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* From the Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Medical University of South Carolina, Charleston, SC.
Correspondence to: Jay T. Heidecker, MD, Department of Pulmonary and Critical Care, Suite 812 CSB, 96 Jonathan Lucas St, PO Box 250630, Charleston, SC 29425; e-mail: heidej{at}musc.edu
Abstract
Study objectives: Pneumothorax following ultrasound-guided thoracentesis is rare. Our goal was to explain the mechanisms of pneumothorax following ultrasound-guided thoracentesis in a setting where pleural manometry is routinely used.
Methods: We reviewed the patient records and procedure reports of 401 patients who underwent ultrasound-guided thoracentesis. When manometry was performed, pleural space elastance was determined. A model assuming dependence of the pleural space elastic properties on respiratory system elastic properties was used to isolate cases with presumed normal pleural space elastance. Elastance outside mean ± SD x 2 of the isolated sample was considered abnormal. Four radiographic criteria of unexpandable lung were used: visceral pleural peel, lobar atelectasis, basilar pneumothorax, and pneumothorax with ipsilateral shift.
Results: There were 102 diagnostic thoracenteses, 192 therapeutic thoracenteses with pleural manometry, and 73 therapeutic thoracenteses without manometry. There was one pneumothorax that occurred from lung puncture and eight unintentional pneumothoraces, all of which showed radiographic evidence of unexpandable lung. Four of eight unintentional pneumothoraces had abnormal elastance; none had excessively negative pleural pressure (< –25 cm H2O).
Conclusions: Unintentional pneumothoraces cannot be prevented by monitoring for symptoms or excessively negative pressure. These pneumothoraces were drainage related rather than due to penetrating lung trauma or external air introduction. We speculate that unintentional pneumothoraces are caused by transient, parenchymal-pleural fistulae caused by nonuniform stress distribution over the visceral pleura that develop during large-volume drainage if the lung cannot conform to the shape of the thoracic cavity in some patients with unexpandable lung. These fistulae appear to be pressure dependent, and the resulting pneumothoraces rarely require treatment. Drainage-related pneumothorax is an unavoidable complication of ultrasound-guided thoracentesis and appears to account for the vast majority of pneumothoraces occurring in a procedure service.
Key Words: pleural manometry • pneumothorax • ultrasound-guided thoracentesis
Pneumothorax is the most common major complication of thoracentesis. The reference investigations12345678910111213 of postthoracentesis pneumothorax focused more on the identification of risk factors rather than pathogenesis. Multiple risk factors have been identified, such as needle type,1914 operator experience,4 presence of emphysema,11 previous thoracentesis,7 mechanical ventilation9 and even ultrasound guidance.13 Ultimately, any of these risk factors must be associated with a mechanism of inadvertent air entry into the pleural space. There are a limited number of pathways by which air can enter the pleural space. Air may enter the pleural space through the lung via a bronchopleural fistula or across the chest wall via the thoracentesis site. A bronchopleural fistula may be caused by direct penetrating lung trauma by the thoracentesis hardware itself or may be created by mechanical factors associated with fluid removal. Air entry via the chest wall may be through the hardware or directly through the wound created during hardware insertion. However, air entry via the thoracentesis site is unlikely due to the collapsibility of the puncture site.
Ultrasonography has been shown to be associated with a low frequency of postthoracentesis pneumothorax,810 and it is reasonable to assume that this is the result of a reduction in penetrating lung trauma.15 Ultrasonography controls one of the pathways leading to pleural air entry; by eliminating lung trauma as cause for a bronchopleural fistula, only air entry through hardware and as a consequence of fluid removal remain as possible mechanisms. Air entry through hardware is either intentional or due to operator error, which may be virtually eliminated by strict attention to technical detail.
The present study reports the findings from 401 thoracenteses performed in a setting where meticulous technique was employed to avoid direct lung injury and errors of equipment handling. In addition, pleural manometry was available, which provides an evaluation of mechanical factors during fluid removal.
