Transport of blood

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Transport of Blood (O₂ and CO₂)

The "transport of blood" in physiology refers primarily to how blood carries oxygen (O₂) from the lungs to tissues and carbon dioxide (CO₂) from tissues back to the lungs. Both gases are transported by two mechanisms: dissolved in plasma and chemically combined.

I. Transport of Oxygen (O₂)

1. Two Forms of O₂ in Blood

O₂ is carried in blood in two forms:

Form	Proportion	Mechanism
Dissolved in plasma	~2%	Henry's law; proportional to PO₂
Bound to hemoglobin	~98%	Chemical combination

Why dissolved O₂ alone is insufficient:

Solubility of O₂ in blood = 0.003 mL O₂/100 mL blood per mm Hg
At a normal arterial PO₂ of 100 mm Hg: dissolved O₂ = only 0.3 mL O₂/100 mL blood
At a resting cardiac output of 5 L/min, this delivers only 15 mL O₂/min
But the body needs ~250 mL O₂/min at rest - a 17-fold shortfall
Therefore, hemoglobin binding is essential for adequate O₂ delivery

(Costanzo Physiology 7th Ed; Medical Physiology)

2. Hemoglobin Structure and O₂ Binding

Normal adult hemoglobin (Hb A) is a tetramer (~68 kDa) with 2α + 2β subunits
Each subunit contains a heme (iron-porphyrin) group + a globin polypeptide
Each heme group binds one O₂ molecule → 4 O₂ per Hb molecule
Iron must be in the ferrous (Fe²⁺) state to bind O₂
1 g of hemoglobin A can bind 1.34 mL O₂
Normal Hb concentration = 15 g/100 mL → O₂-binding capacity = 20.1 mL O₂/100 mL blood

Hemoglobin variants:

Variant	Feature	Clinical Significance
HbA (α₂β₂)	Normal adult	-
HbF (α₂γ₂)	Fetal; higher O₂ affinity	Facilitates O₂ transfer from mother to fetus
HbS (αA₂βS₂)	Deoxygenated form sickles	Sickle cell disease; lower O₂ affinity
Methemoglobin	Fe³⁺ (ferric)	Cannot bind O₂; caused by nitrites/sulfonamides

(Costanzo Physiology 7th Ed)

3. O₂ Content of Blood

The O₂ content (actual O₂ per 100 mL blood) is calculated as:

O₂ content = (O₂-binding capacity × % Saturation) + Dissolved O₂

Normal arterial blood (98% saturated): O₂ content ≈ 20.0 mL O₂/100 mL
O₂ delivery = Cardiac output × O₂ content

4. Diffusion of O₂: Alveoli → Blood → Tissues

At the lungs (alveolar capillaries):

Alveolar PO₂ = 104 mm Hg
Venous blood entering pulmonary capillary PO₂ = 40 mm Hg
Pressure gradient = 64 mm Hg → drives O₂ into blood rapidly
Blood reaches near-equilibrium (~104 mm Hg) after only 1/3 of capillary length

Venous admixture ("shunt"):

~2% of blood passes through bronchial circulation (unexposed to alveolar air), PO₂ ≈ 40 mm Hg
This mixes with oxygenated blood → aortic PO₂ drops slightly to ~95 mm Hg

Uptake of oxygen by pulmonary capillary blood

Figure: O₂ uptake by pulmonary capillary blood - Guyton & Hall

At the tissues (peripheral capillaries):

Arterial blood arrives at PO₂ = 95 mm Hg
Interstitial fluid PO₂ = 40 mm Hg
Intracellular PO₂ = ~23 mm Hg (or even lower near mitochondria)
O₂ diffuses down this gradient into cells

Diffusion of O₂ from peripheral capillary to cells

Figure: PO₂ gradient from capillary to tissue cells - Guyton & Hall

(Guyton & Hall Textbook of Medical Physiology)

5. Factors Affecting O₂-Hemoglobin Dissociation (Bohr Effect)

The oxyhemoglobin dissociation curve describes the sigmoidal relationship between PO₂ and Hb saturation:

Right shift (decreased O₂ affinity, more O₂ released to tissues):

