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BHS116 Fall: Human Physiology and Pathology
Notetaker: Jessica Du
Date: 10/05/2011, 1st hour
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Transport of O2 and CO2 in blood to and from cells
Respiration:
- Goal is to provide oxygen to the tissues and to remove carbon dioxide
- Four major functions
o 1. Pulmonary ventilation (air  lungs)
o 2. Diffusion of O2 and CO2 between alveoli and blood
o 3. Transport of O2 and CO2 in blood to and from cells  Focus on this!
o 4. Regulation of ventilation
Gas Transported in Blood:
- The amount physically dissolved is directly proportional to the partial pressure
- [amt gas dissolved] ∝ Pgas
- The main difference between the transport of O2 and CO2 is that CO2 has a higher solubility coefficient
o Higher solubility coefficient  Higher [gas] dissolved  High partial pressure
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Dissolved O2 is too low to supply the tissues
o Only 15 mL/min, tissues at rest requires 250 mL/min of O2
Hemoglobin binds up the O2 and carries it to the tissues
Hb allows for 30-100 times more O2 transport and 15-20 times more CO2 transport
Hemoglobin:
- 2 α peptides
- 2 β peptides
- Each chain contains a heme group with an iron atom
- The iron atom binds 1 O2 molecules
- A total of 4 O2 can bind a single Hb protein (fully saturated)
Transport of O2 in Blood:
- The % saturation of hemoglobin is directly related to the PO2 of the blood
- Hb binding with O2 is reversible
o Increased PO2 increases Hb saturation (Hb associate more with O2)
o Decreased PO2 decreases Hb saturation (Hb dissociates more O2)
- When alveolar PO2 = Blood PO2 (no Hb)  no diffusion
- When alveolar PO2 > Blood PO2  O2 binds Hb
o Since have O2 bind, now can deliver more O2 systemically
- When alveolar PO = Blood PO2 (saturated Hb) decreased O2 binding to Hb
Oxygen-Hemoglobin Dissociation Curve:
- 100% saturation: 15 g of Hb/100 mL = 20.1 mL of O2/100 mL of blood
- Arterial blood is at 98% saturation = 19.7 mL O2/100 mL of blood
o Pulmonary capillaries
 High PO2  High Hb-O2 association
- Venous blood is at 75% saturation = 14.4 mL O2/100 mL of blood
o Systemic capillaries
 Low PO2  High Hb-O2 dissociation
o 19.7 – 14.4 ~ 5 mL = the amt of O2 delivered per 100 mL of blood
Note: when PO2 < 40 mmHg, very steep Hb-O2 release
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98% of blood entering the left atria from the ling has passed through the alveolar capillaries
o 2% is shunted from the aorta-bronchial circulation-pulmonary veins-left atria and is “not oxygentated”
 This is referred to as the pulmonary shunt blood
 There is blood flow there, but very little exchange occurs
BHS116 Fall: Human Physiology and Pathology
Notetaker: Jessica Du
Date: 10/05/2011, 1st hour
Page2
Diffusion of O2 from Capillaries into Tissues:
- O2 is constantly being consumed by cells. Thus PO2 is low in tissues resulting in the influx O2
o Diffusion gradient:
 PO2 in artery =100 mmHg > PO2 in tissue = 40mmHg
 O2 flows down its concentration gradient, and results in the delivery of O2 to tissues
During Changes in Atmospheric Oxygen:
1) Ascending a mounding
o Alveolar PO2 decreases from 100 mmHg  60 mmHg
o ∆PO2 is 40 mmHg, results in 8% less saturation of Hb than normal
o Venous PO2 decreases from 40 mmHg  35 mmHg
o ∆PO2 is 5 mmHg, saturation is relatively the same
- Still would get 5 mL of O2 deliverer to tissues per 100 mL of blood
- A decrease in alveolar PO2 (40 mmHg) only resulted in a 5 mmHg decreased in the tissue PO2
.`. while climbing a mountain, tissue delivery of O2 is relatively unchanged, despite the changes in the
starting alveolar pressure
2) Diving below sea-level
- If you increase PO2 to 500 mmHg
o Max PO2 can only go potentially 2% higher (it was 98% saturated to begin with)
 .`. not really increasing the amount of O2 bound to Hb very much
o After loss of 5 volumes percent by release to the tissues, PO2 is only 2-3 mmHg greater than normal
