Pneumothorax effects on pulmonary acoustic transmission
Hansen A. Mansy,1 Robert A. Balk,2 William H. Warren,3 Thomas J. Royston,4 Zoujun Dai,5 Ying Peng,5
and Richard H. Sandler1
1Department of Mechanical and Aerospace Engineering and Department of Pediatrics, University of Central Florida,Orlando, Florida; 2Division of Pulmonary and Critical Care Medicine, Rush Medical College, Chicago, Illinois; 3Departmentof Cardiovascular-Thoracic Surgery, Rush Medical College, Chicago, Illinois; 4Department of Bioengineering, University ofIllinois at Chicago, Chicago, Illinois; and 5Department of Mechanical Engineering, University of Illinois at Chicago,Chicago, Illinois
Submitted 23 February 2015; accepted in final form 26 May 2015
Mansy HA, Balk RA, Warren WH, Royston TJ, Dai Z, Peng Y,Sandler RH. Pneumothorax effects on pulmonary acoustic transmis-sion. J Appl Physiol 119: 250–257, 2015. First published May 28,2015; doi:10.1152/japplphysiol.00148.2015.—Pneumothorax (PTX)is an abnormal accumulation of air between the lung and the chestwall. It is a relatively common and potentially life-threatening con-dition encountered in patients who are critically ill or have experi-enced trauma. Auscultatory signs of PTX include decreased breathsounds during the physical examination. The objective of this explor-atory study was to investigate the changes in sound transmission in thethorax due to PTX in humans. Nineteen human subjects who under-went video-assisted thoracic surgery, during which lung collapse is anormal part of the surgery, participated in the study. After subjectswere intubated and mechanically ventilated, sounds were introducedinto their airways via an endotracheal tube. Sounds were then mea-sured over the chest surface before and after lung collapse. PTXcaused small changes in acoustic transmission for frequencies below400 Hz. A larger decrease in sound transmission was observed from400 to 600 Hz, possibly due to the stronger acoustic transmissionblocking of the pleural air. At frequencies above 1 kHz, the soundwaves became weaker and so did their changes with PTX. The studyelucidated some of the possible mechanisms of sound propagationchanges with PTX. Sound transmission measurement was able todistinguish between baseline and PTX states in this small patientgroup. Future studies are needed to evaluate this technique in a widerpopulation.
pneumothorax; acoustic; transmission
PNEUMOTHORAX IS AN ABNORMAL accumulation of air in thepleural space that can result in lung collapse (3, 4, 17).Pneumothorax (PTX) is a relatively common disorder that ispotentially life-threatening, yet treatable with timely diagnosis.More than 20,000 cases of PTX are reported each year in theUnited States, with an estimated cost of �$130,000,000 (4).PTX can develop spontaneously or it can result from trauma orinvasive procedures (34). Spontaneous pneumothoraces areeither primary (i.e., those occurring without obvious cause orunderlying lung disease) or secondary, which develop in pa-tients with underlying lung disease (4, 34). Primary spontane-ous PTX incidence is estimated to be 7.4/100,000 in men and1.2/100,000 in women (29), whereas secondary spontaneousPTX incidence is about 6.3/100,000 in men and 2.0/100,000 inwomen (27). Traumatic PTX is a common encounter withchest injury and occurs in about 20% and 40% of patients withblunt and penetrating trauma, respectively (11).
PTX is also a recognized complication during positive pres-sure ventilatory support (6, 10, 17, 42). Delayed PTX diagnosisand treatment, especially for patients with mechanical ventila-tion, may lead to PTX progression and hemodynamic instabil-ity (5, 12). PTX diagnosis involves evaluating a combination ofmedical history, physical examination, and chest imaging (2, 7,13, 15, 41). History and physical examinations generally lacksensitivity and specificity (21, 27, 28).
