Hypoxemia during apnea in normal subjects: mechanisms and impact of lung volume

1983 ◽  
Vol 55 (6) ◽  
pp. 1777-1783 ◽  
Author(s):  
L. J. Findley ◽  
A. L. Ries ◽  
G. M. Tisi ◽  
P. D. Wagner
Keyword(s):  
Lung Volume ◽  
Compartment Model ◽  
Normal Subjects ◽  
Breath Holding ◽  
Lung Volumes ◽  
Single Compartment ◽  
Single Compartment Model ◽  
Alveolar Hypoventilation ◽  
Arterial O2 Saturation ◽  
Voluntary Breath Holding

Seven normal awake males were studied to define the mechanisms and impact of lung volume on the hypoxemia occurring during apnea. During repeated 30-s voluntary breath holding, these subjects were studied at different lung volumes, during various respiratory maneuvers, and in the sitting and supine body positions. Analysis of expired gases and arterial O2 saturation during these repeated breath holdings yielded the following conclusions. Apnea of 30-s duration at low lung volumes is accompanied by severe arterial O2 desaturation in normal awake subjects. Initial lung volume is the most important determinant of hypoxemia during apnea. The hypoxemia of apnea at most lung volumes can be explained by simple alveolar hypoventilation in a uniform lung. The lung does not behave as a single-compartment model at lung volumes at which dependent airways are susceptible to closure.

Effect of ventilation and diffusion nonuniformity on DLCO (exhaled) in a lung model

1980 ◽  
Vol 48 (4) ◽  
pp. 648-656 ◽  
Author(s):  
D. J. Cotton ◽  
B. L. Graham
Keyword(s):  
Carbon Monoxide ◽  
Lung Volume ◽  
Theoretical Basis ◽  
Normal Subjects ◽  
Lung Model ◽  
Breath Holding ◽  
Lung Region ◽  
Lung Volumes ◽  
Simultaneous Decay ◽  
And Diffusion

Recent studies have shown that diffusing capacities measured at multiple intervals during a single exhalation [DLCO(exhaled)] remained constant with lung volume in normal subjects, but decreased with decreasing lung volume in patients who may have had diffusion nonuniformity. We have examined the theoretical basis of these results by determining what factors affected DLCO(exhaled) in a computerized lung model in which diffusion in each compartment remained constant with lung volume. DLCO(exhaled) decreased with decreasing lung volume when a small lung region lacked diffusion. However, the change in DLCO(exhaled) with lung volume was also affected by nonuniform ventilation and these effects could not be eliminated by correcting the carbon monoxide decay and the simultaneous decay of helium. DLCO(exhaled) values were also influenced by the exhaled flow rate in the presence of nonuniform ventilation and/or nonuniform diffusion. However, prolonging the period of breath holding prior to exhalation reduced DLCO(exhaled) values at all lung volumes when non-uniform diffusion was simulated, but did not affect DLCO(exhaled) when only nonuniform ventilation was simulated.

Breathing at low lung volumes and chest strapping: a comparison of lung mechanics

1981 ◽  
Vol 50 (3) ◽  
pp. 650-657 ◽  
Author(s):  
N. J. Douglas ◽  
G. B. Drummond ◽  
M. F. Sudlow
Keyword(s):  
Lung Volume ◽  
Maximum Flow ◽  
Normal Subjects ◽  
Lung Mechanics ◽  
Lung Volumes ◽  
Flow Rates ◽  
Recoil Pressure ◽  
Forced Expiratory Flow ◽  
Expiratory Flow ◽  
Expiratory Flow Rates

In six normal subjects forced expiratory flow rates increased progressively with increasing degrees of chest strapping. In nine normal subjects forced expiratory flow rates increased with the time spent breathing with expiratory reserve volume 0.5 liters above residual volume, the increase being significant by 30 s (P less than 0.01), and flow rates were still increasing at 2 min, the longest time the subjects could breathe at this lung volume. The increase in flow after low lung volume breathing (LLVB) was similar to that produced by strapping. The effect of LLVB was diminished by the inhalation of the atropinelike drug ipratropium. Quasistatic recoil pressures were higher following strapping and LLVB than on partial or maximal expiration, but the rise in recoil pressure was insufficient to account for all the observed increased in maximum flow. We suggest that the effects of chest strapping are due to LLVB and that both cause bronchodilatation.

Chest wall and trunk muscle activity during inspiratory loading

1992 ◽  
Vol 73 (6) ◽  
pp. 2373-2381 ◽  
Author(s):  
S. J. Cala ◽  
J. Edyvean ◽  
L. A. Engel
Keyword(s):  
Chest Wall ◽  
Lung Volume ◽  
Normal Subjects ◽  
Systematic Difference ◽  
Erector Spinae ◽  
Inspiratory Pressure ◽  
Emg Activity ◽  
Consistent Difference ◽  
Lung Volumes ◽  
Resistive Loading

