Pulmonary embolism caused by a carbon dioxide blower during off-pump coronary artery bypass grafting.

We report a rare case of pulmonary embolism (PE) caused by a carbon dioxide (CO2) blower during off-pump coronary artery bypass grafting (OPCAB). When the anastomosis of the right internal thoracic artery to left anterior descending artery was performed, the operator tore the right ventricle outflow track (RVOT) that was adjacent to the left anterior descending artery. Immediately after the anastomosis and repair of the torn RVOT with CO2 blower, the systolic pulmonary artery pressure (PAP) increased from 28 to 64 mmHg, and end-tidal CO2 decreased from 32 to 12 mmHg. Because transesophageal echocardiograph (TEE) showed numerous gas bubbles in the main pulmonary artery, we diagnosed PE caused by invasion of CO2 gas bubbles via the torn RVOT. Although a CO2 blower is useful to enhance visualization of the anastomosis during OPCAB, it should not be used for the venous system because it may cause CO2 embolism.

Differential effects of propofol and sevoflurane on ischemia-induced ventricular arrhythmias and phosphorylated connexin 43 protein in rats.

BACKGROUND: The effects of anesthetics on ischemia-induced ventricular arrhythmias remain poorly studied. This study investigated the effects of propofol and sevoflurane on the survival rate and morbidity as a result of ventricular arrhythmias, and defined a possible mechanism for the arrhythmogenic properties of anesthetics during acute myocardial ischemia. METHODS: Under anesthesia with intraperitoneal sodium pentobarbital, Sprague-Dawley rats underwent 30 min of left anterior descending coronary artery ligation. The rats were divided into a low-dose propofol (Prop-LD) group (39 mg X kg(-1) X hr(-1), n = 18), a high-dose propofol group (78 mg x kg(-1) x hr(-1), n = 18), a sevoflurane group (2.5%, n = 18) and a control group (n = 18). The survival rate and morbidity as a result of ventricular arrhythmias were determined, and the amount of phosphorylated connexin 43 protein was measured 30 min after coronary artery ligation. RESULTS: The survival rate was 83% (15 of 18), 94% (17 of 18), 89% (16 of 18), and 67% (12 of 18, P = 0.038 vs. Prop-LD) in the control, Prop-LD, high-dose propofol, and sevoflurane groups, respectively. Sustained ventricular tachycardia was observed in 83% (15 of 18), 39% (7 of 18, P = 0.011 vs. control), 50% (9 of 18, P = 0.039 vs. control) and 94% (17 of 18, P < 0.01 vs. Prop-LD) in the control, Prop-LD, high-dose propofol, and sevoflurane groups, respectively. Immunoblotting showed a marked reduction in the amount of phosphorylated connexin 43 in the control and sevoflurane groups, as compared with the Prop-LD and high-dose propofol groups (P < 0.05). CONCLUSION: The authors' results suggest that propofol preserves connexin 43 phosphorylation during acute myocardial ischemia, as compared with sevoflurane, and this might protect the heart from serious ventricular arrhythmias during acute coronary occlusion.

Cardioprotective effects of propofol in isolated ischemia-reperfused guinea pig hearts: role of KATP channels and GSK-3beta.

PURPOSE: Propofol exerts cardioprotective effects, but the involved mechanisms remain obscure. The present study examines the cardioprotective effects of propofol and its role in cardiac function, including its effect on K(ATP) channel opening and the inhibition of GSK-3beta activity in ischemia-reperfused hearts. METHODS: Ischemia-reperfusion (I/R) was produced in isolated guinea pig hearts by stopping coronary perfusion for 25 min, followed by reperfusion. The hearts were incubated for ten minutes, with or without propofol (25 or 50 microM), or for five minutes with 500 microM 5-hydroxydecanoate (a mitochondrial K(ATP) channel blocker) or 30 microM HMR1098 (sarcolemmal K(ATP) channel blocker), followed by five minutes with 50 microM propofol before ischemia. Action potentials on the anterior epicardial surface of the ventricle were monitored using a high-resolution charge-coupled device camera system, and at five minutes after reperfusion, GSK-3beta phosphorylation at the serine residue, Ser9, was examined. RESULTS: After 35 min of reperfusion, propofol (25 and 50 microM) blunted the adverse effects of I/R and reduced infarct size (P < 0.05). In addition, prior incubation with 5-hydroxydecanoate or HMR1098 had no effect on functional recovery improved by 50 microM propofol. At five minutes after reperfusion, propofol (25 and 50 microM) shortened the duration of the action potential and increased the levels of phospho-GSK-3beta (P < 0.05). CONCLUSIONS: Propofol enhanced mechanical cardiac recovery and reduced infarct size. The data further suggest that GSK-3beta play an important role in propofol cardioprotective actions during coronary reperfusion, but mitochondrial K(ATP) channels do not.

