Independent Ventilation and ECMO for Severe Unilateral Pulmonary Edema After SLT for Primary Pulmonary Hypertension

-moment during or after the test, and there were no ischemic ECG changes. Thallium 201 myocardial scintigraphy showed an irreversible perfusion defect in the inferior-posterior segments of the left ventricular wall. Total cholesterol level several weeks after hospital discharge was 5.2 mmol / L Coronary angiography several weeks after scintigraphy demonstrated no coronary stenoses or plaques.

to instruct the patient to consult a physician when he develops persistent chest pain and to insist that he should refrain from smoking during use of the nicotine patch. Since only epidemiologic studies will clarify whether there is an increased risk of cardiovascular events associated with use of the nicotine patch, we recommend the performance of such postmarketing studies.

DISCUSSION

REFERENCES

In view of the temporal relationship between administration of the nicotine patch and acute myocardial infarction in a young patient without previous angina pectoris, and without coronary stenosis, it is possible that the myocardial infarction was caused by the nicotine patch. However, coincidence cannot be excluded. Furthermore, we cannot exclude primary coronary spasm as the cause of the myocardial infarction. Another cardiac side effect, atrial fibrillation, has previously been associated with both the nicotine patch and chewing nicotine gum.3-5 Furthermore, there have been reports of serious cardiovascular adverse reactions, including acute myocardial infarction and cardiac arrest, associated with continued smoking during use of the patches.6-8 Also, the Australian Centre for Adverse Reactions to Drugs received several reports on cardiovascular adverse effects attributed to nicotine patches. 9 Another cardiovascular adverse reaction, stroke, has also been reported.l 0 However, it is difficult to estimate the causal relationship between use of the nicotine patch and these adverse drug reactions in most cases. The effects of nicotine on coronary blood flow can lead to ischemia in patients with coronary heart disease.H This case report now suggests that serious cardiac events also can occur in a patient without a history of heart disease who has stopped smoking during use of the patch. Although serious cardiac events associated with the nicotine patch are probably rare, we advise cautious use of nicotine replacement therapy in patients with known coronary artery disease, in any patient who experiences chest pain during use of this drug, and in patients with a recent history of (increasing) angina pectoris. However, since smoking cessation is a very important treatment of cardiovascular and lung diseases, if the benefits and possible risks (in particular if smoking is continued during use of the patches) are explained to a patient, nicotine replacement therapy may be useful in patients who cannot stop smoking without such therapy.12 It is very important, however,

II

Ill

aVL

aVF

V4

VI

aVR

V2

V3

vs

V6

FIGURE 1. ECG on hospital admission of a 39-year-old man who experienced chest pain while using the nicotine patch. 1766

2

3 4 5 6 7 8 9 10 11 12

Fiore MC, Jorenby DE, Baker TB, et al. Tobacco dependence and the nicotine patch: clinical guidelines for effective use. JAMA 1992; 268:2687-94 Benowitz NL, Fitzgerald GA, Wilson M, et al. Nicotine effects on eicosanoid formation and hemostatic function: comparison of transdermal nicotine and cigarette smoking. J Am Coli Cardiol1993; 22:1159-67 Rigotti N A, Eagle KA. Atrial fibrillation while chewing nicotine gum. JAMA 1986; 255:1018 Ottervanger JP, Stricker BHC, Klomps HC. Atrial fibrillation and the nicotine patch [letter]. JAMA 1993; 269:1940 Stewart PM, Catteral JR. Chronic nicotine ingestion and atrial fibrillation. Br Heart J 1986; 225:1018 Hwang SL, Waldholt M. Heart attacks reported in patch users still smoking. The Wall Street Journal:B1, June 19, 1992 Dacosta A, Guy JM, Tardy R, et al. Myocardial infarction and nicotine patch: a contributing or causative factor? Eur Heart J 1993; 14:1709-11 Warner Jr JG, Little WC. Myocardial infarction in a patient who smoked while wearing a nicotine patch. Ann Intern Med 1994; 120:695 Adverse effects of nicotine patches. Aust Adv Drug React Bull 1994; 13:6-7 Pierce JR Jr. Stroke following application of a nicotine patch. Ann Pharmacother 1994; 28:402 Benowitz NL. Clinical pharmacology of nicotine. Annu Rev Med 1986; 37:21-32 Benowitz NL. Smoking-induced coronary vasoconstriction: implications for therapeutic use of nicotine. J Am Coli Cardiol 1993; 22:648-49

