Fall In Mean Arterial Pressure Research Articles

Impact of anesthetic induction with etomidate, thiopentone, and propofol on regional cerebral oxygenation: An observational study in patients with traumatic brain injury

Abstract Background and Aims: Anesthetic induction plays a pivotal role in determining the operative course and the outcome in patients with acute traumatic brain injury (TBI). The present study compared the effect of anesthetic induction with etomidate, thiopentone, and propofol primarily on systemic hemodynamics and regional cerebral oxygenation (rScO2) and secondarily on the serum cortisol levels in TBI patients. Material and Methods: In this prospective observational study, eligible patients were recruited and divided into three groups as per the induction agent received. Data collected were hemodynamic parameters and rScO2 levels at baseline, following 3 min of preoxygenation, and over 10 min of induction. Serum cortisol levels were measured before and after 24 h of induction. The statistical analysis was done using R software. Results: A total of 115 patients were included: 32, 33, and 50 in thiopentone, propofol, and etomidate groups, respectively. A significant increase (P < 0.001) in bilateral rScO2 was noted in all three groups following anesthetic induction. Intergroup comparison of the propofol and the etomidate groups revealed significantly lesser increase in contralateral rScO2 (P = 0.019) and a greater fall in mean arterial pressure (P = 0.003) on using propofol as an induction agent. Trend changes in bilateral rScO2 and hemodynamic parameters were comparable between thiopentone and etomidate groups. An insignificant fall in serum cortisol was observed in etomidate (P = 0.332) and thiopentone (P = 0.364) groups, but a significant increase was observed in the propofol group (P = 0.004). The Glasgow coma scale (GCS) score at discharge improved significantly in all the groups (P < 0.001). Conclusions: In TBI patients, anesthetic induction with etomidate resulted in least hemodynamic changes compared to induction with thiopentone and propofol. The rScO2 increased in all three groups after induction, with the maximal increase observed with etomidate compared to propofol and thiopentone. Insignificant fall in serum cortisol was observed with etomidate and thiopentone, but not with propofol. Outcome at discharge, assessed with GCS, was comparable in all the groups. Key Messages: Anesthetic induction with etomidate produced least hemodynamic changes compared to induction with thiopentone and propofol in patients with traumatic brain injury. Consequently, maximal increase in cerebral oxygen saturation occurred with etomidate among the three induction agents. An insignificant decrease in serum cortisol was observed with etomidate and thiopentone, but not with propofol. Neurological outcome at discharge was similar with all drugs.

Comparison of Dexmedetomidine and Propofol for Sedation in Patients Undergoing Upper Limb Orthopedic Surgery under Regional Anesthesia with Brachial Plexus Block

Abstract Background: The search for the ideal sedative during regional anesthesia continues. Propofol is widely as a sedative intraoperatively. It may cause troublesome hemodynamic changes. Dexmedetomidine is an α2 agonist with sedative, anxiolytic, and analgesic properties. In this study, we compared dexmedetomidine with propofol as sedatives during surgeries under brachial plexus block. Materials and Methods: In our study, 70 American Society of Anesthesiologists I Class and II patients about to undergo upper limb surgeries under brachial plexus block were blinded and randomly allocated to receive either propofol (Group P) or dexmedetomidine (Group D) infusion. Brachial plexus block was performed, and after confirmation of adequate sensory and motor block, an initial loading dose of the drug was administered over 10 min, followed by a maintenance dose till the end of the surgery. Titration of the rate of infusion was done so as to maintain Ramsay Sedation Score (RSS) of 3–4 and Bispectral Index (BIS) of 60–80. Hemodynamic and respiratory parameters were monitored intraoperatively. Adverse effects such as hypotension, bradycardia, respiratory depression, and incidence of oversedation and undersedation were also noted. The collected data were evaluated using appropriate statistical tests in SPSS version 22®. P <0.05 was considered statistically significant. Results: The RSS remained at 4 in Group P from 20 min onward and for Group D, RSS remained at 3 after 30 min. Post-induction, there was a reduction in BIS in both the groups, but patients in Group P showed statistically significant lower values of BIS when compared with Group D. The fall in mean arterial pressure was more in Group P as compared to Group D. Nine (25.71%) incidences of hypotension were seen in Group P and none in Group D. The decrease in heart rate was more profound in Group D as compared with Group P and one incidence of bradycardia observed in Group D. The respiratory rate was relatively stable in Group D as compared to Group P. The oxygen saturation (SpO2) values in the majority of the patients in both groups were above 92%, but three patients in Group P had SpO2 <92%. In Group P, 6 (17.14%) incidences of oversedation and 8 (22.85%) incidences of undersedation were observed. In Group D, 7 (20%) incidences of undersedation with no incidence of oversedation were observed. Conclusion: Dexmedetomidine at recommended doses has a better sedative property with less effect on hemodynamics and respiration as compared to propofol.

