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Pneumothorax During Laparoscopic Fundoplication: Diagnosis and Treatment with Positive End-Expiratory Pressure

Joris, Jean L. MD; Chiche, Jean-Daniel MD; Lamy, Maurice L. MD

General Article

Pneumothorax can develop during laparoscopy, particularly during laparoscopic fundoplication, since the left parietal pleura is exposed and can be torn during dissection in the diaphragmatic hiatus.Such an event will result in specific pathophysiologic changes, since CO2, under pressure in the abdominal cavity, will pass into the pleural space. The aim of this study was to document the pathophysiologic changes induced by pneumothorax, and to evaluate the benefit of positive end-expiratory pressure (PEEP) to treat pneumothorax. Forty-six ASA physical status I and II patients scheduled for laparoscopic fundoplication were monitored extensively; heart rate, mean arterial pressure, endtidal CO2 (PETCO2), oxygen saturation of hemoglobin (SpO2), minute ventilation, tidal volume, dynamic total lung thorax compliance, and airway pressures were recorded. In 25 patients, oxygen uptake, CO2 elimination and arterial blood gases were also measured. Pneumothorax was diagnosed in seven patients. It resulted in the following pathophysiologic changes: decrease in total lung thorax compliance, increase in airway pressures, and increase in CO2 absorption. Consequently, PaCO2 and PETCO2 also increased. SpO2, however, remained normal. The use of PEEP largely corrected these respiratory changes. None of these pneumothoraces required drainage. These data suggest that pneumothorax is common during laparoscopic fundoplication. Early diagnosis is possible by simultaneous monitoring of PETCO2, total lung thorax compliance, and airway pressures. Finally, treatment with PEEP provides an alternative to chest tube placement when pneumothorax is secondary to passage of peritoneal CO2 into the interpleural space.

(Anesth Analg 1995;81:993-1000)

Department of Anesthesiology and Intensive Care Medicine, University Hospital of Liege, Domaine du Sart Tilman, Liege, Belgium.

Presented in part at the 1994 annual meeting of the European Society of Anaesthesiologists, Brussels, Belgium.

Accepted for publication July 10, 1995.

Address correspondence and reprint requests to Jean L. Joris, MD, Department of Anesthesiology and Intensive Care Medicine, CHU of Liege, Domaine du Sart Tilman, B-4000 Liege, Belgium.

Postoperative benefits and technologic advances explain the effort to extend laparoscopy to more sophisticated surgical procedures [1,2]. During laparoscopy, specific complications may develop, depending on the location of the procedure and the techniques used. During laparoscopic fundoplication for hiatal hernia repair, the peritoneum, which closes the diaphragmatic hiatus, is opened and the esophagus is dissected in the inferior mediastinum. When the left crux of the diaphragm is dissected, the left parietal pleura is exposed and can be torn. Tears of the parietal pleura may allow passage of intraabdominal CO2 under pressure into the pleural cavity and lead to pneumothorax.

Before January 1993, we identified six symptomatic intraoperative pneumothoraces (5%), revealed by mild to moderate decreases in oxygen saturation of hemoglobin (SpO (2)) (from 99% to 93%-94%), increases in airway pressures, and observation by the laparoscopist of abnormal motion of one hemidiaphragm [3]. In most of these cases, this complication was well tolerated, and required only a moderate increase of oxygen concentration and of minute ventilation. All these pneumothoraces disappeared within 1 h after surgery without aspiration of gas [3]. Whereas pneumothorax seems to be more common during laparoscopic fundoplication, spontaneous pneumothorax may also develop during any laparoscopy upon opening of peritoneopleural ducts, which exist as embryonic remnants [4].

Pneumothorax may induce deleterious effects and requires early diagnosis [3-6]. In the previously reported cases, the most frequent signs of intraoperative pneumothorax were, respectively, a decrease in SpO2[3,5-8], an increase in airway pressures [3,5,7-9], an increase in end-tidal CO2 (PETCO2) [7-9], and, rarely, a decrease in arterial blood pressure [7,8]. Therefore, we extensively monitored patients scheduled for laparoscopic fundoplication to document the pathophysiologic changes induced by pneumothorax. More particularly, we focused our monitoring on respiratory mechanics, ventilation, and metabolic and routine hemodynamic variables. Finally, we evaluated the benefit of intraoperative positive end-expiratory pressure (PEEP) to inflate the lung and treat pneumothorax. Indeed, if the pathogenesis of pneumothorax during laparoscopy is flow of intraperitoneal CO2 under pressure into the interpleural space, reduction of the gradient between intraabdominal pressure and intrathoracic end-expiratory pressure should, at least partially, correct pneumothorax.

