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Prof. Mehdi Hasan Mumtaz

Prof. Mehdi Hasan Mumtaz. ACID-BASE BALANCE. Terminology. Physiologic Compensation By Body. Pathophysiologic Disturbances. Practical Approach To Assessment. Biochemical Reports & Case Histories. DEFINITION OF TERMINOLOGY. ACID - STANDARD BICARBONATE. BASE - BUFFER BASE & BASE DEFICIT.

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Prof. Mehdi Hasan Mumtaz

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  1. Prof. Mehdi Hasan Mumtaz

  2. ACID-BASE BALANCE • Terminology. • Physiologic Compensation By Body. • Pathophysiologic Disturbances. • Practical Approach To Assessment. • Biochemical Reports & Case Histories.

  3. DEFINITION OF TERMINOLOGY • ACID - STANDARD BICARBONATE. • BASE - BUFFER BASE & BASE DEFICIT. • ALKALI • BUFFERING & BUFFER. • PH. 24 x PCO2 (mmHg) H+(nmol/L)=- ----------------------------- HCO3 (meq/L) (40nmol/L)

  4. PRODUCT OF METABOLISM • H++ - Anaerobic Metabolism. • CO2 - Aerobic Metabolism.

  5. PHYSIOLOGIC COMPENSATION • HYDROGEN IONS. • Incoporation in water.H++HCO3H2C3O CO2 + H2O. • Loss from body. • Kidney – regeneration of HCO3. • Intestine. • CO2. • Chemoreceptors in hypothalamus. • HCO3. • HCO3 generation by erythrocytes. • HCO3 re-absorption in renal tubules. • HCO3 generation in renal tubules.

  6. BICARBONATE GENERATION BY ERYTHROCYTES HHB Hb Cl— HCO-3 CO2 Cl— -HCO3 +H+ CO2+H2O

  7. HCO3- Na+ Na+ HCO3- HCO3- HCO3- H+ CELL H2CO3 H2CO3 CD CO2 H2O CO2 + H2O BICARBONATE REABSORPTION BY KIDNEY RENAL T. LUMEN STIMULATED BY HCO3- M. ACIDOSIS

  8. BICARBONATE GENERATION IN KIDNEY B- HCO3- Na+ STIMULATED PCO2 (BY RESP ACIDOSIS) & -HCO3 (M. ACIDOSIS) Na+ B- HCO3- H+ CELL H2O HB CO3 H2O

  9. PATHOPHYSIOLOGIC DISTURBANCES Lungs Disturbances of CO2= R. Centre Disturbance of H++HCO3 = Metabolic

  10. Henderson - HosselbalchEQUATION Proton Acceptor (Base) PH=PK+Log = -------------------------------- Proton Donor (Acid) -HCO3 (Metabolic) PH=PK+Log = ---------------------------------- H2CO3 or PCO2 x 0.03 (Respiratory)

  11. ACID-BASE DISTURBANCE -HCO3 PCO2 x 0.03 MEATBOLIC RESPIRATORY ACIDOSIS ALKALOSIS ACIDOSIS ALKALOSIS HCO3 ---------------- PCO2x0.03 HCO3 ---------------- PCO2x0.03 HCO3 ---------------- PCO2x0.03 HCO3 ---------------- PCO2x0.03    RATIO 

  12. Metabolic acidosis = Respiratory acidosis = Metabolic alkalosis = Respiratory alkalosis = Defect HCO3 ---------- PCO2 HCO3 ---------- PCO2 HCO3  ---------- PCO2 HCO3 ---------- PCO2  Correction HCO3 ---------- PCO2  HCO3 ---------- PCO2  HCO3 ---------- PCO2  HCO3 ---------- PCO2 

  13. CAUSES OF M. ACIDOSIS Hyperkalamic M. Acidosis • Glomeralar failure. • Keto-acidosis. • Lactic acidosis. • Intestinal loss. • R. Tubular failure. • Actazolamide therapy. • R. Tubular acidosis. • Ureteric transplantation. • NH4Cl el therapy. Variable Hyppkalamic Acidosis Hyperchloraemic Acidosis

  14. CAUSES M. ACIDOSIS • A.HYPERKALAEMIC M. ACIDOSIS 1, GLOMERULAR FAILURE 2, KETOACIDOSIS 3, LACTIC ACIDOSIS

  15. CAUSES OF M.ACIDOSIS • B.HYPOKALAEMIC M.ACIDOSIS 1.RENAL TUBULAR 2.ACETAZOLAMIDE THERAPY 3.RENAL TUBULAR ACIDOSIS

  16. CAUSES OF M. ACIDOSIS • C.HYPERCHLORAEMIC ACIDOSIS 1.ACATAZOLAMIDE THERAPY 2.RENAL TUBULAR ACIDOSIS 3.URETERIC TRASPLANTATION 4.AMMONIUM CHLORIDE