Materials and Methods
Thoracentesis
The records of all thoracenteses performed by or under the supervision of study investigators (T.H., P.D.) from July 2001 to October 2004 were reviewed. Thoracenteses without postprocedure radiographs were excluded, and the remaining cases were reviewed for the presence of pneumothorax. Complications such as hemothorax, pneumothorax, hypotension, chest pain, and hypoxemia were recorded. The study was approved by the institutional review board for research integrity at our institution.
Technique
Thoracentesis by the pleural disease service in our procedure suite follows a standardized protocol. Thoracentesis is performed under ultrasound guidance (Sonosite Heart Elite; Sonosite; Bothell, WA) with the patient in an upright seated position. Patient position is not changed between ultrasound examination and needle insertion. The presence of fluid is documented by ultrasound dynamic signs including lung flapping, swirling motion of particulate matter in the pleural space, undulating motion of fronds and strands, or dynamic change in the shape of the pleural space during respiration. Accessibility is ascertained, and an access site is marked prior to thoracentesis. In the absence of dynamic signs, the collection may be accessed with a small-bore needle if clinically indicated to distinguish fluid from nondrainable material. Thoracentesis is performed in standard fashion with either a 21-gauge needle for a diagnostic thoracentesis or with a thoracentesis kit (Pleura-Seal; Arrow-Clark; Reading, PA) for therapeutic thoracentesis. Pleural manometry, using an electronic transducer system and a water manometer as described by Doelken and colleagues,16 is performed during most therapeutic thoracenteses. Briefly, the electronic manometer consists of the following in series: pleural catheter, a signal transducer (CDXPRESS 3cc 041576504a; Argon Medical; Athens, TX), a signal conditioner (CD 19A Carrier Demodulator; Validyne Engineering; Northridge, CA), and a personal computer-based data acquisition system (Biobench; National Instruments; Austin, TX). The electronic system is calibrated against a water standard. A water manometer is used in parallel to the electronic manometer during most of the therapeutic thoracenteses. The decision to perform manometry is at the discretion of the clinician performing the procedure.
During therapeutic thoracentesis, complete drainage of the pleural space is usually performed unless curtailed by significant chest pain, hypotension, or a drop in pleural pressure < – 25 cm H2O. When manometry is performed, 100-mL or 250-mL aliquots are removed and pleural pressures measured and recorded following each aliquot. The syringe pump method is employed for fluid withdrawal, allowing precise volumes to be withdrawn. Pleural pressure signals are recorded with the goal to measure at least four respiratory cycles with end-expiratory pressure returning to baseline, indicating quiet breathing with end-expiratory return to functional residual capacity.
Intentional Pneumothorax
During removal of fluid, some patients with negative pleural pressure have significant chest pain. In these patients, we allow air to enter the pleural space to alleviate the pain. This maneuver is termed a therapeutic pneumothorax and is documented in the record.
In patients in whom malignant disease is not suspected who have excessively negative pressures and/or chest pain during drainage with significant remaining fluid, we routinely replace the fluid with air in order to obtain air-contrast CT for the detection of pleural thickening or lobar atelectasis. The air is allowed to enter under manometric control, and the pressure is adjusted to subatmospheric values prior to catheter removal. These pneumothoraces are recorded as diagnostic pneumothoraces.
In all patients with diagnostic pneumothoraces as well as in six of the eight patients with unintentional pneumothoraces detected by postprocedure chest radiography, CT scans were performed. The presence of the following radiographic signs was assessed by an independent radiologist in all patients with pneumothorax: ipsilateral volume loss, defined as a smaller size of the hemithorax containing the pneumothorax in comparison to the contralateral hemithorax; basilar pneumothorax, defined as a pneumothorax present in the inferior lung fields on an upright chest radiograph; visceral pleural peel, defined as a visible visceral pleural line > 1 mm in thickness; and lobar atelectasis, defined as complete atelectasis of a lung lobe seen on CT scan.
