Effect of three opioid-based analgesic protocols on the perioperative autonomic-mediated cardiovascular response in sheep

2018 ◽  
Vol 53 (5) ◽  
pp. 491-499 ◽  
Author(s):  
Luca Bellini ◽  
Giulia Maria De Benedictis
Keyword(s):  
Cardiovascular Response ◽  
Intervertebral Disk ◽  
Noxious Stimulation ◽  
Clinical Effects ◽  
Rescue Analgesia ◽  
Arterial Blood ◽  
Haemodynamic Changes ◽  
End Tidal ◽  
Fixed End ◽  
Surgical Stimulation

Few reports evaluate the clinical effects of opioids in sheep during experimental surgical procedures. Catecholamine-mediated haemodynamic changes resulting from surgical noxious stimulation are blunted by opioids. The aim of this study was to evaluate the efficacy of three opioid-based analgesic protocols in avoiding a 20% increase in heart rate (HR) and/or mean arterial blood pressure (MAP) during experimental intervertebral disk nucleotomy in sheep. Eighteen female Brogna sheep were anaesthetized with propofol and maintained with a fixed end-tidal isoflurane concentration of 1.5 ± 0.1%. Sheep were assigned to one of three groups that intravenously received methadone 0.3 mg/kg (group M), fentanyl 2 µg/kg followed by 10 µg/kg/h (group F), or buprenorphine 10 µg/kg and 30 minutes later ketamine 1 mg/kg followed by 5 mg/kg/h (group BK). Intravenous fentanyl at 2 µg/kg would have been used for rescue analgesia in case HR and/or MAP had increased. During surgery, HR and MAP values did not increase over 20% in all groups. All animals maintained the percentage change between -4 and 7% for both variables; only one sheep in group BK had an increase in MAP superior to 20% after ketamine administration before surgical stimulation. In group M, HR decreased over time and in group BK, MAP tended to increase during surgery. All the opioid-based protocols tested were able to control the cardiovascular response to noxious stimulation in sheep undergoing spinal surgery, although ketamine may have represented a confounding factor.

Fentanyl Augments the Blockade of the Sympathetic Response to Incision (MAC-BAR) Produced by Desflurane and Isoflurane 

1998 ◽  
Vol 88 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Malcolm Daniel ◽  
Richard B. Weiskopf ◽  
Mariam Noorani ◽  
Edmond I. Eger
Keyword(s):  
Nitrous Oxide ◽  
Cardiovascular Response ◽  
Dependent Manner ◽  
Surgical Incision ◽  
Arterial Blood ◽  
Adrenergic Response ◽  
The Mean ◽  
End Tidal ◽  
Inhaled Anesthetic ◽  
Dose Dependent

