1. LABORATORIUM INTERPRETATION OF ACID-BASE & ELECTROLITES DISORDERS dr. Husnil Kadri, M.Kes Biochemistry Departement Medical Faculty Of Andalas University Padang

2. Arterial Blood Gases Aids in establishing a diagnosis Helps guide treatment plan Aids in ventilator management Improvement in acid/base management allows for optimal function of medications Acid/base status may alter electrolyte levels critical to patient status/care

3. Logistics When to order an arterial line -- –Need for continuous BP monitoring –Need for multiple ABGs Where to place – (with antikoagulant) –A. Radial –A. Femoral –A. Brachial –A. Dorsalis Pedis –A. Axillary

4. The Components Desired Ranges: –pH ; 7.35 - 7.45 –PaCO 2 ; 35-45 mmHg –PaO 2 ; 80-100 mmHg –HCO 3 ; 21-27 –O 2 sat ; 95-100% –Base Excess ; +/-2 mEq/L

5. Arterial Blood Gases Reflect oxygenation, gas exchange, and acid- base balance PaO 2 is the partial pressure of oxygen dissolved in arterial blood SaO 2 is the amount of oxygen bound to hemoglobin

6. Base Excess Definition: The amount of a strong acid (like HCl) needed to bring blood to 7.40. Assumes 100% oxygenation, 37 o C, and pCO 2 of 40. Normal = 0 Used to calculate the metabolic component of an acid-base disturbance.

7. Base Excess calculations Calculated the same way, in practice, as SID: Buffer Base (SID) = HCO 3 - + A - HCO 3 calculated by pH & pCO 2 (blood gas machine) BE = Buffer Base – “expected buffer base” (expected if pH = 7.4 and pCO 2 = 40) A - calculated using pH & hemoglobin (whole blood) OR A - calculated using albumin & phos (plasma)

8. 8 Indicators of hypoxaemia and hypoxia Arterial blood gasesLab Findings PO 2 80-100 mm Hg (normal) 60-80 mm Hg (mild hypoxemia) 40-60 mm Hg (moderate hypoxemia) <40 mm Hg (severe hypoxemia) SO 2 95%-97% (normal) <90% (may indicate hypoxemia) pH 7.35-7.45 (normal) <7.35 (acidemia) >7.45 (alkalemia) PCO 2 35-45 mm Hg (normal) >45 mm Hg (hypoventilation) <35 mm Hg (hyperventilation)

9. Is it Respiratory or Metabolic? 1.Respiratory Acidosis 2.Respiratory Alkalosis 3.Metabolic Acidosis 4.Metabolic Alkalosis Increased pCO2 >50 Decreased pCO2<30 Decreased HCO3 <18 Increased HCO3 >30

10. Compensated or Uncompensated—what does this mean? 1.Evaluate pH—is it normal? Yes 2.Next evaluate pCO2 & HCO3 pH normal + increased pCO2 + increased HCO3 = compensated respiratory acidosis pH normal + decreased HCO3 + decreased pCO2 = compensated metabolic acidosis

11. Compensated vs. Uncompensated 1.Is pH normal? No 2.Acidotic vs. Alkalotic 3.Respiratory vs. Metabolic pH 50 + normal HCO3 = uncompensated respiratory acidosis pH<7.30 + HCO3<18 + normal pCO2 = uncompensated metabolic acidosis pH>7.50 + pCO2<30 + normal HCO3 = uncompensated respiratory alkalosis pH>7.50 + HCO3>30 + normal pCO2 = uncompensated metabolic alkalosis

12. Causes of Acidosis Respiratory – Hypoventilation – Impaired gas exchange Metabolic – Ketoacidosis Diabetes – Renal Tubular Acidosis Renal Failure – Lactic Acidosis Decreased perfusion Severe hypoxemia

13. Causes of Alkalosis Respiratory – Hyperventilation due to: Hypoxemia Metabolic acidosis Neurologic – Lesions – Trauma – Infection Metabolic – Hypokalemia – Gastric suction or vomiting – Hypochloremia

14. 14 Mixed Metabolic Acidosis and Chronic Respiratory Alkalosis Examples: Sepsis Addition of respiratory alkalosis to metabolic acidosis further decreases HCO 3 - but pH may remain normal Lactic acidosis plus respiratory alkalosis due to severe liver disease, pulmonary emboli, or sepsis

15. 15 Mixed Metabolic Alkalosis and Chronic Respiratory Acidosis Examples: Patient with COPD receiving glucocorticoids or diuretics pCO 2 and HCO 3 - are increased by both conditions, but pH is neutralized

16. 16 Mixed Alkalosis, Severe Example: Postoperative patient with severe hemorrhage stimulating hyperventilation [respiratory alkalosis] plus massive transfusion and nasogastric drainage [metabolic alkalosis]

17. 17 Mixed Chronic Respiratory Acidosis and Acute Metabolic Acidosis Examples: COPD [chronic respiratory acidosis] with severe diarrhoea [metabolic acidosis]. pH is too low for pCO 2 of 55 mmHg in chronic respiratory acidosis, indicating low pH due to mixed acidosis, but HCO 3 - effect is offset

18. 18 Mixed Metabolic Acidosis and Metabolic Alkalosis Examples: Gastroenteritis with vomiting [metabolic alkalosis] and diarrhoea [metabolic acidosis due to loss of HCO 3 - ]; surprisingly normal findings with marked volume depletion

19. 19 Serum Values in Acid-Base Disturbances ConditionNa + mmol/L Cl - mmol/L HCO 3 - mmol/L pCO 2 mmHg pH Normal 14010525407.40 Metabolic acidosis 14011515317.30 Chronic respiratory alkalosis 13610225407.44 Mixed metabolic acidosis and chronic respiratory alkalosis 13610814247.39 Metabolic alkalosis 1409236487.49 Chronic respiratory acidosis 140100-10228507.37 Mixed metabolic alkalosis and chronic respiratory acidosis 1409040677.40

20. Serum Values in Acid-Base Disturbances 20 ConditionNa + mmol/L Cl - mmol/L HCO 3 - mmol/L pCO 2 mmHg pH Normal136-145100-10624-2635-457.35-7.45 Metabolic alkalosis 139 89  35  47  7.49  Respiratory alkalosis 136102 20  30  7.44 Mixed alkalosis, mild 139 92  32  39 7.53  Mixed alkalosis, severe 139 92  32  30  7.63  Mixed chronic respiratory acidosis and acute metabolic acidosis 136102 22  55  7.22  Mixed metabolic acidosis and metabolic alkalosis 14010325407.40

21. 21 Summary of Pure and Mixed Acid-Base Disorders Decreased pH Normal pHIncreased pH  pCO 2 Respiratory acidosis with or without incompletely compensated metabolic alkalosis or coexisting metabolic acidosis Respiratory acidosis and compensated metabolic alkalosis Metabolic alkalosis with incompletely compensated respiratory acidosis or coexisting respiratory acidosis Normal pCO 2 Metabolic acidosisNormalMetabolic alkalosis Source: Adapted from Friedman HH. Problem-oriented medical diagnosis, 3 rd ed. Boston: Little, Brown. 1983

24. References Anisman, S. Base Excess & Strong Ion Theories. ppt. 2003. Klee, V. Arterial Blood Gas Analysis.ppt. 2012. Perkins, J. ABG Interpretation. ppt. 2012. Rashid, FA. Respiratory Mechanisms in Acid-Base Homeostasis.ppt. 2005.