Acid-Base Analysis - Emory University School of Medicine

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Acid Base Analysis Sources of blood acidsVolatile acids Non volatile acidsH2O dissolved CO2Inorganic Organic.
H2CO3 H HCO3 Lactic Keto Henderson HasselbalchpH pK log HCO3 s 0 0301.
Renal mechanisms Excrete H into urine Resorb filtered HCO3 Active exchange of along with Na Na for H in tubules Excrete H2PO4 using Carbonic anhydrase in phosphate buffer.
renal epithelial cells assures high rate of When phosphatecarbonic acid buffer consumed seeformation H NH3 NH4 1 urine acid is free.
Renal Compensation Metabolic acidosis Phosphate and ammonia buffers used as plasmabicarb 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 toextracellular 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.
substitute increase HCO3 NomenclaturepH pCO2 HCO3 BEUncompensated N metab acidosis.
Compensated N metab acidosisUncompensated N metab alkalosisCompensated N .
metab alkalosis Partial PressureGas Total Partial PressureAir at sea level 760Oxygen 20 9 159.
Nitrogen 79 0 600Alveolar gas at sea levelOxygen 13 3 101Nitrogen 75 2 572CO2 5 3 40.
Water 6 2 470 Atmosphere 16040 alv 100circulationCapillary 47.
54 extravascular fluid 5 55 cells 1 EndotheliumCO2 Dissolved CO2CO2 CO2 Hb CarboxyHgb.
CO2 65 CO2 H2O Utilizes HCO3 H carbonicCO2 Transport Excretion of CO2 Metabolic rate determines how much CO2.
enters blood Lung function determines how much CO 2 minute ventilation alveolar perfusion blood CO2 content.
Hgb dissociation curve Sat Dissociation curve0 20 40 60 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 equalsarterial oxygen 5 shunt in normal lungs Normal Oxygen Levels 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 2 187 40 0 18 7 22.
IF PCO2 18 40 18 227 40 0 22 7 62 Predicting metabolic component Determine predicted pH.
Determine difference between predictedand actual pH 2 3 of that value is the base excess deficit Deficit examples IF pH 7 04 PCO2 76.
Predicted pH 7 227 22 7 40 0 18 18 x 2 3 12 deficit IF pH 7 47 PCO2 18Predicted pH 7 627 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 bicarbonateincreasing by 1 mmol L Acute PaCO2 decrease of 10 torr will decrease.
bicarb by 2 mmol LAcid-Base Analysis Sources of blood acids Henderson-Hasselbalch 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 ...

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