Gas Exchange Asthma Notes

Semester 2

Case 2: Peak Performance

• How does gas transport & gas exchange occur?

[1] Dalton’s Law & Partial Pressures

Air we breathe: N₂ = 78.6%, O₂ = 20.9%, CO₂ = 0.04%, and the rest is mainly water molecules.

Atmospheric pressure is caused by the collision of these gas molecules. Atmospheric pressure = 760mmHg = 100kPa. Each gas contributes to pressure relative to its abundance. This relationship is known as Dalton’s Law. The partial pressure of a gas is the pressure contributed by a single gas in a mixture of gases.

PN₂ + PO₂ + PH₂O + PCO₂ = 760mmHg.

Henry’s Law (Diffusion Between Liquids & Gases)

At a given temperature, the amount of a particular gas in solution is directly proportional to the partial pressure of that gas. When a gas under pressure contacts a liquid, the pressure tends to force gas molecules into (& out of) solution. At a given pressure, the number of dissolved gas molecules will rise until an equilibrium is established. The actual amount of a gas in solution at a given partial pressure & temperature depends on the solubility of the gas in that particular liquid. E.g. In body fluids, CO₂ is highly soluble, O₂ is somewhat less soluble, and N₂ has very limited solubility.

Composition of Alveolar Air

In the nasal cavity, inhaled air becomes warmer & the amount of water vapour increases.

In the pharynx, trachea, & bronchial passageways, humidification & filtration continue.

At alveoli, incoming air mixes with air remaining in the alveoli from the previous respiratory cycle. Therefore, alveolar air contains more CO₂ and less O₂ than does atmospheric air.

Inhaled air: N₂ = 80kPa, O₂ = 21kPa, CO₂ = 0.04kPa, H₂O = 0.49kPa.

Alveolar air: N₂ = 76kPa, O₂ = 13kPa, CO₂ = 5.3kPa, H₂O = 6.3kPa.

Exhaled air: N₂ = 75.9kPa, O₂ = 15.5kPa, CO₂ = 3.7kPa, H₂O = 6.3kPa.

Gas exchange at the respiratory membrane is efficient because:

• The differences in partial pressure across the respiratory membrane are substantial.

• The distances involved in gas exchange are small.

• The gases are lipid-soluble.

• The total surface area is large.

• Blood flow & airflow are coordinated.

Partial Pressures In Alveolar Air & Alveolar Capillaries

Blood arriving in the pulmonary arteries has a lower PO₂ & a higher PCO₂ than does alveolar air. Diffusion between the alveolar air & the pulmonary capillaries increases PO₂ & decreases PCO_2. By the time it reaches the alveolar venules, it has reached equilibrium with the alveolar air. Hence, when blood departs the alveoli PO₂ = 13.3kPa, PCO₂ = 5.3kPa.

Partial Pressures In The Systemic Circuit

As blood enters pulmonary veins, it mixes with blood that flowed through capillaries around conducting passageways of the lungs. Gas exchange only occurs at alveoli, so blood leaving conducting passageways carries relatively little oxygen. Therefore, in pulmonary veins, PO₂ = 12.7kPa. No further changes in partial pressure occur until blood reaches peripheral capillaries.

Normal interstitial fluid: PO₂ = 5.3kPa. As a result, oxygen diffuses out of capillaries & carbon dioxide in, until capillary partial pressures are the same as those in adjacent tissues.

Inactive peripheral tissues: PCO₂ = 6kPa, whereas blood entering peripheral capillaries has PCO₂ = 5.3kPa. So CO₂ diffuses into blood as oxygen diffuses out.

Gas Pickup & Delivery

Oxygen & carbon dioxide have limited solubilities in blood plasma. When plasma oxygen or carbon dioxide concentrations are high, the excess molecules are removed by RBCs. When plasma concentrations are falling, the RBCs release their stored reserves.

Oxygen Transport

98.5% of O₂ in the blood is bound to haemoglobin – specifically to the iron ions in the centre of heme units. Each haemoglobin molecule can bind 4 oxygen molecules, forming oxyhaemoglobin (HbO₂). Haemoglobin with no oxygen bound is called deoxyhaemoglobin. The % of heme units containing bound O₂ at any given moment is called the haemoglobin saturation. The shape & functional properties of haemoglobin change in response to the PO₂ of blood, blood pH, temperature, & ongoing metabolic activity within RBCs. These changes can affect oxygen binding. The poisonous effect of carbon monoxide stems from its competition for the oxygen binding site.

PO₂: At equilibrium, O₂ molecules bind to heme at the same rate that other O₂ molecules are being released. If PO₂ increases, the reaction shifts to the right & more O₂ gets bound to haemoglobin. If PO₂ decreases, reaction shifts to the left & more O₂ is released by haemoglobin. The shape of the Hb molecule changes when an O₂ molecule binds to it, making it easier for the next O₂ to bind. Because each arriving O₂ increases affinity of Hb for the next O₂, the slope rises rapidly after the first O₂ binds. A very small change in PO₂ would result in a large change in % saturation. % then plateaus. Hb will be >90% saturated if exposed to an alveolar PO₂ of >8kPa. When oxygenated blood arrives in peripheral capillaries, the blood PO₂ declines rapidly as a result of gas exchange with the interstitial fluid. This decline causes haemoglobin to give up its oxygen.

pH: Active tissues generate acids, which lower the pH of interstitial fluid. When pH drops, shape of Hb changes & release their oxygen reserves more readily, so saturation declines. This is the Bohr effect. Primary compound responsible = CO₂. When CO₂ diffuses into the blood, it rapidly diffuses into RBCs. In the RBCs:

When PCO₂ rises, more H⁺ is produced, lowering pH.

Temperature: As temperature rises, Hb releases more O₂. As temperature declines, Hb holds onto O₂ more tightly. Temperature effects are significant only in active tissues in which large amounts of heat are being generated.

BPG: RBCs that lack mitochondria produce ATP by glycolysis, in which lactic acid is formed. BPG is also formed. Normal RBCs always contain BPG. For any PO₂, the higher the concentration of BPG, the more O₂ released by Hb, but there...

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