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ABSTRACT |
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This study was directed at assessing changes in bronchial cross-sectional surface areas (BCSA) and in respiratory resistance induced by endotracheal suctioning in nine anesthetized sheep. Cardiorespiratory parameters (Swan-Ganz catheter), respiratory resistance (inspiratory occlusion technique), BCSA, and lung aeration (computed tomography) were studied at baseline, during endotracheal suctioning, and after 20 consecutive hyperinflations. Measurements performed initially at an inspired oxygen fraction (FIO2) of 0.3 were repeated at an FIO2 of 1.0. At an FIO2 of 0.3, endotracheal suctioning resulted in atelectasis, a reduction in BCSA of 29 ± 23% (mean ± SD), a decrease in arterial oxygen saturation from 95 ± 3% to 87 ± 12% (p = 0.02), an increase in venous admixture from 19 ± 10% to 31 ± 19% (p = 0.006), and an increase in lung tissue resistance (DRrs) (p = 0.0003). At an FIO2 of 1.0, despite an extension of atelectasis and an increase in pulmonary shunt from 19 ± 5% to 36 ± 2% (p < 0.0001), arterial O2 desaturation was prevented and BCSA decreased by only 7 ± 32%. A recruitment maneuver after endotracheal suctioning entirely reversed the suctioning-induced increase in DRrs and atelectasis. In three lidocaine-pretreated sheep, the endotracheal suctioning-induced reduction of BCSA was entirely prevented. These data suggest that the endotracheal suctioning-induced decrease in BCSA is related to atelectasis and bronchoconstriction. Both effects can be reversed by hyperoxygenation maneuver before suctioning in combination with recruitment maneuver after suctioning.
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INTRODUCTION |
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ABSTRACT
INTRODUCTION
METHODS
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DISCUSSION
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Endotracheal suctioning in intubated patients is directed at clearing bronchial secretions, which tend to accumulate because tracheal intubation markedly impairs mucociliary transport. The classical procedure for endotracheal suctioning consists of disconnection from mechanical ventilation, followed by insertion of a suction catheter into the trachea for tracheal suctioning under negative pressure. Each step of this maneuver is potentially harmful, and complications reported with it include arterial hypoxemia and atelectasis (1), bronchospasm (2), tracheal mucosal damage (3), cardiac arrhythmias (4), intracranial hypertension (5), and sudden death (6). Most previous studies of endotracheal suctioning have focused on the prevention and treatment of suctioning-induced impairment of arterial oxygenation. Some preventive maneuvers for this have been proposed, such as preoxygenation with an inspired oxygen fraction (FIO2) of 1 (7), hyperinflation before or after suctioning (8, 9), use of a special suction adaptor to avoid disconnection of the patient from the ventilator (10, 11), and insufflation of a constant flow of oxygen during endotracheal suctioning (1).
Recently, it has been shown that endotracheal suctioning may induce a transient bronchoconstrictive response in critically ill patients receiving mechanical ventilation (12). Experimental data suggest that the stimulation of airway irritant receptors produces reflex bronchoconstriction (13), and that this can be prevented with local anesthetic agents that act on sodium channels (14, 15). In ventilated animals or patients, changes in bronchomotor tone can be evaluated by means of the end-inflation airway occlusion technique (16, 17). Unfortunately, this technique provides limited information about the partition between bronchial and parenchymal responses, and no data on the distribution of the regional response. Recent developments in high-resolution computed tomography (HRCT) allow detection and measurement of the cross-sectional surface area of bronchi down to 1 mm in diameter. These developments have been used to assess bronchoconstriction in animal models and in asthmatic subjects (18) at a regional level, and appear to be complementary to the measurement of airway resistance.
The aims of this study, which combined these two approaches, were: (1) to assess the global and regional effects of endotracheal suctioning on bronchoreactivity and lung aeration; (2) to assess whether the endotracheal suctioning- induced increase in bronchoreactivity could be prevented by hyperoxygenation or inhalation of lidocaine; and (3) to assess whether the atelectasis resulting from endotracheal suctioning could be reversed by a postsuction recruitment maneuver. The sheep was used as an experimental model.
