Induction Of Total Intravenous Anesthesia Research Articles

The preventive effect of 5-hydroxytryptamine-3 receptor antagonist on blood pressure reduction and postoperative nausea and vomiting during general anesthesia induction: A double-blinded, randomized controlled trial

Study objectiveAdministering a 5-hydroxytryptamine-3 receptor (5-HT3) at anesthesia induction may aid in achieving hemodynamic stability during general anesthesia induced using opioids. Therefore, we aimed to evaluate the effect of ramosetron, a 5-HT3 antagonist, administered on hypotension at the induction of total intravenous anesthesia (TIVA) with propofol and remifentanil. Additionally, we aimed to compare the impact of ramosetron administration at anesthesia induction versus that at the end of the surgery on postoperative nausea and vomiting (PONV). DesignPatients were randomly allocated to the Induction group (administration of ramosetron [0.3 mg/5 ml] at anesthesia induction and normal saline [5 ml] at the end of the surgery) or End group (administration of normal saline [5 ml] at anesthesia induction and ramosetron [0.3 mg/5 ml] at the end of the surgery). Hemodynamic status, PONV, and postoperative pain were assessed. SettingOperating room, post-anesthetic care unit, and general ward. Patients: In total, 176 non-smoking patients without any past medical history undergoing laparoscopic gynecological surgeries under TIVA were included in the study. MeasurementsBlood pressure (BP), heart rate, PONV, visual analog scale (VAS). Main resultsThe Induction group exhibited significantly higher BP at anesthesia induction and required significantly lower doses of phenylephrine and ephedrine during anesthesia than the End group had. However, PONV and postoperative pain were similar between the two groups. ConclusionsAdministering ramosetron at anesthesia induction resulted in significantly better hemodynamic stability with significantly lesser requirement of phenylephrine and ephedrine than administering at the end of the surgery did. Therefore, we recommend ramosetron administration at anesthesia induction rather than at the end of the surgery to prevent PONV and the decrease in the mean BP during TIVA with propofol and remifentanil.

Propofol/Remifentanil Anesthesia Might Not Alter the Middle Cerebral Artery Diameter by Digital Subtraction Angiography.

Transcranial Doppler (TCD) of the middle cerebral artery (MCA) enables the measurement of the mean blood velocity (MCAVm) and the estimation of the cerebral blood flow (CBF), provided that no significant changes occur in the MCA diameter (MCADiam). Previous studies described a decrease in the MCAVm associated with the induction of total intravenous anesthesia (TIVA) by propofol and remifentanil. This decrease in blood velocity might be interpreted as a decrease in the CBF only where the MCADiam is not modified across TCD examinations. In this observational study, we measured the MCADiam of 24 subjects (almost exclusively females) on digital subtraction angiography under awake and TIVA conditions. Across the two phases, we observed a decrease in the mean arterial blood pressure (from 84 ± 9 to 71 ± 6mmHg; p < 0.001) and heart rate (76 ± 10 vs. 65 ± 8 beats/min; p < 0.001), and a concomitant decrease in the MCAVm (61 vs. 42cm/s; p < 0.001). In contrast, the MCADiam did not vary in association with TIVA (2.3 ± 0.2 vs. 2.3 ± 0.2mm; p = 0.52). Those results suggested that in this population, no significant changes in the MCADiam are associated with TIVA.

Hemodynamic effects of cafedrine/theodrenaline on anesthesia-induced hypotension

There is insufficient knowledge about the hemodynamic effects of cafedrine/theodrenaline (caf/theo), acommercially available drug combination, to treat hypotension. This prospective observational study investigated the hemodynamic effects of caf/theo on anesthesia-induced hypotension in 20patients scheduled for elective major abdominal surgery. After induction of total intravenous anesthesia (TIVA) with propofol and remifentanil, adecrease in mean arterial blood pressure (MAP) below 60 mm Hg (n = 12) was treated with 60 mg/3 mg caf/theo. The systemic vascular resistance index (SVRI), cardiac index (CI), global end-diastolic index (GEDI), maximum pressure increase in the aorta (dPmx) and global ejection fraction (GEF) were assessed by transpulmonary thermodilution (PiCCO2-Monitor). The MAP increased by approximately 60% 10 min after administration of caf/theo. The increase in MAP was a result of the simultaneous effects on various cardiovascular determinants. An increase in peripheral resistance (SVRI +42%) and CI (+17%) could be determined. Data further indicated that the increase in CI was aconsequence of an increase in both dPmx (+31%) and GEDI (+9%) but the GEF remained constant. In anesthesia-induced hypotension caf/theo effectively increased the mean arterial blood pressure by combined effects on preload, contractility, and afterload without altering cardiovascular efficiency.

