Effect of Corticosteroids on Lung Volume-Pressure Curves in Bleomycin-Induced Lung Injury in the Rat

1988 ◽  
Vol 14 (2) ◽  
pp. 183-195 ◽  
Author(s):  
Martin F. Grunze ◽  
Debra Parkinson ◽  
Stephen B. Sulavik ◽  
Roger S. Thrall
2008 ◽  
Vol 36 (6) ◽  
pp. 792-797 ◽  
Author(s):  
H. G. Ryu ◽  
J.-H. Bahk ◽  
H.-J. Lee ◽  
J.-G. Im

The mechanism of oxygenation improvement after recruitment manoeuvres or prone positioning in acute lung injury or acute respiratory distress syndrome is still unclear. We tried to determine the mechanism responsible for the effects of recruitment manoeuvres or prone positioning on lung aeration using a whole lung computed tomography scan in an oleic acid induced acute lung injury canine model. Twelve adult mongrel dogs were allocated into either the supine group (n=6) or the prone group (n = 6). After the establishment of acute lung injury, three recruitment manoeuvres were performed at one-hour intervals. Haemodynamic and ventilatory variables, arterial blood gas analyses and CT scans of the whole lung were obtained 90 minutes after oleic acid injection and five minutes before and after each recruitment manoeuvre. Recruitment manoeuvres in the supine position improved oxygenation (P=0.025) that correlated with increase of the poorly- and well-aerated dorsal (dependent) lung volume (r=0.436, P=0.016). Prone positioning increased oxygenation (P=0.004) that also correlated with increase of the poorly- and well-aerated dorsal (nondependent) lung volume (r=0.787, P <0.001). However, the recruitment manoeuvre in the prone position had no effect on oxygenation despite an increase in ventral (dependent) lung volume. The increase in PO2 after recruitment manoeuvres in the supine position or after prone positioning is related to the increase of the poorly- and well-aerated dorsal lung.


2002 ◽  
Vol 93 (2) ◽  
pp. 705-713 ◽  
Author(s):  
Jason H. T. Bates ◽  
Charles G. Irvin

Recruitment and derecruitment (R/D) of air spaces within the lung is greatly enhanced in lung injury and is thought to be responsible for exacerbating injury during mechanical ventilation. There is evidence to suggest that R/D is a time-dependent phenomenon. We have developed a computer model of the lung consisting of a parallel arrangement of airways and alveolar units. Each airway has a critical pressure (Pcrit) above which it tends to open and below which it tends to close but at a rate determined by how far pressure is from Pcrit. With an appropriate distribution of Pcrit and R/D velocity characteristics, the model able to produce realistic first and second pressure-volume curves of a lung inflated from an initially degassed state. The model also predicts that lung elastance will increase transiently after a deep inflation to a degree that increases as lung volume decreases and as the lung becomes injured. We conclude that our model captures the time-dependent mechanical behavior of the lung due to gradual R/D of lung units.


1989 ◽  
Vol 33 (5) ◽  
pp. 359-368 ◽  
Author(s):  
T. Wetterberg ◽  
E. Svensjö ◽  
A. Larsson ◽  
G. Sigurdsson ◽  
Z. G-Wagner ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Fernando Suárez-Sipmann ◽  
Jesús Villar ◽  
Carlos Ferrando ◽  
Juan A. Sánchez-Giralt ◽  
Gerardo Tusman

Mechanical ventilation (MV) is a lifesaving supportive intervention in the management of acute respiratory distress syndrome (ARDS), buying time while the primary precipitating cause is being corrected. However, MV can contribute to a worsening of the primary lung injury, known as ventilation-induced lung injury (VILI), which could have an important impact on outcome. The ARDS lung is characterized by diffuse and heterogeneous lung damage and is particularly prone to suffer the consequences of an excessive mechanical stress imposed by higher airway pressures and volumes during MV. Of major concern is cyclic overdistension, affecting those lung segments receiving a proportionally higher tidal volume in an overall reduced lung volume. Theoretically, healthier lung regions are submitted to a larger stress and cyclic deformation and thus at high risk for developing VILI. Clinicians have difficulties in detecting VILI, particularly cyclic overdistension at the bedside, since routine monitoring of gas exchange and lung mechanics are relatively insensitive to this mechanism of VILI. Expired CO2 kinetics integrates relevant pathophysiological information of high interest for monitoring. CO2 is produced by cell metabolism in large daily quantities. After diffusing to tissue capillaries, CO2 is transported first by the venous and then by pulmonary circulation to the lung. Thereafter diffusing from capillaries to lung alveoli, it is finally convectively transported by lung ventilation for its elimination to the atmosphere. Modern readily clinically available sensor technology integrates information related to pulmonary ventilation, perfusion, and gas exchange from the single analysis of expired CO2 kinetics measured at the airway opening. Current volumetric capnography (VCap), the representation of the volume of expired CO2 in one single breath, informs about pulmonary perfusion, end-expiratory lung volume, dead space, and pulmonary ventilation inhomogeneities, all intimately related to cyclic overdistension during MV. Additionally, the recently described capnodynamic method provides the possibility to continuously measure the end-expiratory lung volume and effective pulmonary blood flow. All this information is accessed non-invasively and breath-by-breath helping clinicians to personalize ventilatory settings at the bedside and minimize overdistension and cyclic deformation of lung tissue.


