1. Acid-Base Analysis

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

3. Henderson-Hasselbalch
pH = pK + log _[HCO3]_
s x PCO2
pK = 6.1
s =

4. 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+

5. Renal Compensation Metabolic acidosis: Respiratory 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-

6. 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-

7. Other compensation Hyponatremia Chloride
Renals Na+ resorption requires H+ excretion
HCO3 resorbed
Chloride
Freely exchanged across membranes (In=Ex)
When chloride deficient, other anions must “substitute”…increase HCO3-

8. Nomenclature

9. Partial Pressure

10. pCO2 pO2 160 Atmosphere 40 100 alv systemic circulation 45 97 ~47
160
Atmosphere 40
100
alv
systemic
circulation 45 97
~47
Capillary
~47
<39
<54 ~5
extravascular fluid
>55
<1
cells

11. CO2 Transport Endothelium RBC ECF Cells 5% CO2 Dissolved CO2 = pCO2
30%
CO2 + Hb
= HbCO2
CarboxyHgb
CO2
65%
CO2
CO2 + H2O
= HCO3 + H+
Utilizes
carbonic
anhydrase
CO2
CO2 Transport

12. 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

13. Hgb dissociation curve20 %
Sat 40
100 75 50
pO2 25 60 80
100

14. Dissociation curve
% Sat
Shifts
pO2

15. Alveolar oxygen equation
Inspired oxygen = 760 x .21 = 160 torr
Ideal alveolar oxygen =
PAO2 = [PB - PH2O] x FiO2 - [PaCO2/RQ]
= [ ] x [40/0.8]
= [713] x [50]
= 100 torr or 100 mmHg
If perfect equilibrium, then alveolar oxygen equals arterial oxygen.
~5% shunt in normal lungs

16. Normal Oxygen Levels

17. Predicting ‘respiratory part’ of pH
Determine difference between PaCO2 and 40 torr, then move decimal place left 2, ie:
IF PCO2 76:
= 36 x 1/2 = 18
= 7.22
IF PCO2 = 18:
= 22
= 7.62

18. Predicting metabolic component
Determine ‘predicted’ pH
Determine difference between predicted and actual pH
2/3 of that value is the base excess/deficit

19. Deficit examples IF pH = 7.04, PCO2 = 76 Predicted pH = 7.22
= x 2/3 = 12 deficit
IF pH = 7.47, PCO2 = 18
Predicted pH =7.62
= x 2/3 = 10 excess

20. 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

21. 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