A Prospective Randomized Double Blind Comparative Study to Determine the Efficacy of Norepinephrine and Ephedrine to Maintain Arterial Blood Pressure During Spinal Anesthesia for Cesarean Delivery

Background: Spinal Anesthesia Induced Hypotension(SAIH) continues to be the troublesome complication for obstetric patients undergoing cesarean section under subarachnoid block. Vasopressors are emerging as the cornerstone of treating SAIH in cesarean section patients with the evolving evidence of arterial vasodilatation as the primary cause of hypotension. This study was hypothesized to compare the efficacy of norepinephrine and ephedrine boluses to maintain hemodynamics in cesarean section.
 Methods: After approval from institutional ethics committee and registration in Clinical Trials Registry India(CTRI ) and informed consent, study was conducted in 110 healthy parturients aged 18-40 years, belonging to ASA physical status I and II, posted for elective cesarean section under spinal anesthesia, were randomly allocated into group N(n=55) and group E(n=55),who received intravenous boluses of norepinephrine 6 g and ephedrine 10mg respectively as prophylaxis(one dose soon after induction) and in treatment of SAIH. The number of vasopressor boluses were recorded as primary objective and hemodynamics, APGAR scores, adverse events were noted.
 Results: The number of boluses of vasopressor used was 1.9±1.2 for Ephedrine and 4.72±2.9 for Norepinephrine. At 30,40,50 and 60 minutes after anesthesia, there was significant fall in mean arterial pressure in the norepinephrine group compared to ephedrine group. The incidence of tachycardia was more in ephedrine group and incidence of bradycardia was more in norepinephrine group.
 Conclusion: Both the study drugs, ephedrine and norepinephrine are comparably effective in preventing SAIH after prophylactic bolus and effective in maintaining blood pressure intraoperatively, more number of boluses of norepinephrine was required compared to ephedrine.

Intravenous Ascorbic Acid for the Prevention of Postreperfusion Syndrome in Orthotopic Liver Transplantation: Protocol for a Randomized Controlled Trial.

Liver transplantation is the last therapeutic option for patients with end-stage liver disease. Postreperfusion syndrome (PRS), defined as a fall in mean arterial pressure of more than 30% within the first 5 minutes after reperfusion of at least 1 minute, can occur in liver transplantation as a deep hemodynamic instability with associated hyperfibrinolysis immediately after reperfusion of the new graft. Its incidence has remained unchanged since it was first described in 1987. PRS is related to ischemia-reperfusion (I/R) injury, whose pathophysiology involves the release of several mediators from both the donor and the recipient. The antioxidant effect of ascorbic acid has been studied in resuscitating patients with septic shock and burns. Even today, there are publications with conflicting results, and there is a need for further studies to confirm or rule out the usefulness of this drug in this group of patients. The addition of ascorbic acid to preservation solutions used in solid organ transplantation is under investigation to harness its antioxidant effect and mitigate I/R injury. Since PRS could be considered a manifestation of I/R injury, we believe that the possible beneficial effect of ascorbic acid on the occurrence of PRS should be investigated. The aim of this randomized controlled trial is to assess the benefits of ascorbic acid over saline in the development of PRS in adult liver transplantation. We plan to conduct a single-center randomized controlled trial at the Hospital Universitario Ramón y Cajal in Spain. A total of 70 participants aged 18 years or older undergoing liver transplantation will be randomized to receive either ascorbic acid or saline. The primary outcome will be the difference between groups in the incidence of PRS. The randomized controlled trial will be conducted under conditions of respect for fundamental human rights and ethical principles governing biomedical research involving human participants and in accordance with the international recommendations contained in the Declaration of Helsinki and its subsequent revisions. The enrollment process began in 2020. A total of 35 patients have been recruited so far. Data cleaning and analysis are expected to occur in the first months of 2024. Results are expected around the middle of 2024. We believe that this study could be particularly relevant because it will be the first to analyze the clinical effect of ascorbic acid in liver transplantation. Moreover, we believe that this study fills an important gap in the knowledge of the potential benefits of ascorbic acid in the field of liver transplantation, particularly in relation to PRS. European Union Drug Regulating Authorities Clinical Trials Database 2020-000123-39; https://tinyurl.com/2cfzddw8; ClinicalTrials.gov NCT05754242; https://tinyurl.com/346vw7sm. DERR1-10.2196/50091.