Pleural Pressure Data Analysis
Mean pleural pressure measurements during four consecutive respiratory cycles in which the end-expiratory pressure returns to a baseline are analyzed for each aliquot of fluid drained. Mean pleural pressures are the average of dynamically changing pressures during the respiratory cycle and the results of subsequent calculations (see below) are therefore dynamic values.17
Analysis of Pleural Space Pressure/Volume Curves
The manometry curves of each effusion are plotted in SigmaPlot 8.0 (Systat Software; Richmond, CA). In order for a data point to be included, documentation of residual fluid by ultrasonography or documentation of at least 30 mL of fluid drained after the pressure measurement is required. Therefore, artifactual pressure measurements from geometric interaction of the lung and chest wall due to imperfect fit at the end of drainage are excluded. A pleural pressure volume curve may have up to three clearly distinguishable phases separated by inflections. There may be an initial steep section (E0) in tension hydrothoraces followed by a less steep section (E1), occasionally followed by another steep section (E2) during the last part of drainage. Monophasic curves only have E1, which may show a steep or shallow slope. Biphasic curves may have E0 and E1 or E1 and E2, depending on the initial slope in relation to the slope after the first inflection (E0 > E1 < E2). The designations E0, E1, and E2 refer to the slope, and therefore elastance, at different sections of the pressure/volume curve. The sections are identified by visual inspection of the pressure/volume plots, and slopes are subsequently calculated using the volume change over the section. The possible sections of the elastance curve are shown in Figure 1
. Descriptive statistics such as mean, SD, median, percentiles, and student unpaired t tests for elastance values E1 and E2 and symptoms, such as chest pain and cough, are calculated using Excel (Microsoft; Redmond, WA) and SigmaPlot (Systat Software).
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2 distribution, respectively. We defined the normal range of pleural elastance based on this isolated statistical sample. Results
A total of 401 thoracenteses were performed or supervised by two physician sonographers between July 2001 and September 2004. Of these 401 thoracenteses, 367 cases with postprocedure chest radiographs were included in the review. One hundred two thoracenteses were performed with a small-bore (21-gauge) needle, and < 100 mL of fluid was withdrawn (diagnostic thoracenteses). In four of these cases, ultrasonography revealed a hypoechoic region consistent with fluid but without dynamic sonographic signs confirming the presence of fluid. Diagnostic thoracentesis was performed, but no fluid was obtained. An 8F catheter was used in the remaining 265 cases with the intention to drain the pleural space (therapeutic thoracenteses). Figure 2 depicts all types of thoracenteses performed, excluded cases, and relevant outcomes.
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Postprocedure pneumothorax is a rare complication of ultrasound-guided thoracentesis. Our case series documents its absence with diagnostic thoracentesis when ultrasonography is employed in a controlled setting with expert supervision. Small-bore needles are used for all diagnostic thoracenteses in our practice. In the present study, two differences between the diagnostic and therapeutic thoracenteses were needle size and volume of fluid removed. The use of smaller needles has been shown to result in a lower pneumothorax rate,9 possibly because trauma from an inadvertent lung puncture is of less consequence compared to trauma from a large-bore needle. An unexpandable lung will not manifest itself as a postprocedure pneumothorax without a substantial volume change of the pleural space, excluding unexpandable lung as a factor for the development of postprocedure pneumothorax with diagnostic thoracentesis. We suspected from our clinical experience that unexpandable lung may be the major patient-related factor for the development of postprocedure pneumothorax.
There were 14 intentional pneumothoraces in which air was allowed to enter the pleural space for the purpose of performing an air-contrast CT for the radiologic confirmation of unexpandable lung or to relieve chest pain in patients thought due to unexpandable lung. The intentional pneumothoraces are not considered procedure-related complications but simply represent air entry through the drainage hardware. An explanation is required for the remaining eight pneumothoraces, as no air was introduced. The most plausible cause is the development of a peripheral parenchymal-pleural fistula. Air entry through a peripheral parenchymal-pleural fistula as a consequence of pleural fluid removal in the absence of penetrating lung trauma implies the presence of one or more patient related factors favoring fistula development. The most likely factor is the lung failing to expand normally during thoracentesis.