Independent Ventilation and ECMO for Severe Unilateral Pulmonary Edema After SLT for Primary Pulmonary Hypertension* David B. Badesch, MD, FCCP; Martin R. Zamora, MD, FCCP; Steven jones, MD; David W. Campbell, MD, FCCP; and David A. Fullerton, MD, FCCP *From the Divisions of Pulmonary Sciences and Critical Care Medicine (Drs. Badesch and Zamora), and Cardiothoracic Surgery (Drs. Jones, Campbell, and Fullerton) at the Pulmonary Hypertension Center, University of Colorado Health Sciences Center, Denver. Supported in part by a Pfizer Scholar's Award in Cardiovascular Medicine, NIH Clinical Investigator Award HL 02408-04, NIH Vascular Center Award HL02825-01A1, the Pulmonary Hypertension Center at the University of Colorado, American Heart Association of Colorado Grant-in-Aid, Clinical Research Center PHS RG5M01RR00051, and the Burroughs Wellcome Co (Dr. Badesch); injart by the Robert Wood Johnson Foundation (Dr. Zamora); an in part by NIH grant R29HL49398 (Dr. Fullerton). Reprint requests: Dr. Badesch, Box C-272, UCHSC, 4200 E. 9th Avenue, Denver, CO 80262 Selected Reports

Single lung transplantation (SLT) is now accepted therapy for selected cases of severe pulmonary hypertension. A recognized complication is the postoperative development of reperfusion edema in the graft, a potentially fatal cause of respiratory failure. Because reperfusion edema may be a reversible process, temporizing support measures can be life-saving. We report the case of a 48-year-old woman who developed severe reperfusion edema following right SLT for primary (unexplained) pulmonary hypertension. Extracorporeal membrane oxygenation (ECMO) was instituted. Independent lung ventilation was later begun and resulted in markedly improved oxygenation allowing withdrawal of ECMO. We conclude that reperfusion edema following SLT for pulmonary hypertension may be uniquely amenable to treatment with independent lung ventilation and ECMO if needed. (CHEST 1995; 107:1766-70

CPB=cardiopulmonary bypass; ECMO=extracorporeal membrane oxygenation; NO =nitric oxide; PEEP=positive end-expiratory pressure; SLT=single lung transplantation

Key words: extracorporeal membrane oxygenation; independent ventilation; lung transplantation; reperfusion edema edema of the graft is a potentially fatal Reperfusion complication of single lung transplantation (SL T) in

Fick cardiac output, a 51% decrease in total systemic resistance, and a 41 % decrease in total pulmonary resistance. A short-term trial of "high-dose" oral diltiazem therapy with a total dose of 240 mg administered over 4 h resulted in no change in the mean pulmonary artery pressure, a 14% decrease in aortic mean pressure, a 17% decrease in thermodilution cardiac output, no change in systemic vascular resistance, and a 20% increase in total pulmonary resistance. The patient was considered to be refractory to oral vasodilator therapy. Short-term intravenous administration of the investigational agent, prostacyclin (epoprostenol sodium [Flolan; Burroughs Wellcome; Research Triangle Park, NC]), at a maximum dose of 10 ng/ kg/ min, resulted in 33% decrease in total pulmonary resistance and a 47% decrease in total systemic resistance, with no change in mean pulmonary artery pressure. A continuous intravenous infusion of prostacyclin was begun on protocol, and the patient was listed for SL T. The patient underwent right SL T 2 months later. Cardiopulmonary bypass (CPB) was utilized, and intravenous prostacyclin therapy was continued. The donor lung met our standard criteria of a Pa02 of <:::300 mm Hg on an inspired oxygen concentration of 100% with a positive end-expiratory pressure (PEEP) of 5 em H20, and no evidence of infectious or communicable diseases. The recipient and donor were both cytomegalovirus (CMV) seropositive. The surgery was technically uneventful. The cold ischemic time for the donor lung was 2 h 30 min, warm ischemic time was 1 h 14 min, and total ischemic time was 3 h 57 min. The initial CPB time was 1 h 33 min. As the skin was closed, very large amounts of frothy fluid flowed from the right side of the dual-lumen endotracheal tube, progressive hypoxemia and hypotension developed, and CPB was restarted. There was no evidence of venous anastomotic thrombosis or kinking. The second period of CPB lasted 1 h 19 min. When it became clear that CPB could not be withdrawn, the patient was placed on ECMO utilizing both right atrial and femoral vein cannulas, epinephrine,