Abstract P238: Chemerin Is Resident To Vascular Tunicas And Contributes To Vascular Tone

The adipokine chemerin has the potential to support blood pressure, evidenced by a fall in mean arterial pressure following knockdown of chemerin protein by whole-body antisense oligonucleotides (ASO) in rat models of normal and elevated blood pressure. While the liver is the greatest contributor of circulating chemerin, liver-specific (GalNAc) ASOs that abolished hepatic-derived chemerin did not change blood pressure in these models. Thus, other sites must produce the chemerin that supports blood pressure. Presently, we hypothesize that the vasculature—the blood vessel and its perivascular adipose tissue (PVAT)—is a source of chemerin that is independent of the liver and supports arterial tone. RNAScope®, Western blot, ASOs, and isometric contractility were used in the Dahl salt sensitive (SS) rat, male and female, on a normal diet. Species-specific ZZ probes detected Rarres2 mRNA in the smooth muscle, adventitia, and PVAT of the thoracic aorta. Chemerin protein was detected immunohistochemically in the endothelium, smooth muscle cells, adventitia, and PVAT. Chemerin colocalized with the vascular smooth muscle marker a-actin and the adipocyte marker perilipin. Importantly, chemerin protein in the aorta was not reduced when liver-derived chemerin was abolished by a liver-specific ASO against chemerin (thoracic aorta control ASO = 0.62 + 0.03; GalNAc ASO = 0.35 + 0.04; abdominal aorta control ASO = 0.38 ± 0.04, GalNAc ASO = 0.40 ± 0.22). Finally, inhibition of the receptor Chemerin1 by the receptor antagonist CCX832 resulted in aortic vasorelaxation [Media/PVAT + endothelium: -8.8 ± 3.3%; Media/PVAT - endothelium: -14.6 ± 4.2%; Media + endothelium: -1.5 ± 1.3%; and Media - endothelium: -5.1 ± 7.0%, quantified by percentage of initial wakeup to phenylephrine (-152 ± 67 mg of 1660 ± 121 mg; -93 ± 13 mg of 868 ± 171 mg, -20 ± 28 mg of 1906 ± 213 mg; and -59 ± 69 mg of 964 ± 70 mg, respectively)]. These data suggest that vessel-derived chemerin may support vascular tone locally through constitutive activation of Chemerin1 and highlights vascular chemerin as a potential therapeutic target in blood pressure regulation.

Assessment of haemodynamic response to tracheal intubation and prone positioning following clonidine and enalaprilat in lumbar spine surgeries: A double blind randomised controlled trial.

This study evaluates the effectiveness of long-acting antihypertensive drugs (clonidine and enalaprilat) in blunting the intubation response. Also, the study seeks to determine how effectively clonidine and enalaprilat can maintain stable haemodynamics during a change in position. After ethical committee approval and trial registration, a double-blinded, randomised controlled trial was conducted with 71 consenting patients scheduled for elective spine surgery in a prone position under general anaesthesia. Group C received clonidine 2 μg/kg, and Group E received enalaprilat 1.25 mg diluted in normal saline as an intravenous infusion given over 10 min before induction of anaesthesia. The changes in heart rate (HR) and blood pressure (BP) in response to the infusion of the study drugs, induction, tracheal intubation and change in position were recorded. P value <0.05 was considered significant. Statistical analysis was performed using Statistical Package for the Social Sciences (SPSS) version 25. Clonidine infusion caused a significant fall in heart rate post-infusion and post-induction with propofol (p value <0.05). Both clonidine and enalaprilat caused a significant fall in mean arterial pressure (MAP) post-infusion and post-induction (p value <0.05). Clonidine effectively blunted the intubation response with no increase in HR and MAP following intubation. Enalaprilat caused a significant rise in HR in response to intubation. On proning, there was a significant fall in MAP in both groups. Clonidine is effective in blunting the intubation response. Preoperative infusion of clonidine and enalaprilat causes hypotension during a change of position.

Comparison of Bispectral index-guided propofol and etomidate infusion for Supraglottic airway insertion

