BACKGROUND: A new technique resecting the hepatic parenchyma without inflow occlusion using a Cavitron Ultrasonic Surgical Aspirator (CUSA(R) ) reduces intraoperative blood loss and perioperative morbidity. This study was designed to identify the incidence and severity of venous air embolism (VAE) using transesophaseal echocardiography (TEE) in hepatic resection using CUSA(R) . METHODS: Forty patients undergoing hepatic resection using CUSA(R) of ASA class 1 and 2 were selected. After insertion of an epidural catheter for postoperative analgesia, all patients were anesthetized with sevoflurane in 50% air/O2. After the induction of anesthesia, A TEE probe was inserted into the esophagus. Blood pressure, heart rate, central venous pressure, end tidal CO2, and arterial carbon dioxide tension were recorded after induction, and during and after hepatic resection. During hepatic resection, an anesthesiologist evaluated the degree of VAE by transesophageal echocardiography in the 4-chamber view. RESULTS: The mean time of using CUSA(R) was 65.3 +/- 24.4 minutes. Of 40 patients, 9 had VAE grade I, 14 grade II, 14 grade III, and 3 grade IV. However, no significant difference was observed in hemodynamics or PaCO2 after induction, or during or after hepatic resection. The mean amount of blood loss was 887.0 ml +/- 598.8 ml and the mean transfused amount was 123.1 +/- 351.3 ml. CONCLUSIONS: All patients showed air embolism during hepatic resection with CUSA(R) . Serious complications associated with air embolism would occur in patients with an undiagnosed intracardiac right to left shunt. Therefore, meticulous monitoring by transesophageal echocardiography might be recommended in hepatic resection with CUSA(R) .
Analgesia ; Anesthesia ; Blood Pressure ; Carbon Dioxide ; Catheters ; Central Venous Pressure ; Echocardiography* ; Echocardiography, Transesophageal ; Embolism, Air* ; Esophagus ; Heart Rate ; Hemodynamics ; Humans ; Incidence* ; Ultrasonics*

BACKGROUND: Naloxone,an opioidant agonist, has been s hown t o have a c ar di ovascular pressor effect in states of hemorrhagic and endotoxic shock.We determined the direct inotropic effect of naloxone using guinea pig right ventricular papillary muscles. METHODS: With institutional approval,isometric contractile force was measured in normal and 26mM K+ Tyrode's solution at various stimulation rates.Normal and slow action potentials (APs) were measured with conventional microelectrode technique.The effects of naloxone on sarcoplasmic recticulum function were evaluated by measuring rapid cooling contractures (RCCs)in normal Tyrode 's solution and rested-state (RS)contraction in low Na+ (25 mM)Tyrode's solution.Patch clamp study was performed to examine the direct effect on Ca2+ current in myocytes. RESULTS: Naloxone (50,100,200 micro M)caused dose-dependent depression of peak force and maximal rate of peak force (dF/dt-max)by 30,50 and 70%,respectively.Modest depression was shown in RS contraction in low Na+ Tyrode's solution.In 26 mM K+ Tyrode's solution,100 micro M naloxone markedly depressed late force development.100 micro M naloxone depressed RCCs by 20%. While 100 micro M naloxone did not alter amplitude or dV/dt-max in normal and slow APs at 0.25 Hz, AP duration was prolonged significantly.In patch clamp study,50 micro M naloxone depressed Ca2+ current by 50%. CONCLUSIONS: Naloxone depresses contractile force.Myocardial depressant effect partly seems to be caused by depressed Ca2+ influx through cardiac membrane.Rapid release of Ca2+ from the sarcoplasmic reticulum by depolarization and release by rapid cooling seems to be minimally affected.
Action Potentials ; Animals ; Contracture ; Depression ; Guinea Pigs ; Heart ; Microelectrodes ; Muscle Cells ; Myocardial Contraction ; Myocardium ; Naloxone* ; Papillary Muscles ; Sarcoplasmic Reticulum