The resistance of the airways to the airflow through them depends on the radius, length and number of the airways. It has long been apparent (1, 2) that the bronchi are distended as well as lengthened in the inspiratory position of the lung. These two changes in the dimensions of these airways would have opposite effects on their resistance to airflow, lengthening increasing resistance and widening reducing it. More recent measurements of airway resistance have shown that it is reduced in the inspiratory position of the lung (3,4,5) and is more in individuals with small lungs (6).The body plethysmograph affords a good technique for comparing changes in airway resistance with changes in lung volume in an individual, since each measurement of airway resistance includes as an essential stage in its derivation, a measurement of intrathoracic gas volume. It therefore seemed desirable to explore further the relationship between airway resistance and lung volume at different degrees of inflation of the lung in normal subjects. METHODSAirway resistance was measured by the method previously described by DuBois, Botelho and Comroe (7). The method has the advantage that the pressure changes in the body plethysmograph reflect changes in alveolar pressure rather than changes in pleural or esophageal pressure. The resulting measurements are therefore assessments of pure airway resistance uncomplicated by the effects of tissue viscosity which are included with (Figure 1).Each subject sat in the 600 liter body plethysmograph for a few minutes until the air in the box was warm enough and sufficiently saturated with water vapor for spontaneous changes in plethysmograph pressure over a period of 10 seconds to be negligible. During this time the amplification of .the record of plethysmograph pressure was adjusted until a displacement of 30 cc. to or from the plethysmograph gave a deflection of two inches on the oscilloscope face. The subject then put his mouth over the flowmeter shutter assembly which was suspended in the plethysmograph and panted for about six seconds. The observer aligned the plexiglass disc with the midslope of the tracing and read the product (lung volume X airway resistance) off the calibrated scale.The observer then operated a switch, which closed the solenoid shutter at the mouth, and replaced the record of flow rate by one of mouth pressure, on the Y axis of the 5A more detailed description of this modification is being prepared. Meanwhile, the diagram (Figure 1) shows the arrangement of apparatus used in the present study.

In 10 patients with chronic pulmonary emphysema the distribution of ventilation within the lungs was assessed by a nitrogen washout and washin technique. Alveolar ventilation per minute per unit lung volume had a mean value of 5.0 in well ventilated alveoli and 0.19, or 1/26 as much, in poorly ventilated alveoli. Distribution of blood perfusion was estimated by a new method from these data and from O2 consumption and arterial O2 saturation. On the average, poorly ventilated alveoli which constituted 66% of lung volume were perfused by not more than 52% of the cardiac output. Thus poorly ventilated alveoli were underperfused by blood. Ventilation/perfusion ratios averaged 2.24 in well ventilated alveoli and 0.23 in poorly ventilated alveoli. Oxygen saturation averaged 85% in arterial blood and 97frac12% and 76%, respectively, in end-capillary blood leaving well and poorly ventilated alveoli. Inhomogeneity of this degree within the lung invalidates calculations of diffusing capacity based on any single mean PaOO2 and of alveolar ventilation based on identification of mean alveolar Pco2 with arterial blood Pco2. Submitted on March 25, 1960