IntroductionSupraglottic airway devices have become extremely popular for minor therapeutic and surgical procedures. Their insertion requires an adequate depth of anesthesia with suppression of pharyngeal reflexes. Propofol is the most commonly used agent, but has hemodynamic side-effects. Etomidate, although hemodynamically stable, does not suppress pharyngeal reflexes adequately. Moreover, the use of clinical signs to assess the depth of anesthesia has questionable accuracy. Using bispectral index (BIS) monitoring, the hypnotic component of the anesthetic can be measured, with values of 40–60 implying adequate depth of anesthesia. MethodsThis randomized controlled trial included 80 ASA I patients, divided into two groups of 40 patients. Each group received either propofol or etomidate infusion, with BIS monitoring. At BIS 50, infusions were stopped and SGA was inserted. Changes in hemodynamic parameters, time for SGA insertion, number of attempts, and SGA insertion scores were recorded. ResultsWhen BIS reached 50, a statistically significant fall in mean arterial pressure was observed in the propofol group. Time for SGA insertion was less in the propofol group (30.7 ± 8.0 s), with successful SGA insertion observed in 92.5% of patients on the first attempt, compared with 47.9 ± 9.1 s and 32.3% in the etomidate group. ConclusionIn comparison with etomidate, the use of propofol is associated with better conditions for SGA insertion but has the side-effect of hypotension, even with BIS-guided titration of dose for maintaining an adequate depth of anesthesia.

Chemerin is resident to vascular tunicas and contributes to vascular tone.

The adipokine chemerin may support blood pressure, evidenced by a fall in mean arterial pressure after whole body antisense oligonucleotide (ASO)-mediated knockdown of chemerin protein in rat models of normal and elevated blood pressure. Although the liver is the greatest contributor of circulating chemerin, liver-specific ASOs that abolished hepatic-derived chemerin did not change blood pressure. Thus, other sites must produce the chemerin that supports blood pressure. We hypothesize that the vasculature is a source of chemerin independent of the liver that supports arterial tone. RNAScope, PCR, Western blot analyses, ASOs, isometric contractility, and radiotelemetry were used in the Dahl salt-sensitive (SS) rat (male and female) on a normal diet. Retinoic acid receptor responder 2 (Rarres2) mRNA was detected in the smooth muscle, adventitia, and perivascular adipose tissue of the thoracic aorta. Chemerin protein was detected immunohistochemically in the endothelium, smooth muscle cells, adventitia, and perivascular adipose tissue. Chemerin colocalized with the vascular smooth muscle marker α-actin and the adipocyte marker perilipin. Importantly, chemerin protein in the thoracic aorta was not reduced when liver-derived chemerin was abolished by a liver-specific ASO against chemerin. Chemerin protein was similarly absent in arteries from a newly created global chemerin knockout in Dahl SS rats. Inhibition of the receptor Chemerin1 by the receptor antagonist CCX832 resulted in the loss of vascular tone that supports potential contributions of chemerin by both perivascular adipose tissue and the media. These data suggest that vessel-derived chemerin may support vascular tone locally through constitutive activation of Chemerin1. This posits chemerin as a potential therapeutic target in blood pressure regulation.NEW & NOTEWORTHY Vascular tunicas synthesizing chemerin is a new finding. Vascular chemerin is independent of hepatic-derived chemerin. Vasculature from both males and females have resident chemerin. Chemerin1 receptor activity supports vascular tone.

Comparative study of I.V. magnesium sulphate and lignocaine for attenuating the haemodynamic stress during laryngoscopy and intubation

Background: Following induction of general anesthesia, laryngoscopy and endotracheal intubation produce pressor response that are somatic visceral reflexes brought on by stimulation of epipharynx and laryngopharynx. To avoid hemodynamic responses to intubation, several strategies have been tested. Agents like opioids, local anesthetics have been used to attenuate such response. Our study was employed with intravenous magnesium sulphate and lignocaine. Methods: A total of 60 patients of both sexes in the age group between 15-50years, belonging to ASA grade I and II undergoing elective surgery under general anaesthesia. Out of the 60 patients 30 were randomly included in the L group (lignocaine group) and the other 30 were included in the M group (magnesium sulphate group). Results: There was fall in heart rate (p &lt; 0.05) noted following induction, laryngoscopy, and intubation, in Magnesium group and Lignocaine group, but the fall in heart rate was more significant in the Magnesium group when compared with the Lignocaine group Like heart rate there was a significant fall in mean arterial pressure in both the groups, but there was statistically significant fall (p &lt; 0.05) in the Magnesium group when compared with the Lignocaine group.

Antihypertensive Potential of Tartaric Acid and Exploration of Underlying Mechanistic Pathways.

