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PubMed1999

Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of a high inspired oxygen concentration.

BACKGROUND: General anaesthesia impairs the gas exchange in the lungs, and moderate desaturation (SaO2 86-90%) occurred in 50% of anaesthetised patients in a blinded pulse oximetry study. A high FiO2 might reduce the risk of hypoxaemia, but can also promote atelectasis. We hypothesised that a moderate positive end-expiratory pressure (PEEP) level of 10 cmH2O can prevent atelectasis during ventilation with an FiO2 = 1.0. METHODS: Atelectasis was evaluated by computed tomography (CT) in 13 ASA I-II patients undergoing elective surgery. CT scans were obtained before and 15 min after induction of anaesthesia. Then, recruitment of collapsed lung tissue was performed as a "vital capacity manoeuvre" (VCM, inspiration with Paw = 40 cmH2O for 15 s), and a CT scan was obtained at the end of the VCM. Thereafter, PEEP = 0 cmH2O was applied in group 1, and PEEP = 10 cmH2O in group 2. Additional CT scans were obtained after the VCM. Oxygenation was measured before and after the VCM. RESULTS: Atelectasis (> 1 cm2) was present in 12 of the 13 patients after induction of anaesthesia. At 5 and 10 min after the VCM, atelectasis was significantly smaller in group 2 than group 1 (P < 0.005). A significant inverse correlation was found between PaO2 and atelectasis. CONCLUSIONS: PEEP = 10 cmH2O reduced atelectasis formation after a VCM, when FiO2 = 1.0 was used. Thus, a VCM followed by PEEP = 10 cmH2O should be considered when patients are ventilated with a high FiO2 and gas exchange is impaired.

Adult↗
PubMed1998

Airway closure, atelectasis and gas exchange during general anaesthesia.

Airway closure and the formation of atelectasis have been proposed as important contributors to impairment of gas exchange during general anaesthesia. We have elucidated the relationships between each of these two mechanisms and gas exchange. We studied 35 adults with healthy lungs, undergoing elective surgery. Airway closure was measured using the foreign gas bolus technique, atelectasis was estimated by analysis of computed x-ray tomography, and ventilation-perfusion distribution (VA/Q) was assessed by the multiple inert gas elimination technique. The difference between closing volume and expiratory reserve volume (CV-ERV) increased from the awake to the anaesthetized state. Linear correlations were found between atelectasis and shunt (r = 0.68, P < 0.001), and between CV-ERV and the amount of perfusion to poorly ventilated lung units ("low Va/Q", r = 0.57, P = 0.001). Taken together, the amount of atelectasis and airway closure may explain 75% of the deterioration in PaO2. There was no significant correlation between CV-ERV and atelectasis. We conclude that in anaesthetized adults with healthy lungs, undergoing mechanical ventilation, both airway closure and atelectasis contributed to impairment of gas exchange. Atelectasis and airway closure do not seem to be closely related.

Adult↗
PubMed1997

Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study.

BACKGROUND: Respiratory failure after cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. The authors tested the hypothesis that atelectasis is an important factor responsible for the increase in intrapulmonary shunt after CPB. METHODS: Six pigs received standard CPB (bypass group). Six other pigs had the same surgery but without CPB (sternotomy group). Another six pigs were anesthetized for the same duration but without any surgery (control group). The ventilation-perfusion distribution was measured with the inert gases technique, extravascular lung water was quantified by the double-indicator distribution technique, and atelectasis was analyzed by computed tomography. RESULTS: Intrapulmonary shunt increased markedly after bypass but was unchanged over time in the control group (17.9 +/- 6.2% vs. 3.5 +/- 1.2%; P < 0.0001). Shunt also increased in the sternotomy group (10 +/- 2.6%; P < 0.01 compared with baseline) but was significantly lower than in the bypass group (P < 0.01). Extravascular lung water was not significantly altered in any group. The pigs in the bypass group showed extensive atelectasis (32.3 +/- 28.7%), which was significantly larger than in the two other groups. The pigs in the sternotomy group showed less atelectasis (4.1 +/- 1.9%) but still more (P < 0.05) than the controls (1.1 +/- 1.6%). There was good correlation between shunt and atelectasis when all data were pooled (R2 = 0.67; P < 0.0001). CONCLUSIONS: Atelectasis is produced to a much larger extent after CPB than after anesthesia alone or with sternotomy and it explains most of the marked post-CPB increase in shunt and hypoxemia. Surgery per se contributes to a lesser extent to postoperative atelectasis and gas exchange impairment.

