Analysis of difficulty in placement of pulmonary artery catheter through the left internal jugular vein.

PURPOSE: The left internal jugular vein may be an alternative route for the placement of a pulmonary artery catheter when the right jugular vein is not available. Although the placement through the left internal jugular vein is expected to be more difficult, little has been written regarding difficulties in achieving proper placement of the catheter through the left internal jugular vein. METHODS: This prospective and observational study includes patients undergoing cardiac surgery with the catheter placement by monitoring the pressure waveform for 2 years. We measured the time required for the catheter to pass through the tricuspid and pulmonary valves, respectively. The data were analyzed by Mann-Whitney. P < 0.05 was considered significant. RESULTS: The catheter placement through the right and left internal jugular vein was done in 285 (group R) and 10 patients (group L), respectively. The time duration through the tricuspid valve in group L was significantly longer than that in group P (8 [5-14] s vs 70 [19.8-138] s, median [range], P < 0.01), whereas the time duration through the pulmonary valve was comparable between the two groups (15 [10-27.75] s vs 15 [10.25-19] s, median [range], P = 0.62). CONCLUSION: These results indicate that the difficulty in the catheter placement through the left jugular vein may be to pass through the tricuspid valve, not the pulmonary valve.

An analysis of factors influencing pulmonary artery catheter passage through the tricuspid and pulmonary valves.

PURPOSE: A pulmonary artery catheter (PAC) has to pass the tricuspid and pulmonary valves for its proper placement. Although several factors were reported to hinder the placement, there have been no reports to identify the factors that prolong the individual time for passing through each valve. METHOD: We individually measured the time required for a PAC to pass through the tricuspid and pulmonary valves. We examined the effect of the following factors on those times: the patient's age, sex, height, weight, cardiothoracic ratio, tricuspid regurgitation, left ventricular ejection fraction, and the diameters of the sinus of Valsalva and of the sinotubular junction divided by the body surface area which represent the diameter of the aorta. Data were analyzed by multiple linear regression analysis after univariate analysis. RESULTS: The placement of a PAC was successful in all of 100 patients. The time required to pass through the pulmonary valve was significantly longer than that through the tricuspid valve (15 [10-28] s vs 9 [5-16] s, median [range], P < 0.01). The incidence of ventricular arrhythmias during passage through the pulmonary valve was significantly higher than that through the tricuspid valve (17% vs 0%, P < 0.01). Tricuspid regurgitation and the diameter of sinotubular junction had a significant positive association with the time required to advance a PAC through the pulmonary valve, although there was no significant factors that increased the time required to advance a PAC through the tricuspid valve. CONCLUSION: The time required to advance a PAC through the pulmonary valve is much longer than that to pass through the tricuspid valve. The diameter of aortic root and tricuspid regurgitation are significant factors that increased the time required to advance a PAC through the pulmonary valve.

A longer total duration of rapid ventricular pacing does not increase the risk of postprocedural myocardial injury in patients who undergo transcatheter aortic valve implantation.

Rapid ventricular pacing (RVP) is used during transcatheter aortic valve implantation (TAVI). RVP disturbs myocardial oxygen balance, and when prolonged, it may cause procedure-related myocardial injury (PMI). This study investigated whether a longer duration of RVP increased the occurrence of PMI or worsened long-term mortality after TAVI. We retrospectively analyzed data from 188 patients who underwent TAVI in our institute from January 2013 to July 2015. Myocardial injury was represented by the peak value of creatine kinase-myocardial band (CK-MB) within 72 h after the procedure; an increase greater than 5 times the upper reference limit was regarded as PMI. There was no difference in RVP time (RVPT) between patients with and without PMI (median [range]: 57 [9-189] s vs. 54 [0-159] s, p = 0.9). A higher peak CK-MB was significantly correlated with the apical approach for the procedure (p < 0.001) but not with total RVPT (p = 0.22). A subanalysis of 133 patients whose troponin I was tested within 72 h postprocedurally showed no correlation between the peak value and RVPT (p = 0.40). Shortening RVPT did not result in myocardial protection; thus, RVPT during TAVI should be sufficient to optimize valve placement.

