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Ann Thorac Surg 2002;74:1167-1172
© 2002 The Society of Thoracic Surgeons

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Original article: cardiovascular

Lung protection during total cardiopulmonary bypass by isolated lung perfusion: preliminary results of a novel perfusion strategy

^a Departments of Cardiac Surgery, University Hospital Luebeck, Luebeck, Germany
^b Department For Anesthesiology, University Hospital Luebeck, Luebeck, Germany

Accepted for publication June 5, 2002.

* Address reprint requests to Dr Sievers, Klinik fuer Herzchirurgie, Ratzeburger Allee 160, 23538 Luebeck, Germany
e-mail: sievers{at}medinf.mu-luebeck.de

	Abstract

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Background. The present pilot study was conducted to evaluate the effect of isolated short-term lung perfusion during cardiopulmonary bypass (CPB) on inflammatory response and oxygenation.

Methods. A total of 24 patients undergoing elective cardiac surgery with routine CPB were prospectively assigned to three groups. Group I (n = 7), control subjects receiving neither lung perfusion nor ultrafiltration; group II (n = 9), patients undergoing lung perfusion; and group III (n = 8), patients undergoing lung perfusion plus ultrafiltration. Lung perfusion consisted of single-shot hypothermic pulmonary artery perfusion with oxygenated blood. Proteins indicative of leukocyte activation and lung injury were measured in plasma and bronchoalveolar lavage fluid (BALF). The alveolar-arterial oxygen gradient (A-aDO₂) and the oxygenation index (PO₂/FiO₂) were also determined.

Results. Oxygenation values were best preserved in group III, followed by group II. After CPB, elastase-₁-proteinase inhibitor complex had increased in plasma in all groups; in BALF it increased in groups I and II, but not in group III. ₂-Macroglobulin increased significantly in BALF in group I but not in groups II and III.

Conclusions. These preliminary results provide some evidence that single-shot hypothermic lung perfusion with oxygenated blood at the beginning of CPB may have a protective effect on the lungs, especially when combined with ultrafiltration.

	Introduction

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Cardiopulmonary bypass (CPB) has become a commonplace procedure in cardiac operations, and initiates per se a variety of pathophysiological reactions resulting in an inflammatory response [1, 2]. These reactions involve the activation of the contact, complement, coagulation, and fibrinolytic systems and affect the functionality of platelets, the endothelium, and particularly of neutrophils [3]. The release of numerous proinflammatory and antiinflammatory substances contributes to the damaging effects of CPB [4, 5].

Respiratory dysfunction occurs in virtually all patients undergoing CPB [6] and remains a major cause of morbidity and mortality in cardiac surgery [7]. Postoperative lung dysfunction may be related to the inflammatory reactions induced by CPB, to the lung ischemia that occurs during CPB because of either low or no flow in the pulmonary arteries, to reperfusion injury, and to altered postoperative respiratory mechanics [3]. The contribution of lung ischemia to the pathophysiology of postoperative lung dysfunction is poorly understood. We hypothesized that cooling of the lungs at the beginning of CPB by short-term hypothermic pulmonary artery perfusion with oxygenated blood would have a protective effect on the lungs and result in improved oxygenation.

	Material and methods

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Study patients
A total of 24 patients who were designated for routine cardiac surgery were assigned prospectively and alternately to three groups. Emergency cases were excluded. In all, 7 patients were assigned to group I (controls: no lung perfusion, no ultrafiltration), 9 patients to group II (those patients undergoing lung perfusion), and 8 patients to group III (those patients undergoing lung perfusion plus ultrafiltration). The three groups did not differ significantly with regard to demographic or surgical data (Table 1). No patient was treated with steroids or calcium antagonists before the operation.

Anesthesia, CPB, and lung protection
Anesthesia was induced with Etomidat (0.3 mg/kg body weight), sufentanyl (1 µg/kg body weight), and pancuroniumbromide (0.1 mg/kg body weight); and maintained with continuous infusion of propofol (5 mg · kg^-1 · h^-1) and sufentanyl (1 µg · kg^-1 · h^-1). One radial artery and the internal jugular vein were cannulated.

After systemic heparinization (300 IU/kg body weight, ACT >440 seconds), CPB with moderate systemic hypothermia (28° to 30°C nasopharyngeal temperature) was initiated as follows: the ascending aorta was cannulated with an angled 8.0-mm cannula (Sherwood Medical GmbH, Sulzbach, Germany), the right atrial appendage with a two-stage venous cannula (AD 36/51 FR, Jostra Medizintechnik AG, Hirrlingen, Germany). A membrane oxygenator (Monolyth, Sorin Biomedica, Puchheim, Germany) and a roller pump (SIII, Stöckert, München, Germany) for nonpulsatile perfusion were used. The arterial line included a 40-µm filter (AF-1040 Gold, Benteley, Baxter, Irvine, CA). Pump flow was 2.4 l · min^-1 · m^-2 body surface area. Mean arterial pressure was kept between 60 and 70 mm Hg.