Standard portable end expiratory upright chest X-rays arenot always sufficiently sensitive to diagnose PTX (30, 37). Itwas also reported that 30% of 112 pneumothoraces in 88patients who were critically ill were not detectable by routinechest radiographs (41). Another study found 12 patients withunsuspected or untreated tension pneumothoraces (10 of whomwere on positive pressure ventilatory support) among 3,500autopsies (26). In addition, chest X-rays are not always readilyor immediately available and require patient positioning andtiming of respiration to enhance pneumothorax detection. Con-sequently, chest computed tomography (CT) scans have be-come the gold standard for PTX detection (34). The superiorityof a chest CT is, however, offset by expense, increased radia-tion exposure, lack of immediate availability (especially insituations of forward trauma, combat, ambulance, and otheremergency or lower technology settings), and need for patienttransport to the CT scanner (16, 43).
The use of thoracic ultrasonography for PTX detection hasbeen gaining popularity and some now consider the techniqueto be a new gold standard with the advantages of being quickand relatively easy to perform (20). During this test, theabsence of signs of visceral pleural movement (e.g., lungsliding and lung point signs) are suggestive of the presenceof PTX (25). However, the absence of these signs can beobserved in patients with lung fibrosis or pleural adhesionwithout PTX (38).
Misdiagnosis or delayed diagnosis of pneumothoraces incritically ill patients may have severe consequences (2).Several studies suggested that additional tools for PTXdetection and monitoring would be helpful (14, 25, 27, 28,31,39, 40, 44, 48).
Sound transmission in the respiratory system has been stud-ied by many investigators (23, 24, 27, 33, 46, 47). Althoughsome studies have suggested that properties of the thoracicstructures can significantly affect transmission (47), other stud-ies in healthy volunteers (24) reported no changes in peakamplitude or frequency with changes in lung volume or resi-dent gas. More recent investigations (9, 18, 22, 27, 28, 33, 36,46) have demonstrated that certain respiratory system changeshave acoustic correlates. This suggests that only certain (and
Address for reprint requests and other correspondence: H. A. Many, 12760Pegasus Drive, Rm 308, Dept. of Mechanical and Aerospace Engineering,Univ. of Central Florida, Orlando, FL 32816 (e-mail: [email protected]).
J Appl Physiol 119: 250–257, 2015.First published May 28, 2015; doi:10.1152/japplphysiol.00148.2015.
not all) acoustic variables may correlate with respiratory con-ditions and, hence, a high degree of care in data collection andanalysis need to be taken to identify the useful acousticcorrelates of individual pulmonary conditions.
In the current study we hypothesize that the presence of airin the pleural space causes measureable changes in the acousticproperties of the chest structures. Because the acoustic prop-erties of air are significantly different from those of the chestwall tissue and the lungs, acoustic impedance mismatch willoccur at the boundaries of the pleural air pocket. This mis-match will impose acoustic barriers to sound waves and,consequently, cause acoustic transmission changes. This sce-nario was found to cause sound transmission reduction withPTX in earlier animal studies (25, 31). Acoustic changes, ifproven to correlate with the presence of PTX, may serve as anadjuvant patient-monitoring tool with potential operationaladvantages that include being radiation-free, low-cost, provid-ing rapid test results, and having potential utility for continuouspatient monitoring. Although this potential may prove useful inthe future, the authors stress that the objective of this study isto document possible acoustic correlates of PTX and not to testa clinical tool, which would be a possible objective of futureinvestigations.
MATERIALS AND METHODS
This study was approved by the Rush University Medical CenterInstitutional Review Board. Patients were enrolled in the study afterproviding consent. Subjects were recruited from those who were toundergo video-assisted thoracic surgery (VATS) as part of theirnormal care, during which a PTX is induced as a usual part of theprocedure. Patients were sedated and intubated in the usual mannerwith a double-lumen endotracheal (ET) tube. Patients rested on theirnonoperative side with the operative side up, and were ventilated atthe normal rate and tidal volume as deemed appropriate by theattending anesthesiologist.