patients with severe pulmonary hypertension. This may be exacerbated by the large amount of blood flow directed to the graft due to higher vascular resistance in the native lung. This is accompanied by mismatching of ventilation and perfusion , with most perfusion being directed to the graft and effective ventilation occurring predominantly in the native lung. Because reperfusion edema is typically reversible, aggressive supportive measures may significantly alter outcome. We report utilization of extracorporeal membrane oxygenation (ECMO) and independent lung ventilation in the setting of unilateral reperfusion edema following SL T for severe pulmonary hypertension. CASE REPORT

A 48-year-old woman presented with dyspnea on exertion for 6 months. A chest radiograph revealed cardiomegaly and prominent main and proximal pulmonary arteries (Fig 1), and an echocardiogram showed evidence of severe pulmonary hypertension. Right heart catheterization demonstrated the following : right atrial mean pressure, 9; right ventricular pressure, 87 / 2; pulmonary arterial pressure, 92/27 with a mean of 53; mean pulmonary capillary wedge pressure, 11; aortic pressure, 117/ 67 with a mean of 83 mm Hg; measured Fick cardiac output, 2.4 L/ min; pulmonary vascular resistance, 23.4; and total pulmonary resistance, 25.2 Wood units. There was no right-to-left or left-toright shunt by pulmonary artery to aorta and right atrium to aorta indocyanine green dye dilution curves and a pulmonary artery hydrogen curve. Intravenous infusion of iloprost, an investigational prostacyclin analog, to a maximum dose of 5.0 ng/ kg/ min, resulted in a 2%increase in mean pulmonary artery pressure, a 15% decrease in mean aortic pressure, a 33% increase in measured

FIGURE l. Preoperative chest radiograph at time of presentation showing cardiomegaly with prominence of the pulmonary outflow tract and proximal pulmonary arteries, consistent with severe pulmonary hypertension. CHEST / 107/6 / JUNE, 1995

1767

FIGURE 2. Immediately following right SLT, the chest radiograph demonstrates severe edema of the graft. and dopamine. The patient received standard immunosuppression, consisting of preoperative cyclosporine and azathioprine (Imuran; Burroughs Wellcome; Research Triangle Park, NC), methylprednisone sodium succinate (Solu-Medrol; Upjohn; Kalamazoo, Mich), 500 mg, with removal of the pulmonary arterial clamp, and cyclosporine, azathioprine, and methylprednisolone postoperatively . Chest radiography revealed severe edema of the grafted right lung (Fig 2). Fluid was removed as tolerated by ultrafiltration on ECMO. The patient was given exogenous surfactant bronchoscopically into the lobar airways on the right, on a compassionate use basis. She had large amounts of bleeding from her right groin ECMO cannulation site, chest tubes, and nasogastric tube. Inhaled nitric oxide (NO) was given on a compassionate use basis on postoperative day 2. A dual-lumen endotrachael tube remaining in place since surgery allowed trials of NO into both lungs simultaneously, and each lung independently. Although no significant benefit was seen from the NO itself, it was noted that oxygenation improved when her two lungs were ventilated independently. Four hours prior to the NO trial, with an inspired oxygen concentration of 90%, PEEP of 12.5 em H20, and ECMO, the Po2 was 63 (Table 1). The inspired oxygen concentration was decreased to 70% due to the likelihood of a significant shunt

