scholarly journals Phase Lag Entropy as a Surrogate Measurement of Hypnotic Depth during Sevoflurane Anesthesia

Medicina ◽  
2021 ◽  
Vol 57 (10) ◽  
pp. 1034
Author(s):  
Kyung-Mi Kim ◽  
Ki-Hwa Lee ◽  
Jae-Hong Park
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
General Anesthesia ◽  
Phase Lag ◽  
Sevoflurane Anesthesia ◽  
Sedation Scale ◽  
Sevoflurane Concentration ◽  
Anesthetic Concentration ◽  
End Tidal ◽  
The Relationship

Background and Objectives: Phase lag entropy, an electroencephalographic monitor, evaluates the variety in temporal patterns of phase relationship between frontal and prefrontal brain region. Phase lag entropy can reflect the depth of anesthesia induced by propofol, but the association between sevoflurane and phase lag entropy has not been elucidated. This study examined the effect of sevoflurane on phase lag entropy during induction of general anesthesia. We also explored the pharmacodynamic model between end-tidal anesthetic concentration and electroencephalographic monitor. Materials and Methods: A total of 20 patients were enrolled. General anesthesia was produced by escalating the sevoflurane (1 vol% up to 8 vol%). The relationship between phase lag entropy and end-tidal anesthetic concentration was analyzed. A non-linear mixed-effects model was used to get the relationship of pharmacodynamics between the end-tidal sevoflurane concentration and phase lag entropy. Mean blood pressure, heart rate, and the modified observer’s assessment of alertness/sedation scale were also recorded during sevoflurane anesthesia. Results: As level of sedation increased, phase lag entropy decreased. A significant correlation was showed between phase lag entropy and end-tidal sevoflurane concentration (r = −0.759, p < 0.001). The correlation coefficient between the modified observer’s assessment of alertness/sedation scale and phase lag entropy was 0.731 (p < 0.001). The pharmacodynamic factors assessed by the sigmoid Emax model were E0 = 84.9, Emax = 42, Ce50 = 1.81, γ = 4.78, and ke0 = 0.692. The prediction probability of phase-lag entropy for measuring the modified observer’s assessment of alertness/sedation scale and end-tidal sevoflurane concentration were 0.764 and 0.789, respectively. With the increasing concentration of sevoflurane, mean blood pressure decreased, but heart rate did not change. Conclusions: The continuing escalation in end-tidal sevoflurane concentration caused a decline in phase lag entropy. Phase lag entropy can serve as an indicator of hypnotic depth in patients receiving sevoflurane anesthesia.

scholarly journals 1-1-8 one-step sevoflurane wash-in scheme for low-flow anesthesia: simple, rapid, and predictable induction

2020 ◽  
Author(s):  
Sirirat Tribuddharat ◽  
Thepakorn Sathitkarnmanee ◽  
Naruemon Vattanasiriporn ◽  
Maneerat Thananun ◽  
Duangthida Nonlhaopol ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
General Anesthesia ◽  
Gas Flow ◽  
Low Flow ◽  
Target Coverage ◽  
Controlled Ventilation ◽  
One Step ◽  
Low Flow Anesthesia ◽  
End Tidal

Abstract Background Sevoflurane is suitable for low-flow anesthesia (LFA). LFA needs a wash-in phase. The reported sevoflurane wash-in schemes lack simplicity, target coverage, and applicability. We proposed a one-step 1-1-8 wash-in scheme for sevoflurane LFA to be used with both N 2 O and Air. The objective of our study was to identify time for achieving each level of alveolar concentration of sevoflurane (F A S) from 1% to 3.5% in both contexts. Methods We recruited 199 adults requiring general anesthesia with endotracheal intubation and controlled ventilation—102 in group N 2 O and 97 in group Air. After induction and intubation, a wash-in was started using a fresh gas flow of O 2 :N 2 O or O 2 :Air at 1:1 L·min -1 plus sevoflurane 8%. The ventilation was controlled to maintain end-tidal CO 2 of 30-35 mmHg. Results The rising patterns of F A S and inspired concentration of sevoflurane (F I S) are similar, running parallel between the groups. The F A S/F I S ratio increased from 0.46 to 0.72 within 260 sec in group N 2 O and from 0.42 to 0.69 within 286 sec in group Air. The respective time to achieve an F A S of 1%, 1.5%, 2%, 2.5%, 3%, and 3.5% was 1, 1.5, 2, 3, 3.5, and 4.5 min in group N 2 O and 1, 1.5, 2, 3, 4, and 5 min in group Air. The heart rate and blood pressure of both groups significantly increased initially then gradually decreased as F A S increased. Conclusions The 1-1-8 wash-in scheme for sevoflurane LFA has many advantages, including simplicity, coverage, swiftness, safety, economy, and that it can be used with both N 2 O and Air. A respective F A S of 1%, 1.5%, 2%, 2.5%, 3%, and 3.5% when used with N 2 O and Air can be expected at 1, 1.5, 2, 3, 3.5, and 4.5 min and 1, 1.5, 2, 3, 4, and 5 min.

