scholarly journals Effects of Pleural Effusion on Respiratory Function

2004 ◽  
Vol 11 (7) ◽  
pp. 499-503 ◽  
Author(s):  
I Mitrouska ◽  
M Klimathianaki ◽  
NM Siafakas

The accumulation of pleural effusion has important effects on respiratory system function. It changes the elastic equilibrium volumes of the lung and chest wall, resulting in a restrictive ventilatory effect, chest wall expansion and reduced efficiency of the inspiratory muscles. The magnitude of these alterations depends on the pleural fluid volume and the underlying disease of the respiratory system. The decrease in lung volume is associated with hypoxemia mainly due to an increase in right to left shunt. The drainage of pleural fluid results in an increase in lung volume that is considerably less than the amount of aspirated fluid, while hypoxemia is not readily reversible upon fluid aspiration.

1999 ◽  
Vol 91 (5) ◽  
pp. 1221-1221 ◽  
Author(s):  
Paolo Pelosi ◽  
Irene Ravagnan ◽  
Gabriella Giurati ◽  
Mauro Panigada ◽  
Nicola Bottino ◽  
...  

Background Morbidly obese patients, during anesthesia and paralysis, experience more severe impairment of respiratory mechanics and gas exchange than normal subjects. The authors hypothesized that positive end-expiratory pressure (PEEP) induces different responses in normal subjects (n = 9; body mass index < 25 kg/m2) versus obese patients (n = 9; body mass index > 40 kg/m2). Methods The authors measured lung volumes (helium technique), the elastances of the respiratory system, lung, and chest wall, the pressure-volume curves (occlusion technique and esophageal balloon), and the intraabdominal pressure (intrabladder catheter) at PEEP 0 and 10 cm H2O in paralyzed, anesthetized postoperative patients in the intensive care unit or operating room after abdominal surgery. Results At PEEP 0 cm H2O, obese patients had lower lung volume (0.59 +/- 0.17 vs. 2.15 +/- 0.58 l [mean +/- SD], P < 0.01); higher elastances of the respiratory system (26.8 +/- 4.2 vs. 16.4 +/- 3.6 cm H2O/l, P < 0.01), lung (17.4 +/- 4.5 vs. 10.3 +/- 3.2 cm H2O/l, P < 0.01), and chest wall (9.4 +/- 3.0 vs. 6.1 +/- 1.4 cm H2O/l, P < 0.01); and higher intraabdominal pressure (18.8 +/-7.8 vs. 9.0 +/- 2.4 cm H2O, P < 0.01) than normal subjects. The arterial oxygen tension was significantly lower (110 +/- 30 vs. 218 +/- 47 mmHg, P < 0.01; inspired oxygen fraction = 50%), and the arterial carbon dioxide tension significantly higher (37.8 +/- 6.8 vs. 28.4 +/- 3.1, P < 0.01) in obese patients compared with normal subjects. Increasing PEEP to 10 cm H2O significantly reduced elastances of the respiratory system, lung, and chest wall in obese patients but not in normal subjects. The pressure-volume curves were shifted upward and to the left in obese patients but were unchanged in normal subjects. The oxygenation increased with PEEP in obese patients (from 110 +/-30 to 130 +/- 28 mmHg, P < 0.01) but was unchanged in normal subjects. The oxygenation changes were significantly correlated with alveolar recruitment (r = 0.81, P < 0.01). Conclusions During anesthesia and paralysis, PEEP improves respiratory function in morbidly obese patients but not in normal subjects.


1994 ◽  
Vol 76 (5) ◽  
pp. 1993-1998 ◽  
Author(s):  
G. Dechman ◽  
M. Mishima ◽  
J. H. Bates