fraction and concern for oxygen toxicity, with no change in .Po2. While still on ECMO, with the right lung being ventilated manually with 100% oxygen by manual ventilation bag (Ambu Bag; Ambu; Linthicum Heights, Md.), and the left lung being mechanically ventilated, there was marked improvement in oxygenation. The patient was then placed on two ventilators operating independently, with no attempt to synchronize the ventilators. That evening the patient was briefly successfully removed from ECMO for the first time, albeit with a significant decline in oxygenation. Oxygenation improved following reinstitution of ECMO, allowing reduction of inspired oxygen concentrations to nontoxic levels. A chest radiograph demonstrated markedly improved aeration of the right lung (Fig 3). The patient was progressively weaned from ECMO with decannulation on postoperative day 4. The endotracheal tube was changed to a single-lumen tube on postoperative day 5. During the 5 days following transplant, the patient required large amounts of blood products: 54 U of fresh frozen plasma, 125 U of platelets, 64 U of packed red blood cells, and 50 U of cryroprecipitate. In addition to the external bleeding noted above, the patient developed a large right groin hematoma around the ECMO canulation site that extended up the right flank. The bleeding was attributed to the effects of prolonged CPB and ECMO. The patient had been receiving warfarin (Coumadin) preoperatively, but no unusual bleeding occurred during the transplantation procedure itself. Aprotinin was not used during the procedure. The hospital course was complicated by a hemorrhagic cerebral infarct in the left posterior-parietal area, a bland infarct in the left frontal area, and multiple other smaller cerebral infarcts, all believed to be complications of ECMO; recurrent fevers of unknown source; delayed healing of her thoracotomy wound; sepsis; disseminated intravascular coagulation; multiorgan failure, including anuric renal failure requiring dialysis for 6 weeks (including prolonged continuous arteriovenous hemodialysis); and prolonged mechanical ventilation via tracheostomy due to generalized weakness and inability to protect her airway. The patient was discharged from the hospital 4.5 months follo~ing her transplant. She was ambulatory and communicative, with a well-controlled seizure disorder and some residual memory deficit. Following 2 additional months of outpatient rehabilitation, she returned to her hometown in western Colorado. An echocardiogram performed 11 months after SL T revealed normal right atrial and right ventricular size, mild tricuspid regurgitation, mild mitral regurgitation, pulmonic insufficiency, and an estimated pulmonary artery systolic pressure of 30 mm Hg. Thirteen

Table !-Ventilator Settings, ECMO Flow Rates, and Arterial Blood Gases for the Period Immediately Before to and

After the Institution of Independent Lung Ventilation*

Conventional ventilation Conventional ventilation Independent lung ventilation R-L Independent lung ventilation R-L Independent lung ventilation R-L Independent lung ventilation R-L Independent lung ventilation R-L

Hours After Reimplantation

Tidal Volume, mL

Rate, br/ min

22 26.25 27.5

480 480 Ambu-240

10 10 ?-10

4.8 4.8 ?-2.3

28.5

280-320

10-10

2.6-3.2

0.8-0.7

29

280-320

10-10

2.8-3.2

42.5

267-275

10-10

53

220-310

8-8

Min Vent, L/ min

PEEP, em HzO

ECMO Flow Rate, L/min

pH

PaC02, mm Hg

PaOz, mm Hg

2.3 2.3 2.3

7.57 7.57 7.59

33 30 29

63 61 176

12-12.5

0

7.48

38

50

0.8-0.7

12-12.5

2.3

7.54

33

109

2.1-2.3

0.5-0.5

12-12.5

2.2

7.53

34

94

2.0-2.5

0.5-0.6

12-12.5

2.4

7.49

34

160

Fioz

0.9 12.5 0.7 12.5 1-0.8 12.5-12.5

*Times given are for arterial blood gas determinations. Ventilator settings were those recorded closest to the time of blood gas determination. Tidal volumes shown are exhaled. Ambu=Ambu Bag (manual ventilation bag); br=breaths; L=left lung; R=right; Vent=ventilation. 1768

Selected Reports

months after SLT, she is currently well and physically active, with fully recovered memory and deductive abilities according to her spouse. Her resting arterial oxygen saturation is 95% with no supplemental oxygen therapy at an elevation of approximately 135,000 em (4,500 ft.) above sea level. Pulmonary function testing demonstrates an FEV 1 of 1.93 L (89 % of predicted), thoracic gas volume of 2.95 L (102% of predicted), and a diffusing capacity corrected for alveolar volume of 4.31 (86 % of predicted). A recent chest radiograph is shown in Figure 4. DISCUSSION