Previous investigators have suggested unexpandable lung as the main cause of pneumothorax after ultrasound guided thoracenteses. Chest CT in 17 cases revealed evidence of a lung mass, atelectasis, and/or lymphangitic spread of cancer; and the pleural air was eventually replaced by reaccumulation of pleural effusion.18 Attempts at evacuation of some these pneumothoraces with chest tubes under controlled suction were unsuccessful in most cases. The authors18 concluded that treatment of these pneumothoraces was rarely needed. In another study, 28 of 88 patients (31%) had a pneumothorax after small-bore tube insertion into malignant pleural effusions, and their pneumothoraces appeared to be associated with unexpandable lung. The pneumothoraces in this series either resolved slowly or not at all but were not associated with respiratory distress or progression.19
In our series of patients, all eight unintentional pneumothoraces had radiographic evidence of unexpandable lung. Six patients demonstrated a visceral pleural peel or adhesions, one had chronic lower lobe atelectasis, and one had bullous emphysema of the upper lobe with an obstructing endobronchial lesion of the lower lobe. Table 4 shows the radiographic features associated with these patients. Interestingly, in the unintentional pneumothoraces, visceral pleural peel was by far the most common radiographic finding similar to the intentional pneumothoraces (Table 3).
Our experience is similar to previous case series in that radiographic evidence of unexpandable lung is present in all cases of "nontraumatic" postprocedure pneumothorax. Intuitively, one could assume that unexpandable lung should result in excessively negative pleural pressure during fluid withdrawal and that postprocedure pneumothorax from unexpandable lung can be prevented if pressure is monitored. However, this does not always appear to be true, as our cases of unintentional pneumothoraces occurred despite pleural manometry and diligent avoidance of excessively negative pressures. One explanation for this phenomenon may be that pleural pressures are measured intermittently and excessively negative pressures may have occurred but were not measured during the withdrawal of the last aliquot, prior to the development of pneumothorax. An alternative explanation is the development of locally excessive tension and shear forces acting on some areas of the visceral pleura when the lung cannot conform to the shape of the thoracic cavity because of unexpandable lung. Under these conditions of "shape mismatch," the relative uniformity of forces acting on the visceral pleura in the normal physiologic condition may be replaced by significant tension or distortion and localized failure of the visceral pleura may be more likely. The typical finding with manometry when an unintentional pneumothorax develops is recovery of air from the pleural space and an unexpected increase in pleural pressure. Interestingly, the pleural pressure usually remains negative and is relatively constant. A case illustrating this phenomenon is shown in Figure 7 . Despite further withdrawal of fluid the pressure will usually return to the same slightly negative value as a peripheral parenchymal-pleural fistula allows air entry into the pleural space abating the pressure gradient. This phenomenon implies a pressure-dependent parenchymal-pleural fistula and may account for the absence of a progressively enlarging pneumothorax and need for chest tube drainage.
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As the normal range of pleural space elastance has not been documented, we isolated the presumably normal cases using a quantitative and qualitative approach. We assumed that normal pleural space mechanics are determined by overall respiratory system mechanics, provided that geometric distortion is not a factor. This condition may be met with the presence of a small amount of pleural effusion. In experimental hydrothorax, the critical volume is seen at the terminal deflection of the pressure volume curve of the pleural space.20 In the present investigation, care was taken to assure the presence of residual fluid in the pleural space. With the above assumption, pleural space elastance can be predicted from normal respiratory system elastance. The predicted maximal pleural space elastance for a relatively stiff respiratory system with a compliance of 40 mL/cm H2O was calculated as 15.5 cm H2O/L and the expected mean pleural space elastance was calculated as 7.44 cm H2O/L for a respiratory system with normal compliance (100 mL/cm H2O)21 and a ratio of lung and chest wall compliance of 1/2.22
Because of the linearity of the pressure/volume relationship of lung and chest wall around functional residual capacity, linearity of the pressure volume curve of the normal pleural space can also be expected. Our model, therefore, provides a rationale for excluding measurement sets based on quantitative and qualitative criteria, ie, elastance values and linearity of the pressure volume curve throughout the drainage interval.