scholarly journals Effect of intravenous oxycodone on the physiologic responses to extubation following general anesthesia

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Menglu Jiang ◽  
Jiawei Ji ◽  
Xin Li ◽  
Zhenqing Liu
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
General Anesthesia ◽  
Control Group ◽  
Study Group ◽  
Clinical Trial Registry ◽  
Blood Oxygen Saturation ◽  
Blood Concentrations ◽  
Number Of Patients ◽  
Blood Hormones

Abstract Background Endotracheal intubation and extubation may cause undesirable hemodynamic changes. Intravenous oxycodone has recently been introduced and used for relieving hemodynamic alterations in response to intubation, but there is insufficient information regarding its application in stabilizing hemodynamics during extubation in the patients emerging from general anesthesia. Methods One hundred patients, who had undergone assorted laparoscopic surgeries under general anesthesia, were randomly assigned to Control group (saline injection, 50 cases) and Study group (intravenous injection of 0.08 mg/kg oxycodone immediately after completion of the surgical procedure, 50 cases). Blood pressure, heart rate, blood oxygen saturation (SpO2) as well as blood concentrations of epinephrine, norepinephrine, and cortisol were recorded or measured immediately before extubation (T0), during extubation (T1), as well as one minute (T2), 5 min (T3), and 10 min after extubation (T4). In addition, coughing and restlessness, time of eye-opening, and duration from completing surgery to extubation as well as Ramsay Sedation Scale were analyzed. Results Blood pressure and heart rate as well as blood concentrations of epinephrine, norepinephrine, and cortisol were significantly higher in the Control group compared with the Study group at the time of extubation as well as 1, 5, and 10 min after extubation (P < 0.05). When the patients emerged from general anesthesia, 70 % of the Control group had cough, which was significantly higher than that of Study group (40 %, P < 0.05). Significantly higher number of patients manifested restlessness in the Control group before (40 %) and after extubation (20 %) compared with that in the Study group (20 and 2 %, respectively, P < 0.05). In addition, patients of Control group had lower Ramsay score at extubation (1.7 ± 0.7) as well as 30 min after extubation (2.4 ± 0.9) compared to that of the patients of Study group (2.2 ± 0.9, and 3.0 ± 0.8, respectively, P = 0.003 and 0.001). Conclusions Intravenous oxycodone attenuated alterations of hemodynamics and blood hormones associated with extubation during emergence from general anesthesia. Trial registration Chinese Clinical Trial Registry: ChiCTR2000040370 (registration date: 11-28-2020) “‘retrospectively registered”.

Pet CO2 inversely affects MSNA response to orthostatic stress

2001 ◽  
Vol 281 (3) ◽  
pp. H1040-H1046 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Debbie D. O'Leary ◽  
Richard L. Hughson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Orthostatic Intolerance ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Burst Frequency ◽  
Head Up Tilt ◽  
End Tidal ◽  
Combined Data

Arterial hypocapnia has been associated with orthostatic intolerance. Therefore, we tested the hypothesis that hypocapnia may be detrimental to increases in muscle sympathetic nerve activity (MSNA) and total peripheral resistance (TPR) during head-up tilt (HUT). Ventilation was increased ∼1.5 times above baseline for each of three conditions, whereas end-tidal Pco 2 (Pet CO2 ) was clamped at normocapnic (Normo), hypercapnic (Hyper; +5 mmHg relative to Normo), and hypocapnic (Hypo; −5 mmHg relative to Normo) conditions. MSNA (microneurography), heart rate, blood pressure (BP, Finapres), and cardiac output (Q, Doppler) were measured continuously during supine rest and 45° HUT. The increase in heart rate when changing from supine to HUT ( P < 0.001) was not different across Pet CO2 conditions. MSNA burst frequency increased similarly with HUT in all conditions ( P < 0.05). However, total MSNA and the increase in total amplitude relative to baseline (%ΔMSNA) increased more when changing to HUT during Hypo compared with Hyper ( P < 0.05). Both BP and Q were higher during Hyper than both Normo and Hypo (main effect; P < 0.05). Therefore, the MSNA response to HUT varied inversely with levels of Pet CO2 . The combined data suggest that augmented cardiac output with hypercapnia sustained blood pressure during HUT leading to a diminished sympathetic response.

