Diffusion of Gases
dS/dT = D A R T DC
L (MR)1/2
- D = diffusion coefficient which includes solubility of molecule in aqueous solution
- A = surface area for diffusion
- DC = concentration gradient
- L = path length or thickness of membrane
- MR = molecular radius of gas molecule
Pulmonary Blood Flow
- Increased alveolar air PCO2
=> dilate bronchioles and dilate systemic arterioles
- Decreased PCO2 => constrict
bronchioles and constrict systemic arterioles
- Increased PO2 => dilate
pulmonary arterioles and constrict systemic arterioles
- Decreased PO2 => constrict
pulmonary arterioles and dilate systemic arterioles
Respiratory Considerations
- Surface area of capillaries in lung and tissues
- Thin membrane for diffusion
- MR for CO2 and O2 is very similar
- Solubility differs for CO2
and O2
- Gases are warmed as they enter lungs
Respiratory Considerations
Terminology
Hb-O2 Saturation
Curve
- Shift to the right decreases affinity, increases P50, and increases unloading of O2
- Caused by acidity (Bohr effect), increased temperature, and elevated 2,3 - DPG
- Increased by Epi, thyroid hormones, prolonged hypoxia, etc.
CO2 in the
blood
- 7% as dissolved CO2
- 23% as carbamino compounds on Hb
- Protein-NH3+ + CO2 <---> Protein -NH2COOH
- 70% as HCO3- via carbonic anhydrase
Haldane Effect: in the Lungs O2 promotes the unloading of CO2
- As Hb binds O2 , Hb becomes
a stronger acid, i.e., it gives up an H+
- This released H+ binds to
HCO3- -->
HCO3- + H+ ---> H2CO3 ---> CO2
+ H2O
- The CO2 is then released
or blown off in the exhaled air
In the tissues the Bohr effect causes the increased release of O2
- As CO2 increases, H+ is formed and some is buffered by binding to Hb
- This decreases Hb affinity for O2
and promotes the unloading of O2in the tissues
Chloride Shift: RBCs in the systemic capillaries
Chloride Shift

- RBC [Cl-] increases in systemic
capillaries
- RBC volume and blood hematocrit (Hct) increases in systemic capillaries
- Venous Hct is 3% greater than arterial Hct
Chloride Shift Reversed: RBCs in the Lungs

Regulation of Ventilation
Medullary Centers

Respiratory Input from the Pons
- Apneustic Center
- Prolonged inspiration
- Pneumotaxic Center
- Inhibits Apneustic Center
- Receives some input from vagal lung stretch receptors (?)

Inputs
PCO2 (pH receptors)
- CNS: Medulla
- Periphery:Aortic Arch and Carotid Bodies
Increasing Alveolar Ventilation: A Pool Output

Effects of alveolar ventilation on PO2 and PCO2 in the alveoli

O2 Sensing
Glomus Cells of the Carotid Bodies