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After approval of our institution's ethics committee, and with informed consent, 46 ASA physical status I and II patients scheduled for laparoscopic fundoplication from January to July 1993 were enrolled in the study. None had a history of pulmonary or cardiac disease. Laparoscopic fundoplication was performed with patients in the 10 degrees head-up position, as previously described [10]. Intraabdominal pressure was automatically maintained at 14 mm Hg by a CO2 insufflator.

All patients were premedicated with midazolam (5 mg) and atropine intramuscularly (0.25 mg). Anesthesia was induced using propofol (2 mg/kg), sufentanil (15 micro gram), and atracurium (0.6 mg/kg) intravenously (IV). Metabolic monitoring of some patients with a Datex Deltatrac Registered Trademark Metabolic Monitor (Datex Instrument Corporation, Helsinki, Finland) required total IV anesthesia and no N2 O. Anesthesia was maintained in these patients by the continuous infusion of propofol (4-10 mg centered dot kg-1 centered dot h-1). Additional doses of sufentanil (5 micro gram) were administered if needed. In the other patients, anesthesia was maintained with varying concentrations of isoflurane in 50% N2 O/O2, our standard anesthetic technique for laparoscopy [11]. Intraoperative muscle relaxation was provided in all patients by a continuous infusion of atracurium (0.4 mg centered dot kg-1 centered dot h-1).

After tracheal intubation, mechanical ventilation was started in a volume-controlled mode (SERVO 900C; Siemens-Elema, Solna, Sweden). Minute ventilation was initially set at 100 mL centered dot kg-1 centered dot min-1 and adjusted to maintain PETCO2 between 30 and 40 mm Hg. Respiratory rate was kept constant at 10 breaths/min. In the total IV anesthesia group, a mixture of O2/air (FIO2 0.4) was used.

Respiratory mechanics was investigated using a Datex Capnomac Ultima Registered Trademark SVi with Side Stream Spirometry Registered Trademark (Datex Instrument Corporation): PETCO2, SpO2, minute ventilation, tidal volume, dynamic total lung thorax compliance (CLT), and peak and plateau inspiratory pressures (Ppeak, Pplat) were recorded. In addition, pressure-volume (P-V) and flow-volume (F-V) loops both were displayed continuously to allow close analysis during the procedure. Heart rate and arterial pressure were also recorded.

In 25 consenting patients, a radial artery was cannulated to allow arterial blood gas analysis, and a Datex Deltatrac Registered Trademark Metabolic Monitor was used to measure O2 uptake (VO2, in mL/min), CO2 elimination (VCO (2), in mL/min), and respiratory quotient (RQ). Metabolic measurements were recorded at 1-min intervals and the last five measurements of each study period were averaged. Assuming that the ratio between metabolic CO2 production and O2 uptake remained equal to the baseline RQ, metabolic CO2 production (Mb.VCO2) and absorbed VCO2 (Abs.VCO2) were calculated, respectively, as Mb.VCO2 (mL/min) = measured VO2 times baseline RQ and Abs.VCO2 (mL/min) = measured VCO2 - Mb.VCO2. Baseline values were recorded at least 20 min after tracheal intubation but prior to CO2 insufflation. Values were then recorded every 5 min during pneumoperitoneum, and 5 min after exsufflation.

CO2-pneumoperitoneum induces hemodynamic, metabolic, and ventilatory changes [3]. More particularly, CLT decreases, and consequently Ppeak and Pplat increase quickly after the beginning of intraabdominal insufflation. Thereafter, these values remain stable since intraabdominal pressure is maintained constant automatically. During CO2-pneumoperitoneum, absorbed VCO2 and subsequently PETCO2 progressively increase and then plateau after 20-30 min. Any change in these values after their steady state is reached suggests a complication. Therefore, in this study, careful auscultation of both lungs was performed before pneumoperitoneum, 10 min after the beginning of insufflation when intraabdominal pressure was stable, and subsequently, any time a change in one of these variables from their steady state was detected.

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A pneumothorax was diagnosed in 7 of 46 patients (15.2%). Pneumothorax developed on the left side in all cases, and one patient had bilateral pneumothoraces. In all patients, pneumothorax occurred during the dissection of the esophagus in the inferior mediastinum. Pneumothorax was diagnosed in every patient by auscultation of decreased breath sounds over the entire left lung, while fiberoptic bronchoscopy ruled out endobronchial intubation in all patients. Intraoperative fluoroscopy was used in two patients to radiologically confirm the diagnosis. Finally, surgeons observed abnormal motion of the left hemidiaphragm in four patients after we first detected pneumothorax.

