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Ann Thorac Surg 1999;68:181-187
© 1999 The Society of Thoracic Surgeons

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Original Articles

Percutaneous extracorporeal arteriovenous CO₂ removal for severe respiratory failure

^a Department of Surgery, University of Texas Medical Branch and Shriners Burns Institute, Galveston, Texas, USA
^b Department of Medicine, University of Texas Medical Branch and Shriners Burns Institute, Galveston, Texas, USA
^c Department of Radiology, University of Texas Medical Branch and Shriners Burns Institute, Galveston, Texas, USA
^d Division of Pulmonary and Critical Care Medicine, Louisiana State University Medical Center, Shreveport, Louisiana, USA

Address reprint requests to Dr Zwischenberger, Cardiothoracic Surgery, University of Texas Medical Branch, Galveston, TX 77555-0528;
e-mail: jzwische{at}utmb.edu

Presented at the Forty-fifth Annual Meeting of the Southern Thoracic Surgical Association, Orlando, FL, Nov 12–14, 1998.

	Abstract

Top Abstract Introduction Material and methods Results Comment References

 
Background. In previous animal studies, arteriovenous CO₂ removal (AVCO₂R) achieved significant reduction in ventilator pressures and improvement in the PaO₂ to fraction of inspired oxygen ratio during severe respiratory failure. For our initial clinical experience, 5 patients were approved for treatment of severe respiratory failure and CO₂ retention to evaluate the feasibility and safety of percutaneous AVCO₂R.

Methods. Patients were anticoagulated with heparin (activated clotting time, 260 to 300 seconds), underwent percutaneous femoral cannulation (10F to 12F arterial and 12F to 15F venous catheters), and then were connected to a low-resistance, 2.5-m² hollow-fiber oxygenator for 72 hours.

Results. Mean AVCO₂R flow at 24, 48, and 72 hours was 837.4 ± 73.9, 873 ± 83.6, and 750 ± 104.5 mL/min, respectively, with no vascular complications and no significant change in heart rate or mean arterial pressure. Removal of CO₂ plateaued at an AVCO₂R flow of 1086 mL/min with 208 mL/min CO₂ removed. Average CO₂ transfer at 24 and 48 hours was 142 ± 17 and 129 ± 16 mL/min. Use of AVCO₂R allowed a significant decrease in minute ventilation from 7.2 ± 2.3 L/min at baseline to 3.4 ± 0.8 L/min at 24 hours.

Conclusions. All patients survived the experimental period without adverse sequelae. Percutaneous AVCO₂R can achieve approximately 70% CO₂ removal in adults with severe respiratory failure and CO₂ retention without hemodynamic compromise or instability.

	Introduction

Top Abstract Introduction Material and methods Results Comment References

 
Despite recent advances in critical care, the overall mortality of adult respiratory distress syndrome (ARDS) remains approximately 40% to 50% [1]. Until recently, ARDS was treated primarily with mechanical ventilation aimed at restoring normal blood gases by aggressive volume-controlled ventilation and high (> 50%) oxygen concentration while the lungs were recovering from the initial injury or disease process. Volume-controlled ventilation, however, causes iatrogenic injury to the lungs, exacerbating ARDS by inflicting barotrauma and volume trauma [2, 3] to both the injured and uninjured portions of the lung. To reduce the high airway pressures and associated trauma, recent trends in ventilator management limit inflation pressure and tidal volume at the cost of a rise in systemic arterial carbon dioxide (CO₂) levels. This technique, termed permissive hypercapnia, using low tidal volumes and low-pressure pulmonary ventilation, reduces the incidence of barotrauma and volume trauma and possibly improves survival in ARDS [4–8]. Unfortunately, permissive hypercapnia is limited by respiratory acidosis causing substantial changes in hemodynamics, organ blood flow, and intracranial pressure unless arterial pH is controlled [6, 9].

We have previously shown, in a smoke inhalation model of severe ARDS in adult sheep, that arteriovenous carbon dioxide removal (AVCO₂R) allows significant reductions in ventilator pressures without the need for hypercapnia or the complex circuitry and monitoring required for extracorporeal membrane oxygenation (ECMO) [10]. At a shunt flow of up to 29% of cardiac output, AVCO₂R did not significantly change cardiac output [11] or compromise organ blood flow [12]. We have also shown that arterial percutaneous cannulas of 10F or larger allow adequate blood flow to achieve nearly total CO₂ removal without incurring hypercapnia in adult sheep [13, 14].