Background Heart rate (HR) or mean arterial blood pressure (MAP) may increase in response to incision despite the absence of a motor response. The authors hypothesized that the MAC-BAR (minimum alveolar concentration of an anesthetic that blocks adrenergic response to incision) for isoflurane would exceed that for desflurane, and that fentanyl would decrease the MAC-BAR for each anesthetic in a dose-dependent manner. Methods Seventy-one patients were randomly allocated to one of six groups: desflurane or isoflurane without fentanyl or with 1.5 or 3 microg/kg fentanyl given intravenously 5 min before surgical incision. Anesthesia was induced with 2 mg/kg propofol given intravenously, and tracheal intubation facilitated with 0.1 mg/kg given intravenously. The first patient in each group received 1 MAC (end-tidal) of the inhaled anesthetic in 60% nitrous oxide (0.55 MAC), balance oxygen, maintained for at least 10 min before incision. The response was considered positive if the HR or MAP increased 15% or more. If the response was positive, the end-tidal concentration given to the next patient was 0.3 MAC greater; if the response was negative, the end-tidal concentration was 0.3 MAC less. The MAC-BAR level was calculated as the mean of four independent cross-over responses in each group. Results Desflurane and isoflurane anesthesia with 60% nitrous oxide did not change HR (P > 0.05) and decreased MAP (P < 0.05) before incision. Plasma epinephrine and norepinephrine concentrations after anesthesia and before incision were normal in all groups. The MAC-BAR level, without fentanyl, did not differ (P > 0.05) between desflurane (1.30 +/- 0.34 MAC [mean +/- SD]) and isoflurane (1.30 +/- 0.18 MAC). Fentanyl given at 1.5 microg/kg intravenously equivalently (P > 0.05) reduced the MAC-BAR for desflurane (to 0.40 +/- 0.18 MAC; P < 0.05) and isoflurane (to 0.55 +/- 0.00 MAC; P < 0.05), but a further increase in fentanyl to 3 microg/kg caused no greater decrease in the MAC-BAR for desflurane (0.48 +/- 0.16 MAC) and isoflurane (0.40 +/- 0.30 MAC). Conclusions Clinically attainable doses of desflurane and isoflurane, in 60% nitrous oxide (0.55 MAC), block the cardiovascular response to surgical incision at 1.3 MAC. Fentanyl given at 1.5 microg/kg decreases the MAC-BAR for each agent with no further decrease produced by 3 microg/kg fentanyl.

Propofol Fails to Attenuate the Cardiovascular Response to Rapid Increases in Desflurane Concentration

1996 ◽  
Vol 84 (1) ◽  
pp. 75-80 ◽  
Author(s):  
Malcolm Daniel ◽  
Edmond I Eger ◽  
Richard B. Weiskopf ◽  
Mariam Noorani
Keyword(s):  
Heart Rate ◽  
Cardiovascular Response ◽  
Peak Plasma ◽  
Random Order ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
Desflurane Concentration ◽  
End Tidal ◽  
Catecholamine Concentration ◽  
Epinephrine Concentration

Background A rapid increase in desflurane concentration to greater than 1 MAC transiently increases heart rate, arterial blood pressure, and circulating catecholamine concentration. Because propofol decreases sympathetic outflow, it was hypothesized that propofol would blunt these responses. Methods To test this hypothesis, five healthy male volunteers were studied three times. After induction of anesthesia with 2 mg.kg-1 propofol, anesthesia was maintained with 4% end-tidal desflurane in oxygen (0.55 MAC) via an endotracheal tube for 32 min. On separate occasions, in random order, either no propofol or 2 mg.kg-1 propofol was administered either 2 or 5 min before increasing end-tidal desflurane concentration from 4% to 8%. Results Without propofol pretreatment, the increase to 8% desflurane transiently increased heart rate (from 63 +/- 3 beats/min to 108 +/- 5 beats/min, mean +/- SEM; P < 0.01), mean arterial pressure (from 73 +/- 1 mmHg to 118 +/- 6 mmHg; P < 0.01), and epinephrine concentration (from 14 +/- 1 pg.ml-1 to 279 +/- 51 pg.ml-1; P < 0.05). There was no significant change in norepinephrine concentration (from 198 +/- 37 pg.ml-1 to 277 +/- 46 pg.ml-1). The peak plasma epinephrine concentration was attenuated by each propofol pretreatment (158 +/- 35 pg.ml-1, propofol given 2 min before, and 146 + 41 pg.ml-1, propofol given 5 min before; P < 0.05), but neither propofol pretreatment modified the cardiovascular or norepinephrine responses. Conclusions Although able to blunt the increase in epinephrine concentration, propofol 2 mg.kg-1 propofol does no attenuate the transient cardiovascular response to a rapid increase in desflurane concentration to greater than 1 MAC.

