0
Original Research: CRITICAL CARE MEDICINE |

Effect of Thoracentesis on Respiratory Mechanics and Gas Exchange in the Patient Receiving Mechanical Ventilation* FREE TO VIEW

Peter Doelken, MD, FCCP; Ricardo Abreu, MD, FCCP; Steven A. Sahn, MD, FCCP; Paul H. Mayo, MD, FCCP
Author and Funding Information

*From the Division of Pulmonary, Critical Care, Allergy and Sleep Medicine (Drs. Doelken and Sahn), Medical University of South Carolina, Charleston, SC; Department of Medicine (Dr. Abreu), Knapp Medical Center, Weslaco, TX; and Division of Pulmonary and Critical Care Medicine (Dr. Mayo), Beth Israel Medical Center, New York, NY.

Correspondence to: Paul H. Mayo, MD, FCCP, Division of Pulmonary and Critical Care Medicine 7D, Beth Israel Medical Center, First Ave and Sixteenth St, New York, NY 10003; e-mail: pmayo@chpnet.org



Chest. 2006;130(5):1354-1361. doi:10.1378/chest.130.5.1354
Text Size: A A A
Published online

Background: This study reports the effect of thoracentesis on respiratory mechanics and gas exchange in patients receiving mechanical ventilation.

Study design: Prospective.

Setting: University hospital.

Patients: Eight patient receiving mechanical ventilation with unilateral (n = 7) or bilateral (n = 1) large pleural effusions.

Intervention: Therapeutic thoracentesis (n = 9).

Measurements: Resistances of the respiratory system measured with the constant inspiratory flow interrupter method measuring peak pressure and plateau pressure, effective static compliance of the respiratory system (Cst,rs), work performed by the ventilator (Wv), arterial blood gases, mixed exhaled Pco2, and pleural liquid pressure (Pliq).

Results: Thoracentesis resulted in a significant decrease in Wv and Pliq. Thoracentesis had no significant effect on dynamic compliance of the respiratory system; Cst,rs; effective interrupter resistance of the respiratory system, or its subcomponents, ohmic resistance of the respiratory system and additional (non-ohmic) resistance of the respiratory system; or intrinsic positive end-expiratory pressure (PEEPi). Indices of gas exchange were not significantly changed by thoracentesis.

Conclusions: Thoracentesis in patients receiving mechanical ventilatory support results in significant reductions of Pliq and Wv. These changes were not accompanied by significant changes of resistance or compliance or by significant changes in gas exchange immediately after thoracentesis. The reduction of Wv after thoracentesis in patients receiving mechanical ventilation is not accompanied by predictable changes in inspiratory resistance and static compliance measured with routine clinical methods. The benefit of thoracentesis may be most pronounced in patients with high levels of PEEPi.

Figures in this Article

The effect of thoracentesis on respiratory function has been studied in spontaneously breathing patients.14 However, its effect in patients receiving mechanical ventilation has not been well studied. Intuitively, the clinician might assume that thoracentesis would affect bedside respiratory mechanics measurements, especially in the light of the perception that thoracentesis may aid in liberating patients from mechanical ventilation. We have investigated the influence of thoracentesis on simple bedside measurements of respiratory function that may be routinely performed by the intensivist.

Eight patients receiving mechanical ventilation were studied before and after thoracentesis. The institutional review board approved the protocol, and informed consent was obtained from each patient or surrogate. All subjects were hemodynamically stable, were receiving mechanical ventilation via a cuffed tracheal tube, and had large pleural effusions shown on supine anteroposterior chest radiography that were confirmed by sonography. The decision to perform the thoracentesis was made by the clinical team in charge of the patient.

Experimental Procedure

All patients were sedated, paralyzed, and placed on mechanical ventilation (Puritan-Bennett 7200; Puritan-Bennett Corporation; Carlsbad, CA) in continuous mandatory ventilation mode. The patients were studied in supine position. No bronchodilators were administered within 30 min, and no endotracheal suctioning was performed within 15 min of the start of the study. A leak-free, low-compliance circuit (static compliance of the ventilator circuit [Cc] = 1.69 mL/cm H2O) without a humidifier was used. The ventilator was set to fraction of inspired oxygen (Fio2) of 1.0; tidal volume (Vt), 500 mL; inspiratory flow, 60 L/min; square-wave flow pattern; positive end-expiratory pressure (PEEP), 0 cm H2O unless otherwise indicated; plateau, 2 s; and respiratory rate, 8 breaths/min. After reaching steady state on the new settings as evidenced by stable peak pressure (Ppeak) and plateau pressure (Pplat), intrinsic PEEP (PEEPi) was determined using an end-expiratory occlusion maneuver. The goal was to study respiratory mechanics with end-expiratory volume close to the relaxation volume of the respiratory system. PEEP was therefore set at 0 cm H2O, except in patients 3 and 4, who were studied at PEEP of 5 cm H2O. Whenever PEEPi was detected, respiratory rate was lowered to a minimum of 5 breaths/min. As a result, five series of measurements (1, 3, 4, 7a, 7b) were performed in the presence of total PEEP. After determination of study ventilator settings for the individual patient, baseline ventilation was resumed for several minutes; subsequently, study settings were reinstituted. Another end-expiratory occlusion maneuver was performed after reaching stable Ppeak and Pplat, and eight breath cycles were recorded. Measurements were accepted when Ppeak and Pplat were stable during signal acquisition, and measured PEEPi was equal before and after signal acquisition.

