A 22-yr-old woman with Eisenmenger’s syndrome, secondary to a sinus venosus atrial septal defect (ASD), presented for bilateral sequential lung transplantation and ASD repair. A comprehensive prebypass transesophageal echocardiographic (TEE) examination revealed marked right ventricular dilation and hypertrophy, with a large sinus venosus ASD measuring 3.5 cm, with two-way interatrial flow though the ASD throughout the cardiac cycle, and probable anomalous right-sided pulmonary venous drainage. Right and left pulmonary vein (PV) peak velocities were normal (<75 cm/s). There was mild-to-moderate right ventricular impairment.

The ASD repair was achieved with a bovine pericardial patch. The surgeon found no evidence of anomalous pulmonary venous drainage, but during lung allograft implantation the right PV anastomosis required a pericardial patch because of insufficient length. Initial mechanical ventilation and weaning from bypass was uneventful. The initial postbypass TEE examination revealed good left and right ventricular function, no evidence of a residual ASD, and minimal left-sided air. A preliminary color Doppler examination of the left and right PV anastomoses seemed satisfactory. However, a second review at about 5 min after weaning from bypass identified prominent turbulent flow from the left, and to a lesser extent, right PVs, with a peak PV velocity of 267 cm/s, indicating a left PV anastomosis gradient of 28 mm Hg (Fig. 1; Video Clip 1; please see video clip available at www.anesthesia-analgesia.org ). Further TEE examination identified dehiscence of the ASD repair with florid left-to-right flow throughout the cardiac cycle (Video Clip 2; please see video clip available at www.anesthesia-analgesia.org ). The surgeon was notified of these findings and bypass was reinstituted to revise the ASD repair. The anesthesiologist also raised a concern regarding the high-velocity PV flows, indicating probable PV kinking or stenosis and the risk of early pulmonary allograft failure.

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A discussion between the anesthesiologist and surgeon ensued, both considering the possibility that excessive pulmonary blood flow secondary to the left-to-right shunt could explain the high velocity PV flows. A decision was made to wean from bypass after the revised ASD repair, and to repeat the TEE examination and remeasure the PV flows. There was then clear resolution of turbulent flow and normal PV anastomotic diameters (>0.5 cm), and the left and right PV peak velocities reduced to <80 cm/s. Surgery was otherwise completed uneventfully and the patient made a good postoperative recovery.

TEE has become near-routine in lung transplantation, with a special focus on RV function, the existence of a patent foramen ovale and, most importantly, the quality of the pulmonary vascular anastomoses.1–4 Although the left upper PV is commonly evaluated in a four-chamber view at about 10 to 50 degrees, a more comprehensive view of both upper and low left PVs can be achieved with the transducer array at about 110 degrees and the TEE probe rotated to the extreme left. Similarly, the right PVs can be visualized at about 45 to 60 degrees with the TEE probe rotated to the extreme right. Each of these approaches visualizes the respective upper and lower PVs as an inverted “V” and is ideal for Doppler measurements. Continuous wave Doppler is preferable when estimating a maximal gradient.

Restricted pulmonary venous drainage at the anastomosis site may be due to stenosis or kinking, which can result in pulmonary edema and impaired gas exchange after pulmonary allograft implantation. The PV and right pulmonary arterial anastomoses can be visualized with TEE in most cases.1,2 Michel-Cherqui et al.2 evaluated the pulmonary vascular anastomoses in 18 patients during lung transplantation. All right arterial (n = 13) anastomoses were visualized; one had a moderate stenosis but this did not require reoperation. Of the 22 pulmonary venous anastomoses, 16 were considered normal with a diameter more than 0.5 cm and peak systolic flow velocity <100 cm/s. In 5 patients, the PV anastomoses were abnormal but did not require reoperation because of modest PV pressure gradients (<12 mm Hg) and early allograft function being within normal limits. One patient had markedly impaired gas exchange in which severe PV stenosis was identified; this led to revision of the PV anastomosis and resolution of the allograft dysfunction.2

Miyaji et al.4 performed intraoperative TEE on 17 patients during living-donor lobar lung transplantation, using the ratio of peak flow velocities through bilateral PV anastomoses as an indicator of vascular stenosis. By placing the sample volume at the level of each PV anastomosis, they calculated the ratio of the larger to smaller peak velocity as the flow velocity index. Three of 17 patients had a high flow velocity index (>1.5); 2 of these had a kink in a PV anastomosis and 1 had atelectasis of the transplanted lobe.

In our experience, there are some occasions when there is relatively high (80–140 cm/s) peak PV flows during the second lung implantation with bilateral sequential transplant procedures because, with contralateral pulmonary artery clamping, the entire cardiac output is traversing the first implanted ventilated lung. This will artificially increase PV flow and may raise unnecessary concerns regarding the quality of the PV anastomosis. A definitive evaluation of the PV anastomoses is best done with two-lung blood flow and ventilation.

A PV diameter of <0.25 cm has been suggested as the critical threshold for pulmonary allograft failure.3 In any case, unilateral postimplantation pulmonary edema should prompt TEE evaluation of the PV anastomoses. If kinking or stenosis of the PV is demonstrated, then surgical revision can occur before the patient leaves the operating room. We have had several circumstances in our institution when this has occurred. Thus, the importance of the current case study, is that it highlights an alternative explanation for high velocity flow in the PV after lung transplantation. Our patient had high velocity PV flows secondary to a marked left-to-right shunt in the setting of normalized pulmonary vascular resistance after lung transplantation, via a disrupted ASD repair.

REFERENCES
1. Leibowitz DW, Smith CR, Michler RE, Ginsburg M, Schulman LL, McGregor CC, Li Mandri G, Weslow RG, Di Tullio MR, Homma S. Incidence of pulmonary vein complications after lung transplantation: a prospective transesophageal echocardiographic study. J Am Coll Cardiol 1994;24:671–5
2. Michel-Cherqui M, Brusset A, Liu N, Raffin L, Schlumberger S, Ceddaha A, Fischler M. Intraoperative transesophageal echocardiographic assessment of vascular anastomoses in lung transplantation. A report on 18 cases. Chest 1997;111:1229–35
3. Huang YC, Cheng YJ, Lin YH, Wang MJ, Tsai SK. Graft failure caused by pulmonary venous obstruction diagnosed by intraoperative transesophageal echocardiography during lung transplantation. Anesth Analg 2000;91:558–60
4. Miyaji K, Matsubara H, Nakamura K, Kusano KF, Goto K, Date H, Ohe T. Equivalence of flow velocities through bilateral pulmonary vein anastomoses in bilateral living-donor lobar lung transplantation. J Heart Lung Transplant 2005;24:860–4