How does Fick's law tie in with maximised gas transport in the lungs?
List 4 factors which decreases gas transfer from alveoli -> capillaries.
Lungs have large excahnge area, a thin diffusion membrane, a high partial pressure difference, and a high permeability coefficient.
1. decrease in SA (e.g. obstruction, pneumonectomy)
2. increase in thickness of alveolar membrane (e.g. pulmonary fibrosis)
3. decrease in O2 conc (high altitude)
4. inadequate time for gas transfer (lung disease)
What is the rough difference between apical and basal alveolar pO2?
And apical and basal paO2?
What is the difference in partial pressure of O2 between alveolar gas and blood?
Apical: 135mmHg, Basal: 92mmHg so average = 100mmHg
Apical: 130mmHg, basal: 88mmHg (b/c low ventilation pressure relative to perfusion)
About 55mmHg (45%)(alveolar = 100mmHg and blood = 45mmHg) (the lower the diff in pressures, the greater the efficiency of transfer) BUT because of efficient transfer, by the time the blood has reached the end of the pulmonary capillaries, the pO2 is about 95mmHg - nearly arteriolar level.
13% difference so changing breathing rate affects CO2 excretion. Lungs use this to keep pH at desired level without decreasing oxygen saturation of arterial blood.
What do the respiratory muscles do on inhalation?
What 2 forces hold the thoracic wall and lungs in close opposition?
Diaphragm goes down, external inercostals contract = enlarge thoracic cavity.
1. Intrapleural fluid cohesiveness: H2O in intrapleural fluid attracted so pleural membranes stick together, fluid may contain molecules that increase fluid's surface tension
2. Negative intrapleural pressure: creates pressure gradient between lung and chest walls = holds outer suface of lung against inner surface of thorax.
A: hilum - where the 2 pleural layers fuse
B: visceral pleura - attached to thoracic wall
C: parietal pleura - covers lungs
Define lung pleura.
If you stop breathing with an open glottis, what holds the two pleural layers firmly together?
What is Boyle's law? How does it relate to inspiration?
What is Poiseuille's law?
2 layers of serous membrane derived from mesothelium.
Alveolar pressure = atm pressure, and intrapleural pressure is 4mmHg less which holds the 2 layers together.
If the vol of a gas increases, the pressure exerted by the gas decreases. Insipiration: respiratory zone airways forced to expand -> pressure inside decreases -> gas flows in from conducting airways.
As diameter increases, flow of gas into alveoli increases as 4th power of radius of alveolar ducts and respiratory bronchioles
What happens to the size of lungs and alveolar pressure during inspiration and expiration?
What happens to intra-alveolar and intra-pleural pressures during the respiratory cycle?
Inspiration: increase in lung size -> small decrease in alveolar pressure (1mmHg) = v. efficient.
Expiration: normally passive due to inspiratory muscle relaxation (elastic properties), recoil makes intra-alveolar pressure rise above atm (1mmHg)
Inspiration: both pressures decrease, intra-alveolar pressure starts to increase back to atm by mid-inspiration.
Expiration: both pressures increase, intra-alveolar pressure starts to decrease back to atm by mid-expiration.
What 2 factors control lung shrinkage during expiration?
1. elastic CT in lungs
2. alveolar surface tension - attraction between water molecules at water-air interface - produces force in alveoli that woud make them collapse during expiration if not for surfactant.
According to Laplace's law, what happens to alveoli during expiration if no surfactant?
And if surfactant present?
What is surfactant?
Smaller alveoli (with smaller radius) will have a higher tendancy to collapse during expiration (due to surface tension from fluid lining them. Larger = little change).
If surfactant = both alveoli decrease proportionately in size
Mix of lipid + protein secreted by type II pneumatocytes, lowers alveolar surface tension by interspersing between H2O molecules lining alveoli.
What are the 4 different lipoproteins that make different forms of surfactant?
What is respiratory distress syndrome of the newborn?
Why is the baby's first breath important (2 things)?
B and C = classic, decrease surface tension, A and D = coat bacteria and viruses and help immune system deal with (if D deficiency = pulmonary TB risk)
Foetal lungs synthesis surfactant late in pregnancy (premature <28w may not have enough = RDS = lungs hard to inflate and some alveoli fail to open = strenuous inspiratory efforts.
1. enough surfactant? 2. vascular resistance must decrease
Describe the 6 ways of lung function testing.
1. tests of tidal volume (spirometer) - depth and rate, repiratory disease assessment
2. tests of TLC using helium - e.g. if collapse suspected
3. tests of airflow - peak flow meter/vitalograph/bronchodilator improve airflow? Airway obstruction e.g. asthma decreases peak flow? Compare to expected PF values: male = 600L/min female= 450L/min
4. tests of V/Q mismatch using isotopes - causes hypoxaemia if mismatched
5. tests of gas transfer - compare pO2 at diff sites e.g. alveolar and arterial pO2
6. tests of challenge by histamine/exercise