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Abstract |
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A vital capacity maneuver (VCM) (inflating the lungs to 40 cm H2O for 15 s) is effective in relieving atelectasis during general anesthesia or after cardiopulmonary bypass (CPB). The study was undertaken to investigate the safety of one or repeated VCM. Five groups of six pigs were studied. Two groups had general anesthesia for 6 h and one group received a VCM every hour. Three other groups received CPB. VCM was performed after CPB in two of these groups. VCM was then repeated every hour in one of the groups. Lung damage was evaluated by extravascular lung water (EVLW) measurement, light microscopy, and the half-time (T1/2) of disappearance from the lung of a nebulized aerosol containing 99mTc-DTPA. No changes were noted in extravascular lung water. The pigs subjected to VCM decreased their T1/2. In the groups exposed to repeated VCM, T1/2 remained lowered (CPB pigs) or decreased over time (non-CPB pigs). No lung damage could be seen on the morphology study. These results suggest that one VCM is a safe procedure. The increase in lung clearance of 99mTc-DTPA not associated with an increase in lung water when VCM is repeated may have been caused by an increase in lung volume. Therefore, repeated VCM also appears to be safe.
Implications: This study demonstrates in an animal model that inflating the lung once or repeatedly to the vital capacity is a safe procedure. This maneuver, also called the vital capacity maneuver, can be used to relieve lung collapse which occurs in all patients during general anesthesia.
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Introduction |
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The vital capacity maneuver (VCM) is effective in relieving atelectasis during general anesthesia (1). This maneuver has also been effective in preventing atelectasis formation and gas exchange impairment after cardiopulmonary bypass (CPB) in a pig model (2). One VCM is effective for up to 6 h after the end of the CPB. There is no extra benefit in repeating this maneuver every hour, although respiratory compliance increases (3). However, when using high inspired oxygen fraction (FIO2), atelectasis recurs within 5 min after a VCM during general anesthesia (4). In some clinical situations, the administration of 100% O2 is recommended (before intubation or any airway maneuver; during transport of an intubated patient; and after CPB, particularly when the aorta or the heart has been opened); therefore, it could be useful to repeat the VCM. Moreover, in patients with the adult respiratory distress syndrome a "sigh" strategy, comparable to repeated VCM, improves alveolar recruitment and oxygenation (5). However, inflating the lungs to vital capacity carries potential negative effects, such as barotrauma and even temporary hemodynamic depression, if not performed during the CPB. So far, when combining all previous studies, approximately 500 patients have received a VCM without any negative effect. However, there are no reports on repeated VCM and no particular measurement has detected lung damage. The aim of this study was, therefore, to evaluate if one or more VCM, with or without CPB, could produce lung damage.
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Methods |
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After approval by the animal research ethical committee of Uppsala University, 30 pigs were randomly allocated to five different groups (n = 6 each). In the CPB + 1 VCM group, a VCM was performed 5 min before the end of CPB. Another group was subjected to VCM as just mentioned, and the VCM was then repeated hourly for 6 h (CPB + 6 VCM group). A third group had CPB but no VCM (CPB + 0 group). Two groups were not subjected to CPB and had no form of surgery, i.e., in a control group the pigs were anesthetized for 6 h without VCM and in the 6 VCM group, VCM was performed every hour after baseline measurements.
As we have previously shown (2), the pressure necessary (40 cm H2O) to obtain a maximal inflation of the lungs with a closed chest is the same as that required with an open chest at the end of CPB. Therefore, the VCM consisted of inflating the lungs to 40 cm H2O pressure, which was held for 15 s. The same technique was applied to the three groups in which VCM was applied.
After anesthetic induction and muscle relaxation, tracheal intubation was performed and artificial ventilation was started. The tidal volume was 10 mL/kg and the frequency adjusted to maintain an end-tidal CO2 tension between 5.2 and 5.6 kPa (39–42 mm Hg) with a positive end-expiratory pressure of 4 cm H2O. The ventilator settings were kept constant throughout the procedure. The FIO2 was 0.4 balance nitrogen. For further details, see Magnusson et al (2,6). A catheter was inserted in the carotid artery for pressure measurements and blood sampling. A fiberoptic catheter (Pulsiocath 4F FT PV 2024; Pulsion Medical Systems, München, Germany) was inserted in the same artery and advanced into the aorta for lung water measurements. A Swan-Ganz thermodilution catheter was introduced in the external jugular vein and advanced to the pulmonary artery for cardiac output measurements.
