Acid-Base Analysis

Sources of blood acids

H2O + dissolved CO2

H2CO3

Volatile acids Non-volatile acids

Inorganicacid

Organicacid

Lacticacid

Ketoacid

H+ + HCO3-

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

“substitute”…increase HCO3-

Nomenclature

pH pCO2 [HCO3] BE

Uncompensatedmetab acidosis

N

Compensatedmetab acidosis

N

Uncompensatedmetab alkalosis

N

Compensatedmetab alkalosis

N

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

Atmosphere

pCO2 pO2

alv

extravascular fluid

cells

0 160

40 100

Capillary

45 97

~47

~47 <39

<54 ~5

>55 <1

systemiccirculation

Cells ECFEndothelium RBC

CO2

CO2

CO2

CO2

Dissolved CO2

= pCO2

5%

30%

65%

CO2 + Hb= HbCO2

CO2 + H2O= HCO3 + H+

CarboxyHgb

Utilizescarbonicanhydrase

CO2 Transport

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

Hgb dissociation curve

%Sat

pO2

100

75

50

25

20 40

60 80 100

Dissociation curve

0

10

20

30

40

50

60

70

80

90

100

0 20 40 60 80 100

% Sat

pO2

Shifts

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