Risk of Hematoma in Patients With a Bleeding Risk Undergoing Cardiovascular Surgery With a Paravertebral Catheter.

OBJECTIVE: This study aimed to determine the risk of hematoma associated with thoracic paravertebral block (TPVB) in patients undergoing cardiovascular surgery. DESIGN: Retrospective analysis. SETTING: Single university hospital. PARTICIPANTS: The study comprised 141 patients who underwent cardiovascular surgery with TPVB to relieve postoperative pain. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Three patients were excluded and of the remaining 138, TPVB was performed in 135, ages 11 to 96 years, who either had a clotting abnormality or were on anticoagulant or antiplatelet therapy. No paravertebral, epidural, or spinal hematoma was detected, and only 1 case of superficial bleeding was observed. The frequency of hematoma associated with TPVB in patients with a risk of bleeding undergoing cardiovascular surgery was calculated as 0% (95% confidence interval 0-2.7). CONCLUSION: Hematoma did not occur in patients at risk of bleeding who underwent cardiovascular surgery with TPVB for postoperative pain management. However, the risk and benefit in each case still must be considered carefully to determine whether TPVB is indicated.

[Ultrasound-guided Rectus Sheath Block vs Transversus Abdominis Plane Block in Children Undergoing Umbilical Hernia Repair].

BACKGROUND: Although many reports describe the usefulness of the rectus sheath block (RSB) in the umbilical hernia repair, the efficacy of the transversus abdominis plane block (TAPB) is rarely reported. The purpose of this study was to compare the efficacy and technique of ultrasound-guided RSB and TAPB in children undergoing umbilical hernia repair. METHODS: Thirty-four children younger than 12 years of age scheduled for umbilical hernia repair were enrolled in this prospective observer-blinded randomized clinical trial. They were randomly assigned either to RSB group (median age, 3.7 years) or TAPB group (median age, 3.8 years). After the induction of general anesthesia with sevoflurane, nitrous oxide, and oxygen children in both groups received regional anesthesia with 0.3 ml x kg(-1) of 0.25% ropivacaine on each side under ultrasound guidance. Hemodynamic changes at the skin incision, postoperative pain scores and parental satisfaction were recorded. Anesthesiologists rated the quality of ultrasound images and easiness of the block performance. RESULTS: The patients' demographics of the two groups were similar. There were no significant differences in the time needed for the block procedure, quality of ultrasound images and the change of the heart rate and blood pressure at the skin incision between the two groups. Postoperative pain score (immediately, 2 and 4 hours after the operation), need for rescue analgesia and satisfaction of the parents also did not differ. There were no major complications in the patients. CONCLUSION: TAPB provided comparable perioperative analgesia and easiness of block performance to RSB in the pediatric umbilical hernia repair.

Altered Phosphatidylinositol 3-Kinase and Calcium Signaling in Cardiac Dysfunction After Brain Death in Rats.

BACKGROUND: Phosphatidylinositol 3-kinase is involved in myocardial function, including contractility. To date, myocardial regulation by phosphatidylinositol 3-kinase after brain death has not been investigated. The present study using a brain death model was designed to examine the role of phosphatidylinositol 3-kinase in myocardial function after brain death. METHODS: After anesthesia with sevoflurane, a Fogarty catheter was placed intracranially for induction of brain death. A conductance catheter was inserted into the left ventricle for measurement of myocardial function. Rats were assigned to the following groups: one group undergoing sham operation (with catheter placement but no brain death introduction); one group receiving saline before brain death; and one group receiving wortmannin, an inhibitor of phosphatidylinositol 3-kinase, before brain death. Various measurements, including mean blood pressure, heart rate, maximal rate of rise of left ventricular pressure, and ejection fraction, were obtained every 30 minutes for 6 hours after brain death. The phosphorylation status of Akt and phospholamban was determined 360 minutes after brain death. RESULTS: After induction of brain death, rats showed significant decreases in blood pressure, maximal rate of rise of left ventricular pressure, and ejection fraction. Inhibition of phosphatidylinositol 3-kinase using wortmannin significantly improved these measurements, resulting in increased survival. Western blot analysis demonstrated that brain death increased Akt phosphorylation and decreased phospholamban phosphorylation; these effects were abolished by wortmannin. CONCLUSIONS: Inhibition of phosphatidylinositol 3-kinase prevented myocardial dysfunction after brain death in association with inhibition of the decrease in phosphorylation of myocardial phospholamban, characteristic of brain death.