Perfusion was conducted by using a nonpulsatile pump (Gambro®, PMO 10–220; Lund, Sweden) after 400 IU/kg heparin sodium was administered. Ventilation was stopped during CPB, the respirator disconnected, and the airway opened to atmosphere. The aorta was clamped and cardioplegic solution (St. Thomas Type I) with 0.27 mg/L procaine was injected until cardiac arrest. Hypothermia to 30°C was induced with a thermal exchanger (Chiller Thermo Circulator®; Churchill Instruments, Perivale, England) coupled to the oxygenator. During CPB, chest drains were inserted in both pleura, and after chest closure, a negative suction was applied.
The total duration of the cardiac ischemia was 45 min. Rewarming was initiated with the thermal exchanger and continued for 40 min. The pigs were separated from the CPB. The total duration of CPB was 90 min. At 15 min before termination of CPB, ventilation was reinstituted at one-half the tidal volume. Just before termination of the bypass, the VCM was performed for the two VCM groups. Normal tidal volumes were given. The heparin effect was reversed with 1 mg protamine for each 100 IU used. For further details, see Magnusson et al (2,6).
The pigs of the five groups had a basal infusion of 150 mL/hour of NaCl 0.9%. In the three bypass groups, extensive evaporation from the surgical field was estimated to 10–15 mL · kg-1 · h-1. Two hours with an opened sternum and the great vessels, the heart, and the lungs in contact with the atmosphere may have caused a fluid loss of approximately 900 mL. This fluid loss was approximately compensated for by the cardioplegic solution and the priming volume returned to the pig at the end of the CPB. To avoid any differences among the groups in the fluid balance, which could influence gas exchange and lung water measurements, the fluid loss was followed by repeated measurements of hematocrit (Hct). In case of decreasing Hct, perfusion of crystalloid was reduced.
Measurements consisted of arterial blood gases, heart rate, systemic arterial pressures, cardiac output measured by thermodilution, extravascular lung water (EVLW) and intrathoracic blood volume (measured with the double-indicator dilution method) and total respiratory system static compliance (over the tidal volume and including and end-inspiratory pause of two seconds) as previously described (2,6). Lung integrity was evaluated with measurement of the alveolocapillary membrane permeability and morphology examination. Further details are given below.
For lung clearance, a solution of technetium-99m-labeled diethylenetriamine pentaacetate (99mTc-DTPA) was prepared from a commercial kit (DRN 4362 Technescan® DTPA; Mallinckrodt Medical, Petten, Holland) by using 10 mL of 99mTc-sodium pertechnetate labeled at 30 MBq. 99mTc-DTPA was delivered by an ultrasonic nebulizer placed in the inspiratory circuit (ultra-neb 99TM, DeVilbiss, Somerset, UK). This nebulizer enables preferential alveolar deposition of particles with a mass median diameter of 3.1 ± 1.6 µm (7). Nebulization was performed for 5 min until a total count of 1,000 counts per second was obtained. Radioactivity was measured over the entire chest in the anterior view by using a gamma camera with a low-energy, general purpose collimator for 25 min. The time-activity curve from both lungs was obtained. Correction was made for physical decay and background activity. Residual radioactivity from previous measurements remaining in the alveoli and pulmonary lymphatics was measured before each successive nebulization as background activity and eliminated. The half-life of the tracer in the lungs (T1/2) was calculated.
Three animals of each group were used for histological examination of the lungs. The animals were heparinized and the left pulmonary artery was cannulated and ligated proximal to the cannula. The left atrium was cannulated with a large venous bypass cannula. The animals were then killed with an IV injection of KCl. The lungs were inflated to an airway pressure of 20 cm H2O which was maintained during the subsequent perfusion procedure. Lactated Ringer’s solution was first infused into the left pulmonary artery at a pressure of 20 cm H2O until the perfusate was clear. Next, 4% formalin was infused during 20 min at the same pressure. The left lung was then removed and immersed in 4% formalin for 1 mo. After this procedure, the lungs were stiff and remained expanded when the distending pressure was removed. Three samples were taken at different regions from the left lung parenchyma (cranial part of the upper lobe, caudal part of the upper lobe, and the lower lobe). Paraffin sections from these samples, stained with hematoxylin-eosin, were examined by light microscopy with particular reference to the alveolar expansion pattern, hemorrhage, edema, and inflammatory cells. The examination was made by a pathologist blinded to the treatment group from which the tissue sample came.