Animals↗
PubMed1999

Comparable postoperative pulmonary atelectasis in patients given 30% or 80% oxygen during and 2 hours after colon resection.

BACKGROUND: High concentrations of inspired oxygen are associated with pulmonary atelectasis but also provide recognized advantages. Consequently, the appropriate inspired oxygen concentration for general surgical use remains controversial. The authors tested the hypothesis that atelectasis and pulmonary dysfunction on the first postoperative day are comparable in patients given 30% or 80% perioperative oxygen. METHODS: Thirty patients aged 18-65 yr were anesthetized with isoflurane and randomly assigned to 30% or 80% oxygen during and for 2 h after colon resection. Chest radiographs and pulmonary function tests (forced vital capacity and forced expiratory volume) were obtained preoperatively and on the first postoperative day. Arterial blood gas measurements were obtained intraoperatively, after 2 h of recovery, and on the first postoperative day. Computed tomography scans of the chest were also obtained on the first postoperative day. RESULTS: Postoperative pulmonary mechanical function was significantly reduced compared with preoperative values, but there was no difference between the groups at either time. Arterial gas partial pressures and the alveolar-arterial oxygen difference were also comparable in the two groups. All preoperative chest radiographs were normal. Postoperative radiographs showed atelectasis in 36% of the patients in the 30%-oxygen group and in 44% of those in the 80%-oxygen group. Relatively small amounts of pulmonary atelectasis (expressed as a percentage of total lung volume) were observed on the computed tomography scans, and the percentages (mean +/- SD) did not differ significantly in the patients given 30% oxygen (2.5% +/- 3.2%) or 80% oxygen (3.0% +/- 1.8%). These data provided a 99% chance of detecting a 2% difference in atelectasis volume at an alpha level of 0.05. CONCLUSIONS: Lung volumes, the incidence and severity of atelectasis, and alveolar gas exchange were comparable in patients given 30% and 80% perioperative oxygen. The authors conclude that administration of 80% oxygen in the perioperative period does not worsen lung function. Therefore, patients who may benefit from generous oxygen partial pressures should not be denied supplemental perioperative oxygen for fear of causing atelectasis.

Adult↗
PubMed1996

Pulmonary atelectasis after reconstruction with a latissimus dorsi myocutaneous flap.

Atelectasis is the most common postoperative complication encountered in head and neck surgery. Risk factors include preexisting pulmonary disease, type of surgery performed, and the length of anesthetic. It is controversial whether reconstruction of defects with regional myogenous flaps predisposes to atelectasis. The latissimus dorsi myocutaneous flap requires the patient to be placed on his side for a period of time. Whether it is the position or the surgery that contributes to the development of atelectasis has not been examined. Eighteen patients underwent latissimus dorsi myocutaneous flap reconstruction following major ablative procedures for head and neck cancer. The cutaneous area transferred ranged from 70 to 225 cm2 (mean, 128 cm2). The flap size ranged from 7 x 10 to 15 x 15 cm. The majority of flaps were 10 x 15 cm or greater. These patients were compared to 18 patients who did not undergo pedicled myocutaneous chest flap reconstruction. Patients were matched for age, sex, length of operation, site of primary, and stage of disease. Postoperative atelectasis was radiographically detected in 89% of flap patients vs. 79% of controls. Major atelectasis was encountered in 16% of patients undergoing flap surgery vs. 11% of patients in the control group. Patients with large cutaneous paddles on the flaps (> 120 cm2) had significantly more atelectasis than patients with smaller cutaneous paddles (P<.05, chi-squared). The incidence of radiographic postoperative atelectasis in patients having a latissimus dorsi myocutaneous flap is high. The size of the skin paddle harvested as well as the position change may contribute to this.