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METHODS
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Animal Preparation
Nine anesthetized and ventilated sheep (weight: 48 ± 3 kg [mean ± SD]) were studied while in the supine position. Anesthesia was induced and maintained with flunitrazepam (4 mg/h), fentanyl (200 µg/h),
and vecuronium (4 mg/h). The sheep were intubated with an endotracheal tube incorporating a one-sided port that ended at the distal tip
of the tube (Hi-Lo Jet No. 8; Mallinckrodt Inc., Argyle, NY). The animals were ventilated (César Ventilator; Taema, Antony, France) in a
volume-controlled mode with constant inspiratory flow (tidal volume
[VT] = 10 ml/kg, respiratory rate = 12 breaths/min, respiratory duty
cycle (TI/Ttot = 33%, and positive end-expiratory pressure [PEEP] = 5 cm H2O). A fiberoptic thermodilution catheter (Explorer S
O2/CO
[venous oxygen saturation/cardiac output], ComputerTM; Baxter SA,
Maurepas, France) was positioned in the pulmonary artery after denudation of the jugular vein. An arterial carotid catheter was placed after denudation of the artery.
Measurements
Systemic and pulmonary arterial pressures were monitored with calibrated pressure transducers (PX-1X2; Baxter) positioned at the level
of the radiology table on which pressure monitoring was done. The intravascular pressures measured in the right atrium and pulmonary artery were corrected according to the anteroposterior distance between these structures and the table. Airway pressure was measured
with a pressure transducer (P23id; Gould, Maurepas, France) connected to the distal port of the endotracheal tube. A No. 2 Fleisch
pneumotachograph (Fleisch, Lausanne, Switzerland) linked to a differential pressure transducer (Schlumberger, Velizy, France) was
placed at the proximal end of the endotracheal tube to measure flow
() and VT by integration (Integrator 13-4615-70; Gould, Cleveland,
OH). During each of the experimental phases used in the study (see
the subsequent discussion), arterial and pulmonary arterial blood
specimens were sampled for analysis of arterial oxygen tension
(PaO2), arterial carbon dioxide tension (PaCO2), venous oxygen tension
(PvO2), and pH (IL BGE; Instrumentation Laboratory, Milan, Italy);
hemoglobin concentration; and arterial (SaO2) and mixed venous
(SvO2) oxygen saturations (OSM3 hemoximeter, calibrated for sheep
blood; Radiometer, Copenhagen, Denmark). Cardiac output was
measured in triplicate by thermodilution, using a 5-ml injection of an
ice-cold 5% solution of dextrose in water.
The end-inflation airway occlusion technique was used to assess
respiratory mechanics (16): airway pressure, , and VT were recorded
after airflow was interrupted at end-inspiration by clamping of the endotracheal tube just proximal to the pneumotachograph. Occlusion
was relaxed after a plateau in airway pressure was achieved, representing the end-inspiratory elastic recoil pressure of the respiratory
system (Pel,rs). Each measurement of respiratory mechanics was made
in triplicate and recorded with an ES 1000 Gould recorder (Gould Instruments, Longjumeau, France), with measurements made during
the occlusion maneuver being stored in an IBM-compatible personal
computer by a 12-bit analog-to-digital board at a sample frequency of
200 Hz for subsequent data analysis. After the end-inspiratory occlusion, the decrease in airway pressure was analyzed with specifically designed software. The first decrease in pressure during a maximum of 0.1 s after the peak was considered as linear, and was fitted by linear regression. The pressure drop after 0.2 s was considered as exponential (for a period of at least 1 s) and was fitted accordingly. The initial pressure drop, P1, was considered as the pressure corresponding
to the intersection of the first and second pressure-decrease curves.
Calculations
Pulmonary (Rpv) and systemic (Rsv) vascular resistance, venous admixture (
VA/T), true pulmonary shunt (S/T), oxygen delivery
(DO2), and oxygen consumption (O2) were calculated according to
standard formulas. The static compliance of the total respiratory system (Crs) was calculated as: Crs = VT/
Pel,rs, where Pel,rs is the difference between the elastic recoil pressure of the respiratory system
(Pel,rs) and PEEP corrected for the intrinsic PEEP measured at the
end of a prolonged expiratory pause (17, 22). Total respiratory resistance (Rmax,rs) was calculated as Rmax,rs = (PImax 
Pel,rs)/F, where PImax
is the peak inspiratory pressure. Bronchial resistance (Rmin,rs) was calculated as Rmin,rs = (PImax P1)/. Lung tissue resistance (DRrs) was
calculated as DRrs = (P1 Pel,rs)/.