In groups II and III, lung perfusion was started once total pump flow was achieved. The main pulmonary artery was cannulated using an angled 6.0 arterial cannula (Sherwood Medical), and pulmonary artery perfusion was maintained for 10 minutes with 1 L/min of arterial blood from the CPB circuit cooled to 15°C by a separate heat exchanger (D270 P, Dideco, Mirandola, Italy). The lung perfusion line was fitted with a 40-µm arterial filter (D733, Dideco). Figure 1 shows two examples of lung temperature measured by superficial sensors placed between the left lung lobes. Lung temperature decreased during lung perfusion to 18°C, stayed constant for about 15 minutes, and increased to 33°C at the end of CPB. Without lung perfusion, the drop in temperature was less pronounced. During lung perfusion, the heart was beating but empty. If ventricular fibrillation occurred during lung perfusion, the left atrium was vented and cardiac arrest induced by crystalloid cardioplegia (St. Thomas; 800 mL initially, then 200 mL every 20 minutes). During lung perfusion, the lungs were ventilated with 8 mL tidal volume/kg body weight at a rate of 10 respirations/min, a fractional oxygen concentration of 0.4 in the inspired air, and a positive end-expiratory pressure of 5 mm Hg. After lung perfusion had ended, the lungs were no longer ventilated until the end of CPB. In the control group, the lungs were not ventilated during CPB.

View larger version (13K): [in this window] [in a new window]   Fig 1. Effect of lung perfusion on lung temperature as exemplified in 2 patients. Solid line = lung perfusion; broken line = no lung perfusion. (30' ECC = after 30 minutes of ECC; D-clamp = after release of the aortic clamp; ECC = extracorporeal circulation; ECC end = after end of ECC; X-clamp = at the time of aortic cross-clamping.)

Blood sample collection
In all patient groups, blood samples were collected from the radial artery line (after aspiration of 5 mL of blood for dead space) for the various assays at different times: (1) after induction of anesthesia but before surgery, (2) at clamping of the aorta, (3) after 30 minutes of CPB, (4) after declamping of the aorta, and (5) 60 minutes after CPB. A quantity of 2 mL of blood was placed into ethylenediaminetetraacetate-coated tubes, immediately centrifuged for 10 minutes at 3,000 g, and the plasma stored in polypropylene test tubes at -20°C until assayed. Blood samples for determination of the different oxygenation values were taken before anesthesia and 60 minutes after CPB.

Bronchoalveolar lavage
A bronchoalveolar lavage was performed parallel to taking blood samples for the assays. After injection of 10 mL of 0.9% saline into the trachea and two deep breaths of controlled ventilation, the bronchoalveolar lavage fluid (BALF) was collected from the left lower lobe by immediate aspiration through a flexible bronchoscope. After adding triaethanolamine HCl-buffer to the lavage fluid, centrifugation was performed for 10 minutes at 1,000 g. The supernatant was stored in polypropylene test tubes at -20°C until assayed.

Protein measurements
Proteins were measured in plasma and BALF. Elastase-₁-proteinase inhibitor complex [E₁PI] and ₂-macroglobulin [₂MG] were determined by luminescence immunoassay system according to the method described by Wood and colleagues [8]. All measurements were performed twice and the mean value was taken.

Alveolar-arterial oxygen gradient and oxygenation index
Blood samples for arterial gas analysis were processed immediately using a calibrated Ciba-Corning 288 Blood Gas System and a Ciba-Corning 270 CO-Oxymeter (Ciba-Corning Diagnostics, Medfield, MA). The alveolar-arterial oxygen gradient (A-aDO₂) was calculated as follows:

where PAO₂ is the partial pressure of alveolar oxygen and PaO₂ the partial pressure of arterial oxygen. PAO₂ was calculated as follows:

where FiO₂ is the fractional concentration of oxygen in the inspired air, BP the barometric pressure, PH₂O the saturated vapor pressure, PaCO₂ the arterial carbon dioxide tension pressure, and RQ the respiratory exchange ratio. For simplification, the term (BP-PH₂O) - (PaCO₂/RQ) was considered to be constant (760-47)-(36-/0.8) = 679 (mm Hg). To eliminate the influence of the inspired oxygen concentration, we also calculated the oxygenation index PaO₂/FiO₂.