The Change of Severity of Epiblepharon after Induction of Total Intravenous Anesthesia without Muscle Relaxant

Purpose: To investigate the changes of epiblepharon by evaluating the severity of epiblepharon before and after induction of general anesthesia (GA) with a muscle relaxant and total intravenous anesthesia (TIVA) without a muscle relaxant. Methods: Thirteen pediatric patients (26 eyes) underwent surgery for epiblepharon under GA using a muscle relaxant and 19 pediatric patients (38 eyes) underwent surgery for epiblepharon under TIVA without a muscle relaxant. The severity of epiblepharon in each eye was scored according to skin-fold height (scored 1-4) and area of ciliocorneal touch (scored 1-3) while the patient was in the supine position before induction and after induction of GA. Results: Skin-fold height scores and ciliocorneal touch area scores decreased after induction of GA with a muscle relaxant (skin-fold height score before GA: 2.42 ± 0.86, after GA: 1.87 ± 0.88 p-value < 0.001; ciliocorneal touch area score before GA: 2.05 ± 0.70, after GA: 1.61 ± 0.68, p-value < 0.001). In the TIVA group, skin-fold height scores and ciliocorenal touch area scores were not statistically different before and after GA (skin-fold height score before GA: 2.23 ± 1.18, after GA: 2.38 ± 1.10, p-value = 0.212; ciliocorneal touch area score before GA: 2.06 ± 0.74, after GA: 1.94 ± 0.80, p-value = 0.161). Conclusions: The change of epiblepharon severity was significantly reduced by induction of TIVA without a muscle relaxant and there was no recurrence of epiblepharon 3 months after surgery. When using TIVA without a muscle relaxant, the change of epiblepharon severity was reduced and thus, this method can help prevent its undercorrection. J Korean Ophthalmol Soc 2016;57(4):540-545

Electromyographic response of facial nerve stimulation under different levels of neuromuscular blockade during middle-ear surgery

To investigate facial nerve monitoring in patients receiving the partial nondepolarizing neuromuscular blocking agents (NMBAs), remifentanil and propofol. Patients with normal facial function and advanced middle-ear disease were enrolled. For total intravenous anaesthesia (TIVA), propofol and remifentanil were infused as induction/maintenance anaesthesia. Stimulation thresholds and amplitudes were recorded at each train-of-four (TOF) nerve stimulation level. Time differences between start of TOF and electromyographic (EMG) amplitude decreases (Ti), and between complete recovery of TOF and EMG amplitudes (Tr), were calculated. Fifteen patients were enrolled. Mean ± SD Ti was 3.4 ± 1.28 min; Tr was 18.7 ± 4.41 min. Amplitude of stimulation was apparent mostly at TOF level 1. In most cases, no or a weak response (<100 µV) was observed at TOF 0. Mean ± SD threshold of electrical stimulation was 0.31 ± 0.10 mA at TOF 1. At TOF > 2, all cases showed EMG response on electrical stimulation. Induction of TIVA using propofol and remifentanil provided reliable conditions for delicate microsurgery. Minimal NMBA use, considered as producing TOF levels >1, was sufficient for facial nerve monitoring in neuro-otological surgery.

