Gas Exchange Flashcards
Rate of general gas diffusion affected by? (3)
Conc gradient (steeper = better)
SA for diffusion (bigger = better)
Length of diffusion pathway (shorter = better)
Ideal gas equation
P = (nRT )+ V
Grahams Law
“Rate of diffusion is inversely proportional to square root of its molecular mass at identical pressure + temperature”
Smaller mass of gases = more rapid diffusion
Henry’s Law
“Amount of dissolved gas in a liquid is PROPORTIONAL to its partial pressure above liquid”
Fick’s Law (6)
Partial pressure difference across diffusion barrier
Solubility of gas
Cross sectional area of fluid
Distance molecules need to diffuse
Molecular weight of gases
Temperature of fluid (NOT IMPORTANT FOR LUNGS: assumed 37 degrees)
pO2 in alveoli (vs outside envrionement + capillaries)
Compared to external environment = LOW
(due to continuous diffusion of O2 across alveolar membrane)
Compared to capillary = HIGH
(causes net diffusion into the blood)
oxyhaemoglobin?
Transports O2 to respiring tissues via bloodstream
= from binding of haemoglobin + O2
pCO2 (alveolar vs capillaries vs outside environment)
In capillaries = much HIGHER than in alveoli
= net diffusion across into alveoli
CO2 can then be exhaled:
Alveoli = HIGHER than external environment
Layers of diffusion barrier (5)
1) Alveolar epithelium
2) Tissue fluid
3) Capillary endothelium
4) Plasma
5) RBC’s membranes
Factors affecting rate of diffusion at alveoli (4)
Membrane Thickness (Thinner = faster)
Membrane surface areas
Larger = faster
Lungs normal have large SA (due to many alveoli)
Pressure Differences across membrane
Diffusion coefficient of gas
Ventilation rate? (V)
Vol of gas inhaled + exhaled from lungs in a given time period
=tidal volume (amount of air in / out in one breath) x respiratory rate
Perfusion Rate? (Q)
Total volume of blood reaching pulmonary capillaries in a given time period
Ventilation vs perfusion (places in the lung)
Ventilation exceeds perfusion towards apex
Perfusion exceeds ventilation towards base
Why does gravity trigger differences in V/Q in lung? (2)
Pleural Pressure:
Increased at base of lung
Results in more compliant alveoli + increased pressure
Hydrostatic Pressure
Decreased at apex of lungs
Results in decreased flow + decreased perfusion
Management of V/Q mismatch (less ventilation)
Hypoxic vasconsticion = causes blood to be diverted to better ventilated parts of lung
Why does oxygen travel on haemoglobin?
Poorly soluble in blood
Describe haemoglobin
Protein made up of 4 haem groups (containing Fe2+)
Fe2+ ions associated with hemoglobin molecules = chemically react to form oxyhemoglobin
Haemoglobin molecule = can hold 4 O2 molecules
Limiting factor of O2 delivery to tissues
haemoglobin
Cooperative Binding
Haemoglobin changes shaped bases on how many O2 molecules bound to it
Shape change = change in O2 affinity
T-state of haemoglobin
No oxygen bound = hemoglobin in tense state (T state)
Low oxygen affinity
R-state of haemoglobin
At part where 1st oxygen binds hemoglobin alters in shape = relaxed state (R-state)
Higher affinity for oxygen
What influences O2 delivery?
% of oxygen bound to hemoglobin = related to pO2 at given site
How does cooperative binding work at extreme pO2’s
When LOW pO2 locally : don’t want hemoglobin to keep O2 tightly bound
Where HIGH pO2 locally (e.g pulmonary circulation) : `want haemoglobin to take as much O2 as possible
Affect of pH on pO2
Lower pH = more H+
Haemoglobin in T-state it has a higher affinity for H+ than for oxygen
Hemoglobin enters T state + affinity for O2 goes down (more needed to achieve max % saturation)
Bohr Effect = (allows O2 to dissociate with lower pH)
Affect of 2-3,biphosphoglycerate on pO2
Product of ANAEROBIC glucose metabolic pathway
Decrease affinity of hemoglobin + oxygen
2-3BPG = increases while at high altitudes
Helps adjust to relatively low atmospheric O2
More O2 released at tissue
Higher [2,3-BPG] = dissociation curve shifts right
Affect of temperature on pO2?
Higher temperature of O2 = oxygen has more kinetic energy
= more likely to dissociate
More 02 needed for respiring tissues (tend to generate more heat)
Increase in temperature = curve shifts right
CO2 + H20 equation
CO2 + H2O → ← H2CO3 → ← H+ + HCO3-
Why can’t all CO2 be dissolved in blood?
Blood pH will become acidic due to excess H+
Methods of CO2 transportation (3)
CARBAMINO COMPOUNDS
HCO3-
AS DISSOLVED CO2
Carbaminohaemoglobin?
CO2 directly binds to amino acids + amine groups of hemoglobin at high conch
Haldane effect?
Where O2 conc = lower (e.g respiring tissues) the CO2 carrying capacity of blood INCREASES
Release of O2 from hemoglobin = promotes binding of CO2
Carbamino compounds + stabilising pH
CO2 is unable to leave blood cell to contribute to changes in pH (no acidosis!!)
Carbamino compounds + Bohr Effect
Stabilises T-state of hemoglobin
Promoting O2 release from subunits (at most active tissues where CO2 production is highest)
When RBC reaches are of high O2 conc again (e.g lungs) = hemoglobin preferentially binds to O2 again
Stabilises R-state = promotes release of co2 (Haldane effect)
Allows more O2 to be picked up + transported away
HCO3- production (+ its uses)
CO2 diffuses into RBCs
Converted to H+ and HCO3- by carbonic anhydrase
HCO3- = transported back via chloride bicarbonate exchange
HCO3- = can act as buffer against H+ in blood plasma
Deoxyhaemoglobin (what is it + effect)
H+ created by carbonic anhydrase reaction in RBCs = binds to hemoglobin (deoxyhemoglobin)
RBCs rech lungs : O2 binds hemoglobin promoting R-state
Allows release of H+ ions (become free to react with HCO3- (producing CO2 + H2O) where CO2 is exhaled
pC02 at periphery tissues + lower alveoli
PCO2 = high at periphery tissues + lower alveoli (where CO2 is being released)
Allows more CO2 to be dissolved in periphery tissue
Released into gas phase at alveoli where pO2 is lower
