Association between Preoperative Cardiac Left Ventricular Dysfunction and Perioperative Intraaortic Balloon Pump in Patients Undergoing Off-Pump Coronary Artery Bypass Surgery.

BACKGROUND: Prophylactic use of intraaortic balloon pump (IABP) reduces hospital mortality in patients with left ventricular (LV) systolic dysfunction undergoing coronary artery bypass surgery (CABG); however, its association in patients with LV diastolic dysfunction is unclear. This retrospective study investigated the association between preoperative LV function and perioperative use of IABP in patients undergoing off-pump CABG (OPCAB) at a university hospital. METHODS: 100 consecutive patients who underwent OPCAB between January 1, 2011 and August 31, 2014 were studied. Preoperative LV function was categorized into four groups based on LV systolic and diastolic function determined with preoperative transthoracic echocardiography. The use of IABP was reviewed from medical records. The Mann-Whitney test, Pearson chi-square test, or Fisher exact test were used. RESULTS: Patients were categorized into the following groups: normal LV function (n = 43), isolated LV systolic dysfunction (n = 13), isolated LV diastolic dysfunction (n = 21), and combined LV systolic and diastolic dysfunction (n = 14). Intraoperative IABP use was significantly more frequent in patients with isolated LV systolic dysfunction, isolated LV diastolic dysfunction, and combined LV systolic and diastolic dysfunction than in those with normal LV function (P < .05). Furthermore, IABP was used more frequently in patients who developed combined LV systolic and diastolic dysfunction postoperatively (P < .05). Conclusion: Not only the presence of preoperative systolic dysfunction but also LV diastolic dysfunction in the presence of normal LV systolic function were associated with increased use of IABP during and after OPCAB.

[Cardiac asystole in the postanesthetic care unit: a case report].

We report a patient without apparent heart disease who developed asystole postoperatively. A 24-year-old woman was scheduled for acetabulectomy under lumbar epidural anesthesia with intravenous propofol infusion. There was no profound hypotension or arrhythmia during anesthesia and surgery. She complained of nausea 50 minutes after the operation. The ECG showed an abrupt decrease in the heart rate followed by cardiac asystole 30 seconds after the onset of nausea. Prompt cardiac massage resumed the heart beats in eight seconds. There was no neurological deficit.

[Surgical treatment of acute cholecystitis].

Fundamental treatment for acute cholecystitis is cholecystectomy. However, the adoption of a treatment is dependend on degree of a severity of acute cholecystitis in each patient because its degree is influenced by factors such as duration from the onset of symptoms to medical examination. Early laparoscopic cholecystectomy is the preferred procedure for mild acute cholecystitis. Early cholecystectomy is also performed for moderately acute cholecystitis. However, if patients have severe local inflammation (gangrenous and purulent cholecystitis) early gallbladder drainage or open cholecystectomy is indicated. Emergency operation under adequate medical treatment is indicated for a patient with severe local inflammation of the gallbladder, torsion of the gallbladder, emphysematous cholecystitis, gangrenous cholecystitis, and purulent cholecystitis. Pericholecystic abscess, necrosis of the gallbladder wall, and perforation of the gallbladder can be diagnosed accurately by use of imaging diagnosis. The optimal surgical treatment for acute cholecystitis according to grade of severity should be performed referring to imaging findings.

[Landmark method and ultrasound-guided method of internal jugular vein puncture: comparison of residents with staffs].

BACKGROUND: We compared landmark with ultrasound-guided methods of internal jugular vein puncture in residents and staffs. METHODS: Seven residents and five staffs practiced internal jugular vein puncture with landmark and ultrasound-guided methods on a manikin for internal jugular vein cannulation. Thereafter, they performed internal jugular vein cannulation on 42 patients. RESULTS: Number of attempts of internal jugular vein cannulation by the residents was significantly lower with ultrasound-guided method than with landmark method. Three internal jugular veins could not be cannulated by residents with landmark method. The common carotid artery was punctured in one case with either method by residents. CONCLUSIONS: Residents need more practice of internal jugular vein puncture on a manikin before clinical practice.

[Complications of internal jugular vein cannulation under ultrasound guidance: report of three].

Internal jugular cannulation with ultrasound guidance has been advocated to decrease its complications. However, there can be serious complications by in-experienced physicians in even ultrasound-guided internal jugular vein cannulation. We report three cases of complications associated with ultrasound-guided internal jugular vein cannulation: puncture of the common carotid artery in two patients and pneumothorax in one.

[Monitoring of muscle relaxation at the corrugator supercilli muscle in a patient with atrophied upper limbs].

