Effect of chest wall distortion on occlusion pressure and the preterm diaphragm

1983 ◽  
Vol 55 (2) ◽  
pp. 359-364 ◽  
Author(s):  
P. N. LeSouef ◽  
J. M. Lopes ◽  
S. J. England ◽  
M. H. Bryan ◽  
A. C. Bryan
Keyword(s):  
Chest Wall ◽  
Preterm Infants ◽  
Face Mask ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Transdiaphragmatic Pressure ◽  
Airway Occlusion ◽  
Mouth Pressure ◽  
Gastric Pressure ◽  
Mouth Occlusion Pressure

We studied the effect of chest wall distortion (CWD) on transdiaphragmatic pressure (Pdi) and/or mouth pressure during end-expiratory airway occlusions in seven preterm infants. We measured mouth occlusion pressure (Pmo) with a face mask and pressure transducer, gastric pressure (Pga) with a fluid-filled catheter, diaphragmatic electromyogram (Edi) using surface electrodes, and rib cage and abdominal motion using magnetometers. We reasoned that Pdi = Pmo - Pga on airway occlusion. Periods with maximal and periods with minimal CWD were compared. We found that 1) when CWD was minimal, an increase in Edi produced an increase in Pmo and Pdi in all infants; when CWD was greatest, large increases in Edi produced no increase in Pmo or Pdi in four infants; 2) when breaths with the same Pmo or Pdi from each period in each infant were compared, those from the period with greatest CWD had an increased Edi (mean increase 76%, P less than 0.005, and 144%, P less than 0.01, for Pmo and Pdi, respectively). We conclude that in preterm infants, Pmo can be a poor indicator of respiratory drive, and CWD markedly limits the effectiveness of the diaphragm as a force generator.

Relationship between inspiratory drive and perceived inspiratory effort in normal man

1990 ◽  
Vol 78 (5) ◽  
pp. 493-496 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. A. Calverley
Keyword(s):  
Ventilatory Response ◽  
Free Breathing ◽  
Normal Subjects ◽  
Inspiratory Effort ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Resistive Loading ◽  
Mouth Occlusion Pressure ◽  
The Individual ◽  
Induced Changes

1. To examine the relationship between the inspiratory effort sensation (IES) and respiratory drive as reflected by mouth occlusion pressure (P0.1) we have studied loaded and unloaded ventilatory responses to CO2 in 12 normal subjects. 2. The individual coefficient of variation of the effort sensation response to CO2 (IES/Pco2) between replicate studies was 21% and was similar to the variability of the ventilatory response (VE/Pco2) (18%) and the occlusion pressure response (P0.1/Pco2) (22%). 3. IES was well correlated with P0.1 (r >0.9) for both free-breathing and loaded runs. 4. Resistive loading reduced the ventilatory response to hypercapnia from 19.3 1 min−1 kPa−1 (sd 7.5) to 12.6 1 min−1 kPa−1 (sd 3.9) (P <0.01). IES and P0.1 responses increased with resistive loading from 2.28 (sd 0.9) to 3.15 (sd 1.1) units/kPa and 2.8 (sd 1.2) to 3.73 (sd 1.5) cmH2O/kPa, respectively (P <0.01). 5. Experimentally induced changes in Pco2 and respiratory impedance were accompanied by increases in IES and P0.1. We found no evidence that CO2 increased IES independently of its effect on respiratory drive.

