Complications Associated with Membrane Lung Support by Venoarterial Perfusion Jack L. Ratliff, M.D., J. Donald Hill, M.D., Robert J. Fallat, M.D., James Parrot, M.D., and Harvey J. Tucker, M.D. ABSTRACT A series of patients supported with long-term venoarterial perfusion is presented. Gas exchange was achieved with a membrane oxygenatorat flows usually in excess of 50%of the patient's baseline cardiac output. Perfusions were maintained for 7 to 12 days. Two major complications were encountered: thromboembolic myocardial infarction and liquefaction necrosis of the lung. Possible etiologies and suggestions for prevention are discussed.

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embrane lung oxygenators are being used in some centers to support patients with adult respiratory distress syndrome. We undertook a clinical evaluation of several methods of cannulation employed for these perfusions and encountered two problems unrecognized in previous perfusions by other routes of cannulation: myocardial infarction and pulmonary necrosis. Fourteen patients were perfused at Pacific Medical Center by the method described below [23, and experience with 4 patients that underscores these problems is presented.

Case Reports The first patient was a 16-year-oldboy with multiple fractures. Six days after injury his pulmonary function was marginal on maximum support, and cardiopulmonary bypass was instituted. The patient was cannulated as follows: under local anesthesia a 12 mm ID thin-walled wire-reinforced polyvinyl chloride tube was passed up the vena cava from the common femoral vein to the levelof the inferior cavoatrial junction. The distal femoral vein was decompressed into this blood withdrawal line, and blood was then pumped through a gas exchange unit and back into the patient through the common femoral artery. By the tenth day after the injury this patient had improved, and bypass was terminated. However, he died of sepsis, renal shutdown, and secondary deterioration in pulmonary function 16 days after the initial insult. Relevant to this presentation, postmortem examination revealed infarction of that portion of the heart supplied by the anterior descending coronary artery. An embolus was found in the left anterior descending coronary artery just beyond the bifurcation of the main left coronary artery. From the Institutes of Medical Sciences and the Bothin Heart Research Laboratory, and the Department of Cardiovascular Surgery, Pacific Medical Center, San Francisco, Calif. Accepted for publication Dec. 18, 1974. Address reprint requests to Dr. Ratliff, 2009 Buchanan St., San Francisco, Calif. 941 15.

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RATLIFF ET AL. The next patient was a 19-year-oldpregnant woman with blunt injuries to the liver and spleen. Nine days after injury, because of indications similar to those of the first patient, cardiopulmonary bypass was instituted for 12 days; it was terminated because of continued generalized bleeding from all wounds and progressive pulmonary fibrosis and pulmonary tissue destruction proved by open lung biopsy. Postmortem examination revealed heavily fibrosed, infected lungs with large areas of liquefaction necrosis in the right lower lobe. The third patient was a 56-year-old man who underwent bypass 4 days after an episode of what was thought to be sepsis or pancreatitis or a combination of the two. Perfusion was continued for 7 days, at the end of which the patient died of sepsis. Postmortem examination revealed a relatively large area of complete papillary muscle infarction in the left ventricle. The fourth patient, a 41-year-old woman, developed a pneumonialike syndrome while receiving intravenous gold therapy for arthritis. She was placed on cardiopulmonary bypass 10 days after the onset of pulmonary distress, and bypass was continued for 7 days under venoarterial conditions. She died with progressive pulmonary insufficiency and a high-flow bronchopleural fistula. Postmortem examination revealed a liquefied, necrotic right lower lobe. The remainder of the lung was quite heavy, fibrotic, and secondarily infected. The examination also showed a small infarct of the brain without hemorrhage as well as transmural infarction of the entire right ventricle and of a relatively large area of the posterior left ventricle. The unusual postmortem findings in these 4 patients revealed the following: (1) myocardial infarction was observed in 3 patients, with an embolus present in the coronary artery of 1; (2) in 2 patients there was liquefaction necrosis of the lower lobe of the lung; and (3) a cerebral infarct was present in 1 patient.

