Acid-Base Analysis

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Acid-Base Analysis
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Sources of blood acids
Volatile acids
Non-volatile acids
H2O dissolved CO2
Inorganic acid
Organic acid
H HCO3-
H2CO3
Keto acid
Lactic acid
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Henderson-Hasselbalch
pH pK log _HCO3_ s
x PCO2 pK 6.1 s 0.0301
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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
• lt1 urine acid is free H

• Resorb filtered HCO3-, along with Na
• Excrete H2PO4, using phosphate buffer
• When phosphate buffer consumed, see H NH3
  NH4

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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-

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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-

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Other compensation

• Hyponatremia
• Renals Na resorption requires H excretion
• HCO3 resorbed
• Chloride
• Freely exchanged across membranes (InEx)
• When chloride deficient, other anions must
  substituteincrease HCO3-

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Nomenclature
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Partial Pressure
10
Atmosphere
alv
systemic circulation
extravascular fluid
cells
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Endothelium
RBC
ECF
Cells
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CO2
Dissolved CO2 pCO2
30
CO2 Hb HbCO2
CarboxyHgb
CO2
65
CO2
CO2 H2O HCO3 H
Utilizes carbonic anhydrase
CO2
CO2 Transport
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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

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Hgb dissociation curve
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Sat
40
100
75
50
pO2
25
60
80
100
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Dissociation curve
Sat
Shifts
pO2
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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

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Normal Oxygen Levels
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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

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Predicting metabolic component

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

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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

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Hypoxemia - etiology

• Decreased PAO2 (alveolar oxygen)
• Hypoventilation
• Breathing FiO2 lt0.21
• 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

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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