We report a patient whose muscle relaxation was monitored at the corrugator supercilli muscle. In a 51-year-old woman with markedly atrophied upper limbs, anesthesia was induced with propofol and fentanyl. Muscle relaxation was monitored at the adductor pollicis and corrugator supercilli muscles with accelomyography. Train-of-four ratio (TOFR) could be evaluated at the corrugator supercilli muscle; however, it could not be evaluated at the adductor pollicis muscle. The trachea was intubated when the TOFR was 0.09 at the corrugator supercilli muscle after intravenous vecuronium. As the TOFR was 1.44 when the surgery completed, the trachea was extubated without giving neostigmine to antagonize the effect of vecuronium. There was no recurarization after extubation. We conclude that evaluation of TOFR at the corrugator supercilli muscle is useful in some patients who have atrophied adductor pollicis muscle.

[Training of internal jugular vein cannulation: comparison of landmark method with ultrasound-guided method].

We compared training of internal jugular vein cannulation with ultrasound-guided method and that with landmark method in a group of 10 residents and that of 10 staffs. Cannulation was increasingly successful with both methods as the training proceeded, and with increasingly less time and fewer number of punctures. There was no statistically significant difference in time or in number of punctures with ultrasound-guided method between the groups. Ultrasound-guided method needed fewer number of punctures than those with landmark method in both groups.

Neurally Mediated Syncope During Cesarean Delivery: A Case Report.

A 28-year-old woman with preeclampsia at 32 weeks of gestation underwent a cesarean delivery under spinal anesthesia. Administration of nitroglycerin at 200 µg to relax uterine smooth muscles and the application of fundal pressure led to severe bradycardia and loss of consciousness, followed by cardiac arrest. Delivery was completed immediately and recovery was achieved 10 seconds later following cardiopulmonary resuscitation. Neurally mediated syncope was considered the cause of cardiac arrest. Anesthetists should be aware of the potential risk during cesarean delivery following the administration of nitroglycerin, fundal pressure, regional anesthesia, and hypovolemia because of preeclampsia.

[Anesthetic management of a patient with hepatocellular carcinoma with tumor thrombosis extending into the right atrium].

We report a patient with hepatocellular carcinoma whose tumor thrombus was extending into the right atrium. A 55-year-old man underwent extended anterior segmental hepatectomy and removal of the tumor thrombus in the right atrium under cardiopulmonary bypass and general anesthesia using sevoflurane, nitrous oxide and oxygen. End-tidal carbon dioxide was closely monitored to detect pulmonary tumor emboli during the surgery. Intravenous fluid and blood transfusion in large volumes were necessary to avoid circulatory derangement.

[Pulmonary edema due to upper airway obstruction after extubation].

We report a patient who developed pulmonary edema due to airway obstruction after extubation. A 22-year-old man underwent removal of the nails for thoracoplasty under general anesthesia combined with epidural anesthesia. Upper airway obstruction occurred after extubation. SpO2 decreased to 70%. Insertion of an oral airway relieved the airway obstruction. However, inspiratory wheezing was heard over both lung fields. Chest X-ray taken 90 minutes after the event revealed pulmonary edema. Pulmonary edema gradually resolved after intravenous furosemide and oxygen inhalation by mask.

[Propofol suppresses the responses in hypoglossal nerve activity to hypercapnic-hypoxic stimulation].

BACKGROUND: Upper airway obstruction and inadequate ventilation often arise during sedation and anesthesia by propofol. To estimate the influence of propofol (PP) on respiratory control, we studied its effect on the neural activity and the respiratory response caused by a brief (60 sec) respiratory arrest (RA) manifesting in the hypoglossal nerve (HG) and the phrenic nerve (PN) in rabbits. METHODS: Experiments were performed on adult rabbits vagotomized, paralyzed and ventilated artificially with 50% N2O, 50% oxygen and 0.5% sevoflurane. We evaluated and compared the effects of PP on the peak amplitude (AMP) and the root mean square (RMS) of HG and PH, and respiratory cycle (Tc). RESULTS: PP depressed HG activity more than PH activity, and increased Tc in a dose related manner, with 0.25 mg x kg(-1) x min(-1) continuous infusion, propofol soon began to reduce both AMPs without any remarkable changing in Tc. AMP&RMS-HG were reduced to about 35% and AMP&RMS-PN to 80% of control. Administration of propofol 1.5 mg x kg(-1) x min(-1) vanished the activity of HG in all animals. RA made a mixed hypercapnic and hypoxic condition and induced RA response which was characterized by raised AMPs, augmented RMSs (deltaAMPs, deltaRMSs) in activity of both nerves activity and lengthened Tc (deltaTc). PP depressed RA response in HG dose-dependently, but did not do so in PN. Significant depressions in cardiovascular effects with tested dosage of PP occurred, but the values were kept in physiological ranges. CONCLUSIONS: These results suggest that propofol induces respiratory depression by its inhibitory effect on the neural regulation of respiration, especially on the maintenance system of upper airway patency and the reflex related to the chemosensitive upper airway patency control.