In this study we evaluated the initial safety and feasibility of percutaneous AVCO₂R in adults with severe respiratory failure and CO₂ retention.

	Material and methods

Top Abstract Introduction Material and methods Results Comment References

 
Our purpose was to evaluate the safety and feasibility of percutaneous AVCO₂R in patients with severe respiratory failure and CO₂ retention, in a collaborative study between the University of Texas Medical Branch and Louisiana State University Medical Center. For this initial experience, we selected patients with unresponsive, severe ARDS with CO₂ retention despite maximum medical management using the lung protective strategy of "permissive hypercapnia." These patients were either not eligible for or had failed other therapies including inhaled nitric oxide, high-frequency ventilation, prone positioning, partial liquid ventilation, or ECMO. The study was approved by the Institutional Review Boards at each institution, and informed consent was obtained before each study.

We applied a commercially available, low-resistance oxygenator (Affinity, Avecor Cardiovascular, Plymouth, MN) to a femoral-femoral arteriovenous shunt by means of percutaneous access. The AVCO₂R technique includes a femoral-femoral arteriovenous shunt using 10F to 12F arterial and 12F to 15F venous percutaneous cannulas introduced by a modified Seldinger technique. The Affinity oxygenator was chosen for CO₂ removal because of its low-resistance blood flow characteristics. The Affinity membrane oxygenator was primed with normal saline and connected to the vascular cannulas after removing all the air. The patients were systemically anticoagulated with heparin to maintain an activated clotting time (Hemochron 400, International Technidyne, Edison, NJ) between 260 and 300 seconds throughout the study.

The AVCO₂R blood flow was monitored by an ultrasonic flow probe (model H6X, Transonic Systems, Ithaca, NY) placed on the arterial cannula and interfaced with a real-time flowmeter (model HT 109, Transonic Systems) with digital display. The AVCO₂R blood flow was always at the maximum flow achieved by the arteriovenous pressure gradient. Sweep gas flow (100% oxygen) was controlled by an in-line regulator and set at 2 to 4 times AVCO₂R blood flow. Removal of CO₂ by the device was calculated as the product of sweep gas flow and its exhaust CO₂ concentration measured by an in-line capnometer (SaraTrans, Lenexa, KS). Removal of CO₂ by the native lungs was calculated as the product of minute ventilation and the CO₂ concentration in the expired gas collected in a Douglas bag. Blood and expired gases were measured with a blood gas system (System BG3 and Co-Oximeter 482, Instrumentation Laboratory, Lexington, MA).

The ventilator tidal volume or pressure control and respiratory rate were decreased as determined by the investigators at each participating institution. The goal of ventilator management was to decrease the peak inspiratory pressure (PIP) below 35 cm H₂O and continue permissive hypercapnia yet keep the pH greater than 7.2. Each patient had one-on-one nursing care in an intensive care unit. The patients received AVCO₂R for 72 hours, then were returned to mechanical ventilation for total gas exchange while continuing a lung-protective strategy with permissive hypercapnia.

	Results

Top Abstract Introduction Material and methods Results Comment References

 
All patients were successfully cannulated for AVCO₂R at the bedside. Patient number 1 (Table 1) had 10F arterial and 12F venous cannulas, which allowed only 600 mL/min of arteriovenous shunt flow. The subsequent patients, numbers 2 through 5, had 12F arterial and 15F venous cannulas inserted for an average arteriovenous shunt flow of 940 mL/min. All patients completed the 72-hour trial, and 3 of 5 were discharged from the hospital.

View larger version (15K): [in this window] [in a new window]   Fig 1. Total CO2 production simultaneous with CO2 removal by the arteriovenous CO2 removal (AVCO2R) circuit. Production of CO2 ranged from 203.4 ± 54.5 to 128.2 ± 14.3 mL/min as CO2 removal closely paralleled production and ranged from 136.2 ± 48.4 to 77.4 ± 16.1 mL/min.

