C
L (MR)1/2
dS/dT = D A R T C
L (MR)1/2
D = diffusion coefficient which includes solubility of molecule in aqueous
solution
A = surface area for diffusion
C = concentration gradient
L = path length or thickness of membrane
MR = molecular radius of gas molecule
DCO2 >>> DO2 - WHY?
Figure 16.3: Solubility of O2 and CO2 in
water
Figure 16.3: Solubility of O2 and CO2 in
water
Diffusion Capacity of the Lung:
DL = VGAS / P1 - P2
= ml / min / mm Hg
Oxygen Transport:
95% carried by hemoglobin
5% dissolved in plasma
Fig 16.4: O2 and CO2 in the Body
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
C (in mm Hg)
Gas
Air
Alveolar Air
Arterial
Venous
O2
160
100
100
40
CO2
0.25
40
40
46
H2O
0.0
47
N2
600
573
Fig 16.6: Transport of O2
Fig 16.8: Hb - O2 Dissociation Curve
Fig 16.7: Hb - O2 Loading
Hb-O2 Saturation Curve: Review
• 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
Carbonic Anyhydrase Reaction
CO2 + H2O <--> H2CO3
<--> H+ + HCO3-
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 O2 in the tissues
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
See also Figures 16.12 & 13
Fig 16.12: PO2 --> CO2 Transport
Fig 16.11: 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
Gas Transport Summary:
• O2 decreases amount of carbamino, promoting unloading
of CO2 (Haldane Effect)
• CO2 as H+ decreases O2 affintiy
and increases unloading of O2 in systemic capillaries (Bohr
Effect)
Regulation of Ventilation
Medullary Center Respiratory Neurons
Dorsal Respiratory Group (DRG)
Inhalation ---> diaphragm
and external intercostals
Ventral Respiratory Group (VRG)
Shuts off DRG and
promotes active exhalation
Fig 16.15: Brainstem Respiratory Centers
Respiratory Input from the Pons
Apneustic Center: Prolonged inspiration
Pneumotaxic Center: Inhibits Apneustic Center
Receives some input from vagal lung stretch receptors (?)
Fig 16.18: Peripheral Chemoreceptors
Inputs to Medulla
CNS: Medulla
• Sensitive only to pH (due to PCO2)
Periphery:
• Aortic arch
• Carotid bodies
• Sensitive to PO2
and pH
• Oxygen only a factor at
PO2 < 60 mm Hg
Fig 16.19: Chemoreceptor Control
Fig 16.20: Central Chemoreceptors
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
Fig 16.23 Ventilation - perfusion ratios
Pulmonary Blood Flow
• To match perfusion with ventilation:
• 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