Effect of Atropine on Alveolar Gas Mixing in Man

1982 ◽  
Vol 62 (5) ◽  
pp. 549-551 ◽  
Author(s):  
W. Kox ◽  
F. Langley ◽  
K. Horsfield ◽  
G. Cumming

1. Atropine is known to diminish broncho-motor tone. In order to investigate the acute effect of atropine on respiration and alveolar gas mixing, a dose of 2.4 mg was given intravenously. 2. Ten normal male volunteers were each studied three times with a nitrogen washout method, once before administration of atropine and then 20 min and 60 min thereafter. 3. After the administration of atropine there was a reduction in tidal volume, a slight increase in frequency of respiration and an increase in series dead space. The tidal mixing volume showed a fall of 25%. In spite of the reduced alveolar dead space the effective mixing volume fell by 29%. Multi-breath alveolar mixing efficiency fell by 3.5%. 4. Multi-breath alveolar mixing efficiency was found to be less with smaller tidal mixing volumes, a fall of 518 ml in the latter causing a reduction of 17.2% in mixing efficiency. 5. A reduction of 100 ml in tidal volume in normal subjects was associated with a decrease of 6.9% in alveolar mixing efficiency. In the subjects receiving atropine tidal volume reduced by 96 ml, but the observed fall in alveolar mixing efficiency was only 3.5%, This suggests an improvement in alveolar mixing of 3.4% due to the administration of atropine. Despite this small improvement, the mixing efficiency is still only 66%. The residual inefficiency of 34% cannot therefore be explained on the basis of broncho-motor tone.

1988 ◽  
Vol 74 (2) ◽  
pp. 187-192 ◽  
Author(s):  
F. Langley ◽  
K. Horsfield ◽  
G. Burton ◽  
W. A. Seed ◽  
S. Parker ◽  
...  

1. Pulmonary function tests, including alveolar mixing efficiency by the single-breath and multi-breath methods, and ventilation scans were performed on 16 volunteer subjects. The tests were repeated after the inhalation of a methacholine aerosol in sufficient dosage to increase airways resistance. 2. After inhalation of methacholine there was a significant fall in mean series dead space of 31 ml (P < 0.05), and mean multi-breath alveolar mixing efficiency fell from 68% to 36% (P < 0.001), a fall occurring in all subjects. Mean single-breath alveolar mixing efficiency measured on the first breath of the nitrogen washout fell from 76% to 70%, but this change did not reach statistical significance (0.1 > P > 0.05). 3. In eight of the subjects, technically adequate lung scans and pulmonary function tests were obtained both before and not more than 30 min after methacholine inhalation. In seven there were obvious visible defects on the ventilation scans, and in five of these the computer-calculated underventilation score became abnormal. 4. Thus inhalation of methacholine causes maldistribution of ventilation, a fall in alveolar mixing efficiency and a fall in series dead space, presumably brought about by bronchoconstriction. The parallel component of this maldistribution of ventilation, as judged by 81mKr ventilation scanning, does not of itself seem to be sufficient to explain the fall in alveolar mixing efficiency, and therefore a degree of diffusion limitation is probably involved as well.


1982 ◽  
Vol 52 (3) ◽  
pp. 624-633 ◽  
Author(s):  
C. Bowes ◽  
G. Cumming ◽  
K. Horsfield ◽  
J. Loughhead ◽  
S. Preston

An asymmetrical model of the human pulmonary acinus is described, in which elements of volume are represented by nodes joined by conductors permitting convective flow and molecular diffusion. The method of analysis permits simultaneous convection, diffusion, and dimensional change in any direction and requires only simple boundary conditions. Inspiration of O2 into a resident gas of 79% N2 followed by expiration was simulated at two flows. On expiration the slope of the alveolar plateau was 1.7%, and the alveolar N2 mixing efficiency was 97.0%. A symmetrical but otherwise similar model gave a slope of zero and a mixing efficiency of 99.9%. The patterns of gas concentration within the asymmetrical acinus during the respiratory cycle confirm and extend previous observations on the interactions between simultaneous convection and diffusion in asymmetrical structures (16, 21, 22). Even though these in combination within alveolar duct asymmetry can account for the slope of the alveolar plateau, they are insufficient to account for the failure of complete gas mixing found in normal subjects.