We measured the electromyographic (EMG) activity in four chest wall and trunk (CWT) muscles, the erector spinae, latissimus dorsi, pectoralis major, and trapezius, together with the parasternal, in four normal subjects during graded inspiratory efforts against an occlusion in both upright and seated postures. We also measured CWT EMGs in six seated subjects during inspiratory resistive loading at high and low tidal volumes [1,280 +/- 80 (SE) and 920 +/- 60 ml, respectively]. With one exception, CWT EMG increased as a function of inspiratory pressure generated (Pmus) at all lung volumes in both postures, with no systematic difference in recruitment between CWT and parasternal muscles as a function of Pmus. At any given lung volume there was no consistent difference in CWT EMG at a given Pmus between the two postures (P > 0.09). However, at a given Pmus during both graded inspiratory efforts and inspiratory resistive loading, EMGs of all muscles increased with lung volume, with greater volume dependence in the upright posture (P < 0.02). The results suggest that during inspiratory efforts, CWT muscles contribute to the generation of inspiratory pressure. The CWT muscles may act as fixators opposing deflationary forces transmitted to the vertebral column by rib cage articulations, a function that may be less effective at high lung volumes if the direction of the muscular insertions is altered disadvantageously.

A single compartment model of pacemaking in dissasociated Substantia nigra neurons

2013 ◽  
Vol 35 (3) ◽  
pp. 295-316 ◽  
Author(s):  
Febe Francis ◽  
Míriam R. García ◽  
Richard H. Middleton
Keyword(s):  
Substantia Nigra ◽  
Compartment Model ◽  
Single Compartment ◽  
Single Compartment Model

Gravity effects on upper airway area and lung volumes during parabolic flight

1998 ◽  
Vol 84 (5) ◽  
pp. 1639-1645 ◽  
Author(s):  
Maurice Beaumont ◽  
Redouane Fodil ◽  
Daniel Isabey ◽  
Frédéric Lofaso ◽  
Dominique Touchard ◽  
...  
Keyword(s):  
Lung Volume ◽  
Parabolic Flight ◽  
Upper Airway ◽  
Normal Subjects ◽  
Lung Volumes ◽  
Acoustic Reflection ◽  
Volume Functional ◽  
Airway Caliber ◽  
Gravity Effects ◽  
Residual Capacity

We measured upper airway caliber and lung volumes in six normal subjects in the sitting and supine positions during 20-s periods in normogravity, hypergravity [1.8 + head-to-foot acceleration (Gz)], and microgravity (∼0 Gz) induced by parabolic flights. Airway caliber and lung volumes were inferred by the acoustic reflection method and inductance plethysmography, respectively. In subjects in the sitting position, an increase in gravity from 0 to 1.8 +Gz was associated with increases in the calibers of the retrobasitongue and palatopharyngeal regions (+20 and +30%, respectively) and with a concomitant 0.5-liter increase in end-expiratory lung volume (functional residual capacity, FRC). In subjects in the supine position, no changes in the areas of these regions were observed, despite significant decreases in FRC from microgravity to normogravity (−0.6 liter) and from microgravity to hypergravity (−0.5 liter). Laryngeal narrowing also occurred in both positions (about −15%) when gravity increased from 0 to 1.8 +Gz. We concluded that variation in lung volume is insufficient to explain all upper airway caliber variation but that direct gravity effects on tissues surrounding the upper airway should be taken into account.

scholarly journals Respiratory dynamics during laughter

2001 ◽  
Vol 90 (4) ◽  
pp. 1441-1446 ◽  
Author(s):  
Mario Filippelli ◽  
Riccardo Pellegrino ◽  
Iacopo Iandelli ◽  
Gianni Misuri ◽  
Joseph R. Rodarte ◽  
...  
Keyword(s):  
Chest Wall ◽  
Lung Volume ◽  
Dynamic Compression ◽  
Three Dimensional ◽  
Normal Subjects ◽  
Average Frequency ◽  
Abdominal Pressure ◽  
Sudden Increase ◽  
Lung Volumes ◽  
Transdiaphragmatic Pressure

Lung and chest wall mechanics were studied during fits of laughter in 11 normal subjects. Laughing was naturally induced by showing clips of the funniest scenes from a movie by Roberto Benigni. Chest wall volume was measured by using a three-dimensional optoelectronic plethysmography and was partitioned into upper thorax, lower thorax, and abdominal compartments. Esophageal (Pes) and gastric (Pga) pressures were measured in seven subjects. All fits of laughter were characterized by a sudden occurrence of repetitive expiratory efforts at an average frequency of 4.6 ± 1.1 Hz, which led to a final drop in functional residual capacity (FRC) by 1.55 ± 0.40 liter ( P < 0.001). All compartments similarly contributed to the decrease of lung volumes. The average duration of the fits of laughter was 3.7 ± 2.2 s. Most of the events were associated with sudden increase in Pes well beyond the critical pressure necessary to generate maximum expiratory flow at a given lung volume. Pga increased more than Pes at the end of the expiratory efforts by an average of 27 ± 7 cmH2O. Transdiaphragmatic pressure (Pdi) at FRC and at 10% and 20% control forced vital capacity below FRC was significantly higher than Pdi at the same absolute lung volumes during a relaxed maneuver at rest ( P < 0.001). We conclude that fits of laughter consistently lead to sudden and substantial decrease in lung volume in all respiratory compartments and remarkable dynamic compression of the airways. Further mechanical stress would have applied to all the organs located in the thoracic cavity if the diaphragm had not actively prevented part of the increase in abdominal pressure from being transmitted to the chest wall cavity.

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