Chronic airflow obstruction: Evolution of disordered function in cigarette smokers

Abstract

Measurements of the mechanical behaviour of the lung, which reflect lung structure, have been used to elucidate the evolution of chronic airflow obstruction in male cigarette smokers and subjects with pulmonary emphysema. The exponent K, from a single exponential function fitted to static pressure-volume data, is an index of lung distensibility directly related to the size of peripheral airspaces. Elastic recoil pressure is inversely related to K. Conductance measured during forced and interrupted deflations of the lungs reflects the dimensions of airways. K increased abnormally with age in smokers suggesting an increase in the airspace size caused by the effects of cigarette smoke which probably acts by intensifying elastase activity in lung tissue. Decreased conductance implying narrowing of airways is found in young smokers, but conductance rises and airways become more distensible in older smokers. A progressive increase in K (with decrease in recoil pressure) and a decrease in conductance are responsible for the advancement of severe airflow obstruction in cigarette smokers.