We used computed tomography (CT) to examine the effects of infusing 60 ml/kg of saline into the pleural space of four anesthetized paralyzed dogs ventilated with a constant tidal volume at a positive end-expiratory pressure of 0.5 kPa. The dogs were positioned supine, and the thoracic cavity was scanned from apex to base before and immediately after effusate loading. Each CT image was analyzed semi-automatically on a 486 personal computer with custom-designed software. We found that, despite right-side infusion, the effusate was distributed bilaterally no doubt because of the incomplete canine mediastinum. In general, the volume change of the lung was one-third and that of the chest wall was two-thirds that of the total volume infused. Most of the lung volume was contained in the caudal one-third of the lung pre-effusion, and most of the lung volume loss due to effusion was from this same region. Chest wall volume increased and in a more uniform manner post-effusion. The decrease in lung volume resulted in an increase in the mean density of the lung and an increase in its vertical density gradient as the lung was lifted upward toward the sternum by the effusate. The lung lost vertical height while the chest wall increased both its vertical and lateral dimensions after effusate loading. These results suggest that expansion of the chest wall helps preserve lung volume in the presence of acute pleural effusion. We have also demonstrated that CT is a useful tool for assessing changes in volume, shape, and density of the respiratory system.


1993 ◽  
Vol 74 (5) ◽  
pp. 2286-2293 ◽  
Author(s):  
G. M. Barnas ◽  
J. Sprung

Dependencies of the dynamic mechanical properties of the respiratory system on mean airway pressure (Paw) and the effects of tidal volume (VT) are not completely clear. We measured resistance and dynamic elastance of the total respiratory system (Rrs and Ers), lungs (RL and EL), and chest wall (Rcw and Ecw) in six healthy anesthetized paralyzed dogs during sinusoidal volume oscillations at the trachea (50–300 ml; 0.4 Hz) delivered at mean Paw from -9 to +23 cmH2O. Changes in end-expiratory lung volume, estimated with inductance plethysmographic belts, showed a typical sigmoidal relationship to mean Paw. Each dog showed the same dependencies of mechanical properties on mean Paw and VT. All elastances and resistances were minimal between 5 and 10 cmH2O mean Paw. All elastances, Rrs, and RL increased greatly with decreasing Paw below 5 cmH2O. Ers and EL increased above 10 cmH2O. Ecw, Ers, Rcw, and Rrs decreased slightly with increasing VT, but RL and EL were independent of VT. We conclude that 1) respiratory system impedance is minimal at the normal mean lung volume of supine anesthetized paralyzed dogs; 2) the dependency of RL on lung volume above functional residual capacity is dependent on VT and respiratory frequency; and 3) chest wall, but not lung, mechanical behavior is nonlinear (i.e., VT dependent) at any given lung volume.


1999 ◽  
Vol 86 (1) ◽  
pp. 16-21 ◽  
Author(s):  
T. Hirai ◽  
K. A. McKeown ◽  
R. F. M. Gomes ◽  
J. H. T. Bates

To investigate the effect of lung volume on chest wall and lung mechanics in the rats, we measured the impedance (Z) under closed- and open-chest conditions at various positive end-expiratory pressures (0–0.9 kPa) by using a computer-controlled small-animal ventilator (T. F. Schuessler and J. H. T. Bates. IEEE Trans. Biomed. Eng. 42: 860–866, 1995) that we have developed for determining accurately the respiratory Z in small animals. The Z of total respiratory system and lungs was measured with small-volume oscillations between 0.25 and 9.125 Hz. The measured Z was fitted to a model that featured a constant-phase tissue compartment (with dissipation and elastance characterized by constants G and H, respectively) and a constant airway resistance (Z. Hantos, B. Daroczy, B. Suki, S. Nagy, and J. J. Fredberg. J. Appl. Physiol. 72: 168–178, 1992). We matched the lung volume between the closed- and open-chest conditions by using the quasi-static pressure-volume relationship of the lungs to calculate Z as a function of lung volume. Resistance decreased with lung volume and was not significantly different between total respiratory system and lungs. However, G and H of the respiratory system were significantly higher than those of the lungs. We conclude that chest wall in rats has a significant influence on tissue mechanics of the total respiratory system.