[How do diazepam and flumazenil influence respiratory control by the activities of both hypoglossal and phrenic nerves in rabbits?].

BACKGROUND: Upper airway obstruction and inadequate ventilation often arise during sedation and anesthesia by benzodiazepines. To estimate the influence of benzodiazepines on the respiratory control, we studied the effect of diazepam and flumazenil on the neural activity and the respiratory response caused by a brief (60 sec) respiratory arrest (RA) observed in the hypoglossal nerve (HG) and phrenic nerve (PH) in rabbits. METHODS: Experiments were preformed on adult rabbits vagotomized, paralyzed and ventilated artificially with 50% N2O, 50% oxygen and 0.3-0.5% sevoflurane. We evaluated and compared the effects of diazepam and flumazenil on the peak amplitude (AMP-HG&PH) and the root mean square (RMS-HG&PH) of HG and PH, and respiratory cycle (Tc). RESULTS: Diazepam depressed HG activity more than PH activity with no influence on Tc. But it did not cause dose-related depression. Flumazenil 0.2 mg.kg-1 completely reversed the respiratory depressions caused by diazepam with the increased Tc. In addition to augmentation of the hypoglossal activity in inspiration, flumazenil caused a rise in its activity in pan-expiratory period in some cases. Additional administration of diazepam 6 mg.kg-1 following flumazenil depressed PH activity again, but did not affect HG activity any more. There was no significant depression in cardiovascular parameters with tested dosages of diazepam and flumazenil. RA response was characterized by raised AMPs and augmented RMSs (delta AMPs, delta RMSs) with marked prolongation in Tc (delta Tc). Diazepam depressed RA response dose dependently, but flumazenil did not seem to antagonize this depression. CONCLUSIONS: These results suggest that 1) flumazenil is not only a specific antagonist of benzodiazepines but also a potential excitatory agent of hypoglossal nerve activity, and that 2) there is some functional diversity in disposition of benzodiazepine-receptor binding GABAA-receptor responsible for neural respiratory control system.

[Effect of flumazenil on hypoglossal and phrenic nerves activities in rabbits].

BACKGROUND: Upper airway obstruction and inadequate ventilation often arise during sedation and anesthesia by benzodiazepines (Bz). Flumazenil antagonizes these effects of active benzodiazepines on the central nervous system. To estimate the influence of flumazenil on the endogenous Bz system related respiratory control, we studied the effect of flumazenil and diazepam on the neural activity and the respiratory response caused by a brief (60 sec) respiratory arrest (RA) manifested in the hypoglossal nerve (HG) and the phrenic nerve (PH) activities in rabbits. METHODS: Experiments were performed on adult rabbits which were vagotomized, paralyzed and artificially ventilated with 50% N2O, 50% oxygen and 0.5% sevoflurane. We evaluated and compared the effects of the sequential administrations of flumazenil and diazepam on the peak amplitude (AMP) as well as the root mean square (RMS) of HG and PH, and respiratory cycle (Tc). RESULTS: Flumazenil by itself increased HG activity more than PH activity with no influence on Tc. But it was not dose-related. Previous administration of flumazenil in total dose of 0.25 mg x kg(-1) could not prevent the anticipated respiratory depression caused by diazepam 2.0 mg x kg(-1). These depressions are greater in HG activity than in PH activity. Additional flumazenil 0.15 mg x kg(-1) following the administration of diazepam promptly reversed these inhibitory effects on HG activity beyond the control level. The same dose of flumazenil, however, did not reverse PH activity sufficiently. RA response was characterized by raised AMPs and augmented RMSs (deltaAMPs, deltaRMSs) with marked prolongation in Tc (deltaTc). Flumazenil and diazepam did not seem to have any influence upon these RA responses. There was a significant change in cardiovascular parameters with the tested dosages of flumazenil and diazepam, but the change was in the normal physiological range. CONCLUSIONS: These results suggest the possibility that the endogenous benzodiazepine system is likely to play an inhibitory role in the regulation of respiration, especially in the maintenance of upper airway patency but the system is unrelated to the chemosensitive-respiratory control.