Paravertebral block decreases opioid administration without causing hypotension during transapical transcatheter aortic valve implantation.

Paravertebral block (PVB) is feasible for postoperative analgesia in patients who undergo cardiac surgery with unilateral thoracotomy. Postoperative continuous PVB is as effective as thoracic epidural anesthesia and is less likely to cause hypotension. However, the intraoperative utility and safety of PVB remains unclear. Therefore, the present study was conducted to determine the efficacy and hemodynamic influence of intraoperative paravertebral bolus injection during cardiac surgery. We retrospectively compared intraoperative medication use and blood pressure measurements between patients who underwent transapical transcatheter aortic valve implantation (TA-TAVI) with (PVB group, n = 46) or without (non-PVB group, n = 15) intraoperative PVB. Remifentanil administration was lower by more than 40 % in the PVB group compared with that in the non-PVB group (728 ± 319 µg vs. 1240 ± 488 µg, P < 0.001). The average and variability of intraoperative blood pressure showed no significant differences between groups. The duration of hypotension (blood pressure less than 80 % of baseline) was 25.1 ± 21.5 % and 25.4 ± 18.1 % of the entire anesthesia time in the non-PVB and PVB groups, respectively (P = 0.74). The use of inotropic and vasopressor agents was comparable between groups. Intraoperative paravertebral bolus injection decreased remifentanil administration without causing hypotension during TA-TAVI in hemodynamically unstable patients. This result suggests the intraoperative utility of PVB in cardiac surgery.

[A Case of Liver-transplant Recipient who Developed Aggravation of Pulmonary Hypertension during Anhepatic Phase].

Portopulmonary hypertension is a form of pulmo- nary hypertension associated with portal hypertension with/without liver cirrhosis. We describe a case of liver-transplant recipient who developed aggravation of pulmonary hypertension during anhepatic phase of operation. A 31-year-old man with progressive liver failure was scheduled for liver transplantation. He had a history of biliary atresia and underwent Ueda's operation. The patient was diagnosed as having portopulmonary hypertension. Echocardiography revealed pulmonary hypertension. Pulmonary arterial pressure (PAP) mea- sured by right heart catheterization was 52/22 mmHg, which decreased with oxygen inhalation. General anesthesia was induced by infusion of pro- pofol and remifentanil. Arterial pressure (AP) and PAP immediately before surgery were 99/44 mmHg and 51/26 mmHg, respectively. Hemodynamic parameters were stable during hepatectomy phase. During unhepatic phase, PAP and cardiac index gradually increased and AP gradually decreased. The development of hyperdynamic state was suspected, and continuous administration of noradrenaline was commenced. AP was restored ; however, PAP kept increasing to an extent comparable to AP. Inhalation of nitric oxide (NO) 20 ppm was commenced, and then PAP successfully decreased to 46/26 mmHg within 15 minutes. After surgery the patient was mechanically ventilated in the ICU. NO was stopped on the 11th ICU day and extubated on the 13th ICU day.

[Bupivacaine-induced Anaphylaxis in a Parturient Undergoing Cesarean Section].