The experimental setup is shown in Figure 1. A sound source wasconnected to the ventilator tubing via a T-connector, which wasattached to the circuit a few centimeters from the proximal separationof the channels of the double-lumen endotracheal tube. The T-con-nector added a negligible volume (�3 ml) of dead air space to theventilator circuit. The sound source was made of an electromagneticspeaker (Harman Kardon, Mill Valley, CA) that was installed in asealed polyvinyl chloride plastic chamber that was isolated from theventilator circuit via a viral and bacterial filter (Airlife; AllegianceHealthcare, McGaw Park, IL). This system was made air-tight toensure negligible airflow in the tubing that connects to the soundsource. The excitation signal amplitude did not significantly contrib-ute to room noise because it was minimally noticeable in the operatingroom. Similar excitation levels were used in previous studies (1, 8,27). Breathing was not interrupted during sound recording.
An electronic stethoscope (model 04-1060; Labtron Electromax,Hauppauge, NY) was used to record sounds at the chest surface at theintersection of the midaxillary and nipple lines. This location wasapproximately 5–10 cm from the incision site, where the thoracoscopewas to be inserted. The stethoscope was enclosed in a sterile bagbefore placement over the chest surface and was held in place by theattending surgeon or fellow. To measure transpulmonary acoustictransmission, sounds sensed by the stethoscope were recorded for 20s using a digital recorder (model D888; Korg, Japan) while band-limited white noise (50-2,000 Hz) was introduced into the ET tube.Sound recording was performed before PTX was induced. Surgerywas then started, and a PTX was created in the usual manner. After thepresence of a PTX was confirmed using the thoracoscope, the scopewas removed and the incision was covered by Tagaderm to avoid
varying the PTX air volume during the breathing cycle. The stetho-scope was then placed in the same position and sounds were againrecorded for 20 s while the sound source introduced the band-limitedwhite noise into the ET tube. During each sound recording, theelectronic stethoscope output was monitored using the digital re-corder. The amplifier for the input signal was kept at the same settingthroughout each experiment. The recorder saved the acoustic data inthe “wav” file format for post processing. Saved files were transmittedto a computer via the recorder USB port. Sound files were postpro-cessed using a digital signal-processing software package (Matlab;Mathworks, Natick, MA). The sound files contained 20 s of datasampled at 8,192 Hz, resulting in about 164,000 sample for each datafile. The data processing protocol included band-pass filtering (50-1,600 Hz pass band) and spectral analysis using Fast Fourier Trans-form followed by smoothing the spectral curves by a moving averagefilter.
To calculate the power spectral density of the measured signal [x(j),j � 1, 2, 3, . . . , N] that contains N points, we first calculate thediscrete Fourier transform from:
where X(k) is the complex Fourier Transform and k is the index offrequency bins.
The power spectral density, Pxx, is then estimated from:
Pxx�k� � 10 log10� 2
NFs� ��X�k���2�; k � 2, 3, 4, . . . ,
N
2
and
Pxx�k� � 10 log10� 1
NFs� ��X�k���2�; k � 1,
N
2� 1
where these k values correspond to the zero and Nyquist frequencies,respectively, and Fs is the sampling frequency.
Spectral smoothing was performed through a moving averageapproach, which was implemented using a finite impulse-response
A
B
Digital player and recorder
Electronic Stethoscope
Air-tight sound source and filter
To ventilator
Fig. 1. A: experimental setup showing sensor position, and sound source anddata acquisition equipment connections. B: raw and smoothed power spectraldensity for a typical case of pneumothorax. Note the smooth spectra haveconserved the main spectral features.
251Pneumothorax and Acoustic Transmission • Mansy HA et al.
filter. The filter output was calculated from the discrete convolutionformula:
y�n� � �i�0M bix�n � 1�
where y and x are the filtered and unfiltered spectra, bi is the filterweight (i.e., impulse response at the ith instant), and M is the filterorder. In the current study, M was chosen as 5, and bi � 1/M. Thisfiltering was performed in the upward (i.e., from low to high fre-quency) and then in the downward (high to low frequency) directionsto avoid shifting the spectral peaks.
