Right ventricular rupture during off-pump coronary bypass surgery.

ORONARY ARTERY bypass graft surgery (CABG) is increasingly being performed without the use of cardiopulmonary bypass (CPB). This has placed additional responsibilities on the anesthesiologist in terms of monitoring and maintenance of hemodynamics during the procedure, which frequently involves mechanical manipulation of the beating heart. A case of right ventricular (RV) rupture during off-pump CABG (OPCAB) is reported. Possible etiologies and implications for the anesthesiologist are also discussed. CASE REPORT A 78-year-old caucasian male presented for urgent CABG surgery. Cardiac catheterization showed significant 2-vessel coronary artery disease, left mainstem stenosis, and preserved left ventricular (LV) function with an estimated ejection fraction of 59%. There was a history of myocardial infarction. Comorbid conditions included benign essential hypertension and history of chronic atrial fibrillation since the age of 16 years. There was a history of malignant melanoma of the neck, which was successfully surgically treated three months before presentation for cardiac surgery. The patient also reported having a stroke two years before, without residual sequelae. There was no other significant contributory history related to any other organ system. The surgical plan was to proceed with CABG surgery without the use of CPB (OPCAB). The patient was orally premedicated with lorazepam 60 minutes before arrival in the induction room. Intravenous arterial and pulmonary artery catheters were placed before induction. Anesthesia was induced with intravenous bolus of midazolam, fentanyl, and thiopental. Relaxation was achieved with pancuronium bromide, and anesthesia was maintained with isoflurane and supplemental intravenous pancuronium. Transesophageal echocardiography (TEE) before incision revealed normal LV morphology, no hypertrophy, no regional wall motion abnormalities, no intracavitary lesions, and normal papillary muscle structure. Pulsed-wave Doppler evaluation revealed irregular transmitral and pulmonary venous flow velocity profiles consistent with atrial fibrillation. The RV was normal in structure and function. There were no wall motion abnormalities of the RV free wall and no tricuspid regurgitation, reflecting essentially normal RV function. There was no thrombus or mass in the LV, RV, left atrium, or left atrial appendage. Surgery proceeded through a median sternotomy incision and included dissection of the left internal mammary artery and endoscopic harvest of the great saphenous vein (SV) from the left leg. Heparin (15,000 IU) was administered to achieve a target activated coagulation time (ACT) of 300 seconds. Coronary artery grafting was initiated after the ACT had exceeded 300 seconds (first postheparin ACT was 384 seconds). Planned anastomoses included the left internal mammary artery to left anterior descending artery and an SV graft to the first obtuse marginal branch of the left circumflex artery. To optimize exposure to the distal coronary grafting sites, the patient was positioned in a 20° head-down position, and the apex of the heart was suspended using a Guidant Axius Xpose device (Santa Clara, CA; Fig 1). This device consists of a suction cup positioned on the diaphragmatic surface of the cardiac apex and a vacuum seal of 250 mmHg pressure that suspends the heart to expose target vessels. There were no signs of infarction or tissue injury on the ventricular wall before placement of the suction cup. During the surgery, adequate vacuum seal was difficult to achieve, and the device required frequent repositioning for satisfactory exposure. The initial lack of success in suspending the heart appeared to be caused by a small bleeding vein on the apex of the heart, approximately 500 mL of bloodstained fluid collected in the suction container during the surgery. Hemodynamic stability was maintained with intravenous norepinephrine infusion (0.01-0.1 g/kg/min) and intravenous fluid therapy with lactated Ringer’s solution. A background infusion of nitroglycerin (0.5 g/kg/min) was maintained throughout the surgical procedure. The patient was ventilated with 100% oxygen during each anastomosis. Recovery from hemodynamic insult because of manipulation of the heart was facilitated with a 10-minute period of stabilization between anastomoses. There was no regional wall motion abnormality, and TEE revealed normal left ventricular function during this rest period. The second postheparin ACT at this stage was 327 seconds. After the first anastomosis, it was noted that there was increasing bleeding around the LV apex. Closer examination revealed a 0.2- to 0.5-cm tear on the apical surface of the RV. This tear was a small defect in a low-pressure system that could be controlled until completion of the second distal anastomosis and then repaired on the beating heart. The tear was sealed with a portion of the suction cup device applied over the apex covering the tear. The second anastomosis (SV to first obtuse marginal branch) proceeded with the patient in Trendelenburg position and the stabilization devices in place. During the grafting procedure, the patient received a total of 1.5 L of crystalloid solution intravenously and had some episodes of hypotension that required repositioning of the suction cup because of poor response to intermittent bolus doses of vasopressor agents. After successful completion of the distal anastomoses, the suction device was removed. Attempts at surgical repair of the RV tear after removal of the suction cup device were unsuccessful because of inadequate exposure of the tear in the face of significant hemodynamic compromise and concerns over extending the laceration of the RV free wall. This prompted the decision to initiate CPB to