Following measurements before thoracentesis, baseline ventilation as prescribed by the treating physician was resumed and ultrasound-guided thoracentesis was performed. End-expiratory pleural liquid pressure (Pliq) was measured immediately after insertion of the catheter and after withdrawal of 250-mL aliquots until no more fluid could be withdrawn. The measurement system was zeroed at the level of the catheter insertion site. Immediately following thoracentesis, respiratory mechanics were measured again in the same patient position and the same ventilator settings as during the initial measurements.

Measurements

Airway opening pressure was measured through a side port just proximal to the endotracheal tube using a pressure transducer (Validyne MP45 ± 80 cm H2O; Validyne Engineering; Northridge, CA). Flow was measured between the endotracheal tube and the ventilator circuit using a heated pneumotachometer (Hans Rudolph 3700; Hans Rudolph; Kansas City, MO) and a differential pressure transducer (Validyne MP45 ± 2 cm H2O; Validyne Engineering). The flow sensor was calibrated with 100% oxygen over the flow ranges measured. Signals were recorded with a digital storage oscilloscope (Gould Classic 6500; Gould Instrument Systems; Ilford, UK) and stored as the flow-triggered ensemble average of eight breath cycles to attenuate cardiac artifact. Pliqs were measured using a sterile fluid-filled system (Transpac IV; Abbott Critical Care Systems; North Chicago, IL).

Flows were mathematically corrected for body temperature and pressure, saturated; and Vts were obtained by numeric integration. Ppeak, intercept of a computer-fitted third-order polynomial equation of the slow pressure decline and a vertical line indicating the time of onset of valve closure (P1), and Pplat were determined.5Figure 1 depicts a representative plot to calculate respiratory mechanics. Effective interrupter resistance of the respiratory system (Rmax,rs) [(Ppeak − Pplat)/end inspiratory flow], ohmic resistance of the respiratory system (Rinit,rs) [(Ppeak − P1)/end-inspiratory flow], and additional (non-ohmic) resistance of the respiratory system (ΔRrs) [(P1 − Pplat)/end-inspiratory flow] were corrected for equipment resistance6and for volume change (ΔV) after onset of valve closure.78 The flow-dependent ΔV characteristic for the ventilator was ΔV = control flow × 0.026 s + 0.003 L. The effective static compliance of the respiratory system (Cst,rs) was calculated as Vt/(Pplat − PEEP ± PEEPi). The dynamic compliance of the respiratory system (Cdyn,rs) was calculated as Vt/(Ppeak − PEEP). Work of inflation was calculated by numeric integration of the pressure/time curve that was measured from onset of inspiration to end inspiration and expressed in joules per liter. Figure 2 depicts a representative plot used to calculate inflation work (subject 2).

Mixed exhaled Pco2 was measured distal to a mixing chamber connected to the exhalation port of the ventilator with a capnograph (Pryon SC-300; Pryon Corporation; Menomonee Falls, WI). Thirty minutes of baseline ventilation (ventilator settings as prescribed by the treating physician: Vt: median, 500 mL [range, 400 to 650 mL]; respiratory rate: median, 12 breaths/min [range, 10 to 17 breaths/min]; Fio2: median, 0.5 [range, 0.35 to 0.7]) were allowed to establish steady-state conditions in the mixing chamber before simultaneous measurement of mixed exhaled Pco2 and arterial blood gases. Alveolar-arterial oxygen pressure difference (P[A-a]O2) was calculated assuming a respiratory exchange quotient of 0.8. Dead space/Vt (Vd/Vt) ratios were calculated as Vd/Vt = (Paco2 − mixed exhaled Pco2)/Paco2. Mixed exhaled Pco2 was corrected for the circuit compliance and gas compression compensation: Pco2 = mixed exhaled Pco2(Vt + [Ppeak − PEEP]Cc)/Vt.9