[Utility of bicarbonated Ringer's solution as an intraoperative fluid during long-term laparotomy].

BACKGROUND: We compared the effects on intraoperative acid-base balance of bicarbonated Ringer (BR) and those of acetated Ringer (AR) solutions as an intraoperative fluid during long-term laparotomy. METHODS: Forty patients scheduled for laparotomy expected to take more than 5 hours were divided into two groups according to the type of infused solution, BR or AR. Each solution was intravenously administered at a rate between 8 and 10 ml x kg(-1) x hr(-1). Arterial blood gases were analyzed before and during surgery. RESULTS: Intraoperative arterial blood HCO3- and base excess (BE) significantly decreased in the AR group but not in the BR group. HCO3- and BE 2 and 4 hrs after the start of surgery and at the end of surgery were significantly higher in the BR group than in the AR group. CONCLUSIONS: These results suggest that BR has superior effects on the acid-base balance during long-term laparotomy.

Cardioprotective effect and mechanism of action of landiolol on the ischemic reperfused heart.

PURPOSE: The authors examined the cardioprotective effect of landiolol, an ultra short-acting, highly selective beta1-blocker, and its role in cardiac work, antioxidative effect, and sarcoplasmic reticulum (SR) function in hearts subjected to ischemia-reperfusion. METHODS: Isolated guinea pig hearts were subjected to ischemia-reperfusion by stopping the perfusion for 45 min and reperfusing. Before the ischemia, hearts were treated with landiolol (20, 100, or 500 microM) for 15 min (LAN group). In another set of experiments, before ischemia, hearts were washed out for 15 min after treatment with landiolol (WO group). In other hearts, the tissue concentration of malondialdehyde was measured after reperfusion. We also examined the phosphorylation of phospholamban at Ser(16) and Thr(17)residues to evaluate the SR function. RESULTS: After 90 min of reperfusion, left ventricular pressure (LVP) was restored significantly in the LAN-500 microM group regardless of heart rate. However, the improvement in recovery in LVP disappeared in the WO group. The tissue malondialdehyde levels were decreased in the LAN group compared with those in the control group. In the control group, the phosphorylation of phospholamban at Ser(16) and Thr(17) residues was markedly increased after reperfusion. Landiolol at 500 microM suppressed the increase of phosphorylation at Ser(16) residues. CONCLUSION: The present study demonstrated that landiolol had a lipid peroxidation-reducing effect and suppressed the increase in phospholamban phosphorylation at the Ser(16) residue in hearts subjected to ischemia-reperfusion. These findings indicate that landiolol may have an anti-ischemic effect, via an antioxidant effect and/or via preserving SR function during the ischemic period.

[Suspicious case of epidural hematoma due to coagulopathy caused by vitamin K deficiency associated with antibiotics].

We experienced a case of epidural hematoma caused by coagulopathy 3 days after surgery. A 72-year-old man, who had undergone a total gastrectomy, suffered from nausea and vomiting by ileus. He underwent repair of ileus under general anesthesia with thoracic epidural anesthesia. Three days after surgery, abnormal bleeding followed by disorder of prothrombin activity (PT) and activated partial thromboplastin time (aPTT) and paralysis due to thoracic epidural hematoma developed. It was suspected that these coagulopathies were the results of vitamin K deficiency. Vitamin K deficiency in this patient was considered to have been caused by cephem antibiotics containing N-methyl-thiotetrazole (NMTT) side chain and no oral intake of food for a few days preoperatively. The patient was treated with fresh frozen plasma and intravenous menatetrenon, which improved abnormal bleeding and disorder of PT and aPTT within 24hr. After a discussion with orthopedic consultants, we selected a conservative therapy rather than surgical removal of the hematoma. Thoracic epidural hematoma disappeared two months after surgery, but motor paralysis requiring rehabilitation remained. In conclusion, when patients have not eaten anything for a few days and antibiotics with an NMTT sidechain has been administered, care must be taken to prevent vitamin K deficiency and coagulopathy.