Statistical analysis
Not all data for the different groups followed a normal distribution. They are therefore presented as medians (minimum-maximum), and nonparametric tests were applied. To assess changes occurring over time, the Friedmann or Wilcoxon tests were used. At given time points, groups were compared using the Kruskal-Wallis test. Post hoc comparisons were done using the Mann-Whitney U test. To correct for multiple comparisons, Bonferoni’s method was used. Statistical significance was defined at p less than or equal to 0.05. All analyses were performed with SPSS for Windows (SPSS Inc, Chicago, IL).

	Results

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Patients and pulmonary artery pressure
There were no in-hospital deaths. The time until extubation did not differ significantly between the groups (group I, 16 hours [range 13 to 19 hours]; group II, 8.5 hours [range 4 to 21 hours]; group III, 6.5 hours [range 4 to 20 hours]; p = 0.26). No elevation of pulmonary artery pressure was observed in patients with lung perfusion (groups II and III). In all groups, the median stay in the intensive care unit was 1 day (p = 0.52).

Elastase-₁-proteinase inhibitor complex
In BALF, the initial concentration of E₁PI initially did not differ significantly among the three groups (p = 0.80). During the entire study period, the concentration of E₁PI increased significantly in groups I (p = 0.011) and II (p = 0.003), but not in group III (p = 0.273). The time courses of the E₁PI concentrations in BALF for all groups is presented in Figure 2. In group II (patients with lung perfusion alone), the concentration of E₁PI remained low until aortic declamping, but increased thereafter; in group III (patients receiving lung perfusion with ultrafiltration), the concentration remained low even after aortic declamping.

View larger version (26K): [in this window] [in a new window]   Fig 2. Time course of elastase-1-proteinase inhibitor complex (E1PI) in the bronchoalveolar lavage (BAL) fluid. White boxes indicate group I (controls); light gray boxes, group II (patients undergoing lung perfusion); and dark gray boxes, group III (patients undergoing lung perfusion plus ultrafiltration). During the study period, E1PI levels increased significantly in groups I (p = 0.011) and II (p = 0.003), but not in group III (p = 0.273). Boundaries of the boxes indicate 25th and 75th percentiles. Lines in boxes represent median (50th percentile). Bars above and below boxes mark 10th and 90th percentiles. (CPB = cardiopulmonary bypass.)

₂-macroglobulin
In BALF, the initial concentration of ₂MG did not differ significantly among the three groups (p = 0.69). During the further course of the study, ₂MG concentrations increased significantly in the control group (p = 0.004), but remained unchanged in the lung perfusion groups II (p = 0.155) and III (p = 0.810) (Fig 3).

View larger version (22K): [in this window] [in a new window]   Fig 3. Time course of 2-macroglobulin (2MG) in bronchoalveolar lavage (BAL) fluid. White boxes indicate group I (controls); light gray boxes, group II (patients undergoing lung perfusion); and dark gray boxes, group III (patients undergoing lung perfusion plus ultrafiltration). During the study, 2MG levels increased significantly in group I (p = 0.004), but remained unchanged in groups II and III (p = 0.155 and 0.810, respectively). Boundaries of the boxes indicate 25th and 75th percentiles. Lines in boxes represent median (50th percentile). Bars above and below boxes mark 10th and 90th percentiles. (CPB = cardiopulmonary bypass.)

Oxygenation values
Initially A-aDO₂ did not differ significantly between the groups (p = 0.72). After CPB the A-aDO₂ had increased significantly (p < 0.001), but was significantly higher in the no-lung-perfusion control group than in the perfusion groups (p = 0.001). The difference between the latter two groups was not significant (p = 0.083; see Fig 4).

View larger version (15K): [in this window] [in a new window]   Fig 4. Time course of the alveolar-arterial oxygen gradient (A-aDO2) in bronchoalveolar lavage fluid. White boxes indicate group I (controls); light gray boxes, group II (patients undergoing lung perfusion); and dark gray boxes, group III (patients undergoing lung perfusion plus ultrafiltration). After cardiopulmonary bypass (CPB), A-aDO2 had increased significantly (p < 0.001), but it was significantly higher in the control group than in groups II and III (p = 0.001), which did not differ significantly from one another (p = 0.083). Boundaries of the boxes indicate 25th and 75th percentiles. Lines in boxes represent median (50th percentile). Bars above and below boxes mark 10th and 90th percentiles.

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
In the present study, we examined the effect of isolated, single-shot, hypothermic pulmonary artery perfusion with oxygenated blood on the inflammatory response and capillary leakage in lungs as well as on oxygenation. Our findings suggest that this novel strategy for CPB with lung protection—especially when combined with ultrafiltration—reduces lung injury and improves oxygenation.