2006 ◽  
Vol 101 (1) ◽  
pp. 298-306 ◽  
Author(s):  
Masahiko Izumizaki ◽  
Michiko Iwase ◽  
Yasuyoshi Ohshima ◽  
Ikuo Homma

Thixotropy conditioning of inspiratory muscles consisting of maximal inspiratory effort performed at an inflated lung volume is followed by an increase in end-expiratory position of the rib cage in normal human subjects. When performed at a deflated lung volume, conditioning is followed by a reduction in end-expiratory position. The present study was performed to determine whether changes in end-expiratory chest wall and lung volumes occur after thixotropy conditioning. We first examined the acute effects of conditioning on chest wall volume during subsequent five-breath cycles using respiratory inductive plethysmography ( n = 8). End-expiratory chest wall volume increased after conditioning at an inflated lung volume ( P < 0.05), which was attained mainly by rib cage movements. Conditioning at a deflated lung volume was followed by reductions in end-expiratory chest wall volume, which was explained by rib cage and abdominal volume changes ( P < 0.05). End-expiratory esophageal pressure decreased and increased after conditioning at inflated and deflated lung volumes, respectively ( n = 3). These changes in end-expiratory volumes and esophageal pressure were greatest for the first breath after conditioning. We also found that an increase in spirometrically determined inspiratory capacity ( n = 13) was maintained for 3 min after conditioning at a deflated lung volume, and a decrease for 1 min after conditioning at an inflated lung volume. Helium-dilution end-expiratory lung volume increased and decreased after conditioning at inflated and deflated lung volumes, respectively (both P < 0.05; n = 11). These results suggest that thixotropy conditioning changes end-expiratory volume of the chest wall and lung in normal human subjects.


1984 ◽  
Vol 56 (3) ◽  
pp. 681-690 ◽  
Author(s):  
S. B. Gottfried ◽  
A. Rossi ◽  
P. M. Calverley ◽  
L. Zocchi ◽  
J. Milic-Emili

In six spontaneously breathing anesthetized cats (pentobarbital sodium, 35 mg/kg ip), airflow, changes in lung volume, and tracheal and esophageal pressures were measured. Airflow was interrupted by brief airway occlusions during relaxed expirations (elicited via the Breuer-Hering inflation reflex) and throughout spontaneous breaths. A plateau in tracheal pressure occurred throughout relaxed expirations and the latter part of spontaneous expirations indicating respiratory muscle relaxation. Measurement of tracheal pressure, immediately preceding airflow, and corresponding volume enabled determination of respiratory system elastance and flow resistance. These were partitioned into lung and chest wall components using esophageal pressure. Respiratory system elastance was constant over the tidal volume range, divided approximately equally between the lung and chest wall. While the passive pressure-flow relationship for the respiratory system was linear, those for the lung and chest wall were curvilinear. Volume dependence of chest wall flow resistance was demonstrated. During inspiratory interruptions, tracheal pressure increased progressively; initial tracheal pressure was estimated by backward extrapolation. Inspiratory flow resistance of the lung and total respiratory system were constant. Force-velocity properties of the contracting inspiratory muscles contributed little to overall active resistance.


1986 ◽  
Vol 61 (5) ◽  
pp. 1647-1655 ◽  
Author(s):  
W. A. Zin ◽  
A. Boddener ◽  
P. R. Silva ◽  
T. M. Pinto ◽  
J. Milic-Emili

In six spontaneously breathing anesthetized dogs (pentobarbital sodium, 30 mg/kg) airflow, volume, and tracheal and esophageal pressures were measured. The active and passive mechanical properties of the total respiratory system, lung, and chest wall were calculated. The average passive values of respiratory system, lung, and chest wall elastances amounted to, respectively, 50.1, 32.3, and 17.7 cmH2O X l-1. Resistive pressure-vs.-flow relationships for the relaxed respiratory system, lung, and chest wall were also determined; a linear relationship was found for the former (the total passive intrinsic resistance averaged 4.1 cmH2O X l-1 X s), whereas power functions best described the others: the pulmonary pressure-flow relationship exhibited an upward concavity, which for the chest wall presented an upward convexity. The average active elastance and resistance of the respiratory system were, respectively, 64.0 cmH2O X l-1 and 5.4 cmH2O X l-1 X s. The greater active impedance reflects pressure losses due to force-length and force-velocity properties of the inspiratory muscles and those due to distortion of the respiratory system from its relaxed configuration.


