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Chest – expands outwards
Lungs – collapse
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Alveoli – act as bubbles (liquid-air interface)
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P = (2 x surface tension)/radius
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Collapse more likely when surface tension increases or alveolar size decrease
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Surfactant made from Type II pneumocytes decreases surface tension
Compliance – change in volume/change in distending pressure – can be measured for lung, chest wall
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Measures elastic recoil
Total system compliance = 1/Ctotal = 1/Cw +1/CL

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FRC – volume at end of normal exhalation (Vt)
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Inward recoil of lung approx equal to outward recoil of chest – elastic properties determine normal breathing – can be measure by nitrogen washout, helium wash-in, or body plethysmography
Factors affecting FRC: 1) habitus – directly proportional to height. Obesity decreases frc d/t dec chest compliance.
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2) Sex – females 10% less; 3) posture – decreases from upright to sitting to prone – d/t dec chest compliance from abd contents – Greatest change from 0-60 deg of inclination
4)lung dz, 5) diaphragmatic tone
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Decreases 15-20% with induction of anesthesia
Vt – normal breath
IRV – max inspiration above Vt; ERV – max exp below Vt
RV – volume remaining after max exp
TLC – RV+ERV+Vt+IRV
FRC – RV + ERV
VC – max volume expired after max inspiration – dependent on habitus, respiratory muscle strength, chest-lung compliance

 Closing capacity – volume at which small airways begin to close
 small airways depend on elastic recoil of surrounding tissues for patency – dependent on lung volume, especially at bases
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Normally below FRC, but rises with age, leading to shunts
(perfused but not ventilated), probably responsible for agerelated decline in PaO2
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At avg 44, FRC=CC while supine, at 66, CC = or > FRC while upright

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Flow = pressure gradient/Raw
Raw = (8 x length x viscosity)/(pi x radius^4)
Turbulent flow – high gas flows, branching points – sensitive to airway caliber
Reynolds number <1000 – laminar flow = (linear velocity x diameter x gas density)/gas viscosity
Airway resistance highest in medium airways

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Forced expiration of VC to evaluate airway resistance
FEV1 – forced expiratory volume in 1 sec
FEV1/FVC - proportional to degree of obstruction – normally >80%
FEV25-75% - less effort dependent

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Dead space – anatomic + alveolar
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Approx 150cc in adults (2cc/kg)
Shunt vs Dead Space
Hypoxic pulmonary vasoconstriction – shunts blood away from underventilated areas, preventing hypoxemia(alveolar hypoxia more powerful stimulus than pulmonary arterial hypoxia)
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Volatile agents can inhibit this in high doses
Hypercapnia and acidosis – constrict
Hypocapnia – pulmonary vasodilation

 Alveolar Oxygen Tension
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PAO2 = ((Pb – PH20) x FiO2) – (PaCO2/RQ)
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Pb – barometric pressure – 760
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PH20 – vapor pressure of water 47 mmHg at 37 deg
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RQ – usually 0.8
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(760-47) x .21 = 149.7

 PCO2 of 75, RA
 PAO2 for PCO2 of 40, FiO2 100%
 PCO2 of 40, FiO2 50%

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Binding of first 3 O2 to Hgb greatly facilitates binding of last O2 – responsible for linear portion of curve
Rightward shift – decreases O2 affinity, increases availability
Leftward shift – opposite
2,3 DPG – byproduct of glycolysis, builds up in anaerobic metabolism
Important points on O2 curve: P50 – 26.6 mmHG PO2
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SpO2 90% - 60mmHg O2; SpO2 80% - 50mmHg O2; SpO2 70% -
40mmHg O2

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Carbon Monoxide – higher affinity for Hgb, keeps
SpO2 at 100%
Methemoglobin – also displaces O2, sats 85%-90%; treatment is methylene blue
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Hurricane Spray
Oxygen Carrying Capacity
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CaO2 = (Hb x 1.36 x SpO2/100) + (PaO2 x .003)

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Central Receptors – medulla – responds to changes in CSF H+ concentration
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Regulates PCO2, BBB permeable to dissolved Co2, not bicarb
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Increase in H+ concentration increases ventilation to a point (CO2 narcosis)
Peripheral Receptors – carotid, aortic bodies
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Carotid bodies – main receptors – sensitive to PaO2, PaCO2, pH, arterial perfusion pressure (most sensitive to PO2 – activate when PO2<50)
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Communicate with central respiratory centers via glossopharyngeal nerves
Also stimulated by cyanide, doxpram, large doses of nicotine
Dopaminergic neurons – ventilatory response abolished by anti-dopaminergic drugs, b/l carotid surgery
Lung Receptors – transmitted by vagus
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Stretch receptors in bronchial smooth muscle – inhibit inspiration when lung volumes high; shorten exhalation when volumes low
Irritant receptors – in mucosa – noxious stimuli – increases respiratory rate, bronchoconstriction, coughing
J receptors – interstitial space – induce dyspnea in response to expansion of interstitial space volume and chemical mediators after tissue damage