolic disorder can coexist Metabolic and respiratory disorder can coexist Slide 24

25. Slide 25 Pathophysiology of AB disorder Acid-base disorders generally occur via one of three potential mechanisms : a. Abnormal renal function b. Abnormal respiratory function c. Acid or base load which overwhelms the excretory capacity of the kidney or respiratory syste m.

26. Primary events (Primary biochemical change with alter pH) Buffering (blood buffers-Ist line defense) Secondary events( compensation by respiratory system/Kidney) Correction(Slowly by Kidney after removal of underlying cause but not 100%) Biochemical events of AB disorder

27. DisorderpHPrimary Biochemical changes Metabolic acidosis HCO3 pCO2=normal Metabolic alkalosis HCO3 pCO2=normal Respiratory acidosis pCO2 HCO3=normal Respiratory alkalosis pCO2 HCO3=normal Primary events/ Primary Biochemical changes

28. Buffering Different blood buffer specially bicarbonate buffer immediately comes on play to neutralize the disorder If there is increase H+( decrease pH) salt/basic part comes into play If there is decrease H+( increase pH) acid part comes into play Slide 28

29. Secondary events (compensatory changes) Slide 29 It follows primary change (same direction) There is changes in unaffected component Objective is to maintain normal ratio HCO3/pCO2 normal. Cannot fully correct pH

30. Slide 30 DisorderpHPrimary changes Secondary changes Metabolic acidosisHCO3pCO2 Metabolic alkalosisHCO3pCO2 Respiratory acidosis pCO2HCO3 Respiratory alkalosis pCO2HCO3 Secondary events/ compensatory changes

31. Simple ABD Primary event/ defect Unaffected component HCO3 / pCO2 ratio Compensa- tory change or secondary events Mechanism of compensa- tion pHHCO3 after compe- nsation MA HCO3 pCO2 Hyperventil- ation MAL HCO3 pCO2 Hypoventil- ation RA pCO2 HCO3 Renal HCO3 generation RAL pCO2 HCO3 HCO3 excretion All events of ABD

32. Correction of ABD Aim of correction: Removal of primary event/defect by therapeutic intervention Normalize abnormal plasma HCO3- concentration Normalize the AB status Mechanism of correction: Treatment of underlying cause of ABD Renal activity to normalize plasma bicarbonate concentration Slide 32

33. Types of ABDRenal Correction Metabolic acidosis Acid(H+) excretion & HCO3 regeneration(CD),Urine acidic Metabolic alkalosis Serum HCO3- back to normal with simultaneous excretion of HCO3- through decreased reabsorption of HCO3- in PCT. Alkaline urine Respiratory acidosis (Increased) plasma HCO3- back to normal by increasing HCO3- excretion through inhibition of HCO-3 reabsorption from PCT Respiratory alkalosis (Decreased) serum HCO3- back to normal with reduce renal HCO3- excretion. Correction of AB disorder

34. Evaluation of ABD Examine ABG data Examine serum electrolytes Complete clinical assessment by history, physical examination, previous ABGs, serum electrolytes and other lab data Slide 34

35. Electrolyte in ABD Calculation of the anion gap (Na + - [Cl - + CO 2 ]) and the bicarbonate gap can help diagnose mixed acid-base disorders without a blood gas (e.g., metabolic acidosis and metabolic alkalosis occurring at the same time). Slide 35

36. Electrolyte in ABD Anion gap(AG)=Na –[HCO3+Cl] Delta AG=Patients AG-Standard AG Delta CO2=Normal CO2-Standard CO2] Bicarbonate Gap [ Delta AG- Delta CO2] Slide 36

37. ABG analysis Arterial blood gases (ABGs) are an important routine investigation to monitor the acid-base balance of patients in intensive care units (ICUs). Help to make a diagnosis, indicate the severity of a condition and help to assess treatment. ABGs provide the following information: Oxygenation Adequacy of ventilation Acid-base levels Slide 37

38. ABG analysis done by automated ABG analyzer Slide 38

39. ABG parameters/ components ComponentReference value pH7.4 (H=35-40 nmol/L) pO285-100 mm of Hg(95 mm) pCO235-46 mm of Hg(40 mm) HCO3-22-28 mmol/L(24) Slide 39

40. Other AB parameters ParametersReference value Anion gap8-16 meq/L Oxygen saturation >95 % Base excess± 2 mmol/L Slide 40

41. Step wise interpretation/approach to ABD Slide 41

42. Step 1 - Obtain appropriate lab values In order to assess acid-base disorders, the following lab values are necessary:  Arterial blood gas (ABG) - pH value, PaCO 2, PaO 2, HCO 3 - Comprehensive metabolic profile - Sodium (Na + ), Chloride (Cl - ), Carbon dioxide (CO 2 ), Albumin Slide 42

43. pH < 7.35 - primary disorder is an acidosis pH > 7.45 - primary disorder is an alkalosis Slide 43 Step 2- Determine the primary disorder: (Look at pH)

44. Step 3- Determine the source of primary disorde r Acidosis (pH < 7.35)  If the PaCO 2 is > 45 mmHg, then the primary disorder is a respiratory acidosis  If the HCO 3 - is < 22 mEq/L, then the primary disorder is a metabolic acidosis Alkalosis (pH > 7.45)  If the PaCO 2 is < 35 mmHg, then the primary disorder is a respiratory alkalosis  If the HCO 3 - is > 28 mEq/L, then the primary disorder is a metabolic alkalosis Slide 44

45. Step 4-Look for direction of change of both paramete r If both the parameter changed in same direction then there is secondary response or compensatory changes If both parameter changed in opposite direction there is mixed acid base disorder Slide 45

46. Step 5: Determine the nature of mixed ABD Calculation and analysis of Anion gap(AG) Delta AG= Patients AG-Normal AG Delta CO2= Normal CO2-Patients CO2 Bicarbonate Gap [ Delta AG- Delta CO2] Slide 46

47. Step 5: Determine the nature of mixed ABD(contd.) If the anion gap is ≥ 20, then a metabolic acidosis is either the primary or co-primary disorder regardless of the bicarbonate or pH value  The reasoning behind this is that the body will not generate an anion gap ≥ 20 even in the face of chronic alkalosis If the primary disorder is a metabolic acidosis:  Anion gap > 12 mEq/L* - high anion gap metabolic acidosis is present (see high anion gap metabolic acidosis)  Anion gap ≤ 12 mEq/L* - normal anion gap metabolic acidosis is present (see normal anion gap metabolic acidosis) Slide 47

48. Step 5: Determine the nature of mixed ABD(contd.) Diagnostic considerations for “ + ‘’and “-” Bicarbonate gap (delta AG - delta CO 2 ) * If+ bicarbonate gap (> 6 mEq/L) The serum CO 2 is reduced less than predicted by the change in the anion gap, and suggests: a) metabolic alkalosis &/or b) bicarbonate retention as compensation for respiratory acidosis If bicarbonate gap (<-6 mEq/L) The serum CO 2 is reduced more than predicted by the change in the anion gap, and suggests: a) hyperchloremic metabolic acidosis &/or b)bicarbonate excretion as compensation for respiratory alkalosis Slide 48

49. Non invasive alternative of ABG Pulse oximetry plus transcutaneous carbon dioxide measurement by capnography is an alternative method of obtaining approximate information less invasively. Slide 49

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