Dose-finding study comparing three treatments of remifentanil in cats anesthetized with isoflurane undergoing ovariohysterectomy

2017 ◽  
Vol 20 (2) ◽  
pp. 164-171 ◽  
Author(s):  
Marcela L Machado ◽  
João Henrique N Soares ◽  
Maria Alice Kuster de Albuquerque Gress ◽  
Douglas dos Santos e Castro ◽  
Kaleizu Teodoro Rosa ◽  
...  
Keyword(s):  
Dosage Regimen ◽  
Mixed Model ◽  
Cardiovascular Response ◽  
Dose Finding ◽  
Rank Test ◽  
Rescue Analgesia ◽  
Remifentanil Infusion ◽  
Significant Difference ◽  
End Tidal ◽  
Post Hoc

Objectives Three infusion rates of remifentanil were used in isoflurane-anesthetized cats undergoing ovariohysterectomy. The aim of this study was to identify a dosage regimen that would provide optimal anesthetic and surgical conditions, as well as to compare cardiovascular response to surgical stimulation, postoperative analgesia, anesthetic duration and quality of recovery among the tested remifentanil infusion rates. Methods Twenty-seven client-owned, mixed-breed adult healthy female cats were randomized to receive remifentanil 0.1 µg/kg/min (REMI01), remifentanil 0.2 µg/kg/min (REMI02) or remifentanil 0.4 µg/kg/min (REMI04). After premedication with acepromazine and induction of anesthesia with propofol, cats were mechanically ventilated and anesthesia was maintained at approximately 1.0 minimum alveolar concentration (MAC) of isoflurane (1.63% end-tidal isoflurane [ETISO]). Remifentanil infusion rate was increased or decreased by 20% if blood pressure had increased or decreased by 20% from previous values. Pulse rate (PR), systolic arterial pressure (SAP), esophageal temperature, pulse oximetry, end-tidal partial pressure of CO2 and ETISO were recorded at different time points during surgery. Meloxicam was administered before the end of surgery. Data within each treatment group were analyzed using a mixed-model ANOVA and Friedman’s test followed by the Wilcoxon signed rank test. Bonferroni or Dunnett’s post-hoc tests were used. The Kruskal-Wallis test followed by Dunn’s post-hoc test were used to compare data between groups; significance was set at P <0.05. Results Time to sternal recumbency and time to standing were significantly longer in REMI04 than in the other groups. SAP was higher when compared with baseline in REMI01 and REMI02 groups than in REMI04. No significant difference in PR among groups was observed. One cat in REMI01 and another in REMI02 required postoperative rescue analgesia. Conclusion and relevance The dosage regimen of 0.4 µg/kg/min seemed to be the most appropriate to be used in cats undergoing ovariohysterectomy and anesthetized with 1.0 MAC of isoflurane.

scholarly journals Evaluation of Cardiopulmonary, Blood Gases and Clinical Effects of Dexmedetomidine-Ketamine and Midazolam-Ketamine Anesthesia in New Zealand White Rabbits

2021 ◽  
Vol 77 (09) ◽  
pp. 6568-2021
Author(s):  
Ünal YAVUZ ◽  
Kerem YENER ◽  
Adem ŞAHAN ◽  
Pelin Fatoş POLAT DİNÇER ◽  
Ali HAYAT
Keyword(s):  
New Zealand ◽  
Blood Gases ◽  
High Dose ◽  
Clinical Effects ◽  
Arterial Blood ◽  
New Zealand White Rabbits ◽  
Ketamine Anesthesia ◽  
The Difference ◽  
End Tidal ◽  
End Tidal Co2