We describe a case of anaphylaxis that occurred in a 33-year-old gravida 1, para 1 term woman scheduled for cesarean delivery for breech presentation. Her past history was unremarkable except for orciprenaline allergy. Spinal anesthesia was performed at L3-4 using 2.5 ml of 0.5% hyperbaric bupivacaine and 0.1 mg morphine. Seven minutes after spinal anesthesia, she complained of hoarseness and difficulty in breathing and 3 minutes later, blood pressure decreased to 76/51 mmHg, and oxygen saturation to 87% with supplemental oxygen. Skin flushing was noted in the face and trunk of the body and anaphylaxis was diagnosed. She was treated with a rapid intravenous infusion and iv administration of phenylephrine (total dose 0.4 mg), ephedrine (total dose 25 mg), hydrocortisone and famotidine. Cesarean section was started 23 minutes after spinal anesthesia when blood pressure and oxygen saturation recovered. A male infant was delivered (18 minutes after the onset of anaphylactic event) with Apgar scores of 2 and 5 at 1 and 5 min, respectively and resuscitated with mask ventilation. Umbilical artery blood gas analysis revealed pH 6.85, base excess -20.3 mmol x l (-1) and lactate 109 mg x dl (-1). The mother was discharged from the hospital on the 6th postoperative day. The baby's electroencephalogram, however, demonstrated a pattern consistent with mild hypoxic-ischemic encephalopathy. Lymphocyte stimulation test revealed that she was allergic to bupivacaine. If maternal hypotension persists, i.m. or i.v. adrenaline should be administered immediately because maternal hypotension and hypoxemia may cause significant fetal morbidity and mortality and prompt cesarean section should be considered.

Prophylactic antiarrhythmic effect of anesthetics at subanesthetic concentration on epinephrine-induced arrhythmias in rats after brain death.

The present study using brain death model of rats was designed to examine whether prophylactic administration of volatile anesthetics and propofol prevent the epinephrine-induced arrhythmias. A Fogarty catheter was placed intracranially for induction of brain death. After brain death, the rats were randomly assigned to five groups: the control group (no anesthetics), the sevoflurane group (0.8%), the isoflurane group (0.5%), the halothane group (0.3%), and the propofol group (195 µg·kg(-1) ·min(-1)). These anesthetics were about 30% of ED50 of each anesthetic. The arrhythmogenic dose of epinephrine was determined in each anesthetic group. In addition, we examined left ventricular levels of connexin 43 phosphorylation 30 min after administration of each anesthetic with Western blot analysis. The arrhythmogenic dose of epinephrine in the sevoflurane group was significantly higher than that in the control group, while the arrhythmogenic dose of epinephrine in any other anesthetic group was not different. On the other hand, the ratio of phosphorylated-connexin 43/total connexin 43 was also similar among the study groups. Thus, prophylactic administration of subanesthetic dose of sevoflurane is effective in preventing epinephrine-induced arrhythmias after brain death, but phosphorylation of connexin is not involved in the antiarrhythmic property of sevoflurane.

Nicorandil preserves myocardial function following brain death in rats by mitochondrial adenosine triphosphate-sensitive potassium channel-dependent mechanism.

OBJECTIVE: Interventions to preserve myocardial function after brain death may increase the donor pool for heart transplantation. The present study using a brain death model of rats was designed to examine the protective potential of nicorandil, an adenosine triphosphate-sensitive potassium channel opener, on myocardial function after brain death. METHODS: Rats were anesthetized with sevoflurane. A Fogarty catheter was placed intracranially for induction of brain death. The conductance catheter was inserted into the left ventricle for measurement of myocardial function. Rats were assigned randomly to two groups, one receiving nicorandil before brain death and the other receiving saline (control group). Mean blood pressure, heart rate, maximal rate of rise of left-ventricular pressure and ejection fraction were measured every 30 min for 6h after brain death. The same protocol was performed in the presence of nicorandil combined with 5-hydroxydecanoic acid, a mitochondrial adenosine triphosphate-sensitive potassium channel inhibitor. RESULTS: Nicorandil temporally, but significantly, improved ejection fraction compared with the control group. Furthermore, 5-hydroxydecanoic acid inhibited the effects of nicorandil. CONCLUSIONS: Nicorandil was effective to preserve ejection fraction after brain death, and myocardial mitochondrial adenosine triphosphate-sensitive potassium channels may be involved in this action.