Propofol increases pulmonary vascular resistance during alpha-adrenoreceptor activation in normal and monocrotaline-induced pulmonary hypertensive rats.

BACKGROUND: Using isolated perfused lungs of normal or monocrotaline (MCT: 50 mg/kg)-induced pulmonary hypertensive rats, we tested the hypothesis that the pulmonary vascular effects of propofol depend on activation of the alpha-adrenoreceptor. METHODS: Changes in pulmonary perfusion pressure induced by propofol (10(-5) to 10(-4) M) were measured with or without phenylephrine (10(-6) M) pretreatment. Before phenylephrine administration, we assessed the effects of inhibitors of nitric oxide synthase (N(omega)-nitro-l-arginine methylester: 10(-4) M), cyclooxygenase (indomethacin: 10(-5) M), and protein kinase C inhibitor, bisindolylmaleimide I (10(-6) M) or calphostin C (10(-6) M). RESULTS: Changes in pulmonary perfusion pressure by phenylephrine after pretreatment of nitric oxide synthase inhibitor and indomethacin in normal rats were significant (5 +/- 3 and 7 +/- 2 mm Hg), whereas that after pretreatment of bisindolylmaleimide I were small in MCT-rats (2 +/- 1 mm Hg). Propofol caused pulmonary vasoconstriction after phenylephrine pretreatment both in normal and MCT-treated rats. In normal rats, the propofol-induced increase in pulmonary perfusion pressure after indomethacin pretreatment was slightly smaller than that in the non-pretreated lungs (P < 0.05). In MCT-treated rats, the propofol-induced increases in pulmonary perfusion pressure after both protein kinase C inhibitors were smaller than that in the non-pretreated lungs (P < 0.05). CONCLUSIONS: Propofol may increase pulmonary vascular resistance during alpha-adrenoreceptor activation.

[Case of papillary muscle rupture diagnosed by preoperative transesophageal echocardiography].

A 46-year-old man with severe mitral regurgitation (MR) was scheduled for emergency surgery for chordae tendae repairment. Preoperative transesophageal echocardiography (TEE) revealed massive MR due to a rupture in the antero-lateral papillary muscle. We changed the operation procedure to mitral valve replacement. It is difficult to diagnose papillary muscle rupture. Therefore, we should perform TEE on the patient with acute MR of unknown origin.

Effects of ulinastatin on pulmonary artery pressure during abdominal aortic aneurysmectomy.

STUDY OBJECTIVE: Abdominal aortic aneurysmectomy (AAAectomy) results in a general ischemia-reperfusion syndrome accompanied by an acute rise in pulmonary artery pressure (PAP). We examined whether ulinastatin, a urinary trypsin inhibitor, prevents ischemia-reperfusion injury and increase in PAP after aortic unclamping (XU) during AAAectomy. DESIGN: Prospective study. SETTING: Public, university-affiliated hospital. PATIENTS: Sixteen patients (11 males and 5 females) scheduled for AAAectomy. INTERVENTIONS AND MEASUREMENTS: The patients received 300000 IU of ulinastatin intravenously before XU (n = 8) or no additional treatment (n = 8) (control). Heart rate, central venous pressure, PAP, pulmonary arterial wedge pressure, arterial pressure, mixed venous oxygen saturation (Sv(O2)), and cardiac output were monitored. Arterial and mixed venous blood samples were analyzed for pH, Pa(CO2), Pa(O2), hemoglobin, and oxygen saturation, and the physiological shunt function (Qs/Qt) were calculated. Plasma concentrations of malondialdehyde, myeloperoxidase, granulocyte elastase, alpha1-antitrypsine, and thromboxane B2 and the stable hydrolysis products of thromboxane A2 were measured. Measurements were conducted before aortic crossclamping (XC) (baseline) and at 10, 30, and 60 minutes after XU. MAIN RESULTS: A significant increase in PAP was observed 10 minutes after XU in the control group but not in the ulinastatin group. At 60 minutes after XU, Qs/Qt values had increased in the control group but had decreased in the ulinastatin group. There were no significant changes in malondialdehyde, thromboxane B2, granulocyte elastase, and alpha1-antitrypsine levels after XU in either group. A significant decrease in the plasma level of myeloperoxidase after XU was found in both groups. CONCLUSIONS: The present study demonstrated that ulinastatin prevents increase in PAP and shunting after XU during AAAectomy.