Based on the model, 124 E1 values meeting the criteria of an elastance < 15.5 cm H2O/L, linear curve characteristics, and absence of radiographic signs of unexpandable lung (visceral pleural peel, basilar pneumothorax, ipsilateral volume loss, or lobar atelectasis) were extracted. The sample was found to have a Gaussian (normal) distribution and a mean elastance of 7.5 ± 3.5 cm H2O/L (mean ± SD). The distribution is typical for a respiratory mechanics parameter, and the numeric results are in close agreement with the model prediction; therefore, we defined the normal range of pleural elastance to be 0.5 to 14.5 cm H2O/L (mean ± 2 SDs).
The model describes the lung and chest wall as ideal distensible reservoirs; however, the close geometric fit of lung and chest wall may be disturbed by visceral pleural disease, endobronchial obstruction, and possibly severe pulmonary parenchymal fibrosis causing restriction of regional lung expansion. While the normal lung behaves like a semisolid, readily filling the thoracic cavity, the chest wall is geometrically more restricted and cannot conform to the shape of the diseased, distorted lung. Under these conditions, the pleural space elastance is expected to be elevated. A different situation occurs when a large part of the lung is involved with the visceral pleural restriction. Once the lung has achieved its maximal restricted volume and there is no contact with the chest wall; the chest wall will change shape according to its degrees of freedom, and the pleural space elastance becomes essentially the chest wall elastance. Thus, the hemithorax should be expected to behave like a pneumonectomy space that may have pleural elastance in the normal range.
In another scenario, when sufficient fluid accumulates from an active process, the lung will develop relaxation atelectasis, in addition to visceral pleural restriction. In this situation, an inflection of the pleural pressure/volume curve will be seen with two distinctly different slopes, E1 and E2. The inflection point is distinct because an increase of lung elastance occurs once the relaxation atelectasis has resolved during drainage causing a significant increase in the forces required to deform the pleural space boundaries. An example is shown in one of our patients with unexpected pneumothorax, Figure 7. This type of pressure/volume curve may be seen in malignancy with lung entrapment, complex parapneumonic effusion or empyema with lung entrapment or heart failure with coexisting trapped lung.23 Based on our model, E1 in biphasic cases is expected to be in the normal range representing resolution of relaxation atelectasis and E2 is expected to be abnormally high. As predicted by the model, comparison of E1 in the monophasic population (mean elastance, 7.51 ± 3.44 cm H2O/L) with E1 in the biphasic population shows excellent quantitative agreement and reveals a normally distributed E1 in the biphasic group with a mean elastance of 7.44 ± 4.57 cm H2O/L.
The relationships among cough, chest pain, and pleural elastance are shown as box plots of median and 25th to 75th percentiles (Fig 6). Interestingly, cough mirrors the elastance distribution for those patients found to have normal elastance. Thus, the symptom of cough appears to be related to resolution of relaxation atelectasis, which is also supported by clinical experience and observation with ultrasound during thoracenteses and confirms the findings of Feller-Kopman and colleagues.24
In 13 cases of pneumothorax, evidence of unexpandable lung became apparent during drainage through the development of dull chest discomfort and/or excessively negative pressure during drainage, and the pneumothorax was subsequently induced for diagnostic purposes. In all 13 cases, radiographic evidence of unexpandable lung was subsequently demonstrated.
In eight cases, however, neither symptoms nor excessively negative pressure prompting the discontinuation of drainage were noted at the time of the procedure. In four of eight cases, elevated pleural elastance was present, leaving four cases of unintentional pneumothorax in which manometry did not detect any abnormality prior to the development of the pneumothorax. This was in spite of the fact that radiologic criteria of unexpandable lung were present in all cases. It may be that local failure of the pleura from excessive local force development occurred even before pleural pressure was affected, or, alternatively, that during withdrawal of the last aliquot, excessive pressure drops did occur but remained undetected because of air entry into the pleural space.