View larger version (16K): [in this window] [in a new window]   Fig 2. At baseline PaCO2 was 93.6 ± 9.0 mm Hg and decreased to 69.0 ± 10.0 mm Hg on initiation of arteriovenous CO2 removal (AVCO2R). Arteriovenous CO2 removal removed approximately 70% of total CO2 production throughout the 72 hours of the study.

View larger version (15K): [in this window] [in a new window]   Fig 3. Changes in airway pressures from baseline to 48 hours included a decrease in tidal volume from 416.0 ± 29.3 to 284.0 ± 17.2 mL, a decrease in peak inspiratory pressure (PIP) from 33.0 ± 7.4 to 29.0 ± 7.5 cm H2O, and a decrease in minute ventilation from 7.2 ± 2.3 to 4.6 ± 0.9 L/min. (AVCO2R = arteriovenous CO2 removal.)

View larger version (20K): [in this window] [in a new window]   Fig 4. Ratio of PaO2 to fraction of inspired oxygen (PaO2/FiO2) of all patients throughout the 72-hour study. (AVCO2R = arteriovenous CO2 removal.)

View larger version (13K): [in this window] [in a new window]   Fig 5. Throughout the 72-hour study, the heart rate and mean arterial pressure did not significantly change despite the arteriovenous shunt. Heart rate ranged from 97.4 ± 3.7 to 115.4 ± 6.6 beats/min and mean arterial pressure ranged from 81.6 ± 2.4 to 98.6 ± 9.7 mm Hg. (AVCO2R = arteriovenous CO2 removal.)

	Comment

Top Abstract Introduction Material and methods Results Comment References

 
For many years, mechanical ventilation attempted to simulate the normal respiratory cycle, targeting normal blood gases while using tidal volumes of 10 to 15 mL/kg. Conventional mechanical ventilation with high tidal volumes and high PIP causes iatrogenic lung injury in the setting of severe respiratory failure [3]. Kolobow and associates [15] reported that positive airway pressure ventilation with high peak pressures and tidal volumes increases vascular filtration pressures and causes stress fractures of the capillary endothelium, epithelium, and basement membrane. This leads to leakage of fluid, protein, blood, and air, resulting in pulmonary edema, hemorrhage, atelectasis, pneumatoceles, or pneumothorax [16]. Healthy dogs ventilated with PIP of 30 cm H₂O for as little as 2 hours show lung damage (atelectasis, alveolar edema, and hemorrhage) [17]. Tsuno and coworkers [2] ventilated pigs at a PIP of 40 cm H₂O for 24 hours and found histologic changes similar to those seen in early stages of respiratory failure.

When volume-controlled ventilation is used in patients with ARDS, the risk of regional lung overdistention is high, because tidal volumes used to maintain normal blood gases invariably inflict high PIPs to the small fraction of compliant lung capable of gas exchange [16]. To minimize volume distention of healthy alveoli and potentiation of the lung injury [16, 18], pressure-limited ventilation techniques have been proposed. In a prospective, randomized clinical trial [7], patients treated with pressure-limited ventilation had a more rapid increase in static lung compliance and normalization of blood PCO₂ than those with volume-controlled ventilation. Such changes in ventilator strategies to avoid high airway pressures may contribute to the lower mortality recently reported in patients with ARDS [4, 5, 8]. Limiting PIP, and therefore tidal volume depending on lung compliance, may not provide adequate minute ventilation to excrete the produced CO₂ and leads to an increase in systemic PaCO₂, termed permissive hypercapnia.

Use of ECMO provides complete gas exchange and improves survival in neonates [19], pediatric patients [20], and selected adult patients [21, 22]. More than 10,000 cases of ECMO to date reveal an 81% survival in neonates, 49% in children, and 38% in adults in patient populations estimated to have a greater than 80% mortality [22]. Treatment with ECMO, however, involves intensive monitoring, high cost in labor and equipment, and frequent complications [23, 24]. Targeting CO₂ removal, Kolobow and colleagues [25] developed the venovenous extracorporeal technique of extracorporeal CO₂ removal in animals. Gattinoni and associates [26] also reported that low-frequency ventilation combined with extracorporeal CO₂ removal provided sufficient gas exchange and improved survival in patients with ARDS. Although extracorporeal CO₂ removal was effective in reducing ventilatory requirements, extracorporeal CO₂ removal is essentially low-flow venovenous ECMO and has all the inherent disadvantages.

