Acid-Base Analysis

Acid-Base Analysis

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

acid Henderson-Hasselbalch pH = pK + log _[HCO3]_ s x PCO2 pK = 6.1 s = 0.0301 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 HCO3-, along with Na+ Excrete H2PO4, using phosphate buffer When phosphate buffer consumed, see H+ + NH3 = NH4+ 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- 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- Other compensation Hyponatremia Renals Na+ resorption requires H+ excretion HCO3 resorbed Chloride

Freely exchanged across membranes (In=Ex) When chloride deficient, other anions must substituteincrease HCO3- Nomenclature Uncompensated metab acidosis Compensated metab acidosis Uncompensated metab alkalosis Compensated metab alkalosis pH pCO2 [HCO3] BE


N N Partial Pressure Gas % Total

Air at sea level Partial Pressure 760 Oxygen 20.9% 159 Nitrogen 79.0% 600 Alveolar gas at sea level

CO2 Oxygen 13.3% 101 Nitrogen 75.2% 572 CO2 5.3% 40

Water 6.2% 47 pCO2 0 pO2 Atmosphere 160 40 alv

100 45 systemic circulation 97 Capillary ~47 ~47 <54 extravascular fluid <39 ~5 >55 cells <1 Cells CO2 CO2 CO2 Endothelium ECF RBC

5% Dissolved CO2 = pCO2 30% CO2 + Hb = HbCO2 65% CO2 + H2O Utilizes = HCO3 + H+ carbonic anhydrase CarboxyHgb

CO2 CO2 Transport Excretion of CO2 Metabolic rate determines how much CO 2 enters blood Lung function determines how much CO 2 excreted minute ventilation alveolar perfusion blood CO2 content Hgb dissociation curve % Sat 20

40 100 75 50 pO2 25 60 80 100 Dissociation curve % Sat 100 90

80 Shifts 70 60 50 40 30 20 10 0 0 20 40 60

pO2 80 100 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

Normal Oxygen Levels FiO2 PaO2 0.30 >150 0.40 >200 0.50 >250 0.80

>400 1.0 >500 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 Predicting metabolic component Determine predicted pH

Determine difference between predicted and actual pH 2/3 of that value is the base excess/deficit 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 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 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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