Thoracic Computerized Tomographic Scan
With the animal placed in the supine position in a computed tomography (CT) scanner (CE 10000; CGR-General Electric, Brie, France),
lung scanning was done of a series of three contiguous 1.5-mm-thick
sections taken at end-inspiration at the level of the lower lobes. The
appropriate level of the sections was chosen by means of a thoracic
scout view, and was just below the heart in order to reduce cardiac artifacts. No contrast medium was used, and images were photographed at
a window width of 1,600 HU and a level of 700 HU. For each acquisition for each part of the protocol, images from the same anatomic level
were selected by using anatomic landmarks such as vascular and bronchial branching points. The selected CT images were transmitted to a
workstation equipped with software dedicated to the assessment of
bronchial cross-sectional area (BCSA) and lung attenuation. The segmentation of bronchial cross-sections on CT images was obtained
through a method based on mathematical morphology theory, combining morphology filtering, connection cost marking, and conditional watershed techniques. This segmentation procedure was integrated with
a software package (Airway) that had previously been validated with simulated bronchi generated by mathematical modeling (23). The accuracy of measurement of surface BCSA was 95%, 91%, and 77% for
bronchi having a diameter greater than 2 mm and equal to 2 mm and
1 mm, respectively. Analysis included evaluation of changes in surface
BCSA and assessment of parenchymal lung attenuation. We compared the surface BCSA of the same bronchi identified on the three
CT sections for each of the three phases of each condition used in the
study. Lung parenchymal attenuation and pulmonary atelectasis were
assessed by an independent radiologist who was unaware of the study
condition under which CT scanning had been conducted.
Protocol
Animals were studied under one or more of the following three conditions:
Condition 1: FIO2 = 0.3. This condition was directed at evaluating the cardiorespiratory effects of endotracheal suctioning.
Condition 2: pretreatment with pure oxygen (FIO2 = 1). This condition was directed at assessing whether preadministration of pure oxygen could prevent the changes measured in Condition 1, as had already been suggested in humans (7).
Condition 3: pre-treatment with lidocaine (FIO2 = 0.3). This condition was intended to determine whether pretreatment with an aerosol of lidocaine could reverse the endotracheal suctioning-induced bronchoconstriction evidenced under Condition 1. We administered 200 mg of aerosolized 5% lidocaine over a 15-min period, using the jet nebulizer of the César ventilator. The inspiratory flow coming from the ventilator was corrected for the additional flow coming from the nebulizer. Control measurements were made immediately after the end of lidocaine administration.
Nine animals were studied under Condition 1, five under Conditions 1 and 2, and three under Conditions 1, 2, and 3, at 1-h intervals between each condition. Each animal served as its own control.
Each condition was divided into three successive phases, as follows:
Control. Measurements in this phase made after a 1-h steady state of mechanical ventilation with control ventilatory settings.
Endotracheal suctioning. In this phase the sheep was disconnected
from the ventilator. A suction catheter (Argyle; Sherwood Medical, Tullamore, Ireland) was inserted into the airways until resistance was met, and was then pulled back 3 cm. Endotracheal suctioning was begun at a negative suctioning pressure of 100 cm
H2O for 60 s. Measurements were made at the end of the 60-s period, during resumption of mechanical ventilation at control ventilatory settings.
Postsuction recruitment maneuver. A recruitment maneuver in which animals took 20 VT breaths each of 20 ml/kg volume, was applied immediately after endotracheal suctioning, and measurements were made at the end of this recruitment maneuver.
Statistical Analysis
Results are expressed as mean ± SD in the text and tables, and as mean ± SEM in figures. Surface BCSA, hemodynamic, lung mechanical, and blood gas data were compared among the three phases of each study condition through one-way analysis of variance (ANOVA) for repeated measures. Surface BCSA, hemodynamic, lung mechanical, and blood gas data under Condition 1 (FIO2 = 0.3) and under Condition 2 (FIO2 = 1) were compared through two-way ANOVA for the single grouping factor of FIO2, and for the single within-group factor of endotracheal suctioning. Changes in surface BCSA after nebulization of lidocaine were analyzed in 25 bronchi through two-way ANOVA for the two within-group factors of lidocaine and endotracheal suctioning. Relationships between surface BCSA and airway resistance were evaluated through linear regression analysis. A value of p < 0.05 was considered statistically significant.