Arteriovenous CO₂ removal was developed to minimize the foreign surface interactions and blood element shear stress inherent in an extracorporeal circuit with a pump and allow a gas exchange membrane of sufficient surface area for nearly total CO₂ removal. Barthelemy and associates [27] initially achieved significant CO₂ removal using a large membrane in a pumpless circuit with flows in the range of 1200 to 2000 mL/min. More recently, Young and colleagues [28] evaluated AVCO₂R in animals in both a pumped and a pumpless circuit with a large oxygenator membrane and found that despite excellent CO₂ removal, resistance was a limiting factor at low flow rates. To evaluate the potential long-term use of AVCO₂R, Awad and coworkers [29] demonstrated the feasibility of chronic arteriovenous support for 7 days in awake normal sheep without sequelae. However, the major limitation of all these studies was high circuit resistance.

Recent developments in computational fluid dynamics led to a newly designed low-resistance oxygenator commercially available as the Affinity oxygenator [30]. We selected this low-resistance gas exchanger to use with percutaneous arterial and venous cannulas matched to the flow ranges necessary for total CO₂ removal during ARDS induced by severe smoke inhalation and cutaneous flame burn injury in adult sheep [14]. The extremely low resistance of the circuit and gas exchanger (< 10 mm Hg) allowed a blood flow of up to 13% of the cardiac output at a mean arterial blood pressure of 90 mm Hg [31].

During this initial patient experience, AVCO₂R achieved approximately 870 mL/min of flow with a transdevice pressure gradient of consistently less than 10 mm Hg to achieve approximately 70% CO₂ removal of measured CO₂ production. All patients on AVCO₂R achieved either a decrease in ventilator pressures (patients 1 through 3) or a decrease in PaCO₂ (patients 3 through 5) depending on the management strategy. Use of AVCO₂R in patient 1 was associated with an immediate reduction in ventilator requirements and peak airway pressure. Although arterial PCO₂ ranged from 99 to 121 mm Hg during AVCO₂R support, it was still significantly less than it would be without AVCO₂R, as evidenced by a rapid increase of PCO₂ to 214 mm Hg immediately after removal of the cannulas. In patient 2, CO₂ removal up to 208 mL/min, or 94% CO₂ production, was achieved under conditions of moderate hypercapnia. This patient and those subsequent tolerated the 12F arterial cannula without vascular complications. We now recommend a 12F or larger arterial cannula to achieve shunt flows capable of adequate CO₂ removal during periods of high CO₂ production.

Although CO₂ removal was consistent, as shown in Figures 1 and 2, the impact of AVCO₂R on oxygen transfer was patient dependent. Removal of CO₂ allowed reductions in barotrauma and volume trauma from the ventilator; however, the PaO₂ to fraction of inspired oxygen ratio best reflected patient improvement or deterioration during ARDS as shown in Figure 4. In our large animal model of ARDS induced by a smoke inhalation and cutaneous burn injury [32], the PaO₂ to fraction of inspired oxygen ratio showed significant improvement during AVCO₂R [33]. We speculate this improvement in arterial oxygenation with AVCO₂R is likely caused by two separate effects. With resolution of noncardiogenic pulmonary edema associated with the lung injury, one would expect a decrement in the right-to-left shunt fraction. Second, the use of AVCO₂R would be expected to improve the central mixed venous oxygen tensions because of the admixture of well-oxygenated blood from AVCO₂R mixing with the venous return to the right atrium.

Percutaneous AVCO₂R involves much simpler monitoring and maintenance than conventional ECMO. Our technique of AVCO₂R still requires systemic anticoagulation with heparin, increasing the risk of bleeding. Heparin-coated or biopassive circuits and gas exchangers may decrease the blood–foreign surface interactions and decrease the need for anticoagulation. Management issues encountered throughout this feasibility study include two minor complications: (1) an oxygenator thrombosis that required oxygenator change-out, and (2) cannula-site bleeding that could be controlled with a pressure bag. Questions encountered throughout the study included the range of heparin dosing that was ideal for this type of circuit, cannula size selection that would allow minimal access to the femoral artery and vein with adequate blood flow, and best ventilator management in the presence of 70% to 75% CO₂ removal by the AVCO₂R circuit.