Female↗
PubMed1986

Correlation of gas exchange impairment to development of atelectasis during anaesthesia and muscle paralysis.

Pulmonary gas exchange and the development of atelectasis were studied in eight essentially lung-healthy patients, awake and during halothane anaesthesia with mechanical ventilation. Gas exchange was evaluated by a multiple inert-gas elimination technique and conventional blood-gas analysis, and atelectasis was studied by computerized tomography (CT). Ventilation and lung perfusion were well matched in the majority of the patients when awake. In two patients there was low perfusion of poorly ventilated regions (low VA/Q). One patient had a shunt corresponding to 4% of cardiac output. None of the patients showed signs of atelectasis on the CT scans. After 15 min of anaesthesia, shunt had appeared in all patients, ranging from 1% in two patients (unchanged from the awake state) to 17%. The major VA/Q mode was widened and ventilation of poorly perfused regions (high VA/Q) was noted in seven patients. Densities in dependent lung regions (interpreted as atelectasis) were seen on the CT scans in six patients. The extent of atelectasis was significantly correlated both to the magnitude of shunt (r = 0.93, P less than 0.01) and to the impairment of arterial oxygenation (r = 0.99, P less than 0.001). The findings indicate that atelectasis in dependent lung regions during halothane anaesthesia creates shunting of blood flow and that atelectasis is the major or sole cause of impaired gas exchange in the lung-healthy, anaesthetized subject.

Adult↗
PubMed2006

Atelectasis causes alveolar injury in nonatelectatic lung regions.

RATIONALE: Many authors have suggested that the mechanism by which atelectasis contributes to injury is through the repetitive opening and closing of distal airways in lung regions that are atelectatic. However, neither the topographic nor mechanistic relationships between atelectasis and distribution of lung injury are known. OBJECTIVES: To investigate how atelectasis contributes to ventilator-induced lung injury. METHODS: Surfactant depletion was performed in anesthetized rats that were then allocated to noninjurious or injurious ventilation for 90 min. MEASUREMENTS: Lung injury was quantified by gas exchange, compliance, histology, wet-to-dry weight, and cytokine expression, and its distribution by histology, stereology, cytokine mRNA expression, in situ hybridization, and immunohistochemistry. Functional residual capacity, percent atelectasis, and injury-induced lung water accumulation were measured using gravimetric and volumetric techniques. MAIN RESULTS: Atelectasis occurred in the dependent lung regions. Injurious ventilation was associated with alveolar and distal airway injury, while noninjurious ventilation was not. With injurious ventilation, alveolar injury (i.e., histology, myeloperoxidase protein expression, quantification, and localization of cytokine mRNA expression) was maximal in nondependent regions, whereas distal airway injury was equivalent in atelectatic and nonatelectatic regions. CONCLUSIONS: These data support the notion that lung injury associated with atelectasis involves trauma to the distal airways. We provide topographic and biochemical evidence that such distal airway injury is not localized solely to atelectatic areas, but is instead generalized in both atelectatic and nonatelectatic lung regions. In contrast, alveolar injury associated with atelectasis does not occur in those areas that are atelectatic but occurs instead in remote nonatelectatic alveoli.

Animals↗
PubMed2004

Prevention of atelectasis formation during the induction of general anesthesia in morbidly obese patients.