A delay of 30 min was allowed after the surgical preparation before baseline measurements were made. After CPB all of the pigs were kept anesthetized with the same technique for 6 h. Because of the time necessary to remove the CPB cannulas and close the chest, the first postbypass measurements were not taken until 45 min after separation from CPB. The same measurements were then repeated at 3 and 6 h post-CPB. For the two groups not subjected to CPB, measurements were made at 1, 3, and 6 h after baseline. In the groups subjected to repeated VCM, measurements were performed 15 min after a VCM to avoid having a VCM performed during the 25 min measurement of radioactivity.
All data were collected and analyzed in a statistical program (StatView; Abacus Concepts, Berkeley, CA) and are presented in the text, table, and figures as mean ± SD. Analysis of variance was used to evaluate differences among the groups in the hemodynamic, lung fluid, 99mTc-DTPA, etc. When significant, pairwise comparisons were made to locate specific intergroup differences. As a post hoc test, the Bonferroni/Dunn was used to adjust for multiple comparisons. Effect of CPB and different exposure to VCM were evaluated comparing changes within each group over time. P < 0.05 was considered significant.
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Results |
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There were no significant differences in respiratory mechanics, central hemodynamics, gas exchange, EVLW, T1/2, or body weight among the five groups at baseline (Table 1). No significant changes were noted in the hemodynamic variables, the Hct, or in the EVLW during the whole study period (Table 1).
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PaO2/FIO2 decreased directly after CPB from 476 to 265 mm Hg (P < 0.01) in the CPB + 0 group, and not at all in the CPB + 1 VCM and the CPB + 6 VCM groups. Despite a spontaneous improvement in the CPB + 0 group, PaO2/FIO2 remained lower than baseline and lower than in the other groups 6 h after the end of CPB (Table 1). On the other hand, when pigs were not subjected to CPB, PaO2/FIO2 increased significantly after 1 VCM and further improved after 6 VCM (Table 1).
At the end of the CPB, end-inspiratory airway pressure (Peiaw) had increased and respiratory compliance decreased in the three CPB groups. Compliance, on the contrary, progressively increased and Peiaw decreased in the 6 VCM group. These variables were unchanged in the control group (Table 1).
T1/2 was unchanged during the 6 h of general anesthesia in the control group, as well as in the CPB + 0 group (Fig. 1 and 2). Directly after the CPB, T1/2 had significantly decreased in the two CPB groups treated with a VCM. However, T1/2 increased rapidly toward baseline in the CPB + 1 VCM group during the following hours while it remained lowered in the CPB + 6 VCM group (Fig. 2). Finally after three hours of anesthesia and repeated VCM, T1/2 decreased significantly in the 6 VCM group and remained lowered thereafter (Fig. 1).
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No severe lesions, such as alveolar wall rupture, could be seen in any groups. There where no clear signs of interstitial or alveolar edema or hemorrhages. The degree of inflation of the alveoli showed marked differences between the lung regions where it was observed. The lower lobe showed many areas with collapsed alveoli in all groups (Fig. 3). In the cranial part of the upper lobe the alveoli were more expanded in all groups (Fig. 4).
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Discussion |
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A VCM performed during general anesthesia, with or without CPB, had no deleterious effect on the lungs as assessed by EVLW measurements, 99mTc-DTPA clearance, and morphological analysis. Repeated VCM increased the pulmonary clearance of 99mTc-DTPA. Although this finding may indicate increased capillary leak, in this study it is more likely related to other events, as will be discussed below. Indeed, EVLW measurements did not detect significant leakage in the groups receiving multiple VCM. Finally, the lung morphology studies did not reveal evidence of alveolar disruption after repeated VCM. Therefore, repeated VCM is also a safe procedure.
Pulmonary clearance of 99mTc-DTPA (expressed as the half-life of the tracer) is an indicator of the functional integrity of the alveolocapillary barrier. The clearance rate is changed by various factors. Interstitial lung disease increases T1/2 of 99mTc-DTPA (8), as well as high-permeability edema conditions, such as neonatal respiratory distress syndrome and acute respiratory distress syndrome (9). Decreased alveolar surfactant content or function decreases T1/2 (10) and experimentally increased alveolar surfactant content increases T1/2 (11), indicating a role for the surfactant system in limiting the alveolocapillary transfer of solutes. Numerous studies have demonstrated that T1/2 decreases when lung volume is increased (12,13).