When pneumothorax developed, the following characteristics were concomitantly noted in every patient Table 1. Total thorax lung compliance decreased and airway pressures increased. Consequently, the P-V loop displayed on the screen of the Datex Capnomac Ultima Registered Trademark SVi was inclined toward the pressure axis, without any modification of its shape Figure 1A. VCO2, PaCO2, and PETCO2 increased, and consequently minute ventilation had to be increased. Whereas PaO2 decreased, SpO2 exceeded 98% and remained stable in all patients.

Table 1

Table 1

Figure 1

Figure 1

In six of these cases, PEEP was applied to inflate the collapsed lung and allowed us to avoid chest drainage. Despite PEEP and an increase in minute ventilation, Ppeak and Pplat did not increase significantly in most patients. Rather, CLT improved and returned to the values obtained after induction of CO2-pneumoperitoneumFigure 1 B, C. Furthermore, this noninvasive treatment partially corrected the increased CO2 absorption and the decreased PaO2. Intraoperative fluoroscopy used in two patients demonstrated the effectiveness of PEEP for treating pneumothorax Figure 2. Finally, a postoperative chest radiograph did not show residual pneumothorax or major atelectasis.

Figure 2

Figure 2

Two cases (Patients 3 and 5) are reported in detail to precisely document the changes induced by pneumothorax and the benefit of PEEP in treating pneumothorax; the other cases are summarized in Table 1.

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Case-Report 1: Patient 3

A healthy 40-yr-old man (72 kg, 170 cm) was to undergo laparoscopic fundoplication. Total IV anesthesia was performed and the patient was monitored using a Datex Deltatrac Registered Trademark Metabolic Monitor and arterial blood gas analysis. Twenty minutes after the beginning of insufflation, systolic arterial pressure suddenly decreased to less than 70 mm Hg. Concomitantly, PaCO2 increased (37-59 mm Hg), as did PETCO2 (29-44 mm Hg) and VCO2 (138-303 mL/min, Figure 3A). PaO2 decreased from 207 to 143 mm Hg but SpO2 remained stable (99%). Furthermore, CLT decreased from 30 to 20 mL/cm H2 O and airway pressures increased. Pneumothorax was then suspected. Auscultation of the left lung revealed no air entry. Bronchoscopy excluded endobronchial intubation, and intraoperative fluoroscopy revealed a tension pneumothorax. A PEEP of 5 cm H2 O was then applied, and minute ventilation was increased from 7.8 to 10.1 L/min. Consequently, VCO2Figure 3A, PaCO2, and PETCO2 decreased. Despite PEEP and a 35% increase in minute ventilation, Ppeak and Pplat only slightly increased owing to improvement of CLTTable 1. Moreover, systolic arterial pressure quickly returned to normal values. Fifteen minutes later, a second increase in CO2 absorption was observed. No subcutaneous emphysema was clinically detectable and the depth of anesthesia seemed adequate. PEEP was further increased to 8 cm H2 O and attenuated these changes. Thirty-five minutes before the end of the surgical procedure, subcutaneous emphysema developed. Consequently, VCO2 further increased to greater than 400 mL/min. At this time, minute ventilation was 13.2 L/min, Ppeak reached 45 cm H2 O but CLT did not change. The surgeon complained of difficult operative conditions due to exaggerated excursion of the diaphragm. After exsufflation, controlled ventilation with PEEP was maintained until PaCO2 and PETCO2 returned to physiologic values. No residual pneumothorax was detected on the postoperative chest radiograph. Postoperative stay was uneventful.

Figure 3

Figure 3

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Case-Report 2: Patient 5

A 22-yr-old woman (55 kg, 173 cm) was scheduled for laparoscopic fundoplication. General anesthesia was induced with propofol and sufentanil, and atracurium. Controlled ventilation was started, and anesthesia was maintained with 50% N2 O/O2 and isoflurane. CO2-pneumoperitoneum resulted in a decrease in CLT from 49 to 29 mL/cm H2 O, and airway pressures increased. PETCO2 progressively increased and reached a plateau (43 mm Hg) 20 min after the beginning of pneumoperitoneum. Compliance suddenly decreased to 15 mL/cm H2 O and airway pressures increased. PETCO2 increased markedly to 57 mm Hg. Hemodynamics and SpO2 remained stable. At this time, chest auscultation revealed hypoventilation of both lungs, but especially on the left side. Therefore, endobronchial intubation was first ruled out using bronchoscopy. No subcutaneous emphysema was detected. The diagnosis of pneumothorax was then suspected. Fluoroscopy confirmed a bilateral pneumothorax Figure 2A. PEEP (5 cm H2 O) was applied, N2 O was turned off, and minute ventilation was adjusted from 4.7 to 6.8 L/min. Ten minutes after instituting PEEP treatment, CLT and PETCO2 both returned to their values just prior to pneumothorax. Intraoperative fluoroscopy confirmed the disappearance of the pneumothorax with PEEP Figure 2B. There were no subsequent adverse events. The postoperative stay was unremarkable.