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RESULTS |
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Effects of Endotracheal Suctioning on Hemodynamics and Gas Exchange
FIO2-0.3. Endotracheal suctioning induced a significant decrease in PaO2 and a significant increase in VA/T (Figure 1 and Table 1). The decrease in PaO2 was accompanied by a significant increase in mean pulmonary artery pressure and in
Rpv, and by a significant decrease in SaO2 and SvO2. The postsuction recruitment maneuver (PImax = 35 ± 4 [mean ± SD]
cm H2O) reversed these effects and induced a significant decrease in PaCO2. All other values remained unchanged.
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Pretreatment with pure oxygen. Endotracheal suctioning induced a significant decrease in PaO2 associated with a significant increase in S/T (Figure 1 and Table 2). Arterial desaturation was not observed after endotracheal suctioning. The
postsuction recruitment maneuver reversed these deleterious
effects.
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Pretreatment with lidocaine (FIO2-0.3). Aerosolization of lidocaine did not modify the hemodynamic or respiratory responses to endotracheal suctioning.
Effects of Endotracheal Suctioning on Respiratory Mechanics
FIO2-0.3. Endotracheal suctioning induced a significant increase in DRrs (76 ± 45%), Rmax,rs (33 ± 12%) and Rmin,rs (18 ± 40%) (Figure 2, and Table 3). Rmax,rs returned to its baseline value after the postsuction recruitment maneuver. Endotracheal suctioning induced a 27 ± 19% decrease in Crs, associated with a significant increase in PImax and Pel,rs, which returned to control values after the postsuction recruitment maneuver.
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Pretreatment with pure oxygen. Endotracheal suctioning significantly increased DRrs (96 ± 77%) and Rmax,rs (72 ± 63%) (Figure 2). The increase in Rmin,rs was not significant. Endotracheal suctioning-induced changes in Rmax,rs and DRrs were not different from those observed at FIO2 = 0.3.
Pretreatment with lidocaine. Aerosolization of lidocaine prevented the increase in Rmax,rs, and DRrs after endotracheal suctioning (Figure 3).
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Effects on Surface BCSA
FIO2-0.3. Sixty-four bronchi from seven different sheep, with surface BCSA ranging from 1 mm2 to 145 mm2, were found suitable for analysis (Figure 4 and Table 3). As shown in Table 3, a reduction of the surface BCSA was observed after endotracheal suctioning. The reduction was partly reversed by the postsuction recruitment maneuver. An illustrative example is shown in Figure 4, which also shows that the bronchial response to endotracheal suctioning differed according to the size of the airways.
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Pretreatment with pure oxygen. As shown in Figure 5, endotracheal suctioning reduced surface BCSA by only 7 ± 32% at FIO2 = 1, versus a reduction of 38 ± 15% at FIO2 = 0.3 (p < 0.01).
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Pre-treatment with lidocaine. Changes in surface BCSA with and without pretreatment with inhaled lidocaine were compared in 25 bronchi from three sheep (Figure 5). The endotracheal suctioning-induced decrease in BCSA was attenuated by lidocaine (p < 0.05).
Correlation between respiratory resistance and surface BCSA. There was a significant inverse correlation between changes in surface BCSA and DRrs (Figure 6). No correlation of surface BCSA was found with changes in Rminsrs and Rmax,rs.
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Effects of Endotracheal Suctioning on Lung Aeration
FIO2-0.3. Lung aeration could be analyzed in eight sheep. In four of these sheep, endotracheal suctioning induced an increase in areas of nonaerated parenchyma of at least 30% which was entirely reversed by the postsuction recruitment maneuver.
Pretreatment with pure oxygen. At FIO2-1.0, lung aeration could be analyzed in four sheep. Endotracheal suctioning induced an increase in areas of nonaerated parenchyma of more than 30% in one of these four sheep and in more than 60% in the other three sheep. In all animals, the extension of nonaerated lung regions was greater at FIO2-1.0 than at FIO2-0.3. An illustrative example is shown in Figure 7. Atelectasis was completely reversed by the postsuction recruitment maneuver.