 ∆PO2 in tissue = 43 – 40 = 3 mmHg
Hemoglobin Buffers Tissue PO2:
- Upper limit is ~40 mmHg (normal conditions)
o If tissue PO2 was higher, PO2 would not leave Hb
- Lower limit is ~ 15-20 mmHg (exercise)
o Small decrease in PO2, and big increase in O2 released (due to the steep part of the Hb-O dissociation
curve)
Hb-O2 Dissociation Curve Shifts:
- 1) Bohr Effect: Right of Left shift in the curve in response to change circulation levels of:
o 1. PCO2
o 2. H+ (pH)
 Right Shift: Tissue capillaries
 ↑ PCO2  ↑ H2CO3  ↑ H+  ↓ pH
 .`. ↓ O2 Binding
 Left Shift: Pulmonary capillaries

↓ PCO2  ↓ H2CO3  ↓ H+  ↑ pH
 .`. ↑ O2 Binding
 We do not see this often in normal cellular activity
 Could see this at alveolar level, during the recovery from a right shift back to normal
dissociation curve
- Note that the binding of O2 and CO2 to Hb affect the binding of each other
-
2) BPG (2,3-biphosphoglycerate) Effect
o BPG is synthesized in RBC in hypoxic events (eg: when climbing a mountain)
o During hypoxia, BPG may shift the dissociation curve to the right as much as 10 mmHg
 Increases O2 delivery (increase PO2, increase dissociation)
 Because during hypoxia, you need to increase as much O2 release as possible
o Important adaptation during poor tissue blood flow
BHS116 Fall: Human Physiology and Pathology
Notetaker: Jessica Du
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Date: 10/05/2011, 1st hour
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3) Temperature Effect
o Increase in temperature also result in a shift to the right
 Increased O2 dissociation from Hb
 Important during times to illness when fever is present
 Want to increase O2 delivery to tissues, so lymphocytes and macrophages receive
enough O2 to function and fight off infection
4) Exercise Effect
o ↓ pH (due to lactic acid build up)
o ↑ pCO2 (at tissue)
o ↑ temperature (due to ATP used during muscle contraction)
o Results in a right shift of the dissociate curve, resulting in an increase in O2 delivery
CO2 Transport:
- Remember that CO2 is 20x more soluble than O2 in water (blood), due to its higher solubility coefficient
- Carbonic anhydrase is an enzyme which catalyzes conversion of CO2 and H2O  H2CO3 which dissociates
into H+ and HCO3o This occurs 5000x times faster in cell vs plasma, due to the presence of the enzyme
o CO2 is transported at the greatest percentage as HCO3- in the blood (60%)
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HCO3-/Cl- cotransporter (antiporter): found in both tissue RBCs and alveolar RBCs
Results in a Cl- shift between venous and arterial blood RBCs
At tissue:
o PCO2tissue > PCO2blood  causes the diffusion of CO2 into the blood
o This CO2 will combine with Hb, which knocks off some O2, so it can participate in gas exchange at
the tissue
o CO2 also enters the RBC
 CO2 + H2O  H2CO3  H+ + HCO
Increase H+, which also is able to combin with Hb, and knock off more O2 for tissue O2
delivery
At alveoli
o PCO2 blood > PCO2 alveoli  cause diffusion of CO2 into alveoli
o Changes in HCO-/Cl- cotransporter, HCO3- in and Cl- out
BHS116 Fall: Human Physiology and Pathology
Notetaker: Jessica Du
Date: 10/05/2011, 1st hour
Page4
Diffusion of CO2 from the tissues into the capillaries (tissue PCO2 = 46, blood PCO2 = 40)
- CO2 diffuses in the opposite direction of O2
- CO2 diffuses 20x faster than O2
CO2 dissociation curve
- Very narrow range, of only 40-46 mmHg results in 4% of total CO2 being released into alveoli
o Small change in PCO2, relatively high delivery
o Due to high solubility coefficient of CO2
Haldane Effect
- Decreased O2 binding to Hb  increased CO2 and H+ binding to Hb (at tissue capillaries)
- Opposite of Bohr effect
- ** don’t need to know graph for exam
Carbon Monoxide Binding
- Hb has a very high affinity for CO, than O2
o Extremely low PCO can bind Hb easily, due to its higher affinity than O2
o PCO = 0.4 mmHg is enough to complete equally than O2
o PCO = 0.6 mmHg is enough to out compete O2 and cause CO poisoning