Statistical Analysis

The paired t test was used to compare normally distributed data before and after thoracentesis. The t test was used to compare normally distributed groups of data. The Wilcoxon signed-rank test was used for data that was not normally distributed. A difference in measurements was considered statistically significant at p < 0.05. Statistical power was calculated using the following assumptions: For Cst,rs, a 20% change from baseline mean; for Rmax,rs, a 20% change from baseline mean; for Cdyn,rs, a 10% change from baseline mean; and for P(A-a)O2, a change of 36 mm Hg from baseline mean. The assumptions are based on a change of pressure during routine bedside measurements of approximately 3 cm H2O, which should be discernible if the measurements are performed carefully. In the case of P(A-a)O2, 36 mm Hg was chosen, as this value corresponds to a change of Fio2 of 0.05, which is usually the smallest increment or decrement in clinical practice. For Vd/Vt, a change of 0.1 was arbitrarily used, as a change of this magnitude should noticeably affect minute volume requirements. A statistical software package (Sigma Stat 2.0; SPSS; Chicago, IL) was used.

Eight patients were enrolled in the study. One patient underwent bilateral thoracenteses on successive days and was studied twice; the two thoracenteses are referred to as 7a and 7b in Table 1 . The patient characteristics, side of thoracentesis, fluid volume, and characteristics of fluid removed are shown in Table 1. Table 2 shows mean values of respiratory rate, Vt, and constant flow, documenting similar conditions under which measurements of respiratory mechanics were made. There was no significant change of mean Ppeak, mean Pplat, Cdyn,rs, and mean total PEEP. The reduction in mean Pliq was statistically significant (p = 0.008).

Figure 3 shows Pliq at end-expiration while fluid was withdrawn. In subject 5, measurement of Pliq was suspended before negative pressures were measured for technical reasons. Thus, the last data point available was Pliq of 1 cm H2O after withdrawal of 750 mL; after this, another 450 mL could be easily withdrawn. The final value of Pliq in this patient was treated as a missing value for statistical analysis of the overall change in Pliqs.

Figure 4 shows that the input parameters Vt and inspiratory flow are within ± 5% of baseline. The 95% confidence interval of the difference of the means of work performed by the ventilator (Wv) does not overlap 0 and is significantly decreased from baseline. The difference of the means of Cdyn,rs favors improvement, and the difference of Cst,rs indicates a worsening influence on inspiratory airway pressure. The difference of the means of Rmax.rs favors no change. The means of the differences of Cdyn,rs, Rmax,rs, and Cst,rs are all within ± 5% of baseline. The 95% confidence intervals for the difference of the means of Rmax,rs and Cst,rs are well within the assumed range of equivalence of ± 20% for routine bedside measurements.

The results of pleural elastance calculations were as follows: pleural fluid elastance during withdrawal of the first 500 mL of fluid (Est,pl,0.5) was 11.2 cm H2O (SEM 2.3) and mean pleural fluid elastance during the entire thoracentesis (Est,pl) was 12.7 cm H2O (SEM 1.7). In subject 4, Est,pl,0.5 was 27.2 cm H2O and Est,pl was 16.7 cm H2O; this was due to a disproportionate fall of Pliq after withdrawal of the first 250 mL of fluid. Pleural space elastance calculated for the interval of 250 to 1,250 mL was 9.5 cm H2O.

Respiratory mechanics data are shown in Table 3 . There was no statistically significant change of Rmax,rs, Rinit,rs, ΔRrs, or Cst,rs. PEEPi, when present, diminished after thoracentesis; this change was not statistically significant (p = 0.125). Mean Wv during passive inflation decreased significantly after thoracentesis (p = 0.011). Table 4 shows gas exchange data. There were no significant changes of Pao2, P(A-a)O2, Pao2/Fio2 ratio, or Vd/Vt. The statistical power calculated for detecting a change of 10% from baseline of Cdyn,rs was 0.893 (β = 0.107); for a change of 20% of Cst,rs, the power was 0.99 (β = 0.01); for a change of 20% of Rmax,rs, the power was 0.967 (β = 0.033); for a change of 36 mm Hg of P(A-a)O2, the power was 0.956 (β = 0.044); and for a change of 0.1 of Vd/Vt, the power was 0.985 (β = 0.015).

Patients receiving mechanical ventilation commonly have pleural effusions.10Thoracentesis with ultrasound guidance can be safely performed in this patient population.1113 We have investigated the effect of large-volume thoracentesis performed in patients requiring mechanical ventilation on measurements of respiratory physiology that that are easily performed at the bedside.

