acid-base analysis. sources of blood acids h 2 o + dissolved co 2 h 2 co 3 volatile...
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Acid-Base Analysis
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Sources of blood acids
H2O + dissolved CO2
H2CO3
Volatile acids Non-volatile acids
Inorganicacid
Organicacid
Lacticacid
Ketoacid
H+ + HCO3-
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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
– <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+
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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 (In=Ex)– When chloride deficient, other anions must
“substitute”…increase HCO3-
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Nomenclature
pH pCO2 [HCO3] BE
Uncompensatedmetab acidosis
N
Compensatedmetab acidosis
N
Uncompensatedmetab alkalosis
N
Compensatedmetab alkalosis
N
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Partial PressureGas % Total Partial Pressure
Air at sea level 760
Oxygen 20.9% 159
Nitrogen 79.0% 600
Alveolar gas at sea level
Oxygen 13.3% 101
Nitrogen 75.2% 572
CO2 5.3% 40
Water 6.2% 47CO2
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Atmosphere
pCO2 pO2
alv
extravascular fluid
cells
0 160
40 100
Capillary
45 97
~47
~47 <39
<54 ~5
>55 <1
systemiccirculation
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Cells ECFEndothelium RBC
CO2
CO2
CO2
CO2
Dissolved CO2
= pCO2
5%
30%
65%
CO2 + Hb= HbCO2
CO2 + H2O= HCO3 + H+
CarboxyHgb
Utilizescarbonicanhydrase
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
%Sat
pO2
100
75
50
25
20 40
60 80 100
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Dissociation curve
0
10
20
30
40
50
60
70
80
90
100
0 20 40 60 80 100
% Sat
pO2
Shifts
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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
FiO2 PaO2
0.30 >150
0.40 >200
0.50 >250
0.80 >400
1.0 >500
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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 <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
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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