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Pretreatment with lidocaine (FIO2-0.3). Pretreatment with lidocaine did not prevent endotracheal suctioning-induced atelectasis.
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DISCUSSION |
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In mechanically ventilated sheep with normal lungs, endotracheal suctioning induced a significant reduction in the surface BCSA of bronchi of more than 1 mm in diameter. It also induced an increase in respiratory resistance, an impairment of arterial oxygenation, and the appearance of atelectatic lung areas. The reduction of surface BCSA was attenuated by hyperoxygenation before suctioning, and was abolished by the use of aerosolized lidocaine before suctioning. Atelectasis was aggravated by hyperoxygenation before suctioning, and could only be reversed by a postsuction recruitment maneuver.
Endotracheal Suctioning-Induced Reduction of Bronchial Diameter
Following endotracheal suctioning, a significant reduction surface BCSA was observed at FIO2 = 0.3. Two mechanisms are likely to have contributed to this reduction of surface BCSA: (1) a loss of lung volume related to the loss of aeration resulting from the negative pressure applied during the suction procedure; and (2) reflex bronchoconstriction (24).
A constriction of bronchial muscles can be provoked by the
direct stimulation of bronchial stretch receptors caused by
moving a suction catheter in the airways (13). Endotracheal
suctioning-induced arterial oxygen desaturation may also and
independently increase bronchomotor tone (25). Fisher
and colleagues studied the responsiveness of airway smooth
muscle to hypoxia by administering a 10% O2 mixture to paralyzed and ventilated cats (25). They observed a 50% increase in Rmax,rs. Two different mechanisms accounted for the hypoxia-induced bronchoconstriction: direct stimulation of bronchopulmonary afferent branches of the vagal nerve (28), and
the release of bronchoconstrictor mediators by mast cells (29).
The results of the present study strongly suggest that endotracheal suctioning induces a true bronchoconstriction. First, the
endotracheal suctioning-induced decrease in surface BCSA
and increase in respiratory resistance were totally prevented by the administration of lidocaine before suctioning, possibly because of a blockade of stretch receptors. Second, hyperoxygenation before suctioning suppressed the endotracheal suctioning-induced decrease in surface BCSA despite an
extension of atelectatic lung regions. When endotracheal suctioning was performed at FIO2 = 0.3, significant arterial oxygen
desaturation was observed, and was accompanied by a significant reduction of surface BCSA. When endotracheal suctioning was performed at FIO2 = 1.0, arterial oxygenation desaturation and a reduction of surface BCSA were prevented.
These findings suggest that hyperoxygenation before suctioning reverses the component of bronchoconstriction related to
endotracheal suctioning-induced hypoxemia. However, neither lidocaine- nor oxygen-induced blockade of the decrease in
surface BCSA prevented an endotracheal suctioning-induced
increase in S/T, suggesting that atelectasis was largely involved in the impairment of arterial oxygenation.
Endotracheal Suctioning-Induced Atelectasis
Pulmonary atelectasis following endotracheal suctioning and identified by thoracic CT was reported by Brochard and coworkers in patients with acute lung injury (1). In these patients, endotracheal suctioning was associated with an increase in lung CT attenuation and a 400-ml loss of lung volume. In the present study, in which sheep with normal lungs were studied, atelectatic lung areas were observed in half of the animals at an FIO2 of 0.3 and in all animals at an FIO2 of 1. As expected, the loss of lung aeration from atelectasis was associated with a decrease in lung compliance and a significant increase in the resistance of lung tissue.
Atelectasis may have been caused by three mechanisms:
(1) a loss of lung volume related to the high negative pressure
applied during the suctioning procedure; (2) the closure of
bronchi resulting from endotracheal suctioning-induced bronchoconstriction, and (3) the alveolar collapse associated with
the administration of pure O2. Mitzner and coworkers have
clearly shown that lung compliance, TLC, and RV decrease after bronchial constriction, indicating that the conducting airways play an important role in the regulation of lung elasticity
(30). The increase in S/T observed at an FIO2 of 1.0 matched
the greater extension of atelectatic lung regions evidenced in
all sheep, and was in accordance with the notion that pure oxygen can induce alveolar collapse (31, 32).