Passive mechanics of upright human chest wall during immersion from hips to neck

1986 ◽  
Vol 60 (5) ◽  
pp. 1561-1570 ◽  
Author(s):  
M. B. Reid ◽  
S. H. Loring ◽  
R. B. Banzett ◽  
J. Mead
Keyword(s):  
Chest Wall ◽  
Esophageal Pressure ◽  
Vertical Surface ◽  
Repeated Measurements ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Gastric Pressure ◽  
Length Changes ◽  
Accessory Muscles

We have determined the mechanical effects of immersion to the neck on the passive chest wall of seated upright humans. Repeated measurements were made at relaxed end expiration on four subjects. Changes in relaxed chest wall configuration were measured using magnetometers. Gastric and esophageal pressures were measured with balloon-tipped catheters in three subjects; from these, transdiaphragmatic pressure was calculated. Transabdominal pressure was estimated using a fluid-filled, open-tipped catheter referenced to the abdomen's exterior vertical surface. We found that immersion progressively reduced mean transabdominal pressure to near zero and that the relaxed abdominal wall was moved inward 3–4 cm. The viscera were displaced upward into the thorax, gastric pressure increased by 20 cmH2O, and transdiaphragmatic pressure decreased by 10–15 cmH2O. This lengthened the diaphragm, elevating the diaphragmatic dome 3–4 cm. Esophageal pressure became progressively more positive throughout immersion, increasing by 8 cmH2O. The relaxed rib cage was elevated and expanded by raising water from hips to lower sternum; this passively shortened the inspiratory intercostals and the accessory muscles of inspiration. Deeper immersion distorted the thorax markedly: the upper rib cage was forced inward while lower rib cage shape was not systematically altered and the rib cage remained elevated. Such distortion may have passively lengthened or shortened the inspiratory muscles of the rib cage, depending on their location. We conclude that the nonuniform forcing produced by immersion provides unique insights into the mechanical characteristics of the abdomen and rib cage, that immersion-induced length changes differ among the inspiratory muscles according to their locations and the depth of immersion, and that such length changes may have implications for patients with inspiratory muscle deficits.

Respiratory Drive in Nonsmokers and Smokers Assessed by Passive Tilt and Mouth Occlusion Pressure

CHEST Journal ◽  
1985 ◽  
Vol 87 (1) ◽  
pp. 6-10 ◽  
Author(s):  
T.S. Chadha ◽  
E. Lang ◽  
S. Birch ◽  
M. A Sackner
Keyword(s):  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Mouth Occlusion Pressure

Effects of acute exposure to high altitude on ventilatory drive and respiratory pattern

1984 ◽  
Vol 56 (4) ◽  
pp. 1027-1031 ◽  
Author(s):  
N. K. Burki
Keyword(s):  
High Altitude ◽  
Minute Ventilation ◽  
Progressive Increase ◽  
Acute Exposure ◽  
Respiratory Pattern ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Ventilatory Pattern ◽  
Ventilatory Drive ◽  
Mouth Occlusion Pressure

To assess changes in ventilatory regulation in terms of central drive and timing, on exposure to high altitude, and the effects of induced hyperoxia at high altitude, six healthy normal lowland subjects (mean age 19.5 +/- 1.64 yr) were studied at low altitude (518 m) and on the first 4 days at high altitude (3,940 m). The progressive increase in resting expired minute ventilation (VE; control mean 9.94 +/- 1.78 to 14.25 +/- 2.67 l/min on day 3, P less than 0.005) on exposure to high altitude was primarily due to a significant increase in respiratory frequency (f; control mean 15.6 +/- 3.5 breaths/min to 23.8 +/- 6.2 breaths/min on day 3, P less than 0.01) with no significant change in tidal volume (VT). The increase in f was due to significant decreases in both inspiratory (TI) and expiratory (TE) time per breath; the ratio of TI to TE increased significantly (control mean 0.40 +/- 0.08 to 0.57 +/- 0.14, P less than 0.025). Mouth occlusion pressure did not change significantly, nor did the ratio of VE to mouth occlusion pressure. The acute induction of hyperoxia for 10 min at high altitude did not significantly alter VE or the ventilatory pattern. These results indicate that acute exposure to high altitude in normal lowlanders causes an increase in VE primarily by an alteration in central breath timing, with no change in respiratory drive. The acute relief of high altitude hypoxia for 10 min has no effect on the increased VE or ventilatory pattern.

