At the beginning of exhalation, the driving pressure for expiratory gas flow remains the same as in a normal individual. This driving pressure is a combination of the elastic recoil pressure and pleural pressure. However, as exhalation continues, the drop in pressure caused by resistance is greater in individuals with mucus accumulation and inflammation. This results in the collapse of small airways that lack cartilage, known as premature airway closure. This leads to a decrease in maximal expiratory volume and an increase in lung volume, referred to as air trapping. The initial increase in lung volume helps offset the increase in airway resistance caused by mucus accumulation and inflammation. But as the disease progresses and inflammation and mucus accumulation increase further, there is a greater increase in expiratory resistance and a decrease in maximal expiratory flow rates.

In individuals with a decrease in elastic recoil, the driving pressure for expiratory gas flow is reduced at the start of exhalation. While the drop in pressure caused by resistance is normal, the smaller initial driving pressure results in an equal pressure point that occurs closer to the alveolus in airways without cartilage. Premature airway closure occurs again, but for a different reason than in individuals with an increase in airway resistance.

Individuals with premature airway closure often experience crackles, also known as rales, which are popping sounds heard during inspiration upon auscultation. These crackles occur due to the opening of airways during inspiration that were closed (compressed) during the previous exhalation. Crackles can be caused by mucus accumulation, airway inflammation, fluid in the airways, or any mechanism that narrows or compresses the airways. They are also heard in individuals with emphysema, where there is a decrease in lung elastic recoil. In fact, both acute and chronic lung diseases can alter the expiratory flow-volume relationship by changing static lung recoil pressure, airway resistance and its distribution, loss of mechanical tethering of intraparenchymal airways, changes in the stiffness or mechanical properties of the airways, and variations in the severity of these changes in different lung regions.

The mean dynamic compliance of the lung (dyn CL) is calculated as the slope of the line connecting the end-inspiratory and end-expiratory points of no flow. Dynamic compliance is always lower than static compliance and increases during exercise. This is because during tidal volume breathing, a small change in alveolar surface area is insufficient to bring additional surfactant molecules to the surface, making the lung less compliant. However, during exercise, there are large changes in alveolar surface area, leading to increased surfactant availability and greater lung compliance.

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22.6A ).Atthestartofexhalationthedrivingpressureforexpiratorygasflowisthesameasinanormalindividual;thatis,thedrivingpressureisthesumoftheelasticrecoilpressureandpleuralpressure.Asexhalationproceeds,however,theresistivedropinpressureisgreaterthaninthenormalindividualbecauseofthegreaterdecreaseinairwayradiussecondarytotheaccumulationofmucusandtheinflammation.Asaresulttheequalpressurepointnowoccursinsmallairwaysthataredevoidofcartilage.Theseairwayscollapse.Thiscollapseisknownaspremature airway closure, whichresultsinaless-than-maximalexpiratoryvolumeandproducesanincreaseinlungvolumeknownasair trapping.Theincreaseinlungvolumeinitiallyhelpsoffsettheincreaseinairwayresistancecausedbytheaccumulationofmucusandinflammationbecauseitresultsinanincreaseinairwaycaliberandelasticrecoil.Asthediseaseprogresses,however,inflammationandaccumulationofmucusincreasefurther,thereisagreaterincreaseinexpiratoryresistance,andmaximalexpiratoryflowratesdecrease.
Fig.22.6B ).Atthestartofexhalationthedrivingpressureforexpiratorygasflowisreducedsecondarytoalossofelasticrecoil.Whiletheresistivedropinpressureisnormal,thesmallerinitialdrivingpressureresultsinanequalpressurepointthatoccursclosertothealveolusinairwaysthatdonotcontaincartilage.Prematureairwayclosureagainoccursbutforaverydifferentreasonthantheprematureairwayclosureobservedinindividualswithanincreaseinairwayresistance.
Individualswithprematureairwayclosurefrequentlyhavecrackles, alsosometimescalledrales, apoppingsoundusuallyheardduringinspirationonauscultation.Thesecracklesareduetotheopeningofairwaysduringinspirationthatclosed(i.e.,werecompressed)duringthepreviousexhalation.Cracklescanbeduetomucusaccumulation,airwayinflammation,fluidintheairways,oranymechanismresponsibleforairwaynarrowingorcompression.Theyarealsoheardinindividualswithemphysema,inwhichthereisadecreaseinlungelasticrecoil.Infact,acuteandchroniclungdiseasescanchangetheexpiratoryflow-volumerelationshipbychangesin(1)staticlungrecoilpressure,(2)airwayresistanceandthedistributionofresistancealongtheairways,(3)lossofmechanicaltetheringofintraparenchymalairways,(4)changesinthestiffnessormechanicalpropertiesoftheairways,and(5)differencesinseverityoftheaforementionedchangesinvariouslungregions.
mean dynamic compliance of the lung (dyn CL) is calculated as the slope of the line that joins the end-inspiratory and end-expiratory points of no flow (
Fig. 22.7
Dynamic compliance is always less than static compliance, and it increases during exercise. This is because during tidal volume breathing, a small change in alveolar surface area is insufficient to bring additional surfactant molecules to the surface, and thus the lung is less compliant. During exercise the opposite occurs; there are large changes in
Mucus, Edema, Bronchoconstriction PL = 90˜60 = 30 cm H2O
Fig. 22.6 A,Flowlimitationinthepresenceofincreasedairwayresistance.B,Flowlimitationinthepresenceofalossofelasticrecoil.