Effective Dosage of Midazolam to Erase the Memory of Vascular Pain During Propofol Administration.

Intravenous sedation with propofol is often administered to anxious patients in dental practice. Pain on injection of propofol is a common adverse effect. This study aimed to determine the age-adjusted doses of midazolam required to erase memory of vascular pain of propofol administration and assess whether the Ramsay Sedation Scale (RSS) after the pretreatment of midazolam was useful to predict amnesia of the vascular pain of propofol administration. A total of 246 patients with dental phobia requiring dental treatment under intravenous sedation were included. Patients were classified according to their age: 30s, 40s, 50s, and 60s. Three minutes after administration of a predetermined dose of midazolam, propofol was infused continuously. After completion of the dental procedure, patients were interviewed about the memory of any pain or discomfort in the injection site or forearm. The dosage of midazolam was determined using the Dixon up-down method. The first patient was administered 0.03 mg/kg, and if memory of vascular pain remained, the dosage was increased by 0.01 mg/kg for the next patient, and then if the memory was erased, the dosage was decreased by 0.01 mg/kg. The effective dosage of midazolam in 95% of each age group for erasing the memory of propofol vascular pain (ED95) was determined using logistic analysis. The accuracy of RSS to predict the amnesia of injection pain was assessed by receiver operating characteristic (ROC) analysis. The ED95 of midazolam to erase the memory of propofol vascular pain was 0.061 mg/kg in patients in their 30s, 0.049 mg/kg in patients in their 40s, 0.033 mg/kg in patients in their 50s, and 0.033 mg/kg in patients in their 60s. The area under the ROC curve was 0.31. The ED95 of midazolam required to erase the memory of propofol vascular pain demonstrated a downward trend with age. On the other hand, it was impossible to predict the amnesia of propofol vascular pain using the RSS.

Small bolus of esmolol effectively prevents sodium nitroprusside-induced reflex tachycardia without adversely affecting blood pressure.

PURPOSE: Hypotensive anesthesia with sodium nitroprusside (SNP) often is associated with reflex tachycardia. The purpose of this study was to investigate whether a small bolus of esmolol could counteract SNP-induced reflex tachycardia and sympathetic activation without affecting blood pressure. MATERIALS AND METHODS: Using a time-series study design, 27 healthy young patients scheduled for mandibular osteotomy were enrolled in this study. General anesthesia was maintained with 2% sevoflurane and 67% nitrous oxide in oxygen. SNP was administered to decrease the mean arterial pressure to 55 to 65 mm Hg. When heart rate (HR) increased reflexively to higher than 95 beats/min from SNP-induced hypotension, esmolol 0.5 mg/kg was given. Blood pressure and HR were measured, and the low-frequency component (0.04 to 0.15 Hz) of systolic blood pressure variability and high-frequency component (0.15 to 0.4 Hz) of HR variability were calculated to evaluate the autonomic condition. Data were analyzed using 1-way analysis of variance after multiple comparisons or t test. P < .05 was considered statistically significant. RESULTS: Of the 27 patients analyzed, 19 patients (70%) required esmolol. In these patients, SNP caused an increase in the low-frequency component of systolic blood pressure variability and a decrease in the high-frequency component of HR variability, leading to tachycardia (HR range, 95.9 ± 7.3 to 106.7 ± 7.4 beats/min; P < .001). Esmolol suppressed the effects of SNP on the low-frequency component of systolic blood pressure variability and high-frequency component of HR variability, resulting in an immediate decrease in HR to 86.9 ± 6.2 beats/min (P < .001), whereas mean arterial pressure remained unchanged. CONCLUSIONS: A small bolus of esmolol can suppress reflex tachycardia without significantly changing mean arterial pressure. Thus, esmolol restores the autonomic imbalance induced by SNP during hypotensive anesthesia.

Anesthetic Management of a Patient With a Vagal Nerve Stimulator.

Vagal nerve stimulation (VNS) is an established adjunctive treatment for patients with refractory epilepsy. VNS is effective in many cases, but few patients achieve complete elimination of seizures. Furthermore, VNS can cause respiratory complications, such as obstructive sleep apnea. This report describes the successful anesthetic management of a 28-year-old woman with a VNS device who underwent dental treatment under general anesthesia. She was morbidly obese and had undergone placement of a VNS device secondary to drug-resistant epilepsy 2 years prior but continued to experience daily epileptic seizures. Because of concerns about the risk of perioperative epileptic seizures and apneic events, use of the dedicated VNS device magnet was planned if such complications occurred. Total intravenous anesthesia was induced with propofol and remifentanil and a bispectral index sensor was used to help monitor brain wave activity for evidence of seizures along with the depth of anesthesia. Postoperatively, the patient received positional therapy and supplemental oxygen while being closely monitored in recovery. The anesthetic course was completed uneventfully without need of the VNS magnet. A thorough understanding of the mechanics of a VNS device, including proper use of the VNS magnet, is critical for an anesthesiologist during the perioperative period.

The effect of nitrous oxide inhalation on the hypotensive response to propofol: a randomized controlled trial.

OBJECTIVE: Decrease in arterial blood pressure is a prominent adverse reaction during propofol (Disoprivan; AstraZeneca K.K., Osaka, Japan) sedation. The purpose of this prospective randomized study was to explore the effects of nitrous oxide (N2O) on the hypotensive response during propofol sedation. STUDY DESIGN: Twenty-six healthy volunteers received intravenous sedation with propofol alone (group P, n=13) or a combined technique using 20% N2O and propofol (group N+P, n=13). Propofol was administered by a target-controlled infusion system to attain and maintain a plasma propofol concentration of 1.5µg/mL. Hemodynamic and autonomic parameters were measured. RESULTS: Mean arterial pressure decreased in both groups, the hypotensive response in group N+P being significantly smaller than in group P. Reduction in the low-frequency power of systolic blood pressure variability, indicative of sympathetic nervous activity, was also smaller in group N+P than in group P. CONCLUSIONS: Addition of N2O to propofol sedation can attenuate the hypotensive effect of propofol.