Acid-Base Analysis

1. Acid-Base Analysis

2. Sources of acids Non-volatile acids Volatile acids Inorganic acid Organic acid H2O + dissolved CO2 H+ + HCO3- H2CO3 Keto acid Lactic acid

3. Henderson-Hasselbalch pH = pKa + log [A-] [HA] and pH = pKa + log [HCO3-] = 6.1 + log [HCO3-] s x PCO2 0.03 x PCO2 H+ + HCO3- H2CO3 CO2 + H2O Anion Gap [Na+] = [CL- + HCO3-] ~ 10-15

4. Acid-Base States • Acidosis: pH<7.35 • Metabolic: increased acid or decreased in bicarb • Respiratory: increased PCO2 • Alkalosis: pH>7.45 • Metabolic: increased bicarb or loss of H+ • Respiratory: decreased PCO2

5. Compensation • Acute: • Minutes • Respiratory: PCO2 regulation • Chronic • Hours to days • Renal: via regulation of bicarb excretion

6. Acidosis: Respiratory • Decrease PCO2 excretion via hypoventilation • Respiratory etiology • CNS pathology • Intoxication • pH decreases 0.08 unit/10 mmHg increase in PaCO2 • Bicarb and base excess are normal

7. Acidosis: Metabolic • Change in pH by increased in acid or decrease in bicarb • Anion Gap Acidosis: MUD PILES Methanol Paraldehyde Uremia Iron, isoniazid (INH) Diabetic ketoacidosis Lactic acid Ethanol, ethylene glycol Salicylates • Non-Anion Gap Acidosis: USEDCARP Uretorostomy Carbonic anhydrase inhibitors (acetazolamide) Small bowel fistula Adrenal insufficiency Extra Chloride RTA Diarrhea Pancreatic fistula

8. Alkalosis: Respiratory • Decrease in PCO2 by hyperventilation • Compensate by increase renal excretion of HCO3-

9. Alkalosis: Metabolic • Increase in H+ loss or increase in HCO3- • PaCO2 increase by 0.5-1/1 mEq/L of increase in HCO3-

10. Nomenclature

11. Partial Pressure

12. pCO2 pO2 0 160 40 100 45 97 Capillary ~47 ~47 <39 <54 ~5 >55 <1 Atmosphere alv systemic circulation extravascular fluid cells

13. Endothelium RBC ECF Cells 5% CO2 Dissolved CO2 = pCO2 30% CO2 + Hb = HbCO2 CarboxyHgb CO2 65% CO2 CO2 + H2O = HCO3 + H+ Utilizes carbonic anhydrase CO2 CO2 Transport

14. Excretion of CO2 • Metabolic rate determines how much CO2 enters blood • Lung function determines how much CO2 excreted • minute ventilation • alveolar perfusion • blood CO2 content

15. Hgb dissociation curve % Sat 20 40 100 75 50 pO2 25 60 80 100

16. Dissociation curve % Sat Shifts pO2

17. Alveolar oxygen equation • Inspired oxygen = 760 x .21 = 160 torr • Ideal alveolar oxygen = PAO2 = [PB - PH2O] x FiO2 - [PaCO2/RQ] = [760 - 47] x 0.21 - [40/0.8] = [713] x 0.21 -[50] = 100 torr or 100 mmHg • If perfect equilibrium, then alveolar oxygen equals arterial oxygen. • ~5% shunt in normal lungs

18. Normal Oxygen Levels

19. Predicting ‘respiratory part’ of pH • Determine difference between PaCO2 and 40 torr, then move decimal place left 2, ie: IF PCO2 76: 76 - 40 = 36 x 1/2 = 18 7.40 - 0.18 = 7.22 IF PCO2 = 18: 40 -18 = 22 7.40 + 0.22 = 7.62

20. Predicting metabolic component • Determine ‘predicted’ pH • Determine difference between predicted and actual pH • 2/3 of that value is the base excess/deficit

21. Deficit examples • If pH = 7.04, PCO2 = 76 Predicted pH = 7.22 7.22 - 7.40 = 0.18 18 x 2/3 = 12 deficit • If pH = 7.47, PCO2 = 18 Predicted pH =7.62 7.62 - 7.47 = 0.15 15 x 2/3 = 10 excess

22. Hypoxemia - etiology • Decreased PAO2 (alveolar oxygen) • Hypoventilation • Breathing FiO2 <0.21 • Unde rventilated alveoli (low V/Q) • Zero V/Q (true shunt) • Decreased mixed venous oxygen content • Increased metabolic rate • Decreased cardiac output • Decreased arterial oxygen content

23. Blood gases • PaCO2: pH relationship • For every 20 torr increase in PaCO2, pH decreases by 0.10 • For every 10 torr decrease in PaCO2, pH increases by 0.10 • PaCO2: plasma bicarbonate relationship • PaCO2 increase of 10 torr results in bicarbonate increasing by 1 mmol/L • Acute PaCO2 decrease of 10 torr will decrease bicarb by 2 mmol/L

24. Sources of blood acids • INFORMATION

25. Sources of blood acids • INFORMATION