UNLABELLED: Atelectasis caused by general anesthesia is increased in morbidly obese patients. We have shown that application of positive end-expiratory pressure (PEEP) during the induction of anesthesia prevents atelectasis formation in nonobese patients. We therefore studied the efficacy of PEEP in morbidly obese patients to prevent atelectasis. Twenty-three adult morbidly obese patients (body mass index >35 kg/m(2)) were randomly assigned to one of two groups. In the PEEP group, patients breathed 100% oxygen (5 min) with a continuous positive airway pressure of 10 cm H(2)O and, after the induction, mechanical ventilation via a face mask with a PEEP of 10 cm H(2)O. In the control group, the same induction was applied but without continuous positive airway pressure or PEEP. Atelectasis, determined by computed tomography, and blood gas analysis were measured twice: before the induction and directly after intubation. After endotracheal intubation, patients of the control group showed an increase in the amount of atelectasis, which was much larger than in the PEEP group (10.4% +/- 4.8% in control group versus 1.7% +/- 1.3% in PEEP group; P < 0.001). After intubation with a fraction of inspired oxygen of 1.0, PaO(2) was significantly higher in the PEEP group compared with the control group (457 +/- 130 mm Hg versus 315 +/- 100 mm Hg, respectively; P = 0.035) We conclude that in morbidly obese patients, atelectasis formation is largely prevented by PEEP applied during the anesthetic induction and is associated with a better oxygenation. IMPLICATIONS: Application of positive end-expiratory pressure during induction of general anesthesia in morbidly obese patients prevents atelectasis formation and improves oxygenation. Therefore, this technique should be considered for anesthesia induction in morbidly obese patients.

Adult↗
PubMed1999

Effect of combined kinetic therapy and percussion therapy on the resolution of atelectasis in critically ill patients.

BACKGROUND: Some critically ill patients have difficulty in mobilizing their respiratory secretions. These patients can develop pulmonary atelectasis that may result in hypoxemia. There are some data to show that atelectasis may be prevented by turning a patient from side to side utilizing special beds. STUDY OBJECTIVES: To determine the role of kinetic therapy (KT) combined with mechanical percussion (P) in the resolution of established atelectasis of the lungs and hypoxemia in critically ill, hospitalized patients. (KT was defined as rotation of a patient along the longitudinal axis of > or = 40 degrees to each side continuously.) DESIGN: Prospective and randomized study (2:1 test to control group). PATIENTS: Twenty-four patients with respiratory failure, either mechanically ventilated or spontaneously breathing, who demonstrated segmental, lobar, or unilateral entire lung atelectasis were studied. SETTING: Medical ICU and adult respiratory ward in a county hospital in New York. INTERVENTIONS: Seventeen patients were treated with KT combined with mechanical P using a KT system (Triadyne Kinetic Therapy System; KCI; San Antonio, TX). Seven patients received manual repositioning and manual P every 2 h. Both groups received similar conventional therapy with inhaled bronchodilators and suctioning. RESULTS: Partial or complete resolution of atelectasis was seen in 14 of 17 patients (82.3%) in the test group as compared with 1 of 7 patient (14.3%) in the control group. The median duration to resolution of atelectasis was 4 days in the test group. Bronchoscopy was performed in 3 of 7 patients in the control group, but in none of the patients in the test group. A cost of $720 was incurred per patient for utilizing the specialty beds for a mean duration of 4 days. An improvement in oxygenation index occurred in the test group (change in baseline PaO2/fraction of inspired oxygen from 207.4+/-106.7 mm Hg to 318+/-100.7 mm Hg) at the end of therapy, while the control group showed a reduction over a similar duration of time (181.3+/-96.3 mm Hg to 112+/-21.2 mm Hg). CONCLUSIONS: KT and mechanical P therapy resulted in significantly greater partial or complete resolution of atelectasis as compared with conventional therapy. There was a generalized trend toward statistical significance in the improvement of oxygenation and a reduced need for bronchoscopy in the group receiving KT and P therapy.

Aged↗
PubMed2000

Pleural effusion is a cause of round atelectasis of the lung.

OBJECTIVE: The purpose of this study was to determine whether or not pleural effusion could be a cause of round atelectasis of the lung. MATERIALS AND METHODS: The study group consists of 20 patients with round atelectasis who had no evidence of asbestos exposure, who had normal baseline chest radiographs that showed no evidence of preexisting pleural or pulmonary disease, and who developed pleural effusion from a variety of causes. Chest radiographs were examined for signs of round atelectasis at the time of initial presentation of the pleural effusion. Follow-up radiographs, spanning a period of 1 month to 4 years after resolution of the pleural effusion, were also examined in all 20 cases. RESULTS: Round atelectasis was seen initially as a rounded mass-like opacity that produced a focal, upward bulge in the curvilinear meniscus of pleural effusion in 17 cases. In three cases round atelectasis was seen initially as a spherical mass with a comet-tail sign located slightly above the pleural effusion. As the pleural effusion resolved, typical findings of round atelectasis developed in all 20 cases. CONCLUSION: Pleural effusion, in the absence of exposure to asbestos, can cause round atelectasis.

