To determine if a relationship exists between intraoperative regional wall-motio abnormalities (RWMAs) and postoperative adverse outcomes, 87 patients who were undergoing elective coronary artery bypass graft surgery were studied prospectively using continuous transesophageal echocardiography (TEE). New RWMAs occured in 47% (41) of the patients during operation and in 31% (27) during cardio-pulmonary bypass terminating period (WEAN). Thirty patients had abnornal CK-MB level at ICU arrival (ENZ), and there were 10 perioperative myocardial infarctions (PMI) and 17 low-output syndromes (LOS) during ICU stay. RWMA in WEAN was significantly assosiated with all of the postoperative adverse outcomes and had 4.0-fold increase in the odds of PMI (95% confidence interval: 1.03-15.6), 3.3-fold of LOS (C.I.: 1.1-9.7), and 4.8-fold of ENZ (C.I.: 1.8-12.6). We conclude that patient subgroup who are at high risk for developing postoperative adverse outcomes can be identified intraoperatively by TEE.

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This review explains the physiological bases of oxygen transport and evaluation of the heart muscle contractility when we stop the assist circulation of the cardio-pulmonary bypass. When the cardiac index becomes more than two l/min/m² and the pressure of the left atrium becomes less than 18mmHg, we usually stop the assist circulation. And we also know Forrester's indication of the heart failure. However, there are controversies about the timing of the weaning from the assist circulation. We refereed the relationship of cardiac output and oxygen consumption which were obtained both at the resting condition and during mild to severe exercise. Then we interpolated the value of the minimum cardiac output to survive from the results. The value indicates 1.0l/min/m² in the cardiac index. The another limitation may be the maximum pressure of the left atrium to be proof against the lung damage. Forrester noted when the value becomes more than 18mmHg, the congestive lung will occur. But the actual lung can tolerate higher pressures, Judging from our analyois of pulmonary lymphatic drainage, 25mmHg of LAP within 30 minutes will never induce acute pulmonary edema.
In this article, I also introduce the QD and DS time during the cardiac surgery as the indices of the cardiac contractility. QD time is the duration time from R wave of ECG to the arterial end diastolic pressure. DS time is the duration time from the end diastolic pressure to the systolic pressure. When the duration of the DS time decrease less than 200 msec, the patients weaned from the cardio-pulmonary assist circulation. The evaluation of these indicator is not certain now, but the electrical circuit can measure these values easily and we can measure them continuously during and after the cardio-pulmonary bypass.

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We examined the incidence of paroxysmal atrio-ventricular junctional rhythm (AVJR) in 27 patients during general anesthesia with enflurane, sevoflurane and isoflurane. The incidence of paroxysmal AVJR was 3.0% for sevof lurane, 1.8% for enflurane and 1.5% for isof lurane, but these differences were not statistically significant. No significant difference in the incidence of AVJR was seen between general anesthesia alone and general anesthesia combined with epidural anesthesia. We classified the AVJR into three patterns: isorhythmic dissociation (pattern 1), wandering pacemaker (Pattern 2) and atrio-ventricular nodal rhythm (Pattern 3). Pattern 3 was seen most frequently. In all the patterns mean arterial pressure was decreased. In pattern 3, heart rate was increased, whereas it remained unchanged in pattern 1 and 2. In pattern 1, blood pressure was most severely decreased, but heart rate did not change. This study suggests that, of the three patterns, the decrease of cardiac output due to the loss of atrial kick was most marked in pattern 1 during general anesthesia.

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Ten pancreas transplantations to insulin-dependent diabetic patients were performed from Dec. 1990 to Aug. 1993 in our hospital. Seven of these patients received simultaneous kidney and pancreas transplantations and the other three patients received only pancreas transplantation because of a previous kidney transplantation. Pancreas grafts were harvested from the donors under cardiac arrest.
The patients were managed in ICU postoperatively. Duplex-doppler ultrasonography was used to evaluate the blood flow of the graft. The amount, amylase concentration, and cytology of the pancreatic juice was monitored to assess allograft rejection and vascular thrombosis after pancreas transplantation. The immunosuppresive regimen consisted of cyclosporine, methylprednisolone, azathiopurine and antilymphocyte globulin. Gabexate mesilate and prostaglandin E₁ were administered intravenously to prevent vascular thrombosis.
Five of the 10 patients became insulin-free after pancreas transplantation, while the other five patients developed vascular thrombosis or pancreatic graft rejection. Nine patients became dialysis-free. Serum creatinine ranged from 1.5 to 2.0mg/dl. One patient died suddenly nine days after transplantation. The cause of death was unknown. Severe diabetic autonomic neuropathy may have triggered the sudden cardiac death.
Successful management of pancreatic transplantation patients in ICU consists of early detection and prevention of allograft thrombosis and rejection.

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We report two cases of pneumothorax which occurred during laparoscopy under general anesthesia. The trachea was intubated and anesthesia was maintained with nitrous oxide, oxygen and isoflurane in both cases. Right pneumothorax occurred immediately after pneumoperitoneum in a 25-year-old woman who underwent laparoscope for inspection of endometriosis. Left pneumothorax occurred 45 minutes after carbon dioxide insufflation into the abdominal cavity of a 70-year-old man who underwent laparoscopic cholecystectomy. In both patients, an emergent chest drainage was established and they recovered uneventfully. No air leakage from the chest drain was seen after re-expansion of the lung. There was no evidence of iatrogenic damage to the diaphragm in either case. Chest CT was normal in the former case, and carbon dioxide pneumothorax was revealed in the latter case because PCO₂ of the sealed water in the chest drainage bag was 722 mmHg. The existence of some pleuroperitoneal communication (for example, via congenital defect of the diaphragm) was thought to be a possible cause of the pneumothorax.

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