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Although pneumothorax is claimed to be a rare complication of pneumoperitoneum for laparoscopy [9,12,13], several cases of unilateral or bilateral pneumothorax have been described during laparoscopy [4-7,9,14,15]. Most authors speculated that pneumothorax resulted from the passage of gas through congenital or acquired defects of the diaphragm [5,6,9]. Recently, two reports highlighted the need to consider the risk of intraoperative pneumothorax in the course of laparoscopic fundoplication [8,16].

We detected seven pneumothoraces over a 7-mo period. Pneumothorax was diagnosed in every patient by auscultation of reduced breath sounds over the entire left lung. The intensity of breath sounds was diminished not only as compared to the contralateral side, but also to the breath sounds heard over the left lung 10 min after the beginning of pneumoperitoneum. Causes of hypoventilation besides pneumothorax were eliminated. The ventilator tubing was checked, and kinking of the endotracheal tube was excluded. Bronchospasm limited to the left lung was also excluded. Indeed, auscultation of the left lung revealed no wheezing, and the shape of the capnogram did not change relative to that observed before pneumothorax diagnosis. More particularly, no sign of asynchronism (increased slope of the Phase III of the capnogram) was detected. Finally, the shape of the flow-volume loop provided by the Capnomac Ultima Registered Trademark SVi did not change, and the expiratory volume in 1 s continuously displayed on this monitor did not decrease significantly. Fiberoptic bronchoscopy ruled out obstruction of the endotracheal tube, endobronchial intubation, as well as obstruction of the main left bronchus and segmental bronchi. More distal atelectasis involving only the left lung seemed unlikely. Conversely, the location of the surgery and the technique of dissection may explain the fact that pneumothorax developed on the left side in all patients. Indeed, during dissection of the esophagus above the left crux of the diaphragm, the left lung lies in close proximity, and tears of the left parietal pleura can easily occur. Hence, CO2 under pressure in the abdominal cavity can escape into the pleural cavity, since intraabdominal pressure is greater than end-expiratory pleural pressure. Finally, intraoperative fluoroscopy provided radiologic confirmation of the diagnosis in two patients.

The high incidence of pneumothorax during this prospective study (15.2%) contrasts with the 6 of 120 patients observed over the previous 2 yr. We believe that development of undiagnosed pneumothorax may account for this difference. In this study, we would not have been aware of pneumothorax in six or seven patients if we had not closely and simultaneously monitored airway pressures, compliance, and PETCO2. Indeed, monitoring of PETCO2 alone is not sufficient, since an increase in PETCO2 requiring hyperventilation is common during this procedure associated with a high incidence of CO2-subcutaneous emphysema [17]. To diagnose CO2-pneumothorax, a sudden increase in PETCO2 associated with a concomitant decrease in CLT and an increase in airway pressures are required. The presence of all three of these signs, and close analysis of the shape of both P-V and F-V loops will easily rule out other causes of decreased CLT and increased airway pressures (kinking of the endotracheal tube, bronchospasm, etc.): indeed, the shape of the P-V loop and the expiratory limb of the F-V loop are not affected by CO2-pneumothorax.

Pneumothorax probably results from the insufflation of CO2 under pressure through tears in the parietal pleura, since intraabdominal pressure is greater than intrapleural end-expiratory pressure. The increase in PETCO2 during CO (2-pneumothorax) results from an increase in CO2 absorption. During laparoscopy, CO2 absorption notably depends upon the gas-exchange area [18]. When CO2 flows from the peritoneal cavity to the interpleural space, the gas-exchange area and consequently the absorption of CO2 increase. Indeed, in our patients, absorbed CO2 ranged from 78 to 141 mL/min, as compared with 30-40 mL/min during uneventful laparoscopic fundoplication [17]. Furthermore, CO2 is absorbed much more readily from the pleural cavity than from the peritoneal cavity [19].