Adult↗
PubMed2002

[Clinical evaluation of rounded atelectasis induced by exposure to asbestos].

We encountered 15 patients with rounded atelectasis induced by exposure to asbestos from 1992 to 1999. All patients were men whose ages ranged from 42 to 85 years, with a mean age of 64.2 +/- 11.5 years. Rounded atelectasis was present only in the right lung and two patients had 2 rounded atelectasis in the right lung. In eight cases, the rounded atelectasis was found in segment 10, while in the others, it was found in segments 4, 5, 6, 8, and 9. Although evidence of symptoms was absent, rounded atelectasis was detected in six patients through medical examinations. Others complained of chest pain and dyspnea. Thirteen patients displayed pleural plaques and only 2 patients revealed asbestosis. Malignant complications were discovered in 4 patients, of whom 3 showed primary lung cancer and 1 suffered acute myelocytic leukemia. In their occupational histories, 7 patients had been exposed to asbestos in the shipyards and 5 in the construction field. The mean period of the exposure was 25.1 +/- 12.7 years, and the latency period from the first asbestos exposure to the detection of atelectasis was 35.1 +/- 8.8 years. Five autopsied patients had more than 10,000 asbestos bodies in the lung, which indicated heavy exposure to asbestos. These results suggest that rounded atelectasis may appear after high-dose exposure to asbestos.

Adult↗
PubMed2003

Minimally invasive laser contraction myringoplasty for tympanic membrane atelectasis.

OBJECTIVE: We sought to develop a minimally invasive surgical technique using the CO(2) laser to reduce or eliminate tympanic membrane atelectasis in a select group of patients. STUDY DESIGN: Thirty-seven ears with varying degrees of tympanic membrane atelectasis underwent CO(2) laser myringoplasty with the patients under intravenous sedation in the operating room setting. Atelectasis severity was graded for each patient and documented before and after laser myringoplasty through photodocumentation. Patients were followed for 1 year with comparison tympanic membrane photography. SETTING: The study was conducted in a tertiary care private otology-neurotology practice. RESULTS: Laser myringoplasty significantly reduced retraction pocket severity in most patients. No patients required resection of the retraction pocket or tympanoplasty. The most favorable outcomes were observed in patients with atelectasis addressed early rather than later in its more advanced stages. CONCLUSION: Laser contraction myringoplasty can reduce or eliminate atelectatic areas of the tympanic membrane through immediate contraction and "tightening" of the tympanic membrane tissues. Clinicians should use a standardized tympanic membrane atelectasis grading format. SIGNIFICANCE: A minimally invasive surgical technique for addressing tympanic membrane atelectasis is described, and a tympanic membrane atelectasis grading system is presented based on size, location, and depth of the atelectatic region.

Adolescent↗
PubMed1999

Thallium and FDG uptake by atelectasis with bronchogenic carcinoma.

We report a case of bronchogenic carcinoma with atelectasis studied by T1-SPECT and FDG-PET. In the carcinoma, abnormally high uptake of T1 and FDG were detected, but in the region of atelectasis, an abnormally high uptake of T1 with a relatively low uptake of FDG were observed. On quantitative analyses, the T1 retention indexes of the tumor and atelectasis were 29.7 and 42.0. The mean SUVs of FDG of the tumor and the atelectasis were 8.92 and 1.28. T1-SPECT could not distinguish the atelectasis from the carcinoma. FDG-PET was superior to T1-SPECT in this case in detecting malignancy and distinguishing it from atelectasis.

Biological Transport↗
PubMed2002

Effect of maxillomandibular fixation on the incidence of postoperative pulmonary atelectasis.

