1. Acid-Base Analysis

2. Sources of blood acids H 2 O + dissolved CO 2 H 2 CO 3 Volatile acidsNon-volatile acids Inorganic acid Organic acid Lactic acid Keto acid H+ + HCO 3 -

3. Henderson-Hasselbalch pH = pK + log _[HCO 3 ]_ s x PCO 2 pK = 6.1 s = 0.0301

4. Renal mechanisms Excrete H+ into urine –Active exchange of Na+ for H+ in tubules –Carbonic anhydrase, in renal epithelial cells, assures high rate of carbonic acid formation –<1% urine acid is free H+ Resorb filtered HCO 3 -, along with Na+ Excrete H 2 PO 4, using phosphate buffer When phosphate buffer consumed, see H+ + NH 3 = NH 4 +

5. Renal Compensation Metabolic acidosis: –Phosphate and ammonia buffers used as plasma bicarb is deficient Respiratory acidosis: –Increased H+ excretion, HCO 3 - retention Metabolic alkalosis: –Increased urine HCO 3 - excretion Respiratory alkalosis: –Decreased resorption of HCO 3 -

6. Other compensation Hypokalemia –Most K+ is intracellular –When K+ deficient, see redistribution to extracellular space (there K i low) –H+ moves intracellularly to balance –K+ (keep) exchanged for H+ in distal tubules –Excrete H+, resorb HCO 3 -

7. Other compensation Hyponatremia –Renals Na+ resorption requires H+ excretion –HCO 3 resorbed Chloride –Freely exchanged across membranes (In=Ex) –When chloride deficient, other anions must “substitute”…increase HCO 3 -

8. Nomenclature

9. Partial Pressure

10. Atmosphere pCO 2 pO 2 alv extravascular fluid cells 0160 40100 Capillary 4597 ~47 <39 <54~5 >55<1 systemic circulation

11. Cells ECF Endothelium RBC CO2 Dissolved CO 2 = pCO 2 5% 30% 65% CO 2 + Hb = HbCO 2 CO 2 + H 2 O = HCO 3 + H + CarboxyHgb Utilizes carbonic anhydrase CO 2 Transport

12. Excretion of CO 2 Metabolic rate determines how much CO 2 enters blood Lung function determines how much CO 2 excreted –minute ventilation –alveolar perfusion –blood CO 2 content

13. Hgb dissociation curve % Sat pO 2 100 75 50 25 20 40 6080100

14. Dissociation curve % Sat pO 2 Shifts

15. Alveolar oxygen equation Inspired oxygen = 760 x.21 = 160 torr Ideal alveolar oxygen = PAO 2 = [PB - PH 2 O] x FiO 2 - [PaCO 2 /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

16. Normal Oxygen Levels

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

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

19. 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

20. Hypoxemia - etiology Decreased PAO 2 (alveolar oxygen) –Hypoventilation –Breathing FiO 2 <0.21 –Underventilated alveoli (low V/Q) Zero V/Q (true shunt) Decreased mixed venous oxygen content –Increased metabolic rate –Decreased cardiac output –Decreased arterial oxygen content

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