1960 ◽  
Vol 15 (3) ◽  
pp. 359-362 ◽  
Author(s):  
G. Milic-Emili ◽  
J. M. Petit

Simultaneous measurements of mechanical work and energy cost of breathing were performed on four normal subjects with ventilation increased by adding dead space. Mechanical work was obtained from simultaneous records of endoesophageal pressure and tidal volume. The associated energy cost was estimated by measuring oxygen consumption of respiratory muscles by means of a closed-circuit spirometer. In all subjects studied and over the range of ventilations involved (ca. 30–110 l/min.), the mechanical efficiency of breathing was found to be in the order of 0.19–0.25. Submitted on July 6, 1959


1988 ◽  
Vol 64 (2) ◽  
pp. 681-688
Author(s):  
K. I. Arita ◽  
S. M. Lewis ◽  
C. Mittman

The washout of an insoluble tracer from the lung may be represented by a model with two ventilatory compartments representing poorly and better-ventilated regions. Using boli of a second insoluble gas delivered at a given point during inspirations of a multibreath washout test, the proportions of labeled inspired ventilation reaching the poorly and well-ventilated regions may be determined by analyzing the kinetics of the exhaled tracer. We studied eight normal subjects breathing through large-bore solenoid valves controlled to maintain tidal volume at 600 or 900 ml. Boli consisting of 15 ml of 80% He-20% O2 were delivered over 75 ms; this labeled approximately 125 ml of inspired gas. Boli were delivered after 50 ml had been inspired to mark early inspiration and after 300 ml had been inspired to mark midinspiration. Using 900-ml tidal breaths, late inspiration was marked by boli delivered at 600 ml. Subjects were studied in the seated and the supine positions. In both positions, significantly more of the early breath went to the poorly ventilated compartment. Several possible physiological mechanisms, singly or in combination, could account for these observations, but differences in dead space path length are most likely involved.


2000 ◽  
Vol 88 (5) ◽  
pp. 1859-1869 ◽  
Author(s):  
Denis E. O'Donnell ◽  
Harry H. Hong ◽  
Katherine A. Webb

We mimicked important mechanical and ventilatory aspects of restrictive lung disorders by employing chest wall strapping (CWS) and dead space loading (DS) in normal subjects to gain mechanistic insights into dyspnea causation and exercise limitation. We hypothesized that thoracic restriction with increased ventilatory stimulation would evoke exertional dyspnea that was similar in nature to that experienced in such disorders. Twelve healthy young men [28 ± 2 (SE) yr of age] completed pulmonary function tests and maximal cycle exercise tests under four conditions, in randomized order: 1) control, 2) CWS to 60% of vital capacity, 3) added DS of 600 ml, and 4) CWS + DS. Measurements during exercise included cardiorespiratory parameters, esophageal pressure, and Borg scale ratings of dyspnea. Compared with control, CWS significantly reduced the tidal volume response to exercise, increased dyspnea intensity at any given work rate or ventilation, and thus limited exercise performance. DS stimulated ventilation but had minimal effects on dyspnea and exercise performance. Adding DS to CWS further increased dyspnea by 1.7 ± 0.6 standardized Borg units ( P = 0.012) and decreased exercise performance (total work) by 21 ± 6% ( P = 0.003) over CWS alone. Across conditions, increased dyspnea intensity correlated best with decreased resting inspiratory reserve volume ( r = −0.63, P < 0.0005). Dyspnea during CWS was described primarily as “inspiratory difficulty” and “unsatisfied inspiration,” similar to restrictive disorders. In conclusion, severe dyspnea and exercise intolerance were provoked in healthy normal subjects when tidal volume responses were constrained in the face of increased ventilatory drive during exercise.


