[Pulmonary edema due to venous air embolism during craniotomy: a case report].

We present a 35-year-old healthy male patient who developed pulmonary edema (PE) probably due to venous air embolism during craniotomy in the semi-sitting position for arteriovenous malformation (AVM). Anesthesia was maintained with oxygen, nitrous oxide, propofol and fentanyl. During craniotomy, end-tidal carbon dioxide pressure decreased suddenly from 26 to 9 mmHg. Concurrently, a decrease in oxygen saturation from 99% to 91% occurred. There were no serious changes in blood pressure and heart rate. A "mill-wheel murmur" was confirmed. PE due to venous air embolism was suspected. The operation was discontinued and the patient was transferred to the intensive care unit. In the post-operative period, the patient developed PE and made a full recovery within a week. Four months later, the patient was scheduled again for surgical excision of AVM in the semi-sitting position in the same way as the first time. Anesthesia was maintained with oxygen, air, propofol and fentanyl. Transoesophageal echocardiography and pulmonary artery catheter were used. Saline was filled at the surgical site to prevent aspiration of air bubbles and surgical procedure was performed carefully without large vein injury and uneventfully. During neurosurgical intervention in the sitting position, special attention should be paid to entry of air bubbles into the venous system which may lead to PE.

[Effects of landiolol hydrochloride on cardiohemodynamics in patients who underwent coronary artery bypass grafting].

BACKGROUND: It is important to control heart rate for coronary artery bypass grafting. The purpose of this study was to evaluate the effects of landiolol hydrochloride, ultra-short-acting beta-blocker, on cardiohemodynamics in 10 patients who underwent coronary artery bypass grafting. METHODS: Anesthesia was induced and maintained with midazolam and fentanyl. After stabilization of anesthesia, landiolol hydrochloride was administered at a rate of 0.04 mg x kg(-1) x min(-1) for 30 min after 0.125 mg x kg(-1) x min(-1). Hemodynamic measurements were made before and every 5 min after administration of landiolol hydrochloride. RESULTS: Heart rate decreased significantly although arterial pressure was unchanged. There were no changes in cardiac index, left ventricular stroke volume index, systemic vascular resistances and pulmonary vascular resistance after landiolol hydrochloride administration. CONCLUSIONS: These results suggest that landiolol hydrochloride possesses less negative inotropic action than negative chronotropic action. Landiolol hydrochloride did not affect both systemic and pulmonary vascular resistances because of high cardioselectivity.

Hemodynamic profile in rabbits of fospropofol disodium injection relative to propofol emulsion following rapid bolus injection.

The effects of aqueous fospropofol disodium (FP) and propofol emulsion (PE) on hemodynamics and sympathetic nerve activity in rabbits following bolus injection were evaluated. Barodenervated and neuraxis-intact rabbits received PE at 4 mg/kg (PE(4)) or FP equal to 4 or 8 mg/kg propofol equivalents (FP(4) and FP(8), respectively) intravenously as a rapid bolus injection, and mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were recorded for 20 min. The plasma propofol pharmacokinetic behavior from FP and PE was evaluated to support the pharmacodynamic observations. In barodenervated animals, MAP and RSNA decreased significantly in all groups (PE(4) > FP(8) > FP(4)). HR decreased only in the PE(4) group. The time for the maximum reduction of MAP was significantly longer with FP(8) compared with PE(4). MAP decreased, and RSNA and HR increased significantly in the neuraxis-intact animals (PE(4) > FP(8) > FP(4)). The time for maximum reduction of MAP was essentially the same in all neuraxis-intact groups. Plasma propofol levels from FP were lower than those from PE in the first 4 min following administration. The results suggest that the tachycardia observed in humans following injection of FP is not a direct physiological effect of the agent.