Activation of phosphatidylinositol 3-kinase/Akt signaling pathway and endogenous nitric oxide are needed for the antiarrhythmic effect of centrally administered rilmenidine.

Activation of imidazoline receptors in the central nervous system has protective effect on several types of arrhythmias. We demonstrated that centrally administered rilmenidine, a selective imidazoline receptor agonist, prevented adrenaline-induced arrhythmias during halothane anaesthesia. However, detailed myocardial signaling of the antiarrhythmic effect remains to be unexplored. The present study was designed to examine a role of pertussis toxin-sensitive G protein, phosphatidylinositol 3-kinase/Akt signaling pathway and endogenous nitric oxide in the antiarrhythmic effect of rilmenidine. Male Sprague-Dawley rats were anaesthetized with halothane and monitored continuously for arterial blood pressure and premature ventricular contractions. The arrhythmogenic dose of adrenaline was defined as the smallest dose producing 3 or more premature ventricular contractions within 15-s period. Firstly, we confirmed that centrally administered rilmenidine prevented adrenaline-induced arrhythmias during halothane anaesthesia and examined the effect of pertussis toxin, wortmannin (a phosphatidylinositol 3-kinase inhibitor), and nitro-L-arginine methyl ester (L-NAME) (a specific nitric oxide synthesis inhibitors), on the antiarrhythmic effect of rilmenidine. We also performed Western blot analysis to determine phosphorylation of Akt and glycogen synthase kinase 3ß, a direct Akt downstream target, following the central administration of rilmenidine. The antiarrhythmic effect of rilmenidine was significantly inhibited by pertussis toxin, wortmannin and L-NAME. Rilmenidine increased Akt and glycogen synthase kinase 3ß phosphorylation (28±13% and 32±13%, respectively), and this action was abolished by wortmannin. The present results demonstrated that pertussis toxin-sensitive G protein, phosphatidylinositol 3-kinase-Akt-GSK3ß signaling pathway and endogenous nitric oxide may play a key role in antiarrhythmic effect of centrally administered rilmenidine.

[Donor heart preservation].

Heart transplantation is a common procedure for patients with severe heart failure and shortage of donor organs is a significant problem even in Europe and USA. We, anesthesiologists, contribute to transplantation by anesthetic management of a donor and it is essential to maintain cardiac function until the organ harvest for successful organ transplantation. Since cardiac dysfunction occurrs following brain death, it is clinically important to find some interventions to maintain the cardiac function or to delay cardiac deterioration following brain death. We investigated the cardiac function following experimental brain death in rats. Experimental brain death was induced by inflating intracranial balloon. Ejection fraction and dP/dt max significantly decreased earlier than significant blood pressure reduction after brain death. In addition, myocardial sensitization to epinephrine was enhanced following brain death. Preconditioning is a unique phenomenon to prevent cardiac function from ischemic insult. Volatile anesthetics, including sevoflurane and isoflurane, have similar effects in preconditioning. We expect volatile anesthetics to improve cardiac function following brain death due to preconditioning effect.

Bolus administration of landiolol, a short-acting, selective beta1-blocker, to treat tachycardia during anesthesia: a dose-dependent study.