Measurement of Mouth Occlusion Pressure as an Index of Respiratory Centre Output in Man

1977 ◽  
Vol 53 (2) ◽  
pp. 117-123 ◽  
Author(s):  
N. K. Burki ◽  
L. K. Mitchell ◽  
B. A. Chaudhary ◽  
F. W. Zechman
Keyword(s):  
Lung Volume ◽  
Normal Subjects ◽  
Close Correlation ◽  
Regression Coefficients ◽  
Occlusion Pressure ◽  
Mouth Pressure ◽  
Residual Capacity ◽  
Respiratory Centre ◽  
Mouth Occlusion Pressure ◽  
End Tidal

1. Simultaneous measurements of mouth pressure at the end of the first 0·1 s of inspiratory occlusion (P0·1) at functional residual capacity and the maximum rate of rise of this pressure (dP/dt max.) were made repeatedly in five normal subjects during resting respiration; the coefficient of variation of dP/dt max. was 36·2%, compared with 50·6% for P0·1. 2. During both isocapnic hypoxia and hyperoxic hypercapnia in five normal subjects there was a close correlation between ventilation (V̇E) and both P0·1 and dP/dt max., and between end-tidal Pco2 or Po2 and P0·1 and dP/dt max.; during both procedures there was a close correlation between P0·1 and dP/dt max. 3. The time at which dP/dt max. occurred (Tmax.) was not correlated with changes of dP/dt max. in either procedure. Tmax. was greater than 0·12 s in most studies. 4. The regression coefficients of P0·1 and dP/dt max. on V̇E were significantly different in hypoxia as compared with hypercapnia in four out of the five subjects; on repeated hypercapnic stimulation in two out of three subjects these regression coefficients again varied significantly. Changes in lung volume or inspiratory volume-timing relationship were not responsible for these differences. These results suggest that mouth occlusion pressure, as reflected by P0·1 or dP/dt max., is a complex variable, reflecting the motor output of the respiratory centre, but also affected by random variations in the measurements and probably by changes in lung volume.

Respiratory mechanics and timing during sleep in occlusive sleep apnea

1980 ◽  
Vol 48 (3) ◽  
pp. 432-437 ◽  
Author(s):  
R. J. Martin ◽  
B. E. Pennock ◽  
W. C. Orr ◽  
M. H. Sanders ◽  
R. M. Rogers
Keyword(s):  
Sleep Apnea ◽  
Cycle Time ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Respiratory Drive ◽  
Pulmonary Resistance ◽  
Airway Occlusion ◽  
Central Nervous System Activity ◽  
Gastric Pressure ◽  
Obese Subjects

Six human obese subjects with the sleep apnea hypersomnolence syndrome associated with upper airway occlusion (UAO) were studied during sleep to characterize respiration. Measurements included the timing components of ventilation, pulmonary resistance, flow, and esophageal and gastric pressures before and during UAOs. During the period between UAOs, the resistance progressively increased (9.4-18.1 cmH2O/l(-1) . s, P less than 0.05) as the ventilation decreased (1.82-0.77 l/s, P less than 0.05), but without changes in esophageal pressure swings. During this period, inspiratory time-to-total cycle time decreased (0.42-0.25 s, P less than 0.05) due to expiratory phase prolongation. The apnea began after expiration and terminated on inspiration with the maximal swings in esophageal and gastric pressure near the termination. During the UAO, the respiratory cycle time decreased slightly, but the expiratory pause time was significantly shortened immediately before ventilation. We suggest that the UAO is but one aspect of this syndrome and that a decrease in central nervous system activity diminishes the respiratory drive before the onset of the UAO.