We conclude, from our initial clinical experience, that percutaneous AVCO₂R is feasible with only minor complications and achieves approximately 70% CO₂ removal in adults with severe respiratory failure and CO₂ retention to allow decreased barotrauma and volume trauma without hemodynamic compromise. In the future, we will conduct large animal prospective, randomized survival studies of AVCO₂R to evaluate ideal heparin dosing, heparin-coated circuits, and biopassive-coated circuits. Human prospective, randomized, clinical trials will address populations of patients with ARDS with CO₂ retention, severe smoke inhalation and burn-associated ARDS, and CO₂ retention syndromes to avoid intubation.

	Acknowledgments

 
Supported in part by the Constance Marsili Shafer Research Fund and Avecor Cardiovascular, Inc.

	References

Top Abstract Introduction Material and methods Results Comment References

 

1. Demling R.H. The modern version of adult respiratory distress syndrome. Annu Rev Med 1995;46:193-202.[Medline]
2. Tsuno K., Miura K., Takeya M., Kolobow T., Morioka T. Histopathologic pulmonary changes from mechanical ventilation at high peak airway pressures. Am Rev Respir Dis 1991;143:1115-1120.[Medline]
3. Dreyfuss D., Soler P., Basset G., Saumon G. High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. Am Rev Respir Dis 1988;137:1159-1164.[Medline]
4. Hickling K.G., Walsh J., Henderson S., Jackson R. Low mortality rate in adult respiratory distress syndrome using low-volume, pressure-limited ventilation with permissive hypercapnia. Crit Care Med 1994;22:1568-1578.[Medline]
5. Amato M.B.P., Barbas C.S.V., Medeiros D.M., et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998;338:347-354.[Abstract/Free Full Text]
6. Bidani A., Tzouanakis A.E., Cardenas V.J., Jr, Zwischenberger J.B. Permissive hypercapnia in acute respiratory failure. JAMA 1994;272:957-962.[Abstract/Free Full Text]
7. Rappaport S.H., Shpiner R., Yoshihara G., Wright J., Chang P., Abraham E. Randomized, prospective trial of pressure-limited versus volume-controlled ventilation in severe respiratory failure. Crit Care Med 1994;22:22-32.[Medline]
8. Milberg J.A., Davis D.R., Steinberg K.P., Hudson L.D. Improved survival of patients with acute respiratory distress syndrome (ARDS). JAMA 1995;273:306-309.[Abstract/Free Full Text]
9. Cardenas V.J., Jr, Zwischenberger J.B., Tao W., et al. Correction of blood pH attenuates changes in hemodynamics and organ blood flow during permissive hypercapnia. Crit Care Med 1996;24:827-834.[Medline]
10. Tao W., Brunston R.L., Jr, Bidani A., et al. Significant reduction in minute ventilation and peak inspiratory pressures with arteriovenous carbon dioxide removal during severe respiratory failure. Crit Care Med 1997;25:689-695.[Medline]
11. Brunston R.L., Jr, Tao W., Bidani A., Alpard S.K., Traber D.L., Zwischenberger J.B. Prolonged hemodynamic stability during arteriovenous carbon dioxide removal (AVCO₂R) for severe respiratory failure. J Thorac Cardiovasc Surg 1997;114:1107-1114.[Abstract/Free Full Text]
12. Brunston R.L., Jr, Tao W., Bidani A., Traber D.L., Zwischenberger J.B. Organ blood flow during arteriovenous carbon dioxide removal. ASAIO J 1997;43:M821-M824.[Medline]
13. Brunston R.L., Jr, Tao W., Bidani A., Cardenas V.J., Jr, Traber D.L., Zwischenberger J.B. Determination of low blood flow limits for arteriovenous carbon dioxide removal (AVCO₂R). ASAIO J 1996;42:M845-M851.[Medline]
14. Frank B.A., Tao W., Brunston R.L., Jr, Alpard S.K., Bidani A., Zwischenberger J.B. High flow/low resistance cannulas for percutaneous arteriovenous carbon dioxide removal (AVCO₂R). ASAIO J 1997;43:M817-M820.[Medline]