Our results raise the question how pleural manometry impacts the development of unintentional pneumothorax during thoracenteses. Overall, there were 10 thoracenteses in which drainage was terminated in the asymptomatic patient based on excessively negative pleural pressure. We speculate that some of these patients may have had pneumothoraces if drainage had been continued; or chest discomfort may have developed later, prompting termination of drainage. Alternatively, the effusions may have been drained completely without any adverse effects. An interesting possibility is suggested by the four unintentional pneumothoraces in patients with abnormally high elastance in the absence of excessively negative pressure. It is possible that the pneumothoraces may have been prevented if elastances had been calculated during the procedure. However, this was not possible at the time as the range for normal pleural space elastance was not known.
Conclusion
The approximate normal range of pleural space elastance in a typical population referred for thoracenteses as determined in this study may serve as a starting point for further investigations. Our simple model, if our assumptions can be maintained, would allow for calculation of expected pleural space elastance in the individual patient if the predicted respiratory system compliance was known.
We have shown that the vast majority of radiographically detectable pneumothoraces after ultrasound-guided thoracenteses in a controlled setting are drainage related and caused by unexpandable lung. The existence of drainage-related pneumothoraces and their distinction from traumatic pneumothoraces was suspected by previous investigators.181925 Based on our findings and the reports of these authors, we propose that the mechanism for pneumothorax in the majority of patients with properly performed ultrasound-guided thoracentesis is drainage related and should be differentiated from traumatic pneumothoraces. Although we use the syringe pump method for drainage and vacuum bottles are commonly used in clinical practice, our results may well apply to both techniques, as we do not limit the negative pressure applied to the syringe plunger during drainage. Drainage-related pneumothoraces cannot be completely avoided with the employment of pleural manometry, and radiologic criteria appear to be the appropriate means to determine the cause of pneumothorax after thoracentesis. This information has implications for quality control for a thoracentesis service, and we recommend investigating any "unexpected" pneumothorax for the presence of unexpandable lung. These cases must be identified in order to identify pneumothoraces from operator error, which are amenable to quality intervention.
Appendix
Mathematical Model of Normal Pleural Space Elastance
The following assumptions are made for the model:
(1) Pleural space mechanics reflect global respiratory system properties;
(2) Hydrostatic effects of pleural fluid are not considered;
(3) Mechanical properties of each hemithorax are considered equal;
(4) Geometric interaction of lung and chest wall is not considered.
The following abbreviations are used: C = compliance; Cst = static compliance; Cst,cw = static chest wall compliance; Cst,l = static lung compliance; Cst,pl = static pleural space compliance; Cst,rs = static respiratory system compliance; E = elastance; Ecw = chest wall elastance; Edyn,pl,hemithorax = dynamic pleural elastance of a hemithorax; Edyn,rs = dynamic respiratory system elastance; El = lung elastance; Epl = pleural space elastance; Ers = respiratory system elastance; Est = static elastance; Est,cw = static chest wall elastance; Est,l = static lung elastance; Est,pl = static pleural space elastance; Est,pl,hemithorax = static pleural elastance of a hemithorax; Est,pl,left = static left pleural space elastance; Est,pl,right = static right pleural space elastance; Est,rs = static elastance of respiratory system.
Physiologic Calculations
Partitioning of the respiratory system; two elastic elements in parallel:
(1) Est,rs = Est,l + Est,cw.
Pleural space; two elastic elements in series:
(2) Cst,pl = Cst,l + Cst,cw.
Because of E = 1/C,
Est,pl = 1/(Cst,l + Cst,cw),
and
(3) Est,pl = 1/(1/Est,l + 1/Est,cw).
Because of equation (1),
(4) Est,pl = 1/(1/(Est,rs – Est,cw) + 1/Est,cw).
