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Acid-Base Analysis

Acid-Base Analysis. Sources of blood acids. Volatile acids. Non-volatile acids. H 2 O + dissolved CO 2. Inorganic acid. Organic acid. H+ + HCO 3 -. H 2 CO 3. Keto acid. Lactic acid. Henderson-Hasselbalch. pH = pK + log _ [HCO 3 ]_ s x PCO 2

JasminFlorian
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Acid-Base Analysis

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  1. Acid-Base Analysis

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

  3. Henderson-Hasselbalch pH = pK + log _[HCO3]_ s x PCO2 pK = 6.1 s = 0.0301

  4. 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 HCO3-, along with Na+ Excrete H2PO4, using phosphate buffer When phosphate buffer consumed, see H+ + NH3 = NH4+ Renal mechanisms

  5. Renal Compensation • Metabolic acidosis: • Phosphate and ammonia buffers used as plasma bicarb is deficient • Respiratory acidosis: • Increased H+ excretion, HCO3- retention • Metabolic alkalosis: • Increased urine HCO3- excretion • Respiratory alkalosis: • Decreased resorption of HCO3-

  6. Other compensation • Hypokalemia • Most K+ is intracellular • When K+ deficient, see redistribution to extracellular space (there Ki low) • H+ moves intracellularly to balance • K+ (keep) exchanged for H+ in distal tubules • Excrete H+, resorb HCO3-

  7. Other compensation • Hyponatremia • Renals Na+ resorption requires H+ excretion • HCO3 resorbed • Chloride • Freely exchanged across membranes (In=Ex) • When chloride deficient, other anions must “substitute”…increase HCO3-

  8. Nomenclature

  9. Partial Pressure

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

  11. 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

  12. 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

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

  14. Dissociation curve % Sat Shifts pO2

  15. 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

  16. Normal Oxygen Levels

  17. 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

  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 PAO2 (alveolar oxygen) • Hypoventilation • Breathing FiO2 <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 • 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

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