A pinhole method for measuring chest wall compliance

1983 ◽  
Vol 54 (4) ◽  
pp. 1157-1160
Author(s):  
J. L. Grant ◽  
D. P. Moulton
Keyword(s):  
Chest Wall ◽  
Respiratory Muscles ◽  
Esophageal Pressure ◽  
Repeated Measurements ◽  
Needle Valve ◽  
Chest Wall Compliance ◽  
Pressure Line ◽  
Wall Compliance ◽  
The Subject

We describe a method of measuring chest wall compliance (Cw) that readily detects whether respiratory muscles are relaxed. The method simulates a normal slow sigh, with the subject exhaling through a needle valve. Cw is calculated from the slope of the volume-esophageal pressure line. With relaxed subjects, repeated measurements yield similar slopes. When subjects cannot relax, the volume-pressure line is irregular and variable. In 26 subjects who could relax, Cw averaged 0.208 +/- 0.05 (SD) l/cmH2O.

Developmental changes in chest wall compliance in infancy and early childhood

1995 ◽  
Vol 78 (1) ◽  
pp. 179-184 ◽  
Author(s):  
C. Papastamelos ◽  
H. B. Panitch ◽  
S. E. England ◽  
J. L. Allen
Keyword(s):  
Chest Wall ◽  
Respiratory System ◽  
Respiratory Muscles ◽  
Lung Compliance ◽  
Developmental Changes ◽  
System Function ◽  
Manual Ventilation ◽  
Chest Wall Compliance ◽  
Wall Stiffness ◽  
Wall Compliance

Development of chest wall stiffness between infancy and adulthood has important consequences for respiratory system function. To test the hypothesis that there is substantial stiffening of the chest wall in the first few years of life, we measured passive chest wall compliance (Cw) in 40 sedated humans 2 wk-3.5 yr old. Respiratory muscles were relaxed with manual ventilation applied during the Mead-Whittenberger technique. Respiratory system compliance (Crs) and lung compliance (Cl) were calculated from airway opening pressure, transpulmonary pressure, and tidal volume. Cw was calculated as 1/Cw = 1/Crs - 1/Cl during manual ventilation. Mean Cw per kilogram in infants < 1 yr old was significantly higher than that in children > 1 yr old (2.80 +/- 0.87 vs. 2.04 +/- 0.51 ml.cmH2O–1.kg-1; P = 0.002). There was an inverse linear relationship between age and mean Cw per kilogram (r = -0.495, slope -0.037; P < 0.001). In subjects with normal Cl during spontaneous breathing, Cw/spontaneous Cl was 2.86 +/- 1.06 in infants < 1 yr old and 1.33 +/- 0.36 in older children (P = 0.005). We conclude that in infancy the chest wall is nearly three times as compliant as the lung and that by the 2nd year of life chest wall stiffness increases to the point that the chest wall and lung are nearly equally compliant, as in adulthood. Stiffening of the chest wall may play a major role in developmental changes in respiratory system function such as the ability to passively maintain resting lung volume and improved ventilatory efficiency afforded by reduced rib cage distortion.

scholarly journals Calculating the work of breathing during mechanical ventilation.

2021 ◽  
Vol 2 (2) ◽  
pp. 71-72
Author(s):  
Mia Shokry ◽  
Melina Simonpietri ◽  
Kimiyo Yamasaki
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Work Of Breathing ◽  
Esophageal Pressure ◽  
Campbell Diagram ◽  
Chest Wall Compliance ◽  
Wall Compliance ◽  
Left Figure ◽  
Inspiratory Work ◽  
Axis Versus

Left figure: Passive patient esophageal pressure (Pes) in cmH2O on x-axis versus tidal volume in ml on y-axis. Green dashed line represents the chest wall compliance Right figure: same patient actively breathing on pressure support ventilation. (Pes) in cmH2O on x-axis versus tidal volume in ml on y-axis. Green dashed line represents the chest wall compliance. Red shaded area is the Campbell diagram representing the inspiratory work of breathing

THE EFFICIENCY OF THE RESPIRATORY MUSCLES IN OBESITY

1961 ◽  
Vol 39 (8) ◽  
pp. 1215-1222 ◽  
Author(s):  
Reuben M. Cherniack ◽  
Clarence A. Guenter
Keyword(s):  
Chest Wall ◽  
Respiratory Muscles ◽  
Normal Subjects ◽  
Oxygen Cost ◽  
Chest Wall Compliance ◽  
Elastic Resistance ◽  
Lower Lung ◽  
Wall Compliance ◽  
Obese Subjects ◽  
Work Done

The work done to overcome the elastic resistance and the efficiency of the respiratory muscles were determined in normal and obese subjects. The work done was no greater in the obese subjects, but the efficiency of the muscles was low. These findings suggest that the high oxygen cost of breathing in obesity is due to inefficient respiratory muscles rather than to an increased amount of work required to overcome elastic resistance. When an extrapulmonary elastic resistance was applied to the normal subjects, the compliance of the chest wall and the efficiency of the respiratory muscles fell to the level of that in the obese. This suggests that the inefficiency of the respiratory muscles of obese individuals may have been due to the reduced chest wall compliance or to the lower lung volume at which ventilation took place.