Gas Exchange

Thoracentesis had no predictable effect on gas exchange. Pao2 did not change significantly before and after thoracentesis on an identical Fio2, nor did P(A-a)O2. Paco2 did not change to significant extent with constant minute ventilation and with what we assume to be a constant carbon dioxide output. Vd/Vt was unchanged following thoracentesis. It must be said that the patients were receiving a volume mode of ventilation, and no recruitment maneuvers were used that may have influenced the result.

The effect of pleural space drainage on gas exchange in patients receiving mechanical ventilation is limited to one study14that found significant improvement of oxygenation after chest tube drainage in a series of difficult-to-oxygenate patients. The effect of thoracentesis on gas exchange has been studied in spontaneously breathing subjects. Brandstetter and Cohen15reported a decrease in Pao2 after thoracentesis. Others reported increases in Pao2 and decreases in P(A-a)O2 after thoracentesis,17 found Pao2 to increase after thoracentesis without change of P(A-a)O2,,2 or did not demonstrate changes in oxygenation.1819 Neither Perpina et al17 nor Agusti et al19 found an effect on Vd/Vt in spontaneously breathing patients.

Thoracentesis and Pliq

Mean Est,pl,0.5 and Est,pl were at the lower limit of pleural elastances reported in the literature.2021 As shown in Figure 3, there was no rapid decrease to Pliq that would have been indicative of pleural space restriction; we are confident that unexpandable lung was not present.

Compliance

Mean Cst,rs was reduced at baseline, and no significant change was observed following thoracentesis. Cst,rs is a parameter that is readily measured at the bedside and estimates the elastic component of total respiratory impedance. Our measurement strategy was meticulous and included measuring flow and pressure at the airway opening; ensemble averaging of eight consecutive breaths in the passive patient with constant volume history; correcting volumes to body temperature and pressure, saturated; and correcting for valve closure and tubing compliance factors. Figure 4 shows that Vt and inspiratory flow were successfully kept within 5% for each measurement.

The fact that Cst,rs did not increase after thoracentesis is most likely due to the size of pleural effusions removed in this study. It has been shown in a mechanically ventilated dog model that the reciprocal of compliance, elastance, increases with pleural saline solution loading but only when > 30 mL/kg of saline solution was instilled into the pleural space.22This is well above the amount removed in our patients. We conclude that the human respiratory system can accommodate relatively large amounts of pleural fluid before Cst,rs decreases. The effect of a very large pleural effusion has been the subject of a case report23 in which Cst,rs increased considerably after thoracentesis.

Intriguingly, our results indicate a trend toward decreasing Cst,rs after thoracentesis. This may be due to a decrease in compliance of the lung due to newly aerated lung being less compliant, or due to a stiffening effect of thoracentesis on the chest wall. We speculate that restoration of the dome shape of the diaphragm by thoracentesis, which is readily observable by ultrasonography, indicates increased tension of the diaphragm caused by the weight of the abdominal organs in the supine subject. This tension is transmitted to the rib cage, leading to stiffening of the chest wall in the sedated and paralyzed subject.

Resistance

Thoracentesis had minimal effect on Rmax,rs. At baseline, most study subjects had significantly elevated inspiratory resistances. Our results indicate that abnormalities of this parameter do not improve with thoracentesis and, therefore, are not likely to be caused by the presence of pleural effusions of the size studied here. As with the compliance abnormalities present in our patients, the elevated respiratory system resistances most likely are caused by coexisting disease rather than the pleural effusion per se.

Rmax,rs is readily available as a bedside measurement ([Ppeak − Pplat]/inspiratory constant flow); it is an inspiratory measurement when measured with the constant inspiratory flow interruption method. Our results agree with those of Pati et al,3 who also did not find significant changes of inspiratory resistance after thoracentesis in spontaneously breathing patients. As has been shown in a dog model, resistance begins to increase substantially only after a relatively large amount of saline solution has been introduced into the pleural space.22

Rmax,rs is an overall effective resistance that can be partitioned into two subcomponents: Rinit,rs represents ohmic resistance, and ΔRrs represents viscoelastic tissue resistance with a variable contribution from the pendelluft phenomenon. There were no statistically significant changes in Rinit,rs or ΔRrs.