This study aimed to investigate the effects of dexmedetomidine-ketamine and midazolam-ketamine combinations on cardiopulmonary and clinical parameters in New Zealand white rabbits. The DXK group (n=8) received dexmedetomidine (50 µg/kg) and ketamine (20 mg/kg), and the MDK group (n=8) received midazolam (0.6 mg/kg) and ketamine (20 mg/kg) in the same syringe through the intramuscular (IM) route. Before anaesthesia and for 120 minutes, reflexes, haemodynamic values and blood gas changes were monitored. It was determined that anaesthesia was induced within a shorter time and lasted longer in DXK. The difference between the groups in terms of the time of loss of the pedal reflex (2.0 min in DXK, 7.5 min in MDK) was statistically significant (p<0.05). It was observed that, in both groups, the heart rate (HR), mean arterial pressure (MAP), respiratory rate (RR) and oxy-haemoglobin saturation (SpO2) values decreased, and the end-tidal CO2 (EtCO2) values increased, but these changes were greater in DXK. With regard to arterial blood gasses, a reduction in pH and pO2 and an increase in pCO2 were also more noticeable in DXK. Consequently, at the doses applied, dexmedetomidine-ketamine caused more noticeable changes in the haemodynamic values and blood gasses in comparison to midazolam-ketamine. High-dose dexmedetomidine (50 µg/kg) and low-dose ketamine (20 mg/kg) achieved induction in a shorter time but led to a significant reduction in RR. It was concluded that the combination of midazolam (0.6 mg/kg) and ketamine (20 mg/kg) could be regarded as appropriate for the anaesthesia of New Zealand white rabbits.

Isoflurane and Sevoflurane Augment Norepinephrine Responses to Surgical Noxious Stimulation in Humans 

1998 ◽  
Vol 89 (6) ◽  
pp. 1407-1413 ◽  
Author(s):  
Hajime Segawa ◽  
Kenjiro Mori ◽  
Masahiro Murakawa ◽  
Kyomi Kasai ◽  
Gotaro Shirakami ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Response ◽  
Blood Pressure Response ◽  
Volatile Anesthetics ◽  
Plasma Norepinephrine ◽  
Noxious Stimulation ◽  
High Dose ◽  
Plasma Catecholamine ◽  
Arterial Blood ◽  
Plasma Catecholamine Concentrations

Background Suppression of hypertensive response to noxious stimulation by volatile anesthetics may be a result of suppression of the stimulation-induced norepinephrine response or that of the cardiovascular response to catecholamines, or both. The suppression of the cardiovascular response is established, but that of norepinephrine response has not been confirmed. The authors hypothesized that the suppression of cardiovascular response but not that of norepinephrine response plays a major role in suppressing the noxious stimulation-induced hypertensive response by volatile anesthetics. Methods Forty healthy donors for living-related liver transplantation were allocated to four groups: receiving 1.2% (end-tidal) isoflurane in oxygen and nitrogen, 2.0% isoflurane, 1.7% sevoflurane, or 2.8% sevoflurane. The intraoperative plasma norepinephrine and epinephrine concentrations, arterial blood pressure and pulse rate were measured for the first 15 min of surgery and were compared with the preoperative values. Results Norepinephrine and epinephrine concentrations both increased intraoperatively in all four groups. The values of maximum increase and area under the concentration-versus-time curve of norepinephrine were greater in the high dose groups of both anesthetics. The intraoperative blood pressure did not differ by different doses of anesthetics, and the degree of increase of blood pressure was not proportional to the plasma catecholamine concentrations. Conclusion The effects of isoflurane and sevoflurane on the surgical noxious stimulation-induced norepinephrine response were inversely proportional to the dose. The suppression of noxious stimulation-induced blood pressure response by anesthetics that were studied may be the result of suppression of the responses of vascular smooth muscle and myocardium to catecholamines.

HAEMODYNAMIC CHANGES AND ADRENAL FUNCTION IN MAN DURING INDUCED HYPOGLYCAEMIA

1963 ◽  
Vol 44 (3) ◽  
pp. 430-442 ◽  
Author(s):  
B. Arner ◽  
P. Hedner ◽  
T. Karlefors ◽  
H. Westling
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Peripheral Vascular ◽  
Adrenocortical Activity ◽  
Arterial Blood ◽  
Haemodynamic Changes ◽  
The Mean ◽  
Temporary Rise ◽  
Catechol Amines