Effects of L-type Ca2+ channel modulation on direct myocardial effects of diazepam and midazolam in adult rat ventricular myocytes.

PURPOSE: Our objective was to determine whether an L-type Ca2+ channel modulation could alter myocardial depression induced by midazolam or diazepam in adult rat ventricular myocytes. METHODS: Freshly isolated rat ventricular myocytes were loaded with fura-2/AM and field-stimulated (0.3 Hz) at 28 degrees C. Amplitude and timing of intracellular Ca2+ concentration ([Ca2+]i) and myocyte shortening were simultaneously monitored in individual cells. RESULTS: Midazolam (3-100 microM) caused a decrease in both peak [Ca2+]i and shortening. Diazepam (30, 100 microM) increased myocyte shortening and peak [Ca2+]i; however, higher concentration of diazepam (300 microM) decreased shortening and peak [Ca2+]i. Bay K 8644 (0.01-10 microM), an L-type Ca2+ channel agonist, caused dose-dependent increases in peak [Ca2+]i and shortening. In contrast, verapamil (0.1-50 microM), an L-type Ca(2+) channel antagonist, caused dose-dependent decreases in peak [Ca2+]i and shortening. Dose-response curves to benzodiazepines on peak [Ca2+]i and shortening were not affected by pretreatment with Bay K 8644 (0.1 microM) or verapamil (1 microM). Diazepam (30, 100 microM), but not midazolam (3-30 microM), increased shortening and [Ca2+]i in the presence or absence of L-type Ca2+ channel modulators. Diazepam (30 microM) and midazolam (10 microM) had no effect on peak [Ca2+]i of a caffeine-induced [Ca2+]i transient, which was used as a measure of SR Ca2+ content. CONCLUSION: Midazolam and diazepam have differential effects on cardiac E-C coupling. Diazepam, but not midazolam, enhances cardiac E-C coupling independent of L-type Ca2+ channel modulation.

[Anesthetic management in a patient with Goldenhar's syndrome using a perilaryngeal airway and a videolaryngoscope].

A 5-year-old girl with Goldenhar's syndrome was scheduled for reconstruction of her left thumb. Because her preanesthetic X-p had revealed airway abnormality, difficult intubation was anticipated. After induction of anesthesia with thiamylal, the lungs were ventilated easily via a facemask. A perilaryngeal airway (PLA) was inserted after obtaining adequate depth of anesthesia with sevoflurane. Anesthesia was maintained with sevoflurane (2%) plus nitrous oxide (66%) under spontaneous ventilation. The operation was finished uneventfully. However, a re-operation was scheduled for postoperative hemorrhage on that day. In consideration of potential regurgitation of gastric content, endotracheal intubation was scheduled. Her vocal cord was confirmed with a videolaryngoscope, and she was intubated successfully. In conclusion, a PLA and a videolaryngoscope are useful for airway management of patients with Goldenhar's syndrome for whom difficulty in intubation is anticipated.

Experimental conditions are important determinants of cardiac inotropic effects of propofol.