Comment The activated clotting time (ACT) was used to regulate heparin administration. It is rapid, accurate, and simple [ll. The usual procedure is to maintain the ACT around 200 seconds. In the face of major bleeding problems the ACT is reduced to 150 seconds. Insufficient anticoagulation may have promoted thrombosis in these patients or allowed clot propagation once initiated, thus enlarging the ultimate infarction. Several times catheters were passed up the aorta, across the aortic valve, and into the left ventricle to evaluate the true left ventricular end-diastolic pressure. From this position blood samples were taken serially from the left ventricle to the distal abdominal aorta at varying bypass flow rates, the purpose being to determine the mixing pattern of blood returned to the superior vena cava and from there through the heart and lungs and out the aortic root. With minimal venoarterial bypass the interface for the two sources was in the lower abdominal aorta. At full bypass flow the cardiac output and bypass flow usually met in the arch of the aorta. In the first patient the arch vessels were almost entirely supplied from the venoarterial circuit. At maximum bypass flow, a bolus of fluorekein was injected 538

T H E ANNALS OF THORACIC SURGERY

Complications of Venoarterial Perjkion into the bypass return and within a few seconds was seen in the right retinal artery. In the other 3 patients described, and in most of the other perfusions by this route, bypass usually constituted at least 50% of the total perfusion source. Myocardial infarction and other evidence of thromboembolism occurred in areas perfused by blood which did not come from the membrane lung. In our opinion the pulmonary veins themselves were the most likely source for these emboli. Flow through them is very slow; much of total perfusion is diverted around the lesser circulation. In all 4 patients the lungs were heavily infected, and the pulmonary veins lay within semirigid lungs which, because of their low compliance, collapsed little with each expiration. In addition, the pulmonary veins actually should have been held open by the suspensory tissues of the lung since the lungs were consolidated in an inflated position [3]. As discussed below, the pulmonary veins often lie in the substance of infarcted lungs. When the infarcted areas slough, high-flow bronchopleural fistulas are produced which, however, do not hemorrhage. That they do not bleed on sloughing suggests that the vessels in large portions of these sick lungs are in fact thrombosed. We believe that the pulmonary veins are the most likely source of these emboli. Necrosis and liquefaction of the lower lobes have been seen only in patients who were on venoarterial bypass. Probably the lung itself consumes little oxygen under normal conditions, and then mostly from the air ventilating it. These sick lungs are from five to ten times normal weight and are filled with cell-rich infiltrates. They are impossible to ventilate evenly. Zapol and associates noted 1 patient on bypass whose lungs consumed more oxygen than they put into the blood perfusing them on venovenous bypass.* We have likewise noted a patient in whom the aortic Pcoz (above the column of blood returning from bypass) was higher than the pulmonary artery Pcop. We conclude that as the sick lungs in these patients consolidate, they increase their metabolically active cell mass, receiving poor ventilation and uneven perfusion. If venoarterially bypassed, the lungs are even less well perfused and may develop areas of ischemic necrosis and slough as described. Because of the findings reported here, 4 subsequent patients have been perfused with partly venous and partly arterial return. Two have survived, and none sustained infarction of the heart. There was no evidence of peripheral embolization and no major portions of the pulmonary parenchyma sloughed.

References 1.

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3.

Hattersley, P. G. Activated coagulation time of whole blood. JAMA 196:436, 1966. Hill, J. D., Fallat, R., Cohn, K., Eberhart, R., Dontigny, L., Bramson, M. L., Osborn, J. J., and Gerbode, F. Clinical cardiopulmonary dynamics during prolonged extracorporeal circulation for acute respiratory insufficiency. Trans Am SOCArtgZntern Organs 17:355, 1971. Howell, J. B. L., Permutt, S., Proctor, D. F., and Riley, R. L. Effect of inflation of the lung on different parts of the pulmonary vascular bed. J Appl Physiol 16:71, 1961. *Personal communication, 1973.

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Complications associated with membrane lung support by venoarterial perfusion.

A series of patients supported with long-term venoarterial perfusion is presented. Gas exchange was achieved with a membrane oxygenator at flows usual...
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