| Description |
A method utilizing an insoluble inert-gas tracer was developed for measurement of the rates of oxygen consumption, carbon dioxide production, and alveolar ventilation. The measurements are based on the injection of a small constant-volume bolus of tracer gas into the inspired gas flow near the airway opening with each inspiration. Injection timing is controlled to coincide with a fixed pre-selected inspiratory volume with each breath cycle. The concentrations of tracer, oxygen, and carbon dioxide in the expiratory flow were continuously recorded using a mass spectrometer. Calculation of the respective rates is made from the alveolar concentrations as read from the tracings. Since the mathematical model is based, on first principles, on a single-compartment lung, the effects of nonuniformity was examined both by studying subjects with varying pulmonary function abnormalities and by computer simulation. The simulation provided for quantitative estimates of the effects on the error in measurement for variations in the timing of the bolus delivery and the timing of reading the gas concentrations during a single expiration. These techniques allow for the design of an instrumental system in which measurement of the inspired volume can be replaced by thermister temperature measurement for timing the bolus delivery and also for timing a gas sampler which may be substituted for the mass spectrometer, with slower, but less expensive, analyzers for readout of alveolar gas concentrations. The error in the method was quantitated by simultaneous 3-minute gas collection method. The errors in oxygen consumption and carbon dioxide excretion were minimal in normals, of the order of the estimated error by the conventional method, but increased in abnormal subjects with increasing severity of the abnormality according to each of the following pulmonary functions tests: FEV1, FEF25-73, SGaw N2, clearance delay, lung clearance index. By correlating the error with the function test, it was possible to correct the measured values and thereby reduce the errors in measurement on abnormal subjects to one comparable to those on normals. There was no significant difference in the systematic error in resting subjects versus exercising subjects for either normals or abnormals. During washing and washout of the tracer, patterns of changes in the single-breath expiratory contours evolved which, by simulation, could be characterized by the degree and type of non-uniformity of pulmonary mechanical properties, i.e., specific airways conductance and specific compliance. In the stimulation, the dead space was modeled by a non-mixing conducting airway in series with a mixing manifold compartment which communicated immediately with the individual alveolar compartments. Following this, the simulation model was extended to provide for the use of inert gas tracers of finite solubility and thus allow for the added study of the effects of the distribution of pulmonary blood flow. This lead naturally to a consideration of the term "alveolar ventilation" and pointed to possible ambiguities in its meaning and in measurement of its distribution in multi-compartment lungs. |