scholarly journals Contribution of BKCa channels to local metabolic coronary vasodilation: effects of metabolic syndrome

2010 ◽  
Vol 298 (3) ◽  
pp. H966-H973 ◽  
Author(s):  
Léna Borbouse ◽  
Gregory M. Dick ◽  
Gregory A. Payne ◽  
Brittany D. Payne ◽  
Mark C. Svendsen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Heart Rate ◽  
Atherogenic Diet ◽  
Bkca Channels ◽  
Selective Blockade ◽  
Before And After ◽  
Lactate Uptake ◽  
Exercise Induced ◽  
The Relationship

This investigation was designed to examine the hypothesis that impaired function of coronary microvascular large-conductance Ca2+-activated K+ (BKCa) channels in metabolic syndrome (MetS) significantly attenuates the balance between myocardial oxygen delivery and metabolism at rest and during exercise-induced increases in myocardial oxygen consumption (MV̇o2). Studies were conducted in conscious, chronically instrumented Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) that induces many common features of MetS. Data were collected under baseline/resting conditions and during graded treadmill exercise before and after selective blockade of BKCa channels with penitrem A (10 μg/kg iv). We found that the exercise-induced increases in blood pressure were significantly elevated in MetS swine. No differences in baseline cardiac function or heart rate were noted. Induction of MetS produced a parallel downward shift in the relationship between coronary venous Po2 and MV̇o2 ( P < 0.001) that was accompanied by a marked release of lactate (negative lactate uptake) as MV̇o2 was increased with exercise ( P < 0.005). Inhibition of BKCa channels with penitrem A did not significantly affect blood pressure, heart rate, or the relationship between coronary venous Po2 and MV̇o2 in lean or MetS swine. These data indicate that BKCa channels are not required for local metabolic control of coronary blood flow under physiological (lean) or pathophysiological (MetS) conditions. Therefore, diminished function of BKCa channels does not contribute to the impairment of myocardial oxygen-supply demand balance in MetS.

scholarly journals A randomized comparative study of preloading with Ringers lactate and intravenous Ephedrine for the prevention of hypotension due to propofol during induction of general anesthesia

2016 ◽  
Vol 3 (1) ◽  
pp. 22-27 ◽  
Author(s):  
Manisha Pradhan ◽  
Brahma Dev Jha
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Systolic Blood Pressure ◽  
General Anesthesia ◽  
Diastolic Blood Pressure ◽  
Endotracheal Intubation ◽  
Physical Status ◽  
Volume Loading

Background: The ideal method to prevent hypotension due to intravenous propofol for induction of anesthesia is still debatable. The aim of the study was to compare the hemodynamic response of ephedrine and volume loading with ringer lactate in preventing the hypotension caused by propofol as inducing agent in patients scheduled for elective surgeries requiring general anesthesia with endotracheal intubation.Methods: This was prospective randomized study conducted in 40 patients of ASA physical status I, aged 20-50 years, scheduled for elective surgeries requiring general anesthesia with endotracheal intubation. Group I received intravenous ephedrine sulphate (70 mcg/kg) just before induction of anaesthesia, and patients assigned to Group II received preloading with Ringer's lactate (12 ml/kg) over the 10-15 minutes before the administration of propofol. The variables compared were heart rate, systolic blood pressure, diastolic blood pressure, mean arterial pressure following induction of anesthesia till 10 minutes after intubation of trachea.Results: We found that there were increase in systolic blood pressure, diastolic blood pressure and mean arterial pressure after induction in both the groups but the difference between the groups was not significant. The increase in heart rate was found to be significantly higher in ephedrine group in comparison to volume loading group.Conclusion: Our study showed that both the methods used were equally effective in preventing hypotension induced by propofol in the adult ASA physical status I patients requiring general anesthesia with endotracheal intubation. However, the heart rate was significantly higher in patients receiving ephedrine in comparison to volume loading group.

