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Biomedical subjects

T M Nielsen

Publications and source records attributed to T M Nielsen.

9 recordsLinked to original sources
PubMed1977

The compliance curve for the flow limiting segments of the airway. II. Experiments with human subjects.

Maximum effort flow-static recoil curves were obtained in 5 healthy subjects breathing air, He/O2, and SF6/O2 mixtures. In 4 of them maximum effort flows corresponded to really maximal flows and their curves were transformed into compliance curves for the flow limiting segments of the airway and analyzed from the point of view of a previously presented lung model (Pedersen and Nielsen 1976). The results showed, that viscosity dependent pressure losses from the alveoli to the flow limiting segments were minimal for air and SF6/O2, but not for He/O2. When viscosity dependent pressure lossess could be negleted, then expiration of gases of different densities gave almost identical compliance curves for the flow limiting segments. This supported the applicability of the model. The calculated compliance curves for the flow limiting segments were compared with data from the literature, and the findings indicated that flow limitation during expirations with just maximal flows throughout began in the extrapulmonary airways and moved upstream during the expiration.

Adolescent↗
PubMed1977

The compliance curve for the flow limiting segments of the airway. I. Model studies.

By means of a pilot-static tube airway compliance curves describing the cross-sectional area (A) as a function of transmural pressure (Ptm) were constructed for several locations in the elastic airway of a mechanical model of the lung. From these curves local relations between elastic recoil pressure of the lung (Pel) and maximal expiratory flow (Vmax) were calculated and compared with the experimentally determined Pel-Vmax curve for the entire airway, i.e. all parts in series. Theory and experiments showed that the latter was the lower borderline of all the local Pel-Vmax curves. This means that the maximal flow through the entire airway at a given Pel is determined by the segment of the airway, having the smallest Vmax, just as the maximal strength of a chain is determined by its weakest link. The relation between the critical transmural pressure (Ptm-) and the corresponding cross-sectional area (A-) was derived from the experimental Pel-Vmax curve. This Ptm--A- curve had a composed appearance, which was found to reflect parts of the different local Ptm-A curves and transitions between them because of movement of the flow limiting site within the airway. The Ptm--A- curve depends on the elastic properties of the flow limiting segment, and the slope of this curve (dA-/dPtm-) is the compliance of the flow limiting segment. Significant frictional pressure losses upstream from the site of flow limitation caused underestimation of both A- and dA-/dPtm-, but downstream pressure losses had no influence on the Ptm--A- curve.

Airway Resistance↗
PubMed1976

The critical transmural pressure of the abirway.

The critical transmural pressure (Ptm) is defined as the transmural pressure of the airway at the site where and when flow is limited during a forced expiration. According to the presented theory, the maximal expiratory flow (Vmax) can be calculated from the relation between Ptm and the corresponding cross-sectional area of the airway (A). By means of a pitot-static tube, Ptm-A curves were constructed for several locations in the elastic airway of a mechanical model. From these curves local Vmax was calculated at different values of Ptm and compared with actual flow, i.e. measured Vmax for the entire airway. In the downstream part of the airway, the actual flow equalled calculated Vmax at most Ptm values. The site of flow limitation, being the most upstream point where actual flow equals calculated local Vmax could therefore be located. Theory and experiments showed positive as well as negative Ptm not influenced by change in upstream or downstream resistance. Flow limitation could therefore be initiated at distending as well as compressing pressures across the wall of the airway. V was regarded as a function of Ptm and the elastic recoil pressure of the lung (Pel). Measured and calculated iso-Pel, Ptm-V curves agreed well with one major exception: when Ptm less than Ptm measured curves were distorted due to a concomitant downstrean compression of the collapsible airway.

Airway Resistance↗
PubMed1976

A method to correct for the influence of gas density on maximal expiratory flow rate.

Maximal expiratory flow rate (Vmax) was measured at 20, 35, 50, 65, and 80% vital capacity in 4 young healthy subjects breathing air, SF6/O2, and He/O2 mixtures. The flows of SF6/O2 and He/O2 were corrected to normal alveolar gasflow by means of only the density of the gases. The values for normal alveolar gasflow and corrected SF6/O2 flow were identical at 35% VC and larger volumes while the values for normal alveolar gasflow and corrected He/O2 flow were not. The results indicate that in young healthy subjects it is possible to correct Vmax at lung volumes above 35% VC for the changes induced by an increase in density of the gas breathed, provided viscosity is not much changed. Without correction, Vmax after O2-breathing will be underestimated by about 6%, compared with Vmax for normal alveolar gas, whereas a change in alveolar CO2 concentrations between 3 and 9% only causes a 1% decrease of Vmax.

Adolescent↗
PubMed1976

The effect of CO2 on peripheral airways.

In each of ten healthy young subjects breathing different concentrations of CO2 in O2, four alveolar CO2-tension levels were obtained, ranging from about 20 mmHg when hyperventilating in O2 to 50 mmHg. Maximum expiratory flows at 60% total lung capacity were measured at each level and corrected for the influence of the expired gas on the flow. The corrected maximum flow decreased significantly when the alveolar CO2 tension was below 30-35 mmHg, while there was only slight or no influence of CO2 on the maximal flow when the tension was above 35 mmHg. The decrease is taken as evidence of a constrictor effect on peripheral bronchi of hypocapnia.

Adult↗