Vagal Sensory Evoked Potentials Disappear Under the Neuromuscular Block – An Experimental Study

BackgroundTranscutaneous vagal nerve stimulation is a promising treatment modality in patients suffering mood disorders and chronic pain, however, the mechanisms are still to be elucidated. A recently developed technique of EEG responses to electrical stimulation of the inner side of the tragus suggests that these responses are far field potentials, generated in the vagal system – Vagal Sensory Evoked Potentials (VSEP). ObjectiveTo reproduce the VSEP technique free from myogenic artifacts. MethodsFourteen ASA I–II patients scheduled for elective surgery in standardized Total Intravenous Anesthesia (TIVA) were enrolled. Transcutaneous electrical stimulation was applied to the inner side of the right tragus. Averaged EEG responses were recorded from the electrode positions C4-F4 and T4-O2 before and after induction of TIVA, during the maximal effect of the non-depolarizing muscle relaxing agent, cis-atracurium (C-AR) and after recovery from C-AR under TIVA. ResultsTypical response curves with P1, N1 and P2 peaks could be reproduced in all patients before and after anesthesia induction. The response curves disappeared during the C-AR action and re-appeared after recovery from C-AR under TIVA. ConclusionThe disappearance of the scalp responses to electrical tragus stimulation under the neuromuscular block suggests a muscular origin of these potentials.

Angiotensin-converting enzyme inhibition and blood pressure response during total intravenous anaesthesia for minor surgery

This study investigates whether long-term treatment with an angiotensin-converting enzyme inhibitor (ACEI) impairs the haemodynamic regulation during total intravenous anaesthesia (TIVA) for minor surgery. In a prospective, two-armed observational study, 36 patients undergoing TIVA for minor surgery were studied. Seventeen were taking ACEIs regularly but no other antihypertensive medication (ACEI group); 19 patients without any cardiovascular medication served as controls (non-ACEI group). Haemodynamic variables were measured every minute during induction and every 5 min during surgery. The plasma levels of renin, angiotensin II, vasopressin and catecholamines were measured before and 18 min after the induction of anaesthesia. The mean arterial pressure decreased to the same extent in both the groups during the induction of TIVA. There were also no differences between the groups regarding the heart rate, systolic and diastolic arterial pressure, as well as the use of vasoconstrictors, and fluids during induction and throughout surgery. In the ACEI group, the plasma renin concentration was higher at baseline and after the induction of anaesthesia presumably due to the interruption of the negative renin-angiotensin feedback loop (P<0.05). Angiotensin II increased only in the non-ACEI group (6.2 ± 2.2 before vs. 9.6 ± 3.5 pg/ml after induction; P<0.05). In both groups, the plasma norepinephrine concentration decreased after the induction of TIVA (P<0.05). Plasma vasopressin and plasma epinephrine concentrations did not change in either group. Long-term ACEI treatment does not further aggravate the blood pressure decrease under TIVA during minor surgery, provided the induction procedure is slow, the patient is kept well hydrated and vasoconstrictors are promptly applied.

Can intravenous atropine prevent bradycardia and hypotension during induction of total intravenous anesthesia with propofol and remifentanil?

This study was conducted to examine whether pretreatment with intravenous atropine could prevent bradycardia and hypotension during induction of total intravenous anesthesia with propofol and remifentanil in a prospective randomized placebo-controlled manner. Seventy patients, aged 24-78 years, were randomly divided into two groups, and received 0.5 mg atropine or placebo saline 1 min before induction of intravenous anesthesia with remifentanil at 0.4 microg/kg/min, propofol at a target blood concentration of 3 microg/ml, and vecuronium 1.5 mg/kg. Immediately after tracheal intubation, the infusion rate of remfentanil and the target concentration of propofol were reduced to and kept at 0.1 microg/kg/min and 2 microg/ml, respectively, for 10 min. Noninvasive blood pressure (BP) and heartrate (HR) were measured and recorded every minute. Intravenous atropine could prevent a fall in HR, but not a fall in BP, during induction of intravenous anesthesia with propofol and remifentanil of our dosing regimen. Our data suggested that a fall in HR induced by propofol-remifentanil anesthesia was mainly caused by centrally mediated sympatholytic and/or vagotonic actions of propofol and remifentanil, whereas a fall in BP was mainly the result of their direct vasodilating actions.