15. Kolobow T., Moretti M.P., Fumagalli R., et al. Severe impairment in lung function induced by high peak airway pressure during mechanical ventilation. An experimental study. Am Rev Respir Dis 1987;135:312-315.[Medline]
16. Parker J.C., Hernandez L.A., Peevy K.J. Mechanisms of ventilator-induced lung injury. Crit Care Med 1993;21:131-143.[Medline]
17. Barsch J., Birbara C., Eggers G.W.N. Positive pressure as a cause of respiratory failure induced lung disease. Ann Intern Med 1970;72:810.[Abstract/Free Full Text]
18. Hickling K.G. Ventilatory management of ARDS. Intensive Care Med 1990;16:219-226.[Medline]
19. Field D., Davis C., Elbourne D., Grant A., Johnson A., Macrae D., UK Collaborative ECMO Trial Group. UK collaborative randomized trial of neonatal extracorporeal membrane oxygenation. Lancet 1996;348:75-82.[Medline]
20. Zwischenberger J.B., Bartlett R.H. Extracorporeal circulation and oxygenation. In: Civetta J.M., Taylor R.W., Kirby R.R., eds. Critical care. Philadelphia: JB Lippincott, 1992:1629-1637.
21. Kolla S., Awad S.S., Rich P.B., Schreiner R.J., Hirschl R.B., Bartlett R.H. Extracorporeal life support for 100 adult patients with severe respiratory failure. Ann Surg 1997;226:544-566.[Medline]
22. Conrad S.A., Rycus P.T. Extracorporeal life support. ASAIO J 1998;44:848-852.[Medline]
23. Zwischenberger J.B., Nguyen T.T., Upp J.R., Jr, et al. Complications of neonatal extracorporeal membrane oxygenation. Collective experience from the Extracorporeal Life Support Organization. J Thorac Cardiovasc Surg 1994;107:838-849.[Abstract/Free Full Text]
24. Becker J.A., Short B.L., Martin G.R. Cardiovascular complications adversely affect survival during extracorporeal membrane oxygenation. Crit Care Med 1998;26:1582-1586.[Medline]
25. Kolobow T., Gattinoni L., Tomlinson T., Pierce J.E. An alternative to breathing. J Thorac Cardiovasc Surg 1978;75:261-266.[Abstract]
26. Gattinoni L., Pesenti A., Mascheroni D., et al. Low-frequency positive-pressure ventilation with extracorporeal CO₂ removal in severe acute respiratory failure. JAMA 1986;256:881-886.[Abstract/Free Full Text]
27. Barthelemy R., Galletti P.M., Trudell L.A., et al. Total extracorporeal CO₂ removal in a pumpless artery-to-vein shunt. Trans Am Soc Artif Intern Organs 1982;28:354-358.[Medline]
28. Young J.D., Dorrington K.L., Blake G.J., Ryder W.A. Femoral arteriovenous extracorporeal carbon dioxide elimination using low blood flow. Crit Care Med 1992;20:805-809.[Medline]
29. Awad J.A., Deslauriers J., Major D., Guojin L., Martin L. Prolonged pumpless arteriovenous perfusion for carbon dioxide extraction. Ann Thorac Surg 1991;51:534-540.[Abstract]
30. Goodin M.S., Thor E.J., Haworth W.S. Use of computational fluid dynamics in the design of the Avecor Affinity oxygenator. Perfusion 1994;9:217-222.[Free Full Text]
31. Brunston R.L., Jr, Zwischenberger J.B., Tao W., Cardenas V.J., Jr, Traber D.L., Bidani A. Total arteriovenous carbon dioxide removal (AVCO₂R). Ann Thorac Surg 1997;64:1599-1605.[Abstract/Free Full Text]
32. Alpard SK, Zwischenberger JB, Tao W, Deyo DJ, Traber DL, Bidani A. Dose dependent development of severe respiratory failure in an ovine model of smoke inhalation and cutaneous flame burn injury. Crit Care Med 1999 (in press).
33. Alpard SK, Zwischenberger JB, Tao W, Deyo DJ, Bidani A. Reduced ventilator pressure and improved P/F ratio during percutaneous arteriovenous carbon dioxide removal (AVCO₂R) for severe respiratory failure. Ann Surg 1999 (in press).

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