Cdyn,rs and Wv

Cdyn,rs did not change significantly after thoracentesis. Wv, however, decreased significantly. Changes of Cdyn,rs and Wv parallel each other in an ideal system inflated with constant flow, ie, a system with volume-independent inspiratory resistance and linear elastic characteristics. Cdyn,rs evaluates static compliance, viscoelastic resistance, ohmic resistance, and preload of the system in the form of PEEPi. Its limitation lies in it being an end-inspiratory measurement obtained under constant flow conditions. The Wv receives a contribution from the pressure required to accelerate inspiratory flow prior to achievement of constant flow conditions and therefore is susceptible to changes in inertia. It will also be affected by possible nonlinearities of resistance and compliance. Work performed by the ventilator therefore is a more accurate representation of impedance to inflation than Cdyn,rs, but the measurement is unfortunately not readily available at the bedside. Figure 2 shows pre thoracentesis and postthoracentesis pressure/volume curves of subject 2 with virtually identical peak pressure but clearly higher pressures earlier in inflation, resulting in higher Wv.

The largest decreases in Wv were seen in patients with reductions in PEEPi. We can only speculate that in susceptible patients, such as patients with COPD, the presence of a pleural effusion and the resulting decrease in lung volume leads to a further loss of parenchymal tethering of the airways leading to increased air trapping.24 The removal of fluid from the thorax might also reduce respiratory impedance by reducing the effects of inertia related to the fluid mass.

Limitations of the Study

The limitations of the present study are primarily related to the subject population studied, the fact that the subjects were sedated and paralyzed, the size of the effusions removed, the parameters measured, and the fact that postthoracentesis measurements were only performed immediately following the thoracentesis. Our results essentially imply that the volume changes of the lung and chest wall induced by thoracentesis took place on the linear interval of the respective static pressure volume curves, leaving static mechanics parameters nearly unchanged. Consequently, our results do not necessarily apply to patients with excessive thoracic volume, such as emphysema and high levels of PEEPi or with massive effusions. Further study of the effects of thoracentesis under these conditions is needed, especially as our results suggest an effect on expiratory resistance likely mediated by lung volume changes. The effects of thoracentesis on gas exchange parameters may be delayed, and we cannot exclude that clinically significant improvements occur later than in the immediate postthoracentesis period.

Clinical Implications

Rmax,rs, Cst,rs, Cdyn,rs, PEEPi, and measurement of gas exchange derived from arterial blood gases are routinely available to the clinician. It is important for the bedside intensivist to know that therapeutic thoracentesis of fluid volumes described in this study will not predictably affect these parameters. Therapeutic thoracentesis in symptomatic, spontaneously breathing patients is clearly of value in terms of relieving respiratory distress, so that an empiric case can be made to regard the presence of a pleural effusion as a contributing factor to ventilator dependency. However, it is difficult to estimate the contribution of a pleural effusion to ventilator dependency. The reduction of Wv after thoracentesis may be important in patients with impairment of respiratory function due to respiratory muscle dysfunction or dynamic hyperinflation. Although Wv is not necessarily equal to the work to be performed by the patient once breathing spontaneously, a reduction of Wv should lead to a reduction of patient work during spontaneous ventilation.25It also can be expected that thoracentesis will treat the geometric disadvantage that the respiratory pump experiences due to the presence of a pleural effusion. This effect should lead to greater efficiency of respiratory work, ie, more external work performed for similar effort.26 In our opinion, the benefit of thoracentesis in a patient with significant respiratory dysfunction may exceed that suggested by the reduction of Wv as measured in our study. The absence of improvement in the measurements of respiratory function that are readily available at the bedside should not discourage the clinician from performing therapeutic thoracentesis in a patient receiving ventilatory support, as these measurements offer a limited assessment of complex physiology.

Abbreviations: Cc = static compliance of the ventilator circuit; Cdyn,rs = dynamic compliance of the respiratory system; Cst,rs = effective static compliance of the respiratory system; ΔRrs = additional (non-ohmic) resistance of the respiratory system; ΔV = volume change; Est,pl = pleural space elastance during entire thoracentesis; Est,pl,0.5 = pleural space elastance during withdrawal of first 500 mL of fluid; Fio2 = fraction of inspired oxygen; P1 = intercept of a computer-fitted third-order polynomial equation of the slow pressure decline and a vertical line indicating the time of onset of valve closure; P(A-a)O2 = alveolar-arterial oxygen pressure difference; PEEP = positive end-expiratory pressure; PEEPi = intrinsic positive end-expiratory pressure; Pliq = pleural liquid pressure; Ppeak = peak pressure; Pplat = plateau pressure; Rinit,rs = ohmic resistance of the respiratory system; Rmax,rs = effective interrupter resistance of the respiratory system; Vd/Vt = dead space fraction; Vt = tidal volume; Wv = work performed by the ventilator

This work was performed at Beth Israel Medical Center, First Ave and Sixteenth St, New York, NY.