In our pig model, the two groups exposed to a VCM at the end of the CPB showed a decreased T1/2. Various mechanisms can explain this decrease. High permeability edema caused by overstretching of the alveoli or by shear force, as described in one-lung ventilation (14,15) can occur after CPB. However, the absence of increase of the EVLW, the absence of perturbation of the gas exchange, and in-lung morphology make this hypothesis unlikely. A decrease in the amount of surfactant occurs after CPB (16) and this may be a possible cause of the decrease of T1/2 seen directly after CPB. However, repeated VCM stimulates surfactant production in fetal and newborn animals (17,18) and it is likely that the effect of repeated VCM is similar in our pig model. This should prolong the T1/2, not shorten it. An increase in lung volume produced by various mechanisms has been demonstrated to decrease T1/2 (12). The persistence of decreased T1/2 in the CPB + 6 VCM group, as well as the later decrease in the 6 VCM group, may therefore be explained by a progressive increase in the lung volume produced by repeated VCM. This is consistent with our observation of increased pulmonary compliance and improved gas exchange seen in the two groups exposed to repeated VCM (13).
On the other hand, there was no change in the lung clearance after CPB itself, as seen in the CPB + 0 group. In this group, large atelectasis is certainly present at the end of CPB as previously shown (2,6) and functional residual capacity is most likely reduced, as has been shown after cardiac surgery (19). Whether such decrease in lung volume increases T1/2, as does an overall lung volume reduction (12,13), is not clear. The decrease in the surface area caused by atelectasis and the reduced amount of surfactant caused by CPB act on T1/2 of 99mTc-DTPA in an opposite way. These interacting mechanisms may explain the absence of changes in the T1/2 in our pig model. In humans, conflicting results of the effect of CPB on the permeability of the alveolocapillary membrane have been found. One study has shown an increase in the alveolocapillary permeability (20). However, in contrast to our study, continuous positive airway pressure was applied during CPB. Other studies have shown no increase in the permeability (21) or only after prolonged CPB (>120 min) (22).
No lung damage, in particular no alveolar rupture, could be seen in any groups. No differences were observed among the groups.
Alveolar inflation shows considerable difference between the various regions at which the three specimens have been taken. The more cranial the specimens, the more expanded were the alveoli. This confirms our previous finding that atelectasis, measured with computed tomography scan, predominates at the level of the diaphragm (2,6).
Only a few studies have evaluated lung morphology after CPB. The oldest studies have all shown perivascular and interstitial tissue edema with some bleeding in the alveolus or in the perivascular connective tissue (23,24). More recently (25), perivascular and interstitial edema was sometimes seen associated with intraalveolar edema and extravasated corpuscular blood elements. In our study, these histological changes (edema or bleeding) were not seen, whether or not the animals were exposed to CPB or VCM. Our results, compared with those reported in previous studies, probably illustrate the improvement in equipment and management during CPB over the years.
No previous studies have investigated the safety of VCM. In this study, no negative effect was found when one VCM was applied during general anesthesia. This is also true when a VCM is applied at the end of 90 minutes of CPB, despite the probable increased fragility of the lung tissue caused by a period of lung ischemia. An increase in lung clearance of 99mTc-DTPA was seen after repeated VCM, which is best explained by an increase in lung volumes. Therefore, repeated VCM in this pig model is also safe. Nevertheless, repeated VCM in humans should be carefully analyzed with regard to possible beneficial, as well as, negative effects before any application of the technique in the clinical routine.
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Acknowledgments |
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Supported, in part, by grant #5315 from the Swedish Medical Research Council and a grant from the Swedish Heart-Lung Fund.
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Footnotes |
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This work is attributed to the Department of Clinical Physiology, Uppsala University Hospital, Uppsala, Sweden.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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-
Rothen HU, Sporre B, Engberg G, et al. Re-expansion of atelectasis during general anaesthesia: A computed tomography study. Br J Anaesth 1993; 71: 788–95.
[Abstract/Free Full Text] - Magnusson L, Zemgulis V, Tenling A, et al. Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass: An experimental study. Anesthesiology 1998; 88: 134–42.[Web of Science][Medline]
-
Magnusson L, Wicky S, Tyden H, Hedenstierna G. Repeated vital capacity manoeuvres after cardiopulmonary bypass: Effects on lung function in a pig model. Br J Anaesth 1998; 80: 682–4.
[Abstract/Free Full Text] - Rothen HU, Sporre B, Engberg G, et al. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995; 82: 832–42.[Web of Science][Medline]
-
Pelosi P, Cadringher P, Bottino N, et al. Sigh in acute respiratory distress syndrome. Am J Respir Crit Care Med 1999; 159: 872–80.