2001 ◽  
Vol 95 (2) ◽  
pp. 382-389 ◽  
Author(s):  
Hermann Wrigge ◽  
Jörg Zinserling ◽  
Rudolf Hering ◽  
Nico Schwalfenberg ◽  
Frank Stüber ◽  
...  

Background Spontaneous breaths during airway pressure release ventilation (APRV) have to overcome the resistance of the artificial airway. Automatic tube compensation provides ventilatory assistance by increasing airway pressure during inspiration and lowering airway pressure during expiration, thereby compensating for resistance of the artificial airway. The authors studied if APRV with automatic tube compensation reduces the inspiratory effort without compromising cardiovascular function, end-expiratory lung volume, and gas exchange in patients with acute lung injury. Methods Fourteen patients with acute lung injury were breathing spontaneously during APRV with or without automatic tube compensation in random order. Airway pressure, esophageal and abdominal pressure, and gas flow were continuously measured, and tracheal pressure was estimated. Transdiaphragmatic pressure time product was calculated. End-expiratory lung volume was determined by nitrogen washout. The validity of the tracheal pressure calculation was investigated in seven healthy ventilated pigs. Results Automatic tube compensation during APRV increased airway pressure amplitude from 7.7+/-1.9 to 11.3+/-3.1 cm H2O (mean +/- SD; P &lt; 0.05) while decreasing trans-diaphragmatic pressure time product from 45+/-27 to 27+/-15 cm H2O x s(-1) x min(-1) (P &lt; 0.05), whereas tracheal pressure amplitude remained essentially unchanged (10.3+/-3.5 vs. 10.1+/-3.5 cm H2O). Minute ventilation increased from 10.4+/-1.6 to 11.4+/-1.5 l/min (P &lt; 0.001), decreasing arterial carbon dioxide tension from 52+/-9 to 47+/-6 mmHg (P &lt; 0.05) without affecting arterial blood oxygenation or cardiovascular function. End-expiratory lung volume increased from 2,806+/-991 to 3,009+/-994 ml (P &lt; 0.05). Analysis of tracheal pressure-time curves indicated nonideal regulation of the dynamic pressure support during automatic tube compensation as provided by a standard ventilator. Conclusion In the studied patients with acute lung injury, automatic tube compensation markedly unloaded the inspiratory muscles and increased alveolar ventilation without compromising cardiorespiratory function and end-expiratory lung volume.


1965 ◽  
Vol 20 (6) ◽  
pp. 1187-1193 ◽  
Author(s):  
Emilio Agostoni ◽  
Piero Mognoni ◽  
Giorgio Torri ◽  
Ada Ferrario Agostoni

The static relation between lung volume and rib cage circumference has been determined over the vital capacity range, during relaxation and activity of the respiratory muscles with open airway. At small volume the circumference is larger during relaxation; the reverse occurs at large volume. During relaxation at full expiration the cross section of the rib cage becomes more elliptical and in some subjects also greater. Hence the shape of the chest wall during muscular activity is different from that during relaxation. Because of this change of chest wall shape the outward recoil of the passive rib cage at full expiration, in the seven subjects examined, is higher than that given by the conventional volume-pressure curve during relaxation. The volume displacements of the rib cage and of the abdomen-diaphragm have been calculated and the volume-pressure curves of the passive rib cage and abdomen-diaphragm have been constructed, taking into account the changes of the chest wall shape occurring during relaxation. change of chest wall shape during relaxation; relation between lung volume and rib cage circumference during relaxation; relation between pleural pressure and rib cage circumference during relaxation; recoil of the passive rib cage; pressure exerted by the expiratory muscles at full expiration; volume-pressure curve of the passive rib cage; volume-pressure curve of the passive abdomen-diaphragm Submitted on September 14, 1964


Sign in / Sign up

Export Citation Format

Share Document