PURPOSE: Our goal was to assess the role of maxillomandibular fixation (MMF) on postoperative atelectasis. PATIENTS AND METHODS: We examined 64 patients in 2 groups: MMF and non-MMF. Atelectasis was diagnosed by comparing preoperative and postoperative chest radiographs, arterial blood gas analysis, and axial temperatures. Postoperative chest computed tomography scans were also used as the best way to detect atelectasis. RESULTS: Of the MMF and non-MMF patients, 37.5% and 15.6%, respectively, sustained atelectasis (P <.05). Plate type was the most prevalent (71%). The right lung was more involved (59%). Fever was not a significant finding in atelectatic patients (P >.10). PaO(2) was decreased in some cases of atelectasis, especially in patients with extensive involvement. CONCLUSION: MMF should be considered as a contributing factor for postoperative pulmonary atelectasis.

Adolescent↗
PubMed1999

Dynamics of re-expansion of atelectasis during general anaesthesia.

A major cause of impaired gas exchange during general anaesthesia is atelectasis, causing pulmonary shunt. A 'vital capacity' (VC) manoeuvre (i.e. inflation of the lungs up to 40 cm H2O, maintained for 15 s) may re-expand atelectasis and improve oxygenation. However, such a manoeuvre may cause adverse cardiovascular effects. Reducing the time of maximal inflation may improve the margin of safety. The aim of this study was to analyse the change over time in the amount of atelectasis during a VC manoeuvre in 12 anaesthetized adults with healthy lungs. I.v. anaesthesia with controlled mechanical ventilation (VT 9 (SD 1) ml kg-1) was used. For the VC manoeuvre, the lungs were inflated up to an airway pressure (Paw) of 40 cm H2O. This pressure was maintained for 26 s. Atelectasis was assessed by analysis of computed x-ray tomography. The amount of atelectasis, measured at the base of the lungs, was 4.0 (SD 2.7) cm2 after induction of anaesthesia. The decrease in the amount of atelectasis over time during the VC manoeuvre was described by a negative exponential function with a time constant of 2.6 s. At an inspired oxygen concentration of 40%, PaO2 increased from 17.2 (4.0) kPa before to 22.2 (6.0) kPa (P = 0.013) after the VC manoeuvre. Thus in anaesthetized adults undergoing mechanical ventilation with healthy lungs, inflation of the lungs to a Paw of 40 cm H2O, maintained for 7-8 s only, may re-expand all previously collapsed lung tissue, as detected by lung computed tomography, and improve oxygenation. We conclude that the previously proposed time for a VC manoeuvre may be halved in such subjects.

Adult↗
PubMed1983

Pulmonary blood pressure and flow during atelectasis in the dog.

The purpose of the study was to measure the time course, direction, and magnitude of the hypoxic pulmonary vasoconstriction (HPV) response to atelectasis. Six dogs were anesthetized with pentobarbital. With the chest open, each lung was ventilated separately. Pulmonary blood flow was measured with electromagnetic flow probes. Pulmonary arterial, left atrial, and systemic arterial pressures were measured via indwelling catheters. The right lung was ventilated continuously with 100% O2, while the left lung was either ventilated with 100% O2 (control phase), unventilated (4 hours of atelectasis), or ventilated with a gas mixture containing 4% O2, 3% CO2, and 93% N2 (hypoxia phase). Left lung atelectasis resulted in a reduction of the per cent lung blood flow from 43 +/- 4% (mean +/- SE) to 25 +/- 7% at 15 min and to 12 +/- 1% at 60 min which persisted for the remaining four-hour period. The per cent left lung blood flow was significantly lower (8 +/- 1%) and the PaO2 significantly higher (356 +/- 38 mmHg) during the maximal response to atelectasis as compared to 15 min of hypoxic ventilation (23 +/- 5%; 211 +/- 21 mmHg). With atelectasis or hypoxic ventilation, pulmonary perfusion pressure was increased significantly from the control value of 7.9 +/- 0.8 mmHg to approximately 11 mmHg. The present study demonstrated that in the open chest model without systemic hypoxemia, the response to acute atelectasis is a regional increase in pulmonary vascular resistance which develops quickly (15 min) and is maximal by 60 min and is maintained thereafter. As a result, there is a sustained diversion of blood flow away from the atelectatic lung and a generalized increase of pulmonary perfusion pressure.