BACKGROUND: The rationale for this study is that the depressant effect of propofol on cardiac function in vitro is highly variable but may be explained by differences in the temperature and stimulation frequency used for the study. Both temperature and stimulation frequency are known to modulate cellular mechanisms that regulate intracellular free Ca2+ concentration ([Ca2+]i) and myofilament Ca2+ sensitivity in cardiac muscle. The authors hypothesized that temperature and stimulation frequency play a major role in determining propofol-induced alterations in [Ca2+]i and contraction in individual, electrically stimulated cardiomyocytes and the function of isolated perfused hearts. METHODS: Freshly isolated myocytes were obtained from adult rat hearts, loaded with fura-2, and placed on the stage of an inverted fluorescence microscope in a temperature-regulated bath. [Ca2+]i and myocyte shortening were simultaneously measured in individual cells at 28 degrees or 37 degrees C at various stimulation frequencies (0.3, 0.5, 1, 2, and 3 Hz) with and without propofol. Langendorff perfused hearts paced at 180 or 330 beats/min were used to assess the effects of propofol on overall cardiac function. RESULTS: At 28 degrees C (hypothermic) and, to a lesser extent, at 37 degrees C (normothermic), increasing stimulation frequency increased peak shortening and [Ca2+]i. Times to peak shortening and rate of relengthening were more prolonged at 28 degrees C compared with 37 degrees C at low stimulation frequencies (0.3 Hz), whereas the same conditions for [Ca2+]i were not altered by temperature. At 0.3 Hz and 28 degrees C, propofol caused a dose-dependent decrease in peak shortening and peak [Ca2+]i. These changes were greater at 28 degrees C compared with 37 degrees C and involved activation of protein kinase C. At a frequency of 2 Hz, there was a rightward shift in the dose-response relation for propofol on [Ca2+]i and shortening at both 37 degrees and 28 degrees C compared with that observed at 0.3 Hz. In Langendorff perfused hearts paced at 330 beats/min, clinically relevant concentrations of propofol decreased left ventricular developed pressure, with the effect being less at 28 degrees C compared with 37 degrees C. In contrast, only a supraclinical concentration of propofol decreased left ventricular developed pressure at 28 degrees C at either stimulation frequency. CONCLUSION: These results demonstrate that temperature and stimulation frequency alter the inhibitory effect of propofol on cardiomyocyte [Ca2+]i and contraction. In isolated cardiomyocytes, the inhibitory effects of propofol are more pronounced during hypothermia and at higher stimulation frequencies and involve activation of protein kinase C. In Langendorff perfused hearts at constant heart rate, the inhibitory effects of propofol at clinically relevant concentrations are more pronounced during normothermic conditions.

[In vitro evaluation of lubrication properties of a suction catheter].

BACKGROUND: Lubrication is an important factor for passage of a suction catheter through a tracheal tube. This study was carried out to evaluate the effects of lubricants on resistance against removal of a suction catheter from a tracheal tube in an experimental setting. METHODS: A tracheal tube (I.D. of 7.5mm) was inserted into a mannequin, and the resistance against removal of a suction catheter from the tube was measured. RESULTS: Lubrication was improved by using a lubricant (lidocaine jelly or KY jelly), but there was no difference between the effects of the two lubricants. The use of water as lubricant markedly decreased lubrication. Differences in lubrication depending on the type of tracheal tube used, probably due to differences in coating, were also found. CONCLUSIONS: The use of water as a lubricant is not recommended for tracheal suction.

[The use of a Parker Flex-Tip tube in a case of large laryngeal polyps].

A 58-year-old man was scheduled for laryngomicrosurgery for treatment of large laryngeal polyps. Although awake induction was initially attempted to prevent airway obstruction, his vocal cords could not be visualized. We therefore tried intubation with a Parker Flex-Tip (PFT) tube under the guidance of a bronchial fiberscope (BF). After inserting the BF, his trachea was intubated easily. The operation was performed without any complications. We conclude that a PFT tube is useful for endotracheal intubation in a patient with large laryngeal polyps.

[The usefulness of intraoperative TEE monitoring in a patient with renal cell carcinoma].

A 55-year-old man was admitted to our hospital for treatment of renal cell carcinoma. Preoperative MRI showed infradiaphragmatic extension of the tumor thrombus. However, intraoperative transesophageal echocardiography (TEE) revealed intracardiac extension of the thrombus. Therefore, the tumor thrombus was extirpated under cardiopulmonary bypass. The patient recovered without any complications. Intraoperative TEE monitoring is useful not only for the evaluation of cardiac functions but also for intraoperative diagnosis of a tumor thrombus during the operation for renal cell carcinoma.