To quantify the effect of PTX on acoustic transmission at differentfrequencies, the difference in the power spectral density (PSD) be-tween the control and PTX states was calculated. The signal energy incertain frequency bands was also calculated. This was performed byadding the PSD values in the frequency bands under consideration.Energy ratios between the different bands were calculated by dividingthe energy values corresponding to the bands of interest. The spectraltrends were compared using the Wilcoxon rank sum test, with a valueof P � 0.05 indicating significance.
RESULTS
During the course of the study, no significant additionalinterventions were performed for the sole purposes of theexperiment. The main extra needed steps were to connect thesound source, input sounds, and record transmitted sounds atthe chest wall using an electronic stethoscope for 20 s beforeand after lung collapse. All patients exhibited pulmonarypathology. Out of the participating patients, 15 had lungmasses and 4 had lung nodules, 1 of whom also had breastcancer. The operative side was the left side in 10 patients andthe right in 9. This information was taken into consideration bythe attending anesthesiologist when choosing the appropriatedouble-lumen ET tube type (i.e., left- vs. right-sided). Notice-able lung collapse was observed. The air space between thelung surface and chest wall around the sensor location wasvisually estimated to be �2 cm [which is considered a largePTX (19)] in 18 patients and appeared to be �1 cm in onepatient (possibly due to pleural adhesions in the latter case).
An example of the raw and smoothed power spectral den-sities of the transmitted sounds is shown in Figure 1B. Thespectral plot shows that smoothing did not significantly changethe main spectral features. Data for other patients demonstratedsimilar trends.
The spectra of the control and PTX states for all subjectsare shown in Figure 2A, and the mean spectra acrosssubjects are shown in Fig. 2B, with error bars showing the95% confidence interval. Intersubject variability is evident inFig. 2A, but there are common trends. The first trend is a generaldecrease in transmitted sounds as the frequency increases for boththe control and PTX states. Second, the occurrence of PTXseemed to be associated with a drop in sound amplitude, whichwas more noticeable in the mid-frequency (400–900 Hz) range(P � 0.01, Wilcoxon signed rank test).
Figure 3A shows the drop in acoustic spectra when lungcollapse took place relative to the control state. This wascalculated as the difference between the solid and dashed linesin Fig. 2A. The spectral energy for the PTX state was lowerthan that of the control state in most of the frequency ranges ofinterest, but it was higher than the control state for relativelynarrow frequency values that varied among patients. The meanspectral drop with PTX is shown in Fig. 3B with error barsmarking the 95% confidence interval. This figure suggests that,
in the average, the spectral energy drop with PTX is morepronounced in the 400–600 Hz frequency range. The maxi-mum and mean PSD drop in the 400–600 Hz frequency bandis shown in Fig. 4, A and B, respectively, and the maximumspectral increase with PTX is shown in Fig. 4C. In thisfrequency range, no spectral increase with PTX was observed,suggesting that energy increases with PTX took place onlyoutside that frequency band. Some amplitude increase withPTX was observed in computer simulations of a similar phe-nomenon and may be due to resonances (33) that would occurat different frequencies for different subjects as was observedin the current study.
Figure 3, A and B, shows that the PSD drop with PTX tendedto be more pronounced in a certain frequency range (e.g.,around 400–600 Hz) and was smaller at lower and higherfrequencies. A ratio between the acoustic energy of the mid-frequency (e.g., 400–600 Hz) and low-frequency (50–250 Hz)bands was proposed for animal subjects (27) and was calcu-lated in the current study as ER21 � energy in mid-frequencyband � energy in the low-frequency band. In addition, asecond energy ratio between the mid- and high-frequency(1,300–1,500 Hz) bands was also calculated as ER23 � energyin midfrequency band � energy in the high-frequency band.These energy ratios are shown in Fig. 5A, which demonstratesa trend toward a reduction in energy ratios with PTX (P �0.01, Wilcoxon signed rank test). The change in energy ratioswith PTX is shown in Fig. 5B, which demonstrates that a dropin energy ratios in PTX states occurs relative to controls. Thecase with the least drop in energy ratio corresponds to thepatient with the smaller air gap between the lung and chestwall.