Respiratory mechanics in the anesthetized rat

1978 ◽  
Vol 45 (2) ◽  
pp. 255-260 ◽  
Author(s):  
Y. L. Lai ◽  
J. Hildebrandt
Keyword(s):  
Chest Wall ◽  
Respiratory System ◽  
Esophageal Pressure ◽  
Gas Content ◽  
Lung Capacity ◽  
Consistent Change ◽  
Residual Capacity ◽  
Wall Compliance ◽  
The Difference ◽  
Body Plethysmograph

Functional residual capacity (FRC) and pressure-volume (PV) curves of the lung, chest wall, and total respiratory system were studied in 15 anesthetized rats, weighing 307 +/- 10 (SE) g. Pleural pressure was estimated from the esophageal pressure measured with a water-filled catheter. The FRC determined by body plethysmograph was slightly and significantly larger than FRC determined from saline displacement of excised lungs. The difference may be accounted for by O2 uptake by lung tissue, escape of CO2 through the pleura, and abdominal gas. Paralysis in the prone position did not affect FRC, and abdominal gas content contributed only slightly to the FRC measured by body plethysmograph. Values of various pulmonary parameters (mean +/- SE) were as follows: residual volume, 1.26 +/- 0.13 ml; FRC, 2.51 +/- 0.20 ml; total lung capacity, 12.23 +/- 0.55 ml; compliance of the lung, 0.90 +/- 0.06 ml/cmH2O; chest wall compliance, 1.50 +/- 0.11 ml/cmH2O; and respiratory system compliance, 0.57 +/- 0.03 ml/cmH2O. The lung PV curve did not show a consistent change after the chest was opened.

Low-frequency respiratory mechanical impedance in the rat

1987 ◽  
Vol 63 (1) ◽  
pp. 36-43 ◽  
Author(s):  
Z. Hantos ◽  
B. Daroczy ◽  
B. Suki ◽  
S. Nagy
Keyword(s):  
Frequency Dependence ◽  
Chest Wall ◽  
Low Frequency ◽  
Mechanical Impedance ◽  
Total Resistance ◽  
Low Frequencies ◽  
Chest Wall Compliance ◽  
Before And After ◽  
Airway Opening ◽  
Wall Compliance

modified forced oscillatory technique was used to determine the respiratory mechanical impedances in anesthetized, paralyzed rats between 0.25 and 10 Hz. From the total respiratory (Zrs) and pulmonary impedance (ZL), measured with pseudorandom oscillations applied at the airway opening before and after thoracotomy, respectively, the chest wall impedance (ZW) was calculated as ZW = Zrs - ZL. The pulmonary (RL) and chest wall resistances were both markedly frequency dependent: between 0.25 and 2 Hz they contributed equally to the total resistance falling from 81.4 +/- 18.3 (SD) at 0.25 Hz to 27.1 +/- 1.7 kPa.l–1 X s at 2 Hz. The pulmonary compliance (CL) decreased mildly, from 2.78 +/- 0.44 at 0.25 Hz to 2.36 +/- 0.39 ml/kPa at 2 Hz, and then increased at higher frequencies, whereas the chest wall compliance declined monotonously from 4.19 +/- 0.88 at 0.25 Hz to 1.93 +/- 0.14 ml/kPa at 10 Hz. Although the frequency dependence of ZW can be interpreted on the basis of parallel inhomogeneities alone, the sharp fall in RL together with the relatively constant CL suggests that at low frequencies significant losses are imposed by the non-Newtonian resistive properties of the lung tissue.

scholarly journals CAN THEORETICAL VALUES FOR CHEST WALL COMPLIANCE BE USED IN ARDS PATIENTS?

2015 ◽  
Vol 3 (Suppl 1) ◽  
pp. A999
Author(s):  
GQ Chen ◽  
M Xu ◽  
XL Chen ◽  
N Rittayamai ◽  
M Kim ◽  
...  
Keyword(s):  
Chest Wall ◽  
Chest Wall Compliance ◽  
Wall Compliance

μ-Opioid receptor agonist effects on medullary respiratory neurons in the cat: evidence for involvement in certain types of ventilatory disturbances

2003 ◽  
Vol 285 (6) ◽  
pp. R1287-R1304 ◽  
Author(s):  
Peter M. Lalley
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Opioid Receptor ◽  
Membrane Properties ◽  
Respiratory Neurons ◽  
Opioid Agonist ◽  
Chest Wall Compliance ◽  
Wall Compliance ◽  
Μ Opioid Receptor ◽  
Synaptic Drive

μ-Opioid receptor agonists depress tidal volume, decrease chest wall compliance, and increase upper airway resistance. In this study, potential neuronal sites and mechanisms responsible for the disturbances were investigated, dose-response relationships were established, and it was determined whether general anesthesia plays a role. Effects of μ-opioid agonists on membrane properties and discharges of respiratory bulbospinal, vagal, and propriobulbar neurons and phrenic nerve activity were measured in pentobarbital-anesthetized and unanesthetized decerebrate cats. In all types of respiratory neurons tested, threshold intravenous doses of the μ-opioid agonist fentanyl slowed discharge frequency and prolonged duration without altering peak discharge intensity. Larger doses postsynaptically depressed discharges of inspiratory bulbospinal and inspiratory propriobulbar neurons that might account for depression of tidal volume. Iontophoresis of the μ-opioid agonist DAMGO also depressed the intensity of inspiratory bulbospinal neuron discharges. Fentanyl given intravenously prolonged discharges leading to tonic firing of bulbospinal expiratory neurons in association with reduced hyperpolarizing synaptic drive potentials, perhaps explaining decreased inspiratory phase chest wall compliance. Lowest effective doses of fentanyl had similar effects on vagal postinspiratory (laryngeal adductor) motoneurons, whereas in vagal laryngeal abductor and pharyngeal constrictor motoneurons, depression of depolarizing synaptic drive potentials led to sparse, very-low-frequency discharges. Such effects on three types of vagal motoneurons might explain tonic vocal fold closure and pharyngeal obstruction of airflow. Measurements of membrane potential and input resistance suggest the effects on bulbospinal Aug-E neurons and vagal motoneurons are mediated presynaptically. Opioid effects on the respiratory neurons were similar in anesthetized and decerebrate preparations.

Sign in / Sign up

Export Citation Format

Share Document