  17. CAUSES OF M. ACIDOSIS • D.HYPERCHLORAEMIC HYPOKALAEMIC M.ACIDOSIS 1.ACETAZOLAMIDE THERAPY 2.RENAL TUBULAR ACIDOSIS

  18. SCREENING TESTS METABOLIC ACIDOSIS • BLOOD GLUCOSE. • URINE/ BLOOD KETONES. • SERUM CHLORIDE. • SERUM POTASSIUM

  19. RESPIRATORY ACIDOSIS • Acute Respiratory Failure. • Erythrocyte • Chronic Respiratory Failure. • Renal Generation.

  20. METABOLIC ALKALOSIS • Administration of HCO3. • K+ depletion – Generation by kidney. • Pyloric Stenosis.

  21. RESPIRATORY ALKALOSIS • Hysterical Over-breathing. • ICP. • Brain Stem Injury. • Hypoxia. • Pulmonary Oedema. • Lobar Pneumonia. • Pulmonary Collapse. • Excessive Artificial Ventilation.

  22. BALANCE OF ACID-BASE NORMAL VALUES • PCO2 • 30-50mmHg or 4-6.6kPa. • >50mmHg respiratoryor 6.6kPa acidosis • <30mmHg respiratoryor 4kPa alkalosis • PH • 7.30 – 7.50 • >7.50 alkalaemia. • <7.30 acidosis

  23. BALANCE OF ACID-BASE RELATIONSHIP • PCO2 and PH. • PCO2 &ventilation. • PO2 andnormal range. • PO2 and FIO2. • PCO2,and temperature.

  24. TERMINOLOGY • ACIDAEMIA - PH<7.30 • ALKAEMIA - PH>7.50. • ACIDOSIS - Base Deficit Present. • ALKALOSIS - Base Excess Present.

  25. HOW TO ASSESS BLOOD GASES? • STEP-1 Assessment of Acid-Base Balance. • STEP-2 Assessment of Hypoxaemic State. • STEP-3 Assessment of Tissue Oxygenation State.

  26. STEP-1Assessment of Acid-Base BalanceCLASSIFICATION ALKALOSIS ACIDOSIS METABOLIC RESPIRATORY METABOLIC RESPIRATORY CHRONIC ACUTE CHRONIC ACUTE CHRONIC ACUTE CHRONIC ACUTE

  27. STEP-1Assessment of Acid-Base Balance • Acute - Uncompensated. • Chronic - Compensated. -Fully. - Partially. COMPENSATED PH 7.30-7.50 DIAGNOSIS.

  28. DIAGNOSIS SEQUENCE. • PH. • PCO2. • HCO3. PH Normal 7.4 Compensated 7.3-7.5 PCO3 Normal 40mmHg (5.3kPa) Compensated 30-50mmHg (4-6.6 kPa)

  29. DIAGNOSIS • IF PH LOW – acidosis. • Look at PCO2. • If PCO3 high - respiratory acidosis • If PH low - acidosis • Look at PCO2 • If it is normal or low. • Look at HCO3. It is low – metabolic acidosis. • IF PH HIGH - alkalosis • Look at PCO2. • If it is low - respiratory alkalosis • If PH high - PCO2 normal or high. • Look at HCO3. High - metabolic alkalosis. NOW LOOK FOR COMPENSATION

  30. A C I D O S I S A L K A L O S I S Primary change Primary change

  31. PRACTICAL EXAMPLES • PH 7.26 7.38 7.20 7.36 7.60 7.56 • PCO2 56 76 40 25 25 44 • HCO3 24 24 9 15 24 38

  32. STEP-2Hypoxaemic State • Below 60 years of age: • Normal PO2 = 97mmHg.(13 Kpa) • Acceptable range = >80mHg.(10.6Kpa) • Mild hypoxiaemia = <80mmHg.(10.6Kpa) • Moderate hypoxiaemia = <60mmHg.(8) • Severe hypoxiaemia = <40mmHg.(5.3)

  33. STEP-2Hypoxaemic State • Above 60 years of age: • Subtract 1mmHg from minimal 80mmHg for every year over 60; this means acceptable range: • 60 years = >80 mmHg. =>10.6 Kpa • 70 years = >70 mmHg. => 9.3 Kpa • 80 years = >60 mmHg. = > 8.0 Kpa • 90 years = >50 mmHg. = > 6.6 Kpa • New Born: • Acceptable = 40-70 mmHg.= 5.3-9.3 Kpa

  34. STEP-2Hypoxaemic State • Oxygen Therapy FIO2 x 5 = Expected PO2. Uncorrected Hypoxaemia = PO2<Room Air Acceptable Limit. Corrected Hypoxaemia = PO2 > Room Air Acceptable Limit. <100mmHg.=13.3 Kpa Excessively Corrected Hypoxaemia = PO2>100mmHg(13.3Kpa) < minimal predicted.

