Gas exchange lecture 2 +3

How is ventilation tested ? 

Functional tests: lungs X have biomarkers for detecting lung injuries 

	Test
Volume ( amount of air taken in )	Volume time curve  → forced vital capacity  → forced expiratory volume
Flow ( the rate at which air is taken in/ out)	Flow volume loop  → peak expiratory flow rate  → peak inspiratory flow rate  Airflow rate: pressure gradient/ airway resistance

How does airway resistance affect ventilation

Airway resistance

Friction from air moving against walls of airway  Larger diameter → low  resistance  Smaller diameter of airway → high resistance → causes: bronchoconstriction ( asthma ) / mucous/ fluid  Greatest resistance in medium sized bronchi  Lower resistance in small bronchi is ← larger total cross sectional area  Lower resistance in trachea ← larger diameter

How does lung compliance + elastic recoil affect ventilation

Compliance: change in volume per unit change in pressure  → ability for lungs to be stretched  → more compliance → smaller pressure gradient needed to create the same lung volume → easier to breath in  Elastance: tendency to oppose stretch + ability return to return to original configuration after distorting force is removed  High compliance → less elastic recoil/ low compliance → more elastic recoil

How does alveolar surface tension affect ventilation

Water molecules are charged + attracted to each other → tendency to collapse alveoli 

Law of Laplace( calculates the magnitude of inward directed pressure )

→ smaller the radius → greater the magnitude of inward directed pressure 

pulmonary surfactant: lipoprotein complex → amphiphilic → stabilises alveoli + increases lung compliance ( concentration of surfactant is proportional to size of alveoli → magnitude of inward directed pressure of large + small alveoli becomes the same ) 

Infant respiratory distress syndrome

 inadequate surfactant → alveoli collapse during expiration → dyspnea: fatigue from reinflating alveoli

What causes residual volume in lungs

Dynamic small airway closure

1. In forced expiration → muscles contract to lower the pressure in lungs for a greater pressure gradient so air can rush out faster 

2. Pressure in airway becomes lower than the pleural space as air moves out 

3. Airway becomes smaller as the pleural space pressure presses down on the airway 

4. Cause of residual volume

How does matching of alveolar ventilation + pulmonary blood perfusion affect gas movement across respiratory membrane

If other alveolus is poorly ventilated —> ventilation < perfusion ( low V/Q ratio ) —> lower partial pressure of O2 + higher partial pressure of CO2 —> blood vessl is poorly oxygenated —> shunting —> body reaction: constrict blood vessels

If other alveolus has little perfusion —> ventilation > perfusion ( high V/Q ratio ) —> higher partial pressure of O2 + lower partial pressure of CO2 —> blood is fully saturated but X travel to tissue —> physiological dead space —> body reaction: dilate blood vessels

How does structural characteristics of respiratory membrane across respiratory membrane

Surface area: greater surface area —> higher rate of diffusion

Membrane thickness: thinner membrane —> higher rate of diffusion

How does partial pressure gradients + gas solubility across respiratory membrane

Dalton’s law: the partial pressure exerted by a single gas present will be proportional to amount/ percentage of the gas 

breathing in: partial pressure of water vapour increases + air breathed in is mixed with air as residual volume --> partial pressure of oxygen decreases + partial pressure of carbon dioxide increases ( residual volume have higher proportion of carbon dioxide + lower proportion of oxygen ) 

--> blood: lower partial pressure of O2 --> O2 diffuses into the blood 

--> higher partial pressure of CO2 --> CO2 diffuses out of blood

Henry’s law: amount of gas that dissolves in a liquid is directly proportional to partial pressure of the gas

→ gases with higher solubility will have more dissolved molecules than gases with lower solubility

Why is the time taken for O2 + CO2 to diffuse similar?

O2 has steeper pressure gradient than CO2 

diffusion coefficient of CO2 is greater than O2 --> rate of gas transfer for CO2 is faster

O2 transportation

2% dissolved / mostly transported in combination w/ haemoglobin 

→ reduces Hb(4 heme groups w/ iron + globin ) into HbO2

increase in O2 concentration =/= proportional increase in Hb saturation

→ amount of dissolved oxygen determines saturation of haemoglobin

Explain Hb saturation graph

Plateau region of Hb saturation graph: large changes in partial pressure → small changes in percentage of Hb saturation

significance: high altitude → lower partial pressure of oxygen →reduction of only a little saturation of haemoglobin 

Steep region: small changes in partial pressure of O2 → large changes in percentage of Hb saturation → 

significance: small decrease in partial pressure in tissue during exercise → trigger significant offload of oxygen → efficient transfer of oxygen from blood to tissue

CO2 transportation

1. CO2 enters RBC → react s/ H2O + catalysed by carbonic anhydrase → bicarbonate + H+  [ fast] → pumps out bicarbonate + influx of Cl- to balance charges

2. CO2 enters plasma → bicarbonate + H+ [slow] → turns blood acidic

Internal respiration process

In tissues: O2 in oxyhaemoglobin released → O2 diffuses  Hb binds w/ H+ → HHb  CO2 from tissue diffuses into the plasma + RBC Carbonic anhydrase rapidly converts CO2 + water → carbonic acid → bicarbonate + H+  bicarbonate diffuses into plasma from RBCs  Cl- ions rush into RBC from plasma to counterbalance outrush of bicarbonate → electric neutrality ( chloride shift )

External respiration process

In lungs: 

1. Inhaled O2 diffuses from the alveoli into capillaries + RBC → oxyhaemoglobin + H+ 

2. Bicarbonate ions → RBCs + bind w/ H+ → carbonic acid 

3. Cl- diffuses out of cell to plasma ( reverse chloride shift ) 

4. Carbonic acid is split by carbonic anhydrase to release CO2 → diffuses from blood to alveoli for removal

Bohr effect

 

The affinity of oxygen binding of Hb decreases as it binds to carbon dioxide → CO2 + H+ combine reversibly with Hb ( in lungs )→ molecular structure of Hb changes + reduces affinity for O2 

→ decrease in pH / increase in [CO2] → decrease in Hb binding capacity for O2 → offload more O2 ( in tissue environment )

Haldane effect

( in tissue ) increase in [O2] → decreased Hb binding capacity of CO2 → Deoxyhaemoblin has greater affinity for H+ than haemoglobin → unloading of O2 helps Hb pick up CO2 generated H+ ( tissue cells produce CO2 in respiration → CO2 diffuse into blood to form bicarbonate + H+ )→ maintain blood pH