No authors have any personal or financial involvement with organization(s) with financial involvement in the subject matter of this project or any conflict of interest related to this project.

Figure Jump LinkFigure 1. Record of airway opening pressure during constant flow inflation, flow interruption, and a 2-s inspiratory hold maneuver in subject 2 after thoracentesis. The pressure curve shown in an ensemble average of eight interrupter cycles.Grahic Jump Location
Figure Jump LinkFigure 2. Volume/pressure plot of patient 2 before and after thoracentesis. Ppeak and inflation volume are virtually identical, and early inflation pressures are higher before thoracentesis, resulting in higher Wv (larger area) but unchanged Cdyn,rs.Grahic Jump Location
Table Graphic Jump Location
Table 1. Subject Characteristics*
* 

M = male; F = female; CHF = congestive heart failure; ARF = acute renal failure.

Table Graphic Jump Location
Table 2. Summary of Respiratory Mechanics Variables Before and Immediately After Thoracentesis
* 

Paired t test.

 

Wilcoxon signed-rank test.

Figure Jump LinkFigure 3. The relationship of Pliq and fluid withdrawn from the pleural space.Grahic Jump Location
Figure Jump LinkFigure 4. The 95% confidence intervals for the difference of the means are depicted as horizontal bars, and the means of the differences are depicted as diamonds. All values are expressed as percentage of the prethoracentesis (baseline) mean values.Grahic Jump Location
Table Graphic Jump Location
Table 3. Respiratory Mechanics Before and Immediately After Thoracentesis
* 

Paired t test.

 

Wilcoxon signed-rank test, not significant (p = 0.125).

Table Graphic Jump Location
Table 4. Gas Exchange Before and Immediately After Thoracentesis
* 

Paired t test.

Chang-Ting, L, Cellerino, A, Baldi, S, et al (1991) Pulmonary function in patients with pleural effusion of varying magnitude and fibrothorax.Panminerva Med33,86-92. [PubMed]
 
Brown, NE, Zamel, N, Aberman, A Changes in pulmonary mechanics and gas exchange following thoracentesis.Chest1978;74,540-542. [CrossRef] [PubMed]
 
Pati, AR, Pande, JN, Guleria, JS Mechanical properties of the lung in pleural effusion.Ind J Chest Dis Allied Sci1983;25,120-126
 
Light, RW, Stansbury, DW, Brown, SE The relationship between pleural pressures and changes in pulmonary function after therapeutic thoracentesis.Am Rev Respir Dis1986;133,658-661. [PubMed]
 
Bates, JHT, Milic-Emili, J The flow interrupter technique for measuring respiratory resistance.J Crit Care1991;6,227-238. [CrossRef]
 
Behrakis, PK, Higgs, BD, Zin, WA, et al Respiratory mechanics during halothane anesthesia and anesthesia-paralysis in humans.J Appl Physiol1983;55,1085-1092. [PubMed]
 
Kochi, T, Okubo, S, Zin, WA, et al Chest wall and respiratory system mechanics in cats: effects of flow and volume.J Appl Physiol1988;64,2636-2646. [PubMed]
 
Lit, LM, Doelken, P, Mayo, PH Correction of error in respiratory resistance measurements made with the flow-interruption technique during mechanical ventilation: evaluation of the Puritan Bennett 7200 and 840 ventilators.Respir Care2004;49,1022-1028. [PubMed]
 
Forbat, AF, Her, C Correction for gas compression in mechanical ventilators.Anesth Analg1980;59,488-493. [PubMed]
 
Mattison, LE, Coppage, L, Alderman, DF, et al Pleural effusions in the medical ICU: prevalence, causes and clinical implications.Chest1997;111,1018-1023. [CrossRef] [PubMed]
 
Godwin, JE, Sahn, SA A safe procedure in mechanically ventilated patients.Ann Intern Med1990;98,1130-1132
 
Mayo, PH, Goltz, HR, Tafreshi, M, et al Safety of ultrasound-guided thoracentesis in patients receiving mechanical ventilation.Chest2004;125,1059-1062. [CrossRef] [PubMed]
 
Lichtenstein, D, Hulot, JS, Rabiller, A, et al Feasibility and safety of ultrasound-aided thoracentesis in mechanically ventilated patients.Intensive Care Med1999;25,955-958. [CrossRef] [PubMed]
 
Talmor, M, Hydo, L, Gershenwald, JG, et al Beneficial effects of chest tube drainage of pleural effusion in acute respiratory failure refractory to positive end-expiratory pressure.Surgery1998;123,137-143. [CrossRef] [PubMed]
 
