• Air enteres pleural space
• Possible causes:
• Open pneumothorax- i.e. stab wound
• Mediastinal and tracheal shift toward affected side
• Tension pneumothorax- i.e. visceral opening
• Shift toward unaffected side
• Diaphragm displaced inferiorly on affected side
• Lung and chest wall deviate toward respective RV
• Lung- atelectasis
• Chest wall- increases 60%; ~3L air fills pleural space

• FRC- functional residual capacity
• Combination b/t lung's desire to recoil and chest wall's desire to expand
• Recoil ALWAYS passive- unless you forcefully expire, then inspiration is passive b/c you are approaching the FRC
• Emphysema- obstructive lung disease
• Increase lung compliance
• Vol/Pressure curve shifts L
• Expiration dificult
• Fibrosis- stiff lung
• Decrease compliance
• Shift R
• Inspiration difficult
• Muscle work needed

• # and gemoetry of elastic material of lungs (elastin and collagen fibers)
• Responsible for ~ half of elastic recoil of lungs
• Interdependence of alveoli
• Collapse of 1 alveoli causes neighbors to increase in size causing decrease in compliance
• Prevents alveoli collapse

Suface tension and surfactant:

• Surface tension due to air/water interface
• Water wants to decrease total SA exposed to air
• ST increases recoil force- works against surfactant

Surfactant

• Increases compliance/decreases recoil force
• Pressure differences exist b/t small/large alveoli- keeps alveolar exchange equal and prevents collapse along with interdependence of alveli
• Due to hydrophobic tails
• Equalizes ventialtion among alveoli
• Smaller alveoli - more surfactant - allow greater compliance - expand more
• Larger alveoli - less surfactant - less compliance - expand less
• Made by Type II alveolar cells (pneumocytes)

• The majority of the lung resistance occurs closer to the mouth- specifically the first 16 branching generations (anatomical dead space)
• Therefore, less TOTAL resistance in periphery of lungs
• *Silent Lung Disease- tumor in periphery of lung may go unnoticed due to relatively low change in lung function because of such low resistance and high volume in periphery of lung

• Equal to or greater than anatomical dead space
• Alveoli in last 7 generations may have collapsed or not be perfused with blood- functionalyl behave like anatomical dead space

• RV, residual volume- volume that is left over after max forced expiration
• *Cannot be measured with spirometer
• Tidal volume- normal amount of inhalation/exhalation 
  
• Expiratory reserve volume- amount of air we can exhale after tidal volume
  
• Inspiratory resrve volume- amount of more air we are able to inhale after tidal volume

• Measures mobilized air- NOT RV (residual volume)
• Tidal volume- 0.5 L
• IRV (inspiratory reserve volume)- extra air we can breathe in after normal V_T inhalation=2.5L
• ERV (experitory reserve volume)- extra volume of air we can breathe in after tidal volume exhalation (1.5L

Inert gas method

• (% of He) x (V_spirometer) = (new % of He) x (V_spirometer + V_Lung)

• Inspiratory capacity (IC)- tidal volume + Inspiratory reserve volume = total amount we can breathe in after REGULAR expiration
• Functional residual capacity (FRC)- amount of extra air in our lungs, after regular tidal expiration
• Highest compliance
• Total lung capacity- inspiratory capacity + functional reserve capacity
• Vital Capacity- everything we mobilize during max breathing
• Largest breath that can be taken and expired
• IRV + V_T + ERV
• Inspiratory capacity= (IRV + V_T)

• Up until age 20, all lung volumes increase
• After 20:
• Total lung capacity levels off
• Residual volume continues to slowly increase
• Therefore, vital capacity decreases with age

(Because TLC = RV + ERV + V_T + IRV= FRC + IC = VC + RV)

• Obstructive (COPD)
• Large increase RV 
• Increase TLC
• Increase RV/TLC
• Restrictive (asthma)
• Decrease RV
• Decrease TLC
• Same/slight decrease VC/TLC

• Equal volume changes require increased P_TM
• Steeper the slope, greater the compliance; similarly the flatter the slope the lower the compliance