Relationships Between Respiratory Resistance and Surface BCSA
We combined HRCT scanning and the constant inspiratory flow occlusion method to assess the bronchial effects of endotracheal suctioning. The HRCT method has the advantages of being quantitative, reproducible, and noninvasive, allowing an accurate assessment of the surface BCSA of different-sized airways down to a diameter of 1 mm. In addition, it is the only existing method that can show locoregional differences in airway reactivity (33, 34). Classically, in animals or humans whose lungs are mechanically ventilated, resistance of the respiratory system, including respiratory tubing and conducting airways, is measured by applying an end-inspiratory occlusion after the administration of a constant inspiratory flow (16, 17). In the present study, we preferred to do this by manual clamping rather than automatic interruption from the ventilator in order to eliminate errors in the measurement of respiratory resistance related to excessive closing time and incomplete sealing by the automatic interrupter device (35). In addition, we measured airway pressure at the distal tip of the endotracheal tube, and Rmax,rs therefore reflected only the resistive properties of conducting airways and lung tissue. In the study, we showed that an endotracheal suctioning-induced decrease in surface BCSA was associated with a predominant increase in DRrs. After endotracheal suctioning, some parts of the lungs became atelectatic, and various degrees of bronchoconstriction were observed in the bronchial tree. As a consequence, lung elasticity decreased, regional time constants of the lungs became more heterogeneous, and DRrs increased. Very logically, a good correlation was found between changes in DRrs and changes in surface BCSA.
Prevention and Treatment of Endotracheal Suctioning-Induced Hypoxemia, Bronchoconstriction and Atelectasis
Different maneuvers have been proposed to prevent endotracheal suctioning-induced hypoxemia in patients with acute lung injury (ALI). It has been shown that a constant insufflation of 12 L/min of O2 administered throughout the period of endotracheal suctioning prevents arterial O2 desaturation and loss of lung aeration. However, this procedure requires the reintubation of critically ill patients with a special endotracheal tube incorporating multiple side ports. The use of a closed suctioning system has been proposed as an alternative (36). However, this may result in partial obstruction of the endotracheal tube and may cause an increase in respiratory resistance (37).
A recruitment maneuver after suctioning has also been recommended to prevent arterial oxygen desaturation during and after endotracheal suctioning (8, 32). The present study confirms that a recruitment maneuver consisting of 20 consecutive breaths, each of 20 ml/kg volume and applied immediately at the end of endotracheal suctioning, reverses atelectasis and the increase in respiratory resistance. It should be pointed out that this beneficial effect was obtained in sheep with normal lungs, and that it may not be observed in animals or patients with ALI. Because bronchial reactivity is often increased and nonaerated pulmonary parenchyma is already present before endotracheal suctioning, these effects could increase hypoxemia and bronchoconstriction and render the recruitment maneuver less efficient. Additional studies are required to determine the type of postsuctioning recruitment maneuver that would be the most effective for reversing endotracheal suctioning-induced loss of lung aeration and bronchoconstriction in the presence of ALI.
In summary, we found that in normal sheep, hyperoxygenation before suctioning prevents endotracheal suctioning-
induced bronchoconstriction and arterial oxygen desaturation,
but not atelectasis or an increase in S/T. Aerosolized lidocaine
prevents the bronchoconstriction related to suctioning-induced
reflex bronchial stimulation, but does not prevent atelectasis
or impairment of arterial oxygenation. A recruitment maneuver after suctioning appears to be the only method that can reverse bronchoconstriction, the increase in S/T and atelectasis resulting from endotracheal suctioning.
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Footnotes |
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Correspondence and requests for reprints should be addressed to Pr. J.-J. Rouby, Réanimation Chirurgicale Pierre Viars, Department of Anesthesiology, La Pitié- Salpêtrière Hospital, 47-83, Boulevard de l'Hôpital, 75013 Paris, France. E-mail: jjrouby.pitie{at}invivo.edu
(Received in original form March 16, 2000 and in revised form June 22, 2000).
Acknowledgments: Supported by grant 920908 from the Institut National de la Sante et de la Recherche Medicale, France.
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References |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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