ABSTRACT Observations were made on healthy volunteers during insulin induced hypoglycaemia (10 cases) and infusion of adrenaline (3 cases) or cortisol (1 case). In all cases a rise in the cardiac output was registered during insulin hypoglycaemia. The mean arterial blood pressure was relatively unchanged and the calculated peripheral vascular resistance decreased in all cases. A temporary rise in plasma corticosteroids was observed. After infusion of adrenaline similar circulatory changes were observed but no rise in plasma corticosteroids was found. Infusion of cortisol caused an increased plasma corticosteroid level but no circulatory changes. It is concluded that liberation of catechol amines and increased adrenocortical activity following hypoglycaemia are not necessarily interdependent.

scholarly journals 217 The end-tidal and arterial carbon dioxide gradient in serious traumatic brain injury after pre-hospital emergency anaesthesia: a retrospective observational study

2020 ◽  
Vol 37 (12) ◽  
pp. 847.1-847
Author(s):  
James Price ◽  
Daniel Sandbach ◽  
Ari Ercole ◽  
Alastair Wilson ◽  
Ed Barnard
Keyword(s):  
Carbon Dioxide ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Thoracic Injury ◽  
Secondary Brain Injury ◽  
Hospital Emergency ◽  
Hospital Arrival ◽  
Arterial Blood ◽  
End Tidal ◽  
Emergency Anaesthesia

Aims/Objectives/BackgroundIn the United Kingdom (UK), 20% of patients with severe traumatic brain injury (TBI) receive pre-hospital emergency anaesthesia (PHEA). Current guidance recommends an end-tidal carbon dioxide (ETCO2) of 4.0–4.5kPa to achieve a low-normal arterial partial pressure of CO2 (PaCO2), and reduce secondary brain injury. This recommendation assumes a 0.5kPa ETCO2-PaCO2 gradient. However, the gradient in the acute phase of TBI is unknown. Our primary aim was to report the ETCO2-PaCO2 gradient of TBI patients at hospital arrival.Methods/DesignA retrospective cohort study of adult patients with serious TBI, who received a PHEA by a pre-hospital critical care team in the East of England between 1st April 2015 to 31st December 2017. Linear regression was performed to test for correlation and reported as R-squared (R2). A Bland-Altman plot was used to test for paired ETCO2 and PaCO2 agreement and reported with 95% confidence intervals (95%CI). ETCO2-PaCO2 gradient data were compared with a two-tailed, unpaired, t-test.Results/Conclusions107 patients were eligible for inclusion. Sixty-seven patients did not receive a PaCO2 sample within 30 minutes of hospital arrival and were therefore excluded. Forty patients had complete data and were included in the final analysis; per protocol.The mean ETCO2-PaCO2 gradient was 1.7 (±1.0) kPa, with only moderate correlation of ETCO2 and PaCO2 at hospital arrival (R2=0.23, p=0.002). The Bland-Altman bias was 1.7 (95%CI 1.4–2.0) kPa with upper and lower limits of agreement of 3.6 (95%CI 3.0–4.1) kPa and -0.2 (95%CI -0.8–0.3) kPa respectively. There was no significant gradient correlation in patients with a co-existing serious thoracic injury (R2=0.13, p=0.10), and this cohort had a larger ETCO2-PaCO2 gradient, 2.0 (±1.1) kPa, p=0.01. Patients who underwent pre-hospital arterial blood sampling had an arrival PaCO2 of 4.7 (±0.2) kPa.Lower ETCO2 targets than previously recommended may be safe and appropriate. The use of pre-hospital PaCO2 measurement is advocated.

scholarly journals Cerebral blood flow autoregulation in ischemic heart failure

2017 ◽  
Vol 312 (1) ◽  
pp. R108-R113 ◽  
Author(s):  
J. R. Caldas ◽  
R. B. Panerai ◽  
V. J. Haunton ◽  
J. P. Almeida ◽  
G. S. R. Ferreira ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Healthy Volunteers ◽  
Neurological Complications ◽  
Ischemic Heart ◽  
Step Response ◽  
Ischemic Heart Failure ◽  
Arterial Blood ◽  
End Tidal

