MECHANISM OF PRODUCTION OF CRACKLES AFTER ATELECTASIS DURING LOW-VOLUME BREATHING

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Abstract
Effects of shallow breathing of air (LVB-air) and O2 (LVB-O2) at low lung volumes (below closing capacity) and tidal breathing at FRC [functional residual capacity] (FRC-air, FRC-O2) on the production of crackles were compared in 5 normal [human] volunteers. Two microphones were attached on the right posterior chest wall in the midclavicular line 10 and 20 cm from the apex of the right lung, respectively (M10 and M20), to record crackles during various breathing maneuvers. After LVB-air and LVB-O2, there were changes in residual volume as measured by the body plethysmograph. Inspiratory and expiratory limbs of the quasi-static pressure volume curve were shifted to the right. Occasionally, some subjects coughed after LVB-air and/or LVB-O2. Inspiratory crackles occurred mostly at the upper third of vital capacity (VC) after LVB-air and LVB-O2 and were confined almost exclusively to the dependent lung zones (M20). The inspiratory transpulmonary pressure at 25% (PL25) and 50% (PL50) of VC correlated with the volume of trapped gas that was absorbed (.DELTA.Vtg) (P < 0.001 and P < 0.001, respectively). The quantity of crackles correlated with .DELTA.Vtg (P < 0.01). During low lung volume breathing airways in the dependent lung regions are closed. There is absorption of trapped O2, which causes reversible atelectasis. Upon reinflation, inspired air will go to the lung regions with open airways first and subsequently to the closed dependent regions, producing crackles recorded by th M20 microphone at the upper third of VC. The crackles are produced by inflation of atelectatic lung.

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