Hypoxemia raises muscle sympathetic activity but not norepinephrine in resting humans

1989 ◽  
Vol 66 (4) ◽  
pp. 1736-1743 ◽  
Author(s):  
L. B. Rowell ◽  
D. G. Johnson ◽  
P. B. Chase ◽  
K. A. Comess ◽  
D. R. Seals
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous Activity ◽  
Plasma Concentrations ◽  
Random Order ◽  
Sympathetic Nervous Activity ◽  
Severe Hypoxemia ◽  
Arterial Blood ◽  
End Tidal ◽  
Venous Plasma

The experimental objective was to determine whether moderate to severe hypoxemia increases skeletal muscle sympathetic nervous activity (MSNA) in resting humans without increasing venous plasma concentrations of norepinephrine (NE) and epinephrine (E). In nine healthy subjects (20–34 yr), we measured MSNA (peroneal nerve), venous plasma levels of NE and E, arterial blood pressure, heart rate, and end-tidal O2 and CO2 before (control) and during breathing of 1) 12% O2 for 20 min, 2) 10% O2 for 20 min, and 3) 8% O2 for 10 min--in random order. MSNA increased above control in five, six, and all nine subjects during 12, 10, and 8% O2, respectively (P less than 0.01), but only after delays of 12 (12% O2) and 4 min (8 and 10% O2). MSNA (total activity) rose 83 +/- 20, 260 +/- 146, and 298 +/- 109% (SE) above control by the final minute of breathing 12, 10, and 8% O2, respectively. NE did not rise above control at any level of hypoxemia; E rose slightly (P less than 0.05) at one time only with both 10 and 8% O2. Individual changes in MSNA during hypoxemia were unrelated to elevations in heart rate or decrements in blood pressure and end-tidal CO2--neither of which always fell. We conclude that in contrast to some other sympathoexcitatory stimuli such as exercise or cold stress, moderate to severe hypoxemia increases leg MSNA without raising plasma NE in resting humans.

OP-224: THE RELATIONSHIP BETWEEN CIRCADIAN BLOOD PRESSURE PATTERN AND HEART RATE TURBULENCE

2011 ◽  
Vol 147 ◽  
pp. S90
Author(s):  
S. Okutucu ◽  
U.N. Karakulak ◽  
G. Kabakci ◽  
E. Demiri ◽  
S.G. Fatihoglu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Turbulence ◽  
Pressure Pattern ◽  
Circadian Blood Pressure ◽  
The Relationship

Phase I Safety Assessment of Intrathecal Neostigmine Methylsulfate in Humans 

1995 ◽  
Vol 82 (2) ◽  
pp. 331-343 ◽  
Author(s):  
David D. Hood ◽  
James C. Eisenach ◽  
Robin Tuttle
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Side Effects ◽  
Healthy Volunteers ◽  
Nausea And Vomiting ◽  
Severe Nausea ◽  
End Tidal Carbon Dioxide ◽  
End Tidal ◽  
Ice Water

Background In dogs, sheep, and rats, spinal neostigmine produces analgesia alone and enhances analgesia from alpha 2-adrenergic agonists. This study assesses side effects and analgesia from intrathecal neostigmine in healthy volunteers. Methods After institutional review board approval and informed consent, 28 healthy volunteers were studied. The first 14 volunteers received neostigmine (50-750 micrograms) through a #19.5 spinal needle followed by insertion of a spinal catheter. The remaining 14 volunteers received neostigmine through a #25 or #27 spinal needle without a catheter. Safety measurements included blood pressure, heart rate, oxyhemoglobin saturation, end-tidal carbon dioxide, neurologic evaluation, and computer tests of vigilance and memory. Analgesia in response to ice water immersion was measured. Results Neostigmine (50 micrograms) through the #19.5 needle did not affect any measured variable. Neostigmine (150 micrograms) caused mild nausea, and 500-750 micrograms caused severe nausea and vomiting. Neostigmine (150-750 micrograms) produced subjective leg weakness, decreased deep tendon reflexes, and sedation. The 750-micrograms dose was associated with anxiety, increased blood pressure and heart rate, and decreased end-tidal carbon dioxide. Neostigmine (100-200 micrograms) in saline, injected through a #25 or #27 needle, caused protracted, severe nausea, and vomiting. This did not occur when dextrose was added to neostigmine. Neostigmine by either method of administration reduced visual analog pain scores to immersion of the foot in ice water. Conclusions The incidence and severity of these adverse events from intrathecal neostigmine appears to be affected by dose, method of administration, and baricity of solution. These effects in humans are consistent with studies in animals. Because no unexpected or dangerous side effects occurred, cautious examination of intrathecal neostigmine alone and in combination with other agents for analgesia is warranted.

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