Patients with ischemic heart failure (iHF) have a high risk of neurological complications such as cognitive impairment and stroke. We hypothesized that iHF patients have a higher incidence of impaired dynamic cerebral autoregulation (dCA). Adult patients with iHF and healthy volunteers were included. Cerebral blood flow velocity (CBFV, transcranial Doppler, middle cerebral artery), end-tidal CO2 (capnography), and arterial blood pressure (Finometer) were continuously recorded supine for 5 min at rest. Autoregulation index (ARI) was estimated from the CBFV step response derived by transfer function analysis using standard template curves. Fifty-two iHF patients and 54 age-, gender-, and BP-matched healthy volunteers were studied. Echocardiogram ejection fraction was 40 (20–45) % in iHF group. iHF patients compared with control subjects had reduced end-tidal CO2 (34.1 ± 3.7 vs. 38.3 ± 4.0 mmHg, P < 0.001) and lower ARI values (5.1 ± 1.6 vs. 5.9 ± 1.0, P = 0.012). ARI <4, suggestive of impaired CA, was more common in iHF patients (28.8 vs. 7.4%, P = 0.004). These results confirm that iHF patients are more likely to have impaired dCA compared with age-matched controls. The relationship between impaired dCA and neurological complications in iHF patients deserves further investigation.

Abstract 119: Influence of Anesthetics on the Hemodynamic Response in a Rat Model of Hemorrhagic Shock

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Claudius Balzer ◽  
Franz J Baudenbacher ◽  
Susan S Eagle ◽  
Michele M Salzman ◽  
William J Cleveland ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Rat Model ◽  
Cardiovascular Response ◽  
Femoral Vein ◽  
Blood Pressure Measurement ◽  
Experimental Models ◽  
Sprague Dawley ◽  
Compensatory Mechanisms ◽  
Arterial Blood

Introduction: Experimental models of hemorrhagic shock (HS) in rats are important to test new treatments that may improve outcomes in humans, and general anesthesia is required during these experiments. The volatile anesthetic Isoflurane is known for its beneficial effects in rat HS models. Focusing on cardiovascular compensatory mechanisms, we wanted to evaluate Isoflurane versus the injectable anesthetic Pentobarbital in our rat model of mild HS (class 2). We hypothesize that Isoflurane during development of HS improves hemodynamics compared to Pentobarbital. Methods: Twelve Sprague-Dawley rats were initially anesthetized with an intraperitoneal (IP) injection of Pentobarbital (45 mg/kg) and intubated (1 L/min, FiO 2 0.25); heart rate (HR) was monitored by subcutaneous ECG needles. Femoral artery and vein were cannulated for continuous blood pressure measurement and delivery of fluids, respectively. In one group (n=7), anesthesia was continued with repeated IP injections of Pentobarbital (dose mg/kg), the other group (n=5) received continuous Isoflurane (1%). After 30 min of stabilization and administration of Heparin (100 IU/kg), HS was induced by removal of 1 ml of blood over 1 min via the femoral vein, repeated every 3 min until a volume of 5 ml of blood was removed. Mean arterial blood pressure (MAP) and HR were recorded and analyzed in LabChart. Results: During baseline, rats showed no significant differences in HR and MAP between both groups. After 5 ml of hemorrhage, both groups showed significant changes compared to baseline, with significantly higher MAP and HR in rats given only Pentobarbital. Conclusions: In our rat model of HS, Isoflurane dampens the physiologic response to compensate for mild hemorrhage. The cardiovascular response of rats in the Isoflurane group was a decrease of HR and MAP to every ml of hemorrhage, while rats given only Pentobarbital were able to maintain their MAP by raising their HR until decompensation.

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