DISCUSSION
The current study investigated the effects of PTX on acous-tic transmission through the chest in patients with pulmonaryconditions such as lung nodules and masses. To perform thesemeasurements, controlled acoustic signals with low amplitudewere introduced via an ET tube into the airways of subjects.The excitation amplitude was minimally noticeable in theoperating room and did not interfere with clinical activities.Similar sound transmission measurements were used in previ-ous studies to monitor lung conditions in which broad-bandsounds are usually introduced via ET tubes. It is to be notedthat the acoustic transmission properties of these tubes canaffect the actual signal input to airways. A careful study (35) ofsound transmission in ET tubes documented the existence ofspectral peaks and valleys (at the ET tube tip) that are depen-dent on ET tube length and diameter changes.
In the current study the spectra of the sound delivered intothe airways were calculated from the acoustic signal measuredover the neck of one patient. The results showed a spectraluniformity of �3 dB in the 100–1,600 Hz range. This spectralvariability is relatively low, possibly because of the smalldiameter changes (�25%) in our sound-delivery ducts includ-ing the ET tube. This variability value is also comparable to thetheoretical estimates at the tip of the endotracheal tube usingexisting theoretical estimates (35) for cases involving smalldiameter changes. This relatively small variability likely ex-isted in similar ways in both the control and PTX states andmay have only a minor influence on the observed PTX effect
252 Pneumothorax and Acoustic Transmission • Mansy HA et al.
on acoustic transmission. To assess the effect of this variabilitymore quantitatively, future studies may be performed to furtherdocument the spectral content of the sound inputted from theET tube in both the control and PTX states.
There was no need to pause breathing during the experiment.Because sound signals were acquired without breath hold, theycontained low-amplitude breaths sounds. Typical breath soundamplitudes in the current study were at least 10 dB lower thanthe measured signals and, hence, likely had a small effect onthese signals. The study subjects were those who underwentVATS, during which a lung collapse was created as a routinepart of the procedure. Sound waves that reached the chest wallwere measured before and after lung collapse, which wasconfirmed by thoracoscopy. The described sound introductionapproach may be termed “active forcing” because it involvesactively inputting external signals. Earlier studies have eluci-
dated some of the useful acoustic parameters that correlatedwith respiratory system conditions (9, 18, 22, 27, 28, 33, 36).
The primary hypothesis in the current study is that propertychanges in the tissue structures along the sound transmissionpath cause measureable changes in the sounds measured at thechest surface. In turn, these acoustic changes may be used as anadjuvant to the methods of detecting or following the progres-sion of certain pulmonary conditions.
Sound transmission in the respiratory system involves a setof relatively complex frequency-dependent processes includ-ing sound transmission through the airway tree; coupling tosurrounding tissue; and transmission through 1) the paren-chyma, 2) the PTX air pocket (if it exists), and 3) the chestwall. Earlier studies suggested that most of the low-frequencysounds (below about 600 Hz) efficiently couple from the largeairways to the surrounding tissue (24). As the frequency
Fig. 2. A: spectra of sounds transmitted fromthe mouth to chest wall of all study subjectsfor the control (solid line) and pneumothorax(PTX) (dashed line) states. A spectral dropin acoustic transmission due to PTX can beseen at certain frequencies. B: average spec-tra of transmitted sounds in the control (solidline) and PTX (dashed line) states. Error barsshow the 95% confidence interval.