↑ PCO₂
↑ [H⁺] (acidosis / ↓ pH) - Bohr effect
↑ Temperature
↑ 2,3-DPG (diphosphoglycerate)

Left shift (increased O₂ affinity, O₂ held tighter):

↓ PCO₂
↓ [H⁺] (alkalosis / ↑ pH)
↓ Temperature
Fetal hemoglobin (HbF)
CO poisoning (carboxyhemoglobin)

II. Transport of Carbon Dioxide (CO₂)

CO₂ is produced by cellular metabolism and must be carried from tissues to lungs. Average transport: 4 mL CO₂ per 100 mL blood. CO₂ is transported in three forms:

1. Dissolved CO₂ (~7%)

PCO₂ venous = 45 mm Hg; arterial = 40 mm Hg
Dissolved CO₂ at 45 mm Hg = 2.7 mL/100 mL; at 40 mm Hg = 2.4 mL/100 mL
Difference = 0.3 mL/100 mL transported this way

2. As Bicarbonate Ion (HCO₃⁻) - the MAJOR form (~70%)

This is the most important mechanism, driven by carbonic anhydrase inside RBCs:

CO₂ + H₂O  →[carbonic anhydrase]→  H₂CO₃  →  H⁺ + HCO₃⁻

Carbonic anhydrase accelerates this reaction 5,000-fold
H⁺ ions are buffered by hemoglobin inside RBCs
HCO₃⁻ diffuses out of RBCs into plasma in exchange for Cl⁻ (chloride shift / Hamburger phenomenon)
The venous RBC thus has higher chloride content than arterial RBC

Importance: Blocking carbonic anhydrase (e.g., acetazolamide) raises tissue PCO₂ to ~80 mm Hg (vs. normal 45 mm Hg)

3. Carbaminohemoglobin (~20-30%)

CO₂ binds directly to amine (-NH₂) groups on hemoglobin → carbaminohemoglobin (CO₂Hb)
Reaction is reversible; CO₂ released easily in alveoli where PCO₂ is lower
A small amount also binds to plasma proteins (less significant - only 1/4 the protein mass of Hb)

Form	% of CO₂ Transported
Dissolved CO₂	~7%
Bicarbonate (HCO₃⁻)	~70%
Carbaminohemoglobin	~20-23%

(Guyton & Hall Textbook of Medical Physiology)

Figure: CO₂ dissociation curve showing normal operating range (arterial 40 mmHg, venous 45 mmHg) - Guyton & Hall

The Haldane Effect

Oxygenation of Hb in the lungs displaces CO₂ - this is the reverse of the Bohr effect:

When O₂ binds to Hb in alveolar capillaries, Hb releases CO₂ more readily
This increases CO₂ unloading from blood to alveolar air
The Haldane effect is actually quantitatively more important than the Bohr effect in enhancing gas exchange

III. Summary: The Full Transport Cycle

LUNGS
  Alveolar PO₂ = 104 mm Hg  →  O₂ loads onto Hb
  Alveolar PCO₂ = 40 mm Hg  →  CO₂ unloads from blood
         ↓
ARTERIAL BLOOD
  PO₂ = 95 mm Hg
  PCO₂ = 40 mm Hg
  O₂ content ≈ 20 mL/100 mL
         ↓
TISSUES
  Interstitial PO₂ = 40 mm Hg  →  O₂ unloads from Hb
  Intracellular PCO₂ rises  →  CO₂ loads into blood
         ↓
VENOUS BLOOD
  PO₂ = 40 mm Hg
  PCO₂ = 45 mm Hg
  CO₂ content rises ~4 mL/100 mL
         ↓
Back to LUNGS

Key numbers to remember:

Parameter	Arterial	Venous
PO₂	95 mm Hg	40 mm Hg
PCO₂	40 mm Hg	45 mm Hg
O₂ content	~20 mL/100 mL	~15 mL/100 mL
Hb O₂ saturation	~98%	~75%

Sources:

Guyton and Hall Textbook of Medical Physiology (Chapter 41)
Costanzo Physiology, 7th Edition
Medical Physiology (Boron & Boulpaep)

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