1978 ◽  
Vol 44 (3) ◽  
pp. 416-423 ◽  
Author(s):  
S. M. Lewis ◽  
J. W. Evans ◽  
A. A. Jalowayski

We describe a new technique for recovering continuous distributions of ventilation (V) as a function of tidal ventilation/volume ratio (V/V0) from the nitrogen washout. The analysis yields a continuous distribution of V as a function of V/V0 represented as fractional ventilations of 50 compartments plus dead space. The procedure was verified by recovering known distributions from data to which noise had been added. Using an apparatus to control the subject's tidal volume and FRC, mixed expired N2 data gave the following results: a) the distributions of young, normal subjects were narrow and unimodal with a mean ln standard deviation of 0.56 plus or minus 0.13; b) those of subjects over age 40 were broader (ln SD 0.86 plus or minus 0.19) with more poorly ventilated units; c) patients with pulmonary disease of all descriptions showed enlarged dead space; d) patients with cystic fibrosis showed multimodal distributions with the bulk of the ventilation going to overventilated units; and e) patients with obstructive lung diseases fell into several classes, three of which are illustrated. These results suggest that our approach is well suited for clinical investigation.


1964 ◽  
Vol 19 (4) ◽  
pp. 683-692 ◽  
Author(s):  
Domingo M. Gómez ◽  
William A. Briscoe ◽  
Gordon Cumming

An analytical method is presented which, applied to nitrogen washout data from the lung, describes a continuous distribution of specific tidal volume (or ventilation) throughout the air phase of the lung. The technique of computation is described in some detail. Curves of distribution of specific tidal volume are studied for 12 washout data from normal subjects and for 20 washout data from patients with pulmonary emphysema. In normal subjects the pattern of continuous distribution is an asymmetrical one in which the function starts at zero or very nearly so, increases continuously until it reaches a maximum value, then decreases progressively and becomes negligible for comparatively high values of the specific tidal volume. The formulation expressing this law of distribution is neither that of a normal frequency distribution nor that of a log normal one. With increasing over-all tidal volume in normal subjects the curve is progressively displaced toward the right. In contrast, in pulmonary obstructive diseases the maximum amplitude takes place for very low values of the specific tidal volume and tends to vanish slowly toward values that are higher than in the normal subjects. apparent volume of lung Submitted on June 20, 1963


1960 ◽  
Vol 15 (5) ◽  
pp. 826-828 ◽  
Author(s):  
Philip Samet ◽  
Eugene M. Fierer ◽  
William H. Bernstein

The basic purpose of this investigation was to determine whether salicylates increase the sensitivity of the respiratory center to inhaled CO2. The problem was approached by noting the effect of salicylates upon ventilation and arterial blood Co2 tension and pH during inhalation of compressed air and 3% and 5% Co2 in air. These studies were performed in 30 subjects, 15 of whom ingested 2.1 gm salicylate; the other 15 ingested 3.6 gm. The results demonstrate that the ventilatory response to CO2 was increased only by the larger dose of salicylate. Variations in dead-space volume secondary to increments in tidal volume were observed. Dead-space volume increased in approximately linear fashion with increase in tidal volume. Submitted on October 28, 1959


1991 ◽  
Vol 70 (1) ◽  
pp. 55-62 ◽  
Author(s):  
C. McParland ◽  
J. Mink ◽  
C. G. Gallagher

We examined the effects of dead space (VD) loading on breathing pattern during maximal incremental exercise in eight normal subjects. Addition of external VD was associated with a significant increase in tidal volume (VT) and decrease in respiratory frequency (f) at moderate and high levels of ventilation (VI); at a VI of 120 l/min, VT and f with added VD were 3.31 +/- 0.33 liters and 36.7 +/- 6.7 breaths/min, respectively, compared with 2.90 +/- 0.29 liters and 41.8 +/- 7.3 breaths/min without added VD. Because breathing pattern does not change with CO2 inhalation during heavy exercise (Gallagher et al. J. Appl. Physiol. 63: 238–244, 1987), the breathing pattern response to added VD is probably a consequence of alteration in the PCO2 time profile, possibly sensed by the carotid body and/or airway-pulmonary chemoreceptors. The increase in VT during heavy exercise with VD loading indicates that the tachypneic breathing pattern of heavy exercise is not due to mechanical limitation of maximum ventilatory capacity at high levels of VT.


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