253Pneumothorax and Acoustic Transmission • Mansy HA et al.
increases, the airways become more rigid due to their mass,and the acoustic energy travels deeper into the smaller airwaysbefore coupling to the parenchyma (24). Other relevant acous-tic phenomena include increased acoustic attenuation in tissuewith increasing frequency, ET tube acoustics, possible reso-nances of thoracic structures, and reflections of sound waves atinterfaces between different tissues and between tissue andPTX air (27). All these factors contribute to increasing thetransmission complexity. Although each phenomenon involvedcan be studied separately, the current study focuses on inves-tigating the acoustic effect of one main structural change;namely, the abnormal existence of PTX air between the lungand chest wall.
The measured spectra in the current study showed a generaltrend toward decreased amplitude with frequency, which is
consistent with data from previous studies (24, 27, 46). Thespectral distributions, however, varied among subjects in thecontrol state as well as the PTX state. This may be due at leastin part to differences among subjects in size and pathology. Forexample, the body mass index of subjects varied from 25 to 40.In addition, 15 subjects had lung masses and 4 had lungnodules, 1 of whom had breast cancer. In an earlier study thatreported intersubject variability, this variability was suggestedas evidence for the dependence of acoustic transmission onpulmonary structures (47). But variability can also make itmore challenging to identify pulmonary conditions withoutbaseline measurements. It is to be noted, however, that ifcertain acoustic signatures are found to correlate with pulmo-nary system changes, these features may be useful for contin-uously monitoring the prognosis of subjects at risk for devel-
Fig. 3. A: spectral drop in acoustic transmis-sion with PTX for all study participants.There was a relatively consistent drop inacoustic energy (P � 0.01, Wilcoxon signedrank sum test) for frequencies �300 Hz.There appears to be a smaller change inamplitude in the 0–300 Hz range. B: averagedrop in transmitted spectra with PTX for allstudy participants. Error bars show the 95%confidence interval. It appears that the dropin spectral energy with PTX is most pro-nounced in the 400–600 Hz range. The dropin energy was smaller outside this frequencyrange.
254 Pneumothorax and Acoustic Transmission • Mansy HA et al.
oping these conditions. This may be possible, even in thepresence of significant intersubject variability, as long as base-line measurements are available. To further study this possi-bility, future studies need to assess intrasubject variability.Evidence from the current study suggests that the effects ofPTX air were noticeable even in the presence of variability.
The study results showed a general trend toward a frequen-cy-dependent drop in sound amplitude when PTX was induced,with the largest drop in the 400–600 Hz range (Fig. 3). Similartrends were observed in dog and pig PTX models of otherwisehealthy subjects (27, 33). The drop in sound amplitude is alsoconsistent with the clinical experience of decreased sounds andtactile fremitus with PTX. Selective filtering of different fre-quency sounds is known to occur with some lung conditions;for example, selective enhancement of high frequencies(known as egophony) may present with lung consolidation dueto fluid accumulations, which can enhance sound transmissionat these frequencies.
It is worth mentioning that when PTX takes place, an airpocket is formed between the affected lung and the chest wall.At the air pocket boundary, relatively strong acoustic reflec-tions take place due to large acoustic impedance mismatchbetween the air on one hand and the lung parenchyma andchest wall on the other hand. Due to these reflections, the airpocket is expected to act as a sound barrier. Reflected sounds(at the air and parenchymal surface) will travel again throughthe parenchyma and undergo more attenuation. Portions of thesounds that are blocked by the air pocket, however, will travelalong the longer path around the pocket and further attenuatebefore they reach the chest surface. Acoustic damping in softtissue is lower at low frequencies (8, 33, 45–47) and, hence,low-frequency waves will travel around the PTX air pocketmore efficiently (27) (i.e., they will suffer less attenuation).
The data collected in the current study consistently showed lesssound attenuation with PTX below 300 Hz (Fig. 3B).