OBJECTIVES: The purpose of this study was to clarify the clinical efficacy of landiolol, a selective beta(1)-blocker, in patients developing tachycardia during anesthesia. DESIGN: A prospective, randomized, and placebo-controlled study. SETTING: A single university hospital. PARTICIPANTS: Patients undergoing resection of intracranial or maxillofacial tumors under general anesthesia. INTERVENTIONS: Intravenous bolus administration of landiolol. MEASUREMENTS AND MAIN RESULTS: Patients with heart rates exceeding 90 beats/min for more than 5 minutes received an intravenous bolus dose of landiolol. These patients who developed tachycardia were randomized into 4 groups receiving landiolol in the dose of 0, 0.1, 0.2, or 0.3 mg/kg. Heart rate and blood pressure were recorded before drug injection and 1, 3, 5, 7, 10, 15, 20, 25, and 30 minutes after the injection. Heart rate was significantly reduced with each dose of landiolol compared with the placebo group between 3 and 20 minutes after drug injection. The lowest heart rate was 93 +/- 4, 80 +/- 8, 79 +/- 8, and 77 +/- 6 beats/min (mean +/- standard deviation) in the landiolol 0, 0.1, 0.2, and 0.3 mg/kg groups, respectively. On the other hand, reduction of blood pressure was not as remarkable as that of heart rate. Landiolol, 0.1 and 0.2 mg/kg, did not significantly reduce systolic or diastolic blood pressure during the study period, although significant reduction of blood pressure was observed in the landiolol 0.3-mg/kg group between 5 and 10 minutes after drug injection. CONCLUSION: The results showed that bolus administration of landiolol was effective in the treatment of tachycardia during anesthesia in surgical patients. Landiolol was more efficacious in reducing heart rate than blood pressure.

Diabetes mellitus reduces the antiarrhythmic effect of ion channel blockers.

We designed the present study to examine whether diabetes mellitus affects the antiarrhythmic effect of flecainide, a sodium channel blocker, E-4031, a potassium channel blocker, and verapamil, a calcium channel blocker, in diabetic rats. The experiments were performed in intact and diabetic rats 2, 4, and 6 wk after administration of streptozotocin. Rats were anesthetized with halothane and monitored continuously for arterial blood pressure and premature ventricular contractions. The arrhythmogenic dose of epinephrine was defined as the smallest dose producing 3 or more premature ventricular contractions within a 15-s period. The arrhythmogenic doses of epinephrine in the presence of flecainide were 8.2 +/- 2.2 (mean +/- sd), 7.4 +/- 6.1, 5.5 +/- 2.8, and 2.0 +/- 0.5 microg/kg in intact and diabetic rats 2, 4, and 6 wk after streptozotocin administration, respectively. Similarly, the arrhythmogenic doses of epinephrine in the presence of E-4031 were 7.7 +/- 2.6, 2.3 +/- 0.7, 2.0 +/- 0.7, and 1.2 +/- 0.5 microg/kg, and those in the presence of verapamil were 8.2 +/- 2.1, 3.1 +/- 1.2, 2.3 +/- 0.9, and 1.5 +/- 0.5 microg/kg. Insulin partially recovered the antiarrhythmic effect of the blockers. We concluded that diabetes mellitus reduces the antiarrhythmic effects of flecainide, E-4031, and verapamil.

Identification of the central imidazoline receptor subtype involved in modulation of halothane-epinephrine arrhythmias in rats.

We previously reported that imidazoline receptors in the central nervous system are involved in modulation of halothane-epinephrine arrhythmias. These receptors have been subclassified as I1 and I2 subtypes, but it is not known which receptor subtype is involved in halothane-epinephrine-induced arrhythmias. We designed the present study to clarify the involvement of central imidazoline receptor subtype in the modulation of halothane-epinephrine-induced arrhythmias. Rats were anesthetized with halothane and monitored continuously for systemic arterial blood pressure and premature ventricular contractions. The arrhythmogenic dose of epinephrine was defined as the smallest dose that produces three or more premature ventricular contractions within a 15-s period. Intracisternal moxonidine dose-dependently inhibited the epinephrine-induced arrhythmias during halothane anesthesia. Intracisternal efaroxan, a selective I1 antagonist with little affinity for I2 subtype, but not rauwolscine, an alpha2 antagonist without affinity for imidazoline receptors, blocked the antiarrhythmic effect of moxonidine. Intracisternal BU 224 and 2-BFI, selective I2 ligands, also inhibited the epinephrine-induced arrhythmias dose-dependently; however, these effects were abolished by efaroxan. We conclude that central I1, but not I2, receptors play an important role in inhibition of halothane-epinephrine arrhythmia.