We performed multiple-breath N2 washouts (MBNW) with tidal volumes of 1 liter at 8-16 breaths/min and constant flow rates in six normal subjects. For each breath we computed the slope of the alveolar plateau, normalized by the mean expired N2 concentration (Sn), the Bohr dead space (VDB), an index analogous to the Fowler dead space (V50), and the normalized slope of phase II (S2). In four subjects helium (He) and sulfur hexafluoride (SF6) were washed out after equilibration with a 5% gas mixture of each tracer. The Sn for He and SF6 increased in consecutive breaths, but the difference (delta Sn) increased only over the first five breaths, remaining constant thereafter. In all six subjects Sn, VDB, and V50 increased progressively in consecutive breaths of the MBNW, the increase in Sn being the greatest, approximately 290% from the first to the 23-25th breath. In contrast, S2 was unchanged initially and decreased after the sixth breath. The results indicate that after the fifth breath the increase in Sn during a MBNW is diffusion independent and may constitute a sensitive index of convection-dependent inhomogeneity (CDI). Subtraction of this component from the first breath suggests that Sn in a single-breath washout is largely due to a diffusion-dependent mechanism. The latter may reflect an interaction of convection and diffusion within the lung periphery, whereas CDI may comprise ventilation inequality among larger units, subtended by more centrally located branch points.
To examine the mechanism of hyperinflation in bronchial asthma we studied lung and chest wall mechanics in 7 asymptomatic patients in whom progressive bronchoconstriction was induced by doubling the amount of inhaled aerosolized histamine. An increase in pulmonary resistance (RL) from 2.5 +/- 0.3 cmH2O . 1-1 . s (mean, +/- 1 SE) to 12.3 +/- 0.9 cmH2 was associated with a linear increase in functional residual capacity (FRC) up to 74.7 +/- 1.7% of control total lung capacity (TLCc). The mean regression coefficient was 2.3% TLCc . cmH2O-1 . 1 . s-1. At each level of hyperinflation the most positive expiratory pleural pressures measured during spontaneous breathing were generally less than the predicted chest wall relaxation pressures, indicating persistent inspiratory muscle contraction throughout expiration. This was predominantly due to inspiratory intercostal and accessory muscle activity, because measurements of transdiaphragmatic pressure indicated complete diaphragmatic relaxation early in expiration. Recruitment of abdominal muscles during expiration, inferred from measurements of gastric pressure (Pg) and abdominal antero-posterior (A-P) diameter, was progressively more apparent with increasing bronchoconstriction. We concluded that the increase in FRC in induced asthma is substantially influenced by persistent inspiratory intercostal and accessory muscle activity during expiration. Concomitant abdominal muscle recruitment results in a chest wall configuration that tends to optimize diaphragmatic function.
We examined the movements of the vocal cords during tidal breathing, panting, and large changes in lung volume in 12 normal subjects. The glottis was observed with a fiber-optic bronchoscope, and the glottic image was recorded together with flow, volume, and a time marker onto videotape. Phasic respiratory swings in glottic width (dg) and glottic area (Ag) were reproducible in all subjects but differed substantially between subjects. In the group as a whole dg and Ag increased during inspiration to 10.1 +/- 5.6 mm and 126 +/- 8 mm2 (mean +/- SE), respectively, whereas during expiration the lowest values were 5.7 +/- 0.5 mm and 70 +/- 7 mm2, respectively. These extreme dimensions corresponded closely to the midtidal volume points in the respiratory cycle. Glottic width during vital capacity (VC) expirations was nearly 30% greater at a flow of 1.2 l/s than at 0.5 l/s, but the relationship between dg and lung volume differed between subjects. When swings in dg were minimized by panting, there was no difference in dg between functional residual capacity (FRC) and a volume corresponding to midinspiratory capacity. However, tidal breathing at this lung volume was associated with a 20% decrease in dg compared with breathing at FRC. Our observations indicate a tight coupling between the pattern of glottic movement and the respiratory volume cycle. The results suggest that during voluntary respiratory maneuvers both intrinsic laryngeal and respiratory muscles are recruited, participating as effector organs in ventilatory and respiratory control.
We examined the relationship between the pressure-time product (Pdt) of the inspiratory muscles and the O2 cost of breathing (VO2 resp) in five normal subjects breathing through an external inspiratory resistance with a tidal volume of 800 ml at a constant end-expiratory lung volume [functional residual capacity, (FRC)]. Each subject performed 30-40 runs, each of approximately 30 breaths, with inspiratory flow rates ranging from 0.26 +/- 0.01 to 0.89 +/- 0.04 l/s (means +/- SE) and inspiratory mouth pressures ranging from 10 +/- 1 to 68 +/- 4% of the maximum inspiratory pressure at FRC. In all subjects VO2 resp was linearly related to Pdt when mean inspiratory flow (VI) was constant, but the slope of this relationship increased with increasing VI. Therefore, Pdt is an accurate index of VO2 resp only when VI is constant. There was a linear relationship between the VO2 resp and the work rate across the external resistance (W) for all runs in each subject over the range of W 10 +/- 1 to 137 +/- 21 J/min. Thus, at a constant tidal volume the VO2 resp was related to the mean inspiratory pressure, independent of flow or inspiratory duration. If the VO2 resp were determined mainly during inspiration, then for a given rate of external work or O2 consumption, VI would be inversely related to mean inspiratory pressure. Efficiency (E) was 2.1 +/- 0.2% and constant over a large range of VI, pressure, work rate, or resistance and was not altered by the presence of a potentially fatiguing load. The constant E over such a wide range of conditions implies a complex integration of the recruitment, mechanical function, and energy consumption of the muscles utilized in breathing.
To examine the effect of preinspiratory lung volume (PILV) on ventilation distribution, we performed multiple-breath N2 washouts (MBNW) in seven normal subjects breathing 1-liter tidal volumes over a wide range of PILV above closing capacity. We measured the following two independent indexes of ventilation distribution from the MBNW: 1) the normalized phase III slope of the final breaths of the washout (Snf) and 2) the alveolar mixing efficiency during that portion of the washout where 80-90% of the lung N2 had been cleared. Three of the subjects also performed single-breath N2 washouts (SBNW) by inspiring 1-liter breaths and expiring to residual volume at PILV = functional residual capacity (FRC), FRC + 1.0, and FRC - 0.5, respectively. From the SBNW we measured the phase III slope over the expired volume ranges of 0.75-1.0, 1.0-1.6, and 1.6-2.2 liters (S0.75, S1.0, and S1.6, respectively). Between a PILV of 0.92 +/- 0.09 (SE) liter above FRC and a PILV of 1.17 +/- 0.43 liter below FRC, Snf decreased by 61% (P less than 0.001) and alveolar mixing efficiency increased from 80 to 85% (P = 0.05). In addition, Snf and alveolar mixing efficiency were negatively correlated (r = 0.74). In contrast, over a similar volume range, S1.0 and S1.6 were greater at lower PILV. We conclude that, during tidal breathing in normal subjects, ventilation distribution becomes progressively more inhomogeneous at higher lung volumes over a range of volumes above closing capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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