Animals↗
PubMed1994

Phrenic nerve stimulation during halothane anesthesia. Effects of atelectasis.

BACKGROUND: Atelectasis formation during anesthesia may be due to loss of respiratory muscle tone, in particular that of the diaphragm. This was tested by tensing the diaphragm by phrenic nerve stimulation (PNS) and observing the effect on atelectasis. METHODS: Twelve patients (mean age 48 yr) without preexisting lung disease were studied during halothane anesthesia. PNS was executed with an external electrode on the right side of the neck. Chest dimensions and area of atelectasis were studied by computed tomography of the chest. RESULTS: Right-sided PNS against an occluded airway at functional residual capacity reduced the atelectatic area in the right lung from 5.1 to 3.8 cm2. The atelectasis was reduced to 1.1 cm2 after application of positive end-expiratory pressure (PEEP) of 10 cmH2O and large tidal volumes but increased to 2.5 cm2 within 1 min after discontinuation of PEEP. Commencement of PNS immediately after PEEP prevented the atelectasis from increasing, the mean area being 0.9 cm2. In seven patients, in whom the trachea was intubated with a double-lumen endobronchial catheter the atelectatic area was smaller during PNS with an open airway than during positive pressure inflation of the lung with the same volume as inspired during PNS (3.5 and 5.2 cm2, respectively. CONCLUSIONS: The findings indicate that contracting the diaphragm in the anesthetized subject reduces the size of atelectasis.

Adult↗
PubMed1995

Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia.

BACKGROUND: Atelectasis, an important cause of impaired gas exchange during general anesthesia, may be eliminated by a vital capacity maneuver. However, it is not clear whether such a maneuver will have a sustained effect. The aim of this study was to determine the impact of gas composition on reappearance of atelectasis and impairment of gas exchange after a vital capacity maneuver. METHODS: A consecutive sample of 12 adults with healthy lungs who were scheduled for elective surgery were studied. Thirty minutes after induction of anesthesia with fentanyl and propofol, the lungs were hyperinflated manually up to an airway pressure of 40 cmH2O. FIO2 was either kept at 0.4 (group 1, n = 6) or changed to 1.0 (group 2, n = 6) during the recruitment maneuver. Atelectasis was assessed by computed tomography. The amount of dense areas was measured at end-expiration in a transverse plane at the base of the lungs. The ventilation-perfusion distributions (VA/Q) were estimated with the multiple inert gas elimination technique. The static compliance of the total respiratory system (Crs) was measured with the flow interruption technique. RESULTS: In group 1 (FIO2 = 0.4), the recruitment maneuver virtually eliminated atelectasis for at least 40 min, reduced shunt (VA/Q < 0.005), and increased at the same time the relative perfusion to poorly ventilated lung units (0.005 < VA/Q < 0.1; mean values are given). The arterial oxygen tension (PaO2) increased from 137 mmHg (18.3 kPa) to 163 mmHg (21.7 kPa; before and 40 min after recruitment, respectively; P = 0.028). In contrast to these findings, atelectasis recurred within 5 min after recruitment in group 2 (FIO2 = 1.0). Comparing the values before and 40 min after recruitment, all parameters of VA/Q were unchanged. In both groups, Crs increased from 57.1/55.0 ml.cmH2O-1 (group 1/group 2) before to 70.1/67.4 ml.cmH2O-1 after the recruitment maneuver. Crs showed a slow decrease thereafter (40 min after recruitment: 61.4/60.0 ml.cmH2O-1), with no difference between the two groups. CONCLUSIONS: The composition of inspiratory gas plays an important role in the recurrence of collapse of previously reexpanded atelectatic lung tissue during general anesthesia in patients with healthy lungs. The reason for the instability of these lung units remains to be established. The change in the amount of atelectasis and shunt appears to be independent of the change in the compliance of the respiratory system.

Adult↗