2020 ◽  
Vol 2 (1) ◽  
pp. 69-78
Author(s):  
Ni Putu Nita Pranita

Pleural effusion is a common problem. Pleural effusion developed as a sequel to the underlying disease process, including pressure/volume imbalance, infection, and malignancy. In addition to pleural effusion, persistent air leak after surgery and bronchopleural fistula remain a challenge by a physician. An understanding of the pleural disease, including its diagnosis and management, has made an extraordinary step. The introduction of molecular detection of organism-specific infections, risk stratification, and improvement in the non-surgical treatment of patients with pleural infection are all within reach and maybe the standard of care shortly. This article discusses the role of existing techniques, and some of the more recent ones, which are now available for establishing the diagnosis of pleural disease. The initial approach to diagnosis usually begins by distinguishing between transudates and exudates, based on the concentration of protein and lactate dehydrogenase (LDH) in pleural fluid. The exact role of amylase and LDH can provide additional information towards the differential diagnosis of various exudative pleural effusions. With newer cytochemical staining techniques in pleural fluid, diagnostic results of malignant pleural effusion can increase by up to 80%. Ultrasound (US) and thoracic computed tomographic (CT) scans have further improved the diagnosis of undiagnosed pleural effusion. The reappearance of thoracoscopy as the latest diagnostic and therapeutic tool (e.g., Pleurodesis) for undiagnosed or recurrent pleural effusions. Management of malignant pleural effusion continues to develop with the introduction of tunneled pleural catheters and chemical pleurodesis procedures. Advances in the diagnostic and therapeutic evaluation of pleural disease and what appears to be an increasing multidisciplinary interest in a doctor managing patients with pleural disease.


1990 ◽  
Vol 69 (6) ◽  
pp. 2050-2056 ◽  
Author(s):  
R. D. Hubmayr ◽  
J. Sprung ◽  
S. Nelson

We measured the transdiaphragmatic pressure (Pdi) during bilateral phrenic nerve stimulation and evaluated the determinants of its change with lung volume, chest wall geometry, and respiratory system impedance in supine dogs. Four rows of radiopaque markers were sewn onto muscle bundles of the costal and crural diaphragm between their origin on the central tendon and their insertion on the rib cage and spine. The length of the diaphragm (L) was determined from the projection images of marker rows using biplane fluoroscopy. Measurements were made at lung volumes between total lung capacity and functional residual capacity before and after the infusion of Ringer lactate solution into the abdominal cavity. In contrast to relaxation, during tetanic stimulation the active lengths of the muscle bundles were similar at all volumes, but the diaphragm assumed different shapes. Although the small differences in active muscle length with volume and liquid loads are consistent with only small changes in muscle force output, Pdi varied by a factor of greater than or equal to 5. There was no single L/Pdi curve that fitted all data during 50-Hz stimulations. We conclude that under these experimental conditions Pdi is not a unique measure of the force produced by the diaphragm and that lung volume, chest wall geometry, and respiratory system impedance are important determinants of the mechanical efficiency of the diaphragm as a pressure generator.


Author(s):  
Ayyali Ambresh ◽  
Mallanna S Mulimani

Background: Pleural effusion is one of the common condition encountered in day to day practise. Pleural effusions represent a very common diagnostic task to the physician. A correct diagnosis of the underlying disease is essential to rational management. Today there are a number of laboratory tests available to differentiate exudates and transudates which are considered cost effective to the patients, so this study was designed for the measurement of pleural fluid cholesterol to differentiate transudative and exudative pleural effusions (sensitivity-97.8%, specificity-100%) with the advantage that a contemporary blood sample is not required, thereby lowering cost of diagnostic procedure. Objectives: To study the diagnostic value of Pleural fluid Cholesterol in differentiating transudative and exudative pleural effusions. Methodology: This cross sectional descriptive study was conducted on patients of pleural effusion (n=60)age >18 years patients with definitive clinical diagnosis and evidenced by radiological diagnosis of pleural effusion were taken as inclusion criteria. Results: The results showed majority of the patients were males (63.3%) and females (36.7%). According to lights criteria 46 patients were exudates and 14 patients were transudates and according to Pleural fluid Cholesterol criteria 45 patients were exudates and 15 patients were transudates with sensitivity of 97.8% and specificity of 100% and accuracy of 98.3%.Conclusion: The pleural fluid cholesterol criteria were found to be the most efficient criteria. Since this parameter involves the measurement of only pleural fluid values of cholesterol, it has following advantages-Economically it reduces number of biochemical tests and Simpler as there is no need to take simultaneous blood sample at the time of thoracocentesis.


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