Reperfusion edema frequently complicates SL Tin patients with pulmonary hypertension and may contribute to the increased perioperative risk apparent in these patients compared with nonpulmonary hypertensive patients undergoing SLT. Because reperfusion edema is typically reversible, temporizing measures may significantly alter outcome. This case illustrates potential roles for ECMO and independent lung ventilation in the setting of severe reperfusion edema following SL T for pulmonary hypertension. Although it is not possible to separate the effects of ECMO, ultrafiltration, healing of the acute lung injury, and independent ventilation, it was our impression that the dramatic improvement seen in oxygenation and aeration of the graft was at least partially attributable to the effects of independent ventilation. Ultrafiltration likely also contributed to the improvement seen over the first 3 to 4 days. Decreasing the inspired oxygen concentration prior to beginning independent lung ventilation had little effect on oxygenation, suggesting the presence of a large shunt. It is therefore unlikely that the increase in inspired oxygen concentration when the manual ventilation bag (Ambu Bag) was applied to the right lung and independent lung ventilation initiated totally accounted for the dramatic improvement in the Po2 . A more likely explanation is that the shunting through the right lung decreased significantly when it was effectively inflated and ventilated. Effective inflation and ventilation of the right lung may have been crucial due to the disproportionate amount of blood flow through it, secondary to its lower vascular resistance as compared with the native lung. We did not see significant benefit from trials of exogenous surfactant or NO. In contrast, independent lung ventilation appeared to lead to significant improvement, and earlier use may be indicated in similar situations. The application of independent ventilation was not difficult. While we were concerned regarding the potential adverse effects of mediastinal pendulluft shortly following SLT, there were no apparent complications due to asynchrony of the two ventilators. The tidal volumes utilized were somewhat arbitrarily chosen, and were roughly one half the total tidal volume prior to independent ventilation. Whether volume-cycled or pressure-cycled ventilation is preferable in this situation remains to be determined. It may be desirable to limit peak and mean airway pressures in the graft with reperfusion edema and / or acute lung injury to minimize barotrauma. ECMO can provide temporary circulatory support, and improve critically low oxygenation. It is perhaps most appropriately applied in a situation that is potentially quickly reversible. ECMO has been successfully utilized in neonates and children for respiratory failure, persistent pul-

FIGURE 3. Postoperative day 3, following the institution of independent ventilation on postoperative day 2, and with ongoing ECMO and net fluid removal by ultrafiltration, the chest radiograph demonstrates some aeration of the graft.

FIGURE 4. Eleven months after right SLT, the chest radiograph demonstrates a near-normal cardiac silhouette and good aeration of the graft. monary hypertension of the newborn, and following cardiac surgery. 1-6 Although ECMO has been utilized in adult patients, the outcome is often less favorable, which may in part be due to the fact that severe illness in adults often involves multiple organs and frequently is not quickly reversible. Furthermore, ECMO may be complicated by a severe bleeding diathesis. Nevertheless, ECMO has been utilized successfully in special situations in adults, such as patients with cardiomyopathy and unstable angina underCHEST /1 07 /6/ JUNE, 1995

1769

going angioplasty, 7 ARDS, "extended indications" including graft failure following heart or lung transplantation, and as a bridge to subsequent retransplantation of either the heart or one lung. When ECMO was used in these "extended indications," 2 of 13 patients were long-term survivors.8 Acute pulmonary failure following lung and heart-lung transplantation is a potentially reversible disorder that may be particularly amenable to treatment with ECM0. 9·10 ECMO has also been utilized during and prior to transplantation. Differential perfusion is a potential complication of femoral-femoral bypass during SLT. 11 Successful lung transplantation has been accomplished for posttraumatic ARDS after ECM0. 12 The same group reported lung transplantation in five patients after ECMO support. 13 Independent lung ventilation after SL T for emphysema has been previously reported. 14 In this setting, there is a significant mechanical discrepancy between the two lungs, with the overly compliant emphysematous lung being prone to overdistention and air-trapping, possibly with the development of auto-PEEP. This may result in mediastinal shift and compression of the graft, potentially compromising graft function. It may also result in impaired venous return with hemodynamic compromise. Graft failure due to reperfusion edema, acute rejection, or development of ARDS increases the mechanical discrepancy in compliance between the two lungs and worsens ventilation-perfusion mismatching. Independent ventilation allows tailoring of ventilator settings to achieve optimal ventilation of each lung despite mechanical differences. Independent lung ventilation following SL T has also been reported in a patient with lymphangioleiomyomatosis.15 This patient developed hyperexpansion of the native lung 6 days postoperatively with moderate mediastinal shift, marked atelectasis of the graft, progressive dyspnea on exertion, and arterial hypoxemia. She required reintubation and then demonstrated significant auto-PEEP. The right lung failed to reexpand, and the patient became hemodynamically unstable. A double-lumen endotracheal tube was placed, and independent ventilation was begun, resulting in reexpansion of the graft and immediate hemodynamic improvement. While the mechanical discrepancies seen following SL T in the patient with emphysema are quite different from the situation occurring in the patient with pulmonary hypertension who develops reperfusion edema following SL T, both situations share the problem of an enormous difference in compliance between the native lung and graft. It is therefore understandable that independent ventilation might have utility in both situations, allowing optimization of ventilator settings for each lung. In the pulmonary hypertensive patient with reperfusion edema following SL T, the situation is further complicated by the majority of blood flow going to the graft, and the majority of ventilation going to the more compliant and nonedematous native lung. This leads to severe ventilation-perfusion mismatching, perhaps making restoration of adequate ventilation to the graft even more critical. We conclude that ECMO and independent ventilation can provide life-saving support in the patient who devel-

