“…Accordingly, not only compliance but also resistance can be expected to influence gas distribution. Resistance has been shown to be volume dependent (ZAMEL et al 1974), and in the present study an increase in FRC (non-dependent lung) decreased and a decrease in FRC (dependent lung) increased resistance. The product of compliance and resistance yields the time constant, which is an important determinant of gas distribution ( OTIS et al 1956).…”
The distribution of ventilation in man during halothane anesthesia was studied in a two-compartment lung model in which each lung was ventilated separately by means of a double-lumen tracheal tube. Eight subjects were studied prior to scheduled surgery. Tidal volume distribution was even between the lungs in the supine position (horizontal distribution) as was distribution of dynamic lung compliance, resistance and dead space. The vertical distribution was assessed when the patient was in the left lateral position. Dependent dynamic lung compliance and dead space were lower and lung resistance was higher than in the non-dependent lung. These factors favoured a non-dependent lung ventilation and, moreover, caused a re-distribution from dependent to non-dependent lung during an end-inspiratory pause (EIP), thus increasing the inhomogeneity of ventilation. The application of a positive end-expiratory pressure (PEEP) of 10 cmH2O improved dependent ventilation and abolished redistribution between the lungs. In conclusion, uneven distribution of dynamic lung compliance and lung resistance causes inhomogeneous ventilation distribution, favouring the non-dependent lung. An EIP enhances and a PEEP reduces the inhomogeneity of ventilation.
“…Accordingly, not only compliance but also resistance can be expected to influence gas distribution. Resistance has been shown to be volume dependent (ZAMEL et al 1974), and in the present study an increase in FRC (non-dependent lung) decreased and a decrease in FRC (dependent lung) increased resistance. The product of compliance and resistance yields the time constant, which is an important determinant of gas distribution ( OTIS et al 1956).…”
The distribution of ventilation in man during halothane anesthesia was studied in a two-compartment lung model in which each lung was ventilated separately by means of a double-lumen tracheal tube. Eight subjects were studied prior to scheduled surgery. Tidal volume distribution was even between the lungs in the supine position (horizontal distribution) as was distribution of dynamic lung compliance, resistance and dead space. The vertical distribution was assessed when the patient was in the left lateral position. Dependent dynamic lung compliance and dead space were lower and lung resistance was higher than in the non-dependent lung. These factors favoured a non-dependent lung ventilation and, moreover, caused a re-distribution from dependent to non-dependent lung during an end-inspiratory pause (EIP), thus increasing the inhomogeneity of ventilation. The application of a positive end-expiratory pressure (PEEP) of 10 cmH2O improved dependent ventilation and abolished redistribution between the lungs. In conclusion, uneven distribution of dynamic lung compliance and lung resistance causes inhomogeneous ventilation distribution, favouring the non-dependent lung. An EIP enhances and a PEEP reduces the inhomogeneity of ventilation.
“…We assumed adiabatic conditions in the pump. When measurements are made in subjects, the heat dissipation is efficient and the conditions are isothermal, as discussed by Zamel et al (11). Assuming isothermal conditions, they found good agreement between measured esophageal pressure and derived alveolar pressure during forced expirations in subjects with use of the plethysmograph.…”
Section: Discussionmentioning
confidence: 88%
“…where PA is alveolar pressure, PB is barometric pressure, PH 2 O is the pressure of saturated water vapor at 37°C, TLC is the total lung capacity from which the expiration starts, and Vb is the volume entering the box during the expiration. This equation is essentially the same as was applied by Ingram and Schilder (5) and Zamel et al (11). Validation of pressure measurements.…”
It has recently been shown (O. F. Pedersen T. R. Rasmussen, O. Omland, T. Sigsgaard, P. H. Quanjer. and M. R. Miller. Eur. Respir. J. 9: 828-833, 1996) that the added resistance of a mini-Wright peak flowmeter decreases peak expiratory flow (PEF) by approximately 8% compared with PEF measured by a pneumotachograph. To explore the reason for this, 10 healthy men (mean age 43 yr, range 33-58 yr) were examined in a body plethysmograph with facilities to measure mouth flow vs. expired volume as well as the change in thoracic gas volume (Vb) and alveolar pressure (PA). The subjects performed forced vital capacity maneuvers through orifices of different sizes and also a mini-Wright peak flowmeter. PEF with the meter and other added resistances were achieved when flow reached the perimeter of the flow-Vb curves. The mini-Wright PEF meter decreased PEF from 11.4 +/- 1.5 to 10.3 +/- 1.4 (SD) l/s (P < 0.001), PA increased from 6.7 +/- 1.9 to 9.3 +/- 2.7 kPa (P < 0.001), an increase equal to the pressure drop across the meter, and caused Vb at PEF to decrease by 0.24 +/- 0.09 liter (P < 0.001). We conclude that PEF obtained with an added resistance like a mini-Wright PEF meter is a wave-speed-determined maximal flow, but the added resistance causes gas compression because of increased PA at PEF. Therefore, Vb at PEF and, accordingly, PEF decrease.
“…It was used here as an indicator of the strength of the expiratory muscles [18]. It can be readily calculated and is obtained from noninvasive measurements using a plethysmograph, as described previously [6,19].…”
The aim of this study was to estimate, in patients with chronic obstructive pulmonary disease (COPD), the maximal strength of the expiratory muscles, its correlation with exercise performance and the effects of a specific physiotherapy. In 38 COPD men, aged 54 ± 7 years, pulmonary function data, maximal alveolar pressure (Palv, max) developed during forced vital capacity, were measured using a whole-body plethysmograph and the maximal tolerated power (MTP), i.e. the highest power maintained for at least 3 min, was determined by a progressive test on a treadmill. Airway obstruction was severe (FEV1/FVC: 54 ± 10%), Palv, max was lower than normal (74 ± 36 vs. 130 ± 48 hPa in 20 healthy men of the same age; p < 0.01) and increased with airway resistance values (Raw); mean MTP was low: 115 ± 30 W and individual values were inversely related to Raw values. Then, two subgroups of 14 patients were chosen at random. One subgroup received an abdominal muscle physiotherapy during 3 weeks. The other subgroup only received usual medical treatment. No modification in any parameter was found in the second subgroup. Specific physiotherapy of abdominal muscles improves significantly both Palv, max (118 ± 45 hPa) and MTP (171 ± 38 W; p < 0.01), without any variation in other respiratory function parameters. We conclude that abdominal muscle weakness is common in COPD patients and can participate in the limitation in exercise performance. Specific physiotherapy increases abdominal muscle strength and seems to improve exercise tolerance by a still unexplained mechanism
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