A comparison of the failure times of pulse oximeters during blood pressure cuff-induced hypoperfusion in volunteers.

Important information may not be obtained if the pulse oximetry signal is lost during inflation of a cuff for blood pressure measurement, particularly in patients with hemodynamic instability. In the present study, we compared the failure times of pulse oximeters during cuff-induced hypoperfusion in volunteers. A pulse oximeter sensor was attached to the index finger, and a blood pressure cuff was attached to the same arm of each volunteer. MasimoSET Radical (Masimo), Nellcor N-395 (N-395), Nellcor N-20PA, and Nellcor D-25 were tested. To evaluate the failure time of each pulse oximeter, time to peak of cuff pressure, time to loss of signal, time to recovery of signal, and failure interval were measured. All measurements were performed three times for each pulse oximeter and were averaged. There were no differences in hemodynamic measurements among the groups. Time to loss of signal was longer in Masimo than the other pulse oximeters. Masimo and N-395 showed significantly shorter times to recovery of signal than those of the other two pulse oximeters. Failure interval was in the order of Masimo << N-395 < Nellcor D-25 = Nellcor N-20PA. Masimo did not lose a signal as rapidly as the other oximeters studied. Masimo was similar in performance to the N-395 at providing useful data sooner than conventional technology after a loss of the signal. These observations suggest that data will be more available with fewer false-positive alarms when using the Masimo oximeter followed by the N-395 when compared with conventional oximeters.

Differential pressor response to intravenous ephedrine during recovery from deliberate hypotension.

STUDY OBJECTIVE: To determine whether nitroglycerin or trimethaphan alters pressor response to intravenous (i.v.) ephedrine. DESIGN: Prospective, randomized study. SETTING: Operating room of a university hospital. PATIENTS: 60 ASA physical status I female patients scheduled for mastectomy. INTERVENTIONS: Patients were assigned to one of six groups (n = 10 in each). Group 1: nitroglycerin + normal saline (NS) i.v., Group 2: nitroglycerin + ephedrine 0.1 mg/kg i.v., Group 3: nitroglycerin + ephedrine 0.15 mg/kg i.v., Group 4: trimethaphan + NS i.v., Group 5: trimethaphan + ephedrine 0.1 mg/kg i.v., and Group 6: trimethaphan + ephedrine 0.15 mg/kg i.v. MEASUREMENTS: Hemodynamic responses to ephedrine following withdrawal of vasodilators were observed for 15 minutes. MAIN RESULTS: Ephedrine increased heart rate and mean blood pressure. After ephedrine 0.1 mg/kg i.v., the maximum pressor response in the trimethaphan group was approximately twofold that of the nitroglycerin group (p = 0.038). CONCLUSIONS: Ephedrine restored BP more easily in those patients who had received trimethaphan compared with those who had received nitroglycerin for deliberate hypotension.

Forehead is as sensitive as finger pulse oximetry during general anesthesia.

PURPOSE: To compare the performance of a forehead probe to a conventional finger pulse oximetry probe in anesthetized patients. METHODS: Eighteen patients participated in the study. Each probe was connected to a Nellcor N-550 pulse oximeter. Anesthesia was induced and maintained with propofol. After intubation, the patients received air to achieve a steady-state of peripheral arterial oxygen saturation (SpO(2)). Ventilation was interrupted to induce a hypoxic state. As soon as one of the two SpO(2)'s decreased to 90%, the patients' lungs were ventilated with 100% oxygen. To evaluate the performance of the two pulse oximeters, time to the lowest (TL), time of recovery (TR) and lag times to beginning of SpO(2) decrease (Lag) were measured. RESULTS: There were no significant differences in TL and TR between forehead and finger pulse oximetry under normal perfusion conditions during general anesthesia. When the axillary artery was compressed to mimic reduced peripheral perfusion, SpO(2) in the forehead decreased sooner than in the finger during hypoxia. The forehead and finger TLs were similar, however, TR was significantly longer in the finger. CONCLUSION: The forehead SpO(2) sensor can be used as an alternative to the conventional finger sensor during general anesthesia.