The rationale for PEEP therapy was to decrease the pressure gradient between the abdominal and pleural cavities not only during inspiration (controlled mechanical ventilation) but also during expiration, and subsequently to inflate the lung. Indeed, if the gradient is reduced or reversed, CO2 should leave the pleural space. Furthermore, because it is highly diffusible, CO2 should be quickly absorbed from the pleural space when pleural entry of intraperitoneal CO2 is prevented. Reexpansion of the lung with PEEP might also mechanically seal the surgically induced tear in the parietal pleura. Our data suggest that this noninvasive treatment was effective for treating pneumothorax and its pathophysiologic consequences. Indeed, intraoperative fluoroscopy confirmed the disappearance of pneumothorax within 5-10 min when PEEP was applied Figure 2B. Moreover, CLT and airway pressures quickly improved when PEEP was applied. Finally, PEEP not only reversed pneumothorax-induced alterations of respiratory mechanics and hemodynamics when present (Patient 3), but it also improved arterial blood gases. Due to inflation of the collapsed lung, CO (2) passage into the pleural space was reduced, and consequently CO2 absorption decreased when PEEP was applied Table 1. Accordingly, PaCO2 and PETCO2 decreased in our patients.

Pneumothorax during laparoscopy creates specific and controversial therapeutic issues. In most of the published cases, thoracocentesis was performed [5,6,8,16] and many authors recommend performing tube thoracostomy when pneumothorax is diagnosed [8,9]. However, this procedure is not without complications, and insertion of a chest tube can compromise the maintenance of the pneumoperitoneum, and therefore the laparoscopy. Rarely, other clinicians have converted laparoscopy to an open procedure [7,8]. In our study, PEEP therapy allowed us to successfully manage six patients who developed a pneumothorax. In all patients, thoracocentesis was avoided. Postoperative chest radiograph excluded residual pneumothorax, and the postoperative course was uneventful. In case of residual pneumothorax, conservative management is also recommended, since CO2 will be quickly absorbed from the pleural cavity after abdominal desufflation [3,4].

Most of these pneumothoraces were hemodynamically well tolerated and SpO2 remained normal. The main consequence of CO2-pneumothorax is the increased VCO2, PaCO2, and PETCO2 which can be corrected by increasing minute ventilation. One may question whether PEEP is necessary in these pneumothorax. We believe that PEEP treatment can be of benefit for the following reasons: first, PEEP will treat pneumothorax, and will therefore prevent pneumothorax from extending and resulting in serious consequences; second, the treatment of these pneumothoraces reduces CO2 absorption, and consequently limits the hyperventilation necessary to correct hypercapnia. This can be particularly relevant in patients with chronic obstructive pulmonary disease, in whom ventilation with high volumes and high pressures may be deleterious. Finally, the exaggerated excursion of the diaphragm, which may disturb the surgeon operating in the diaphragmatic hiatus, is thereby avoided.

Given the high incidence of pneumothorax during laparoscopic fundoplication and the effectiveness of PEEP treatment, prophylactic PEEP during this procedure may be proposed. However, the advantages of prophylactic PEEP remain speculative and PEEP during laparoscopy can induce hemodynamic side effects [20]. Therefore, we do not recommend prophylactic PEEP, and wait for the early signs of pneumothorax before applying this treatment.

The pathogenesis and the pathophysiologic changes of pneumothorax reported in this article, as well as its treatment with PEEP, are only relevant to pneumothorax secondary to the passage of CO2 from the peritoneal cavity into the interpleural space. However, the hyperventilation sometimes required during CO2-pneumoperitoneum may induce volotrauma and/or barotrauma, and result in the rupture of preexisting pulmonary bullae leading to pneumothorax. In this case, CO2 absorption is not increased. A decrease in cardiac output usually results in a decrease in PETCO2; under these circumstances, PEEP must not be applied and thoracocentesis is mandatory.

In summary, we report seven cases of pneumothorax during laparoscopy for diaphragmatic hiatal hernia repair. Pneumothorax during laparoscopic fundoplication probably occurs more frequently than we had originally thought, most often on the left side. The diagnosis should be considered any time PETCO2 increases abnormally while CLT decreases and airway pressures increase. Careful monitoring of these variables is thus strongly recommended. If pneumothorax is confirmed by lung auscultation, N2 O should be turned off and PEEP should be applied. This treatment usually results in a substantial improvement of gas exchange and respiratory mechanics. These preliminary findings have been confirmed by a prospective animal study [21,22].

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