1770

ops severe reperfusion edema of the graft following SLT for pulmonary hypertension. As illustrated by the case presented, ECMO and the associated coagulation disturbances may lead to severe complications, including bleeding and centralnervous system embolic phenomena. Early consideration of single lung ventilation may eliminate the need for ECMO in some cases. Further work is needed to evaluate the cost-effectiveness of these very expensive and resource-consuming therapies. ACKNOWLEDGMENTS: The authors thank the following for their invaluable assistance in the care of the patient: Joan Balik, RRT; Betty Booker, RRT; Maren Diercks, RN , MSN; James Fisher, MD; Fredrick Grover, MD; Bertron Groves, MD; Susan Leone, RN; Fran Piedalue, BS, RRT; and Kristinne Wynne, RN, BA. REFERENCES

1 B~rtl~tt RH, Gazzaniga AB, Toomasian J, et al. Extracorporeal membrane oxygenation (ECMO) in neonatal respiratory failure: 100 cases. Ann Surg 1987; 205:llA 2 Klein MD, Andrews AF, Wesley JR, et al. Venovenous perfusion in ECMO for newborn respiratory insufficiency: a clinical comparison with venoarterial perfusion. Ann Surg 1985; 201 : 520-26 3 DeLemos R, Yoder B, McCurnin D, et al. The use of high-frequency oscillatory ventilation (HFOV ) and extracorporeal membrane oxygenation (ECMO) in the management of the term / near term infant with respiratory failure. Early Hum Dev 1992; 29:299-303 4 Suddaby EC, O'Brien AM. ECMO for cardiac support in children. Heart Lung 1993; 22:401-07 5 Donn SM. ECMO indications and complications. Hosp Pract 1990; 25:143-50, 153-57 6 Kelly RE Jr, Phillips JD, Foglia RP, et al. Pulmonary edema and fluid mobilization as determinants of the duration of ECMO support. J Pediatr Surg 1991; 26:1016-22 7 Ott RA, Mills TC, Tobis JM, et al. ECMO assisted angioplasty for cardiomyopathy patients with unstable angina. ASAIO Trans 1990; M483-5 8 Jurmann MJ, Haverich A, Demertzis S, et al. Extracorporeal membrane oxygenation (ECMO): extended indications for artificial support of both heart and lungs. Int J Artif Organs 1991; 14:771-74 9 Slaughter MS, Nielsen K, Bolman RM. Extracorporeal membrane oxygenation after lung or heart-lung transplantation. ASAIO J 1993; 39:M453-6 10 Ichiba S, Okabe K, Date H, et al. Experimental study on venavenous extracorporeal membrane oxygenation for respiratory failure after lung transplantation. Acta Med Okayama 1992; 46:213-21 11 Sikela ME, Noon GP, Holland VA, et al. Differential perfusion: potential complication of femoral-femoral bypass during single lung transplantation. Heart Lung Transplant 1991; 10:322-24 12 Demertzis S, Haverich A, Ziemer G, et al. Successful lung transplantation for posttraumatic adult respiratory distress syndrome after extracorporeal membrane oxygenation support. J Heart Lung Transplant 1992; 11:1005-07 13 Jurmann MJ, Schaefers HJ, Demertzis S, et al. Emergency lung transplantation after extracorporeal membrane oxygenation. ASAIO J 1993; 39:M448-52 14 Gavazzeni V, lapichino G, Mascheroni D, et al. Prolonged independent lung respiratory treatment after single lung transplantation in pulmonary emphysema. Chest 1993; 103:96-100 15 Popple C, Higgins TL, McCarthy P, et al. Unilateral auto-PEEP in the recipient of a single lung transplant. Chest 1993; 103: 297-99

Selected Reports