As the sound frequency increases, the air pocket blockssound waves more efficiently (because these frequencies sufferstronger attenuation when they go around the air pocket)causing a more pronounced sound amplitude drop with PTX atthese frequencies. This trend was observed in the current studyfor frequencies in the 300–900 Hz range (P � 0.01, Wilcoxonsigned rank test). When the frequency further increased, themeasured sound amplitudes tended to decrease (due to in-creased tissue damping) and the drop in their amplitudes withPTX also tended to diminish. This trend was observed atfrequencies above about 1,000 Hz in the current study. Thedetected drop in acoustic energies and energy ratios (Figs. 4and 5) was consistent (P � 0.01 for both, Wilcoxon signedrank test). This may warrant further testing of this approach ina larger patient population. If proved successful, and due to therelative ease of repeating the acoustic measurements (com-pared with imaging methods such as chest ultrasonography andX-ray), the described method may be helpful as a complemen-tary tool for continuous monitoring of patients at risk fordeveloping PTX. In that respect, candidate patient populationswho may benefit from this approach include patients in inten-sive care units who are on positive pressure ventilation andwho may be at an increased risk for developing PTX. In thiscase, the transpulmonary transmission measurements may beintegrated in ventilators that can monitor patients and alertwhen this potentially lethal condition develops. Such an alertwould help healthcare providers decide whether further testingor intervention is needed in light of other clinical variables.
Conclusions. This study demonstrated that there are detect-able spectral changes in pulmonary acoustic transmission withPTX. The spectral changes include transmitted energy levels
Fig. 4. Difference between the control andPTX power spectral density in the 400–600Hz frequency range. A: maximum drop withPTX. B: mean drop with PTX. C: maximumincrease with PTX. One can observe a con-sistent spectral drop with PTX and no spectralincrease in this frequency range because alldata points in A and B are positive, whereasthose in C are negative.
Fig. 5. The acoustic spectrum was divided intothree bands. Band 1 � 50–250 Hz; band 2 �400–600 Hz; band 3 � 1,300–1,500 Hz. Theenergy ratio between bands 1 and 2 (ER21 �energy in band 2 � energy in band 1); and thatbetween bands 2 and 3 (ER23 � energy in band2 � energy in band 3) were calculated for thecontrol and PTX states. A: ER21 and ER23;dashed lines connect data points for the samesubject. There is a trend toward decreased ratioswith PTX. B: change in ER21 and ER23 withPTX. All data fell in the third quadrant, whichcorresponds to a decrease in both energy ratios.The borderline case (the case where E23 changeis close to zero) corresponds to the case with therelatively smaller PTX air pocket.
255Pneumothorax and Acoustic Transmission • Mansy HA et al.
and energy ratios between different frequency bands. Usingthese and other clinical signs may potentially provide the basisfor a rapid, safe, easy-to-use, and inexpensive bedside PTXmonitoring tool. On the basis of these preliminary results,further evaluation may be warranted.
GRANTS
This study was supported by National Institute of Biomedical Imaging andBioengineering Grant R01 EB-012142.
DISCLOSURES
H.A. Mansy and R.H. Sandler founded a company in 1997 that wasawarded a patent in 2002 that is related to the technology used in this article.The patent was never sold, licensed, or commercialized. The company did notcommercialize any devices that are based on this technology.
AUTHOR CONTRIBUTIONS
H.A.M., R.A.B., W.H.W., T.J.R., and R.H.S. conception and design ofresearch; H.A.M., W.H.W., and R.H.S. performed experiments; H.A.M., Z.D.,and Y.P. analyzed data; H.A.M., R.A.B., W.H.W., T.J.R., and R.H.S. inter-preted results of experiments; H.A.M. prepared figures; H.A.M. and R.A.B.drafted manuscript; H.A.M., R.A.B., W.H.W., T.J.R., Z.D., Y.P., and R.H.S.edited and revised manuscript; H.A.M., R.A.B., W.H.W., T.J.R., Z.D., Y.P.,and R.H.S. approved final version of manuscript.
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