Tartaric acid is capable of balancing blood pressure. It is the main constituent of antihypertensive agents (grapes and wine) and has not been scientifically explored as an antihypertensive remedy. This study aimed to investigate the antihypertensive effect of a low-dose tartaric acid in vivo and explore underlying mechanisms in vitro. Intravenous administration of tartaric acid at the dose of 50 µg/kg caused a % fall in mean arterial pressure (MAP) in normotensive and hypertensive rats [51.5 ± 1.7 and 63.5 ± 2.9% mmHg]. This hypotensive effect was partially inhibited by atropine (1 mg/kg) and L-NAME (100 µg/kg) pretreatment. In hypertensive rats, oral administration of tartaric acid (.1, .5, 1, 5, and 10 mg/kg) for 2 weeks resulted in 65 ± 7.3 mmHg MAP at 10 mg/kg. This antihypertensive effect was comparable to the orally administered verapamil (10 mg/kg) for 2 weeks which caused a decrease in MAP 60.4 ± 3.8 mmHg. Tartaric acid relaxed phenylephrine (PE) and High K+-induced contractions with EC50 values of .157 (.043-.2) and 1.93 (.07-2) µg/mL in vitro. This endothelium-dependent relaxation was inhibited with atropine (1 µM) and L-NAME (10 µM) pretreatment. Tartaric acid also suppressed phenylephrine contractions in Ca+2 free/EGTA medium and on voltage-dependent calcium channels, causing the concentration–response curves toward right. Tartaric acid induced negative inotropic and chronotropic effects with EC50 values of .26 (.14-.4) and .60 (.2-.8) in rat atria. It showed its effect by complete blockade against atropine and partially in propranolol pretreatment. These findings provide scientific basis to low-dose tartaric acid as an antihypertensive and vasodilatory remedy through muscarinic receptor-linked nitric oxide (NO) pathway and Ca+2 channel antagonist.

Abstract 115: Soluble (pro)renin Receptor Contributes To Endotoxin-induced Septic Shock And Aki In Mice

Sepsis associated acute kidney injury (S-AKI) is a life-threating disease with poorly defined mechanisms and limited therapeutic options. Here we examined the role of site-1 protease (S1P)-derived soluble PRR (sPRR) in the S-AKI model induced by lipopolysaccharide (LPS). Male 10-week-old B6129SF1/J mice were pretreated with a S1P inhibitor PF-429242 (PF) at 20 mg/kg/day via minipump and treated with a single s.c. injection of LPS at 10 mg/kg and monitored for 24 hours. By radiotelemetry, LPS induced fall in mean arterial pressure (MAP) (Δ mmHg: -14.98 ± 4.13 in LPS+PF group vs . -23.15 ± 1.82 in LPS+ Vehicle group; n = 6, p &lt; 0.05) and heart rate (HR) (Beats/min: -78.60 ± 20.73 in LPS+PF group vs . -133.35 ± 30.92 in LPS group, n = 6, p &lt; 0.05), which was significantly attenuated by PF treatment. In parallel, renal dysfunction as reflected by the rises in plasma creatinine and BUN along with albuminuria, urinary excretion of NGAL and Kim-1 were all improved. Similar improvement was observed for infiltration of macrophage as assessed by immunofluorescence detection of F4/80 as well as renal mRNA expression of M1 markers such as iNOS, IL-1β, IL-6, and TNFα. The results from the pharmacological study were validated using a recently generated mouse model of mutagenesis of the cleavage site of PRR (termed Mutant mice). LPS-induced hypotensive response, renal dysfunction, the markers of renal injury and inflammation and M1 activation were all improved in Mutant mice as seen with PF treatment. LPS induced a 3.35-fold increase in plasma sPRR which was attenuated by PF or in Mutant mice. By immunofluorescence, LPS-induced PRR expression was largely restricted to renal medullary intercalated dells. In cultured RAW264.7 macrophage cells, recombinant sPRR treatment at 30 nM directly promoted macrophage migration and stimulated mRNA levels of M1 markers, all of which were attenuated by losartan. Taken together, the present study suggests that (1) S1P-derived sPRR contributes to LPS-induced septic shock and AKI, and (2) within the kidney, LPS-induced sPRR originates from intercalated cells and may act in a paracrine manner to activate AT1R on macrophages to induce pro-inflammatory response.

Abstract 124: Angiotensin-(1-12) Immunoneutralization: A New Approach To Hypertension Treatment

There is a critical need to identify new therapeutic targets and treatments, given emerging data documenting the limited effectiveness of current antihypertensive drugs to have a marked impact in preventing target organ damage and cardiovascular death. While monoclonal antibodies (mAb) are revolutionizing the treatment of human diseases, including severe hypercholesterolemia, their applicability to long-term hypertension control remains unexplored. Identification of angiotensin-(1-12) [Ang-(1–12)] as a non-renin-dependent substrate for Ang II generation in rodents and humans led us to engineer a mAb directed against the C-terminus of human Ang-(1–12) [h-Ang-(1-12)] sequence. We utilized a model of hypertension expressing the human angiotensinogen (AGT) gene in the rat genome [TGR(hAGT)L1623 rats] to address the effectiveness of endogenous