Equation (4) is a function with a maximum (for Est,rs > 0) at
Est,rs – Est,cw = Est,cw,
or
(5) Est,rs/2 = Est,cw.
Solving equation (4) using equation (5),
Est,pl = 1/(1/Est,rs/2 + 1/Est,rs/2),
or
(6) Est,pl = Est,rs/4
for the maximum Est,pl at a given Est,rs.
The pleural space is anatomically divided into two reservoirs that may be modeled as two elastic elements in series. Thus, relation of the overall pleural elastance to the pleural elastance of each hemithorax is as follows:
(7) 1/Est,pl = 1/Est,pl,right + 1/Est,pl,left.
Assuming the pleural space elastances of the right and left hemithorax are equal, then
1/Est,pl = 2/Est,pl,hemithorax;
thus,
Est,pl = Est,pl,hemithorax/2,
and
(8) Est,pl,hemithorax = 2Est,pl.
Using equation (6),
Est,pl,hemithorax = Est,rs/2.
The solution represents the maximum static pleural space elastance of one hemithorax for a given static respiratory system elastance because of equation (4). Pleural space elastance calculated using mean pleural pressure results in an overestimate of 3 cm H2O/L over static pleural space elastance.17
Thus, maximum dynamic pleural space elastance (Edyn,pl, hemithorax) becomes:
(9) Edyn,pl,hemithorax = Est,rs/2 + 3 cm H2O/L.
Solving equation (9) for a respiratory system with a static compliance of Cst,rs = 40 mL/cm H2O, which is actually a fairly stiff, noncompliant respiratory system yields:
Edyn,pl,hemithorax = 15.5 cm H2O/L,
as the maximum predicted dynamic pleural space elastance for one hemithorax in the model.
For computation of the mean dynamic elastance, we select a value of 100 mL/cm H2O for mean normal respiratory system compliance.21 In the linear section of the pressure/volume curve of the respiratory system, the chest wall is approximately twice as compliant as the lung22; therefore, the elastance of the lung is twice the elastance of the chest wall:
(10) Est,l = 2Est,cw.
In calculation of the normal mean pleural elastance, we use equation (2) using the value of 0.1 L/cm H2O for compliance of the respiratory system. Thus,
Est,rs = 1/0.1 L/cm H2O = 10 cm H2O/L.
Solving for Est,rs with equation (1):
10 cm H2O/L = Est,l + Est,cw; using equation (10),
10 cm H2O/L = 2Est,cw + Est,cw;
thus,
Est,cw = (10 cm H2O/L)/3 = 3.33 cm H2O/L;
and using equation (10),
Est,l = 6.66 cm H2O/L.
Using our values for Est,l and Est,cw, we can solve for the normal Est,pl using equation (3):
Est,pl = 2.22 cm H2O/L; and using equation (8),
Est,pl,hemithorax = 4.44 cm H2O.
Given that dynamic elastance is 3 cm H2O/L higher than static elastance,17 the mean dynamic measured pleural elastance in a group of normal adults should be 7.44 cm H2O/L with a maximal value of 15.5 cm H2O/L if the model assumptions are suitable.
Acknowledgements
We would like to acknowledge James G. Ravenel, MD, Professor of Radiology, Medical University of South Carolina. Dr. Ravenel provided radiographic interpretation of the chest radiographs and CT scans of the patients with pneumothoraces; Lisa K. Kaiser, BS, Respiratory Therapist, Medical University of South Carolina. Ms. Kaiser performed or assisted in almost all pleural manometry procedures and provided technical expertise in all aspects of pleural manometry; and Bronchoscopy Staff, Medical University of South Carolina. The bronchoscopy staff provided a controlled, efficient environment for pleural interventions allowing assessment of outcomes, fidelity of data collection and, above all, patient safety and comfort.
Footnotes
Abbreviation: CI = confidence interval
None of the authors have any conflicts of interests to disclose.
Received for publication January 5, 2006. Accepted for publication March 20, 2006.
References
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