Respiratory dysfunction is a well-known sequela of CPB, covering a wide spectrum of gas exchange abnormalities. In the worst case, adult respiratory distress syndrome may develop, particularly after operations using circulatory arrest or in patients with preexisting lung dysfunction. Several variables are known to be associated with respiratory dysfunction after CPB. One major determinant that is scarcely addressed in the literature is lung ischemia-reperfusion injury [9–11]. Nutrition for the lung parenchyma is provided by a dual system of blood supply through the bronchial and pulmonary arteries. In human subjects, the flow in the bronchial arteries during CPB varies considerably and was measured to be 3.23% ± 4% of cardiac output [12]. Kowalsky and colleagues [13] found an inverse correlation between bronchial artery flow during lung ischemia and the lung wet-to-dry ratio after reperfusion. Friedman and colleagues [10] demonstrated in a sheep model that levels of thromboxane B₂ are elevated after total CPB. Moreover, Serraf and associates [14] showed in neonatal piglets that CPB results in ischemia-reperfusion injury of the pulmonary vascular bed. Our study confirms these findings inasmuch as levels of E₁PI (an indirect measure of leukocyte activation [15, 16]) and ₂MG (an indicator of capillary leakage and thus of lung injury) in BALF were significantly increased in the control patients.

This growing body of evidence that the lungs are at risk of ischemia-reperfusion injury after CPB underscores the need for protective measures. In the present study, we used cold oxygenated blood for lung perfusion similar to a technique reported for lung transplantation [17]. Serraf and associates [14] reported that pulmonary artery perfusion with blood prevented hemodynamic alterations after CPB but failed to prevent any of the biochemical disturbances. In that study, however, the lungs were perfused with venous blood at 28°C. In our study, the lungs were cooled to lower temperatures using oxygenated blood while undergoing simultaneous ventilation, which might also influence pulmonary function and hemodynamics after reperfusion [9]. We cannot rule out the possibility that the beneficial effects observed in our groups II and III were caused by ventilation and not by the lung perfusion. However, lung ventilation was performed for only 10 minutes, which we think is insufficient to decrease capillary leakage and improve oxygenation. This, however, is a point that must be investigated in further studies.

Our technique of lung perfusion had a positive effect on capillary leakage, as indicated by the low ₂MG levels in the BALF and improved oxygenation values in group III. After CPB, however, the concentration of E₁PI was significantly elevated in group II, indicating that damage to the lung occurs in part after aortic declamping and cannot easily be prevented by lung perfusion. It can be hypothesized that application of systemic antiinflammatory strategies (eg, administration of methyprednisolone, aprotinin, or neutrophil elastase inhibitors, or use of leukocyte filtration or heparin-bonded circuits) or of more extensive local measures (eg, controlled continuous or intermittent perfusion of the lungs with special solutions [11, 18]) might better protect the lungs.

We could further demonstrate that ultrafiltration significantly reduces the inflammatory response in the lungs. The ability of ultrafiltration to remove inflammatory mediators such as interleukins, tumor necrosis factor, and activated complement components may account for this effect [19]. The low E₁PI levels in BALF of group III after CPB indicates that lung perfusion plus ultrafiltration were highly effective at preventing leukocyte-derived proteolytic enzymes from appearing in air space fluids. Leukocytes-derived elastase in the BALF is considered to be a strong indicator of lung tissue damage and is particularly elevated at the onset of adult respiratory distress syndrome [20]. No clear effect of ultrafiltration on the systemic inflammatory response as measured by plasma E₁PI levels was found.

₂-Macroglobulin is a protein of high molecular weight that passes through the capillary membrane only if damage had increased its permeability. Thus, our results suggest that lung perfusion during CPB—especially when combined with ultrafiltration—attenuates damage to alveolar epithelium and endothelial barriers. Oxygenation values improved when lung perfusion was combined with ultrafiltration (group III), and the time until extubation showed a trend towards shorter duration of ventilation. Whether these salutary effects have any impact on clinical events such as long-term respiratory function or the incidence of pneumonia remains to be established.

In summary, we were able to demonstrate that short-term hypothermic pulmonary artery perfusion with cold oxygenated blood during CPB—especially if combined with ultrafiltration—has a beneficial effect on the inflammatory response and capillary leakage in the lungs and improves oxygenation. Because of the study limitations (such as the small number of patients, nonrandomized protocol, heterogeneity of surgical procedures, and lack of clinical endpoints), this must be regarded as a pilot study and its results must be viewed as preliminary. However, the present findings underscore the rationale for lung protection during CPB and, it is hoped, will promote further research into measures to achieve it.

	Acknowledgments

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We are grateful to Dr H. J. Friedrich, Department of Medical Biometry and Statistics, for his statistical assistance; to Sabine Ziesewitz for performing the immunoassays; and to U. Schubert for preparing the manuscript.

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 

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