  35. OXYGENATION STATUS • FIO2 ----PIO2 • PAO2 = PIO2-PACO2 • PaO2 • P(A-a)O2=PAO2-PaO2 • PaO2/PAO2=0.67 ------------------------------------------------------ • DO2 520—720ml/min/m2 • VO2 110—160 ml/min/m2 • Lactate

  36. PRACTICAL EXAMPLES • PH 7.24 7.42 7.54 7.16 7.36 7.48 • PCO2 32 28 29 83 83 33 • HCO3 14 18 24 29 48 24 • BE -13 -5 +3 -3 +15 +1 • PO2 100 50 65 30 45 75 • FIO2 21 40 21 40 21 50 • AGE 40 50 45 40 80 70

  37. PRACTICAL EXAMPLES • PH 7.24 7.46 7.40 7.48 7.48 7.55 • PCO2 28 26 56 33 33 20 • HCO3 12 18 34 24 24 18 • BE -15 -4 +7 +1 +1 -3 • PO2 90 70 55 50 160 45 • FIO2 21 21 21 50 50 21 • AGE 40 75 60 30 30 40

  38. STEP-3Assessment of Tissue Oxygenation • Cardiac Status. • Peripheral Perfusion Status. • Blood Oxygen Transport Mechanism. Depends on: • Vital Signs • Physical Examination.

  39. STEP-3Assessment of Tissue Oxygenation • BP. • Pulse Pressure. • Heart Rate • ECG. • Skin Color & Condition. • Capillary Fill. • Senosrium. • Electrolyte Balance. • Urine Out Put. • If Above 1,2 Good Only 3 Interfering. • Arterial Oxygen Tension Po2. • Blood Oxygen Content. • Hb Oxygen Affinity.

  40. SUMMARY • ASSESS ACID/BASE STATUS. • ASSESS HYPOXAEMIC STATE • ASSESS TISSUE OXYGENATION. • TRY TO FIND OUT THE CAUSE. • SEE FOR THE NEED OF HCO3.

  41. SUMMARY Acidosis Metabolic 6. If Cl- K+ Think of actazolamide therapy and R. Tubul Acidosis. 7. If Cl-N K+  Proximal Tubul Failure. OTHERWISE THINK ABOUT GIT INVOLVEMENT Look at 1. Blood urea If  and K+  G.F. 2. Blood Glucose/ ketones If  and K+  ketoacidosis. 3. PO2 If K+  Lactic acidosis 4. Serum HCO3. If only H/o Therapy 5. If  K+  think of NH4Cl therapy + G. Transplantation

  42. SUMMARY Respiratory Alkalosis Lung Functions will Help METABOLIC Look at K+ & Cl- K+  Cl-  H/o vomiting Pyloric stenosis If K+  find cause. H/o bicarb therap. RESPIRATORY - H/o H. Injury - L. Infection - IPPV

  43. PRACTICAL EXAMPLES • PH PCO2 HCO3 Na K Cl UREA G • 7.25 40 20 130 5.5 100 95 120 • 7.29 35 20 135 4.5 118 40 90 • 7.58 40 37 145 4.3 100 40 100 • 7.52 42 35 130 2.7 85 58 100 • 7.35 37 18 136 2.9 117 25 90

  44. BUFFER BASE/BASE DEFICIT “Sum of the Buffer anions; 44--55 meq/l PREDICTED RESPIRATORY PH? PCO2 -- PH RELATIONSHIP  PCO2 20mmHg =  0.1PH.  PCO2 10mmHg =  0.1PH

  45. BASE EXCESS/ DEFICITPredicted Respiratory PH • Calculate difference between measured PCO2 and 40mmHg. Move decimal 2 places to left. • If PCO2 > 40 subtract ½ difference from 7.4. • If PCO2 < 40 add the difference to 7.40. • PH 7.21 PCO2 90 • 90-40 = 50 = 0.50 = 0.50x ½ = 0.25 • 7.40-0.25 =7.15 • PH 7.47 PCO2 18 • 40-18 = 22= 0.22 • 7.40 + 0.22 =7.62 Predicted Resp PH.

  46. METABOLIC COMPONANT METABOLIC PH CHANGE = Measured PH -- Predicted Respiratory PH

  47. DETERMINATION OF METABOLIC COMPONENT Determine predicted PH Determine difference between measured and predicted PH Move two decimal point to the right Multiply by 2/3 Base excess if measured Ph > predicted PH Base deficit if measured PH<predicted PH

  48. EXAMPLE • PH 7.04 PCO2 76 Predicted PH= 76-40=36 =.36=1/2*36 = 18=.18=7.4-.18=7.22 Base Excess/deficit=7.22-7.04=0.18= 18*2/3=12 As measured PH is less than predicted,so it is Base deficit

  49. PaCO2/HCO3 Relationship • A.Respiratory acidosis. Expected HCO3=24+0.1*(Paco2-40) • Chronic Respiratory acidosis. Expected HCO3=24+0.35*(Paco2-40) • A.Respiratory alkalosis. Expected HCO3=24-0.2*(40-Paco2) • Chronic respiratory alkalosis. Expected HCO3=24-0.5*(40-Paco2)

  50. EXPECTED PaCO2 • METABOLIC ACIDOSIS Expected PaCO2=1.5*(HCO3) + 8 METABOLIC ALKALOSIS Expected PaCO2=40+0.6*(HCO3)

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