Yoonki Lee, et al. Fig. 3. Chest AP taken the morning after surgery shows clear lungs without an enlarged heart. Three hours after admission to the intensive care unit, the ventilator was disconnected and her trachea was extubated. She was alert, and her BP was 110/70 mmHg, her heart rate was 95 bpm, her respiration rate was 20/min, and her SpO2 was 99% with a facemask. The next morning, the chest AP showed clear lungs (Fig. 3). DISCUSSION The initial sign in this case included an abrupt and transient increase in the ETCO2 to 85 mmHg, which likely was related to the acute increase in the CO2 level in the vascular system followed by exhalation from the respiratory system.7 Sub- sequently, there was a decrease in the ETCO2 to 13 mmHg. In addition, there was a deterioration of the hemodynamic parameters with a decrease in the BP and heart rate, as well as a mill-wheel murmur consistent with the manifestation of a gas embolism. These manifestations can be explained by the increased CO2 causing overcrowding in the right heart and the occluded right outflow tract of the heart, which was observed in the gas embolism.8 However, Geissler et al.9 have proposed that the primary mechanism for cardiac dysfunction after venous embolism is increased right ventricular afterload and arterial hypoten- Yonsei Med J Vol. 49, No. 4, 2008 sion, possibly with subsequent right ventricular ischemia, rather than right ventricular outflow obstruction by an airlock. In this case, the presence of the CO2 in the right ventricle was the primary etiology causing cardiac dysfunction. It is believed that the immediate termination of laparoscopic gas insufflation blocked any further CO2 entry into the vascular system, and the immediate resuscitative measures were useful in preventing any devastating events. The manner in which CO2 entered the vessels during the laparoscopic surgery is unclear. When a CO2 embolism is encountered, it normally occurs at the beginning of or immediately after the completion of CO2 insufflation.2 In addition, the risk of an embolic episode decreases after the completion of the pneumoperitoneum because increased intra-abdominal pressure can cause the collapse of the injured vessel. In contrast, our case occurred more than an hour after the insufflation of CO2. There are several possible reasons for this embolism. First, the previous lower abdominal surgery might have caused peritoneal adhesions that could have ruptured during the forceful irrigation. This may have caused CO2 to enter into the circulatory system through the injured vessels and then led to the CO2 embolism.2 Another possibility is inadvertent use of the laparoscopic machine. In our case, irrigating solutions were introduced into the intraperitoneal cavity by CO2 pressure; an unnoticed empty irrigation bottle or a CO2 mixed irrigation solution could have allowed for the entry of CO2 into the open venous sinuses under pressure. The coincidence of the occurrence of CO2 embolism with the irrigation and bleeding control in this case support this possibility. Additionally, CO2 might have become trapped in the portal system after transperitoneal absorption and later might have been released into the circulation.4 Finally, although direct injury to a vessel with a Veress needle might be possible, this possibility is less likely because the embolus occurred one hour after completing the pneumoperitoneum. Although short-lived, the patient developed pulmonary edema in the operating room and required intensive therapy even after surgery in the intensive care unit. The cause of pulmonary