Configuration of the chest wall and occlusion pressures in awake humans

1981 ◽  
Vol 50 (1) ◽  
pp. 134-142 ◽  
Author(s):  
A. E. Grassino ◽  
J. P. Derenne ◽  
J. Almirall ◽  
J. Milic-Emili ◽  
W. Whitelaw
Keyword(s):  
Chest Wall ◽  
Abdominal Pressure ◽  
Intercostal Muscle ◽  
Elastic Recoil ◽  
Transdiaphragmatic Pressure ◽  
Sitting Posture ◽  
Supine Posture ◽  
Mouth Pressure ◽  
Simultaneous Change ◽  
Diaphragm Activity

During CO2 rebreathing in sitting position seven of nine conscious men showed a progressive fall in expiratory reserve volume, most of it due to a decrease in abdominal volume. Diaphragm length at end expiration was thus increased, and some elastic recoil pressure became available to drive inspiration. In four out of six subjects, when CO2 tension was greater than 55 Torr, there was a dip in abdominal pressure at the beginning of inspiration, and the change in transdiaphragmatic pressure during the first 100 ms of an occluded inspiration was smaller than the simultaneous change in mouth pressure (P0.1). In the subjects who showed the smallest diaphragmatic pressure in this 100 ms, electromyogram recordings showed that abdominal activity ceased before the onset of inspiration, and diaphragm activity did not appear until later than 100 ms into inspiration. We conclude that, in four our of our six subjects in the sitting posture, P0.1 can be generated in whole or in part by release of chest wall elastic recoil or in intercostal muscle contraction. In the supine posture, there was no change by end-expiratory chest wall configuration, and onset of diaphragm contraction coincided with beginning of inspiration in the two subjects in whom diaphragm electromyogram was recorded.

Microcomputer-assisted on-line measurement of breathing pattern and occlusion pressure

1984 ◽  
Vol 56 (1) ◽  
pp. 235-239 ◽  
Author(s):  
F. G. Lind ◽  
A. B. Truve ◽  
B. P. Lindborg
Keyword(s):  
Breathing Pattern ◽  
Low Cost ◽  
Occlusion Pressure ◽  
Flexible System ◽  
Analog Signals ◽  
Occlusion Device ◽  
Mouth Pressure ◽  
Line Measurement ◽  
On Line ◽  
Mouth Occlusion Pressure

A flexible system has been developed for on-line breath-by-breath measurements of variables commonly included in studies of breathing pattern and mouth occlusion pressure (P0.1). The system, utilizing analog signals for mouth pressure and inspiratory flow as inputs, includes a breathing pattern monitor and a pneumatically driven occlusion device designed to be compatible with a low-cost microcomputer and analog and/or digital readout instruments. The design of the system permits accurate breathing pattern and P0.1 measurements even at the highest flow and breathing frequency encountered in muscular exercise studies.

Dynamics of chest wall in preterm infants

1987 ◽  
Vol 62 (1) ◽  
pp. 170-174 ◽  
Author(s):  
G. P. Heldt ◽  
M. B. McIlroy
Keyword(s):  
Chest Wall ◽  
Preterm Infants ◽  
Dynamic Compliance ◽  
Older Children ◽  
Additional Degree ◽  
Airway Occlusion ◽  
Paradoxical Movement ◽  
Volume Relationship ◽  
Pressure Volume Relationship ◽  
Wall Compliance

The chest wall of the preterm infant has visible paradoxical movement during breathing, because of its greater flexibility than those of older children and adults. We studied the dynamics of the chest wall in 10 preterm infants to describe the interaction of the chest wall volume, as partitioned by the inductance plethysmograph, and the transthoracic and abdominal pressures. There was considerable hysteresis between the chest wall volume and the transthoracic pressure, and it had linear pressure-volume behavior during airway occlusion, late inspiration, and early expiration. The slope of this pressure-volume relationship, or the instantaneous chest wall compliance, averaged 0.89 +/- 0.16 and 0.94 +/- 0.18 ml/cmH2O for the respiratory effort during airway occlusion and early expiration, respectively. The dynamic compliance was considerably greater, averaging 7.8 +/- 2.3 ml/cmH2O. This resistive pressure-volume behavior was not related to the absolute value of or the rate of development of the esophageal or abdominal pressures. This additional degree of freedom of motion of the chest wall suggests that its linkage to the diaphragm is flexible, which provides a braking force for expiration and allows free movement of the diaphragm for breathing movements before birth.

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