[Abstract/Free Full Text] - Magnusson L, Zemgulis V, Wicky S, et al. Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: An experimental study. Anesthesiology 1997; 87: 1153–63.[Web of Science][Medline]
- Lagerstrand L, Dahlback M, Hedenstierna G. Gas exchange during simulated airway secretion in the anaesthetized rabbit. Eur Respir J 1992; 5: 1215–22.[Abstract]
-
Chinet T, Jaubert F, Dusser D, et al. Effects of inflammation and fibrosis on pulmonary function in diffuse lung fibrosis. Thorax 1990; 45: 675–8.
[Abstract/Free Full Text] - Coates G, O’Brodovich H. Measurement of pulmonary epithelial permeability with 99mTc-DTPA aerosol. Semin Nucl Med 1986; 16: 275–84.[Web of Science][Medline]
-
Evander E, Wollmer P, Jonson B, Lachmann B. Pulmonary clearance of inhaled 99mTc-DTPA: Effects of surfactant depletion by lung lavage. J Appl Physiol 1987; 62: 1611–4.
[Abstract/Free Full Text] -
Bos JA, Wollmer P, Bakker W, et al. Clearance of 99mTc-DTPA and experimentally increased alveolar surfactant content. J Appl Physiol 1992; 72: 1413–7.
[Abstract/Free Full Text] -
Cooper JA, van der Zee H, Line BR, Malik AB. Relationship of end-expiratory pressure, lung volume, and 99mTc-DTPA clearance. J Appl Physiol 1987; 63: 1586–90.
[Abstract/Free Full Text] -
Marks JD, Luce JM, Lazar NM, et al. Effect of increases in lung volume on clearance of aerosolized solute from human lungs. J Appl Physiol 1985; 59: 1242–8.
[Abstract/Free Full Text] - Mahfood S, Hix WR, Aaron BL, et al. Reexpansion pulmonary edema. Ann Thorac Surg 1988; 45: 340–5.[Abstract]
-
Matsuura Y, Nomimura T, Murakami H, et al. Clinical analysis of reexpansion pulmonary edema. Chest 1991; 100: 1562–6.
[Abstract/Free Full Text] - Marcatili S, Guarino C, Giannattasio A, et al. Alterations of the endoalveolar surfactant after surgery with extracorporeal circulation. Respiration 1990; 57: 233–8.[Web of Science][Medline]
- Corbet A, Voelker R, Murphy F, Owens M. Effect of calcium and calcium antagonists on phospholipid secretion induced by lung inflation in newborn rabbits. Am J Med Sci 1991; 301: 102–14.[Web of Science][Medline]
- Faridy EE, Thliveris JA. Rate of secretion of lung surfactant before and after birth. Respir Physiol 1987; 68: 269–77.[Web of Science][Medline]
-
Jonmarker C, Nordstrom L, Werner O. Changes in functional residual capacity during cardiac surgery. Br J Anaesth 1986; 58: 428–32.
[Abstract/Free Full Text] - Royston D, Minty BD, Higenbottam TW, et al. The effect of surgery with cardiopulmonary bypass on alveolar-capillary barrier function in human beings. Ann Thorac Surg 1985; 40: 139–43.[Abstract]
- Macnaughton PD, Braude S, Hunter DN, et al. Changes in lung function and pulmonary capillary permeability after cardiopulmonary bypass. Crit Care Med 1992; 20: 1289–94.[Web of Science][Medline]
-
Raijmakers PG, Groeneveld AB, Schneider AJ, et al. Transvascular transport of 67Ga in the lungs after cardiopulmonary bypass surgery. Chest 1993; 104: 1825–32.
[Abstract/Free Full Text] -
Asada S, Yamaguchi M. Fine structural change in the lung following cardiopulmonary bypass: Its relationship to early postoperative course. Chest 1971; 59: 478–83.
[Abstract/Free Full Text] - Ratliff NB, Young WG, Hackel DB, et al. Pulmonary injury secondary to extracorporeal circulation: An ultrastructural study. J Thorac Cardiovasc Surg 1973; 65: 425–32.[Web of Science][Medline]
- Anyanwu E, Dittrich H, Gieseking R, Enders HJ. Ultrastructural changes in the human lung following cardiopulmonary bypass. Basic Res Cardiol 1982; 77: 309–22.[Web of Science][Medline]
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