Brandstetter, RD, Cohen, RP Hypoxemia after thoracentesis.JAMA1979;242,1060-1061. [CrossRef] [PubMed]
 
Wang, JS, Tseng, CH Changes in pulmonary mechanics and gas exchange after thoracentesis on patients with inversion of a hemidiaphragm secondary to large pleural effusion.Chest1995;107,1610-1614. [CrossRef] [PubMed]
 
Perpina, M, Benlloch, E, Marco, V, et al Effect of thoracentesis on pulmonary gas exchange.Thorax1983;38,747-750. [CrossRef] [PubMed]
 
Karetzky, MS, Kothari, GA, Fourre, JA, et al Effects of thoracocentesis on arterial oxygen tension.Respiration1978;36,96-103. [CrossRef] [PubMed]
 
Agusti, AGN, Cardus, J, Roca, J, et al Ventilation-perfusion mismatch in patients with pleural effusion: effects of thoracentesis.Am J Respir Crit Care Med1997;156,1205-1209. [PubMed]
 
Light, RW, Jenkinson, SG, Vu-Dinh, M, et al Observations on pleural fluid pressures as fluid is withdrawn during thoracentesis.Am Rev Respir Dis1980;121,799-804. [PubMed]
 
Lan, R-S, Lo, SK, Chuang, M-L, et al Elastance of the pleural space: a predictor for the outcome of pleurodesis in patients with malignant pleural effusion.Ann Intern Med1997;126,768-774. [PubMed]
 
Dechman, G, Sato, J, Bates, JHT Effect of pleural effusion on respiratory mechanics, and the influence of deep inflation, in dogs.Eur Respir J1993;6,219-224. [PubMed]
 
Yaylali, YT, Nassar, NK, Manthous, CA Tension hydrothorax.South Med J1997;90,1156-1158. [CrossRef] [PubMed]
 
Pride, NB, Macklem, PT Lung mechanics in disease. Macklem, PT Mead, J eds.Handbook of physiology1986,659-692 American Physiological Society. Bethesda, MD:
 
Marini, JJ, Rodriguez, RM, Lamb, V The inspiratory workload of patient-initiated mechanical ventilation.Am Rev Respir Dis1986;134,902-909. [PubMed]
 
Estenne, M, Yernault, J-C, De Troyer, A Mechanism of relief of dyspnea after thoracocentesis in patients with large pleural effusions.Am J Med1983;74,813-819. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1. Record of airway opening pressure during constant flow inflation, flow interruption, and a 2-s inspiratory hold maneuver in subject 2 after thoracentesis. The pressure curve shown in an ensemble average of eight interrupter cycles.Grahic Jump Location
Figure Jump LinkFigure 2. Volume/pressure plot of patient 2 before and after thoracentesis. Ppeak and inflation volume are virtually identical, and early inflation pressures are higher before thoracentesis, resulting in higher Wv (larger area) but unchanged Cdyn,rs.Grahic Jump Location
Figure Jump LinkFigure 3. The relationship of Pliq and fluid withdrawn from the pleural space.Grahic Jump Location
Figure Jump LinkFigure 4. The 95% confidence intervals for the difference of the means are depicted as horizontal bars, and the means of the differences are depicted as diamonds. All values are expressed as percentage of the prethoracentesis (baseline) mean values.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Subject Characteristics*
* 

M = male; F = female; CHF = congestive heart failure; ARF = acute renal failure.

Table Graphic Jump Location
Table 2. Summary of Respiratory Mechanics Variables Before and Immediately After Thoracentesis
* 

Paired t test.

 

Wilcoxon signed-rank test.

Table Graphic Jump Location
Table 3. Respiratory Mechanics Before and Immediately After Thoracentesis
* 

Paired t test.

 

Wilcoxon signed-rank test, not significant (p = 0.125).

Table Graphic Jump Location
Table 4. Gas Exchange Before and Immediately After Thoracentesis
* 

Paired t test.

References

Chang-Ting, L, Cellerino, A, Baldi, S, et al (1991) Pulmonary function in patients with pleural effusion of varying magnitude and fibrothorax.Panminerva Med33,86-92. [PubMed]
 
Brown, NE, Zamel, N, Aberman, A Changes in pulmonary mechanics and gas exchange following thoracentesis.Chest1978;74,540-542. [CrossRef] [PubMed]
 
Pati, AR, Pande, JN, Guleria, JS Mechanical properties of the lung in pleural effusion.Ind J Chest Dis Allied Sci1983;25,120-126
 
Light, RW, Stansbury, DW, Brown, SE The relationship between pleural pressures and changes in pulmonary function after therapeutic thoracentesis.Am Rev Respir Dis1986;133,658-661. [PubMed]
 
Bates, JHT, Milic-Emili, J The flow interrupter technique for measuring respiratory resistance.J Crit Care1991;6,227-238. [CrossRef]
 
Behrakis, PK, Higgs, BD, Zin, WA, et al Respiratory mechanics during halothane anesthesia and anesthesia-paralysis in humans.J Appl Physiol1983;55,1085-1092. [PubMed]
 
Kochi, T, Okubo, S, Zin, WA, et al Chest wall and respiratory system mechanics in cats: effects of flow and volume.J Appl Physiol1988;64,2636-2646. [PubMed]
 
Lit, LM, Doelken, P, Mayo, PH Correction of error in respiratory resistance measurements made with the flow-interruption technique during mechanical ventilation: evaluation of the Puritan Bennett 7200 and 840 ventilators.Respir Care2004;49,1022-1028. [PubMed]
 
Forbat, AF, Her, C Correction for gas compression in mechanical ventilators.Anesth Analg1980;59,488-493. [PubMed]
 
Mattison, LE, Coppage, L, Alderman, DF, et al Pleural effusions in the medical ICU: prevalence, causes and clinical implications.Chest1997;111,1018-1023. [CrossRef] [PubMed]
 
Godwin, JE, Sahn, SA A safe procedure in mechanically ventilated patients.Ann Intern Med1990;98,1130-1132
 
Mayo, PH, Goltz, HR, Tafreshi, M, et al Safety of ultrasound-guided thoracentesis in patients receiving mechanical ventilation.Chest2004;125,1059-1062. [CrossRef] [PubMed]
 
Lichtenstein, D, Hulot, JS, Rabiller, A, et al Feasibility and safety of ultrasound-aided thoracentesis in mechanically ventilated patients.Intensive Care Med1999;25,955-958. [CrossRef] [PubMed]
 
Talmor, M, Hydo, L, Gershenwald, JG, et al Beneficial effects of chest tube drainage of pleural effusion in acute respiratory failure refractory to positive end-expiratory pressure.Surgery1998;123,137-143. [CrossRef] [PubMed]
 
Brandstetter, RD, Cohen, RP Hypoxemia after thoracentesis.JAMA1979;242,1060-1061. [CrossRef] [PubMed]
 
Wang, JS, Tseng, CH Changes in pulmonary mechanics and gas exchange after thoracentesis on patients with inversion of a hemidiaphragm secondary to large pleural effusion.Chest1995;107,1610-1614. [CrossRef] [PubMed]
 
Perpina, M, Benlloch, E, Marco, V, et al Effect of thoracentesis on pulmonary gas exchange.Thorax1983;38,747-750. [CrossRef] [PubMed]
 
Karetzky, MS, Kothari, GA, Fourre, JA, et al Effects of thoracocentesis on arterial oxygen tension.Respiration1978;36,96-103. [CrossRef] [PubMed]
 
Agusti, AGN, Cardus, J, Roca, J, et al Ventilation-perfusion mismatch in patients with pleural effusion: effects of thoracentesis.Am J Respir Crit Care Med1997;156,1205-1209. [PubMed]
 
Light, RW, Jenkinson, SG, Vu-Dinh, M, et al Observations on pleural fluid pressures as fluid is withdrawn during thoracentesis.Am Rev Respir Dis1980;121,799-804. [PubMed]
 
Lan, R-S, Lo, SK, Chuang, M-L, et al Elastance of the pleural space: a predictor for the outcome of pleurodesis in patients with malignant pleural effusion.Ann Intern Med1997;126,768-774. [PubMed]
 
Dechman, G, Sato, J, Bates, JHT Effect of pleural effusion on respiratory mechanics, and the influence of deep inflation, in dogs.Eur Respir J1993;6,219-224. [PubMed]
 
Yaylali, YT, Nassar, NK, Manthous, CA Tension hydrothorax.South Med J1997;90,1156-1158. [CrossRef] [PubMed]
 
Pride, NB, Macklem, PT Lung mechanics in disease. Macklem, PT Mead, J eds.Handbook of physiology1986,659-692 American Physiological Society. Bethesda, MD:
 
Marini, JJ, Rodriguez, RM, Lamb, V The inspiratory workload of patient-initiated mechanical ventilation.Am Rev Respir Dis1986;134,902-909. [PubMed]
 
Estenne, M, Yernault, J-C, De Troyer, A Mechanism of relief of dyspnea after thoracocentesis in patients with large pleural effusions.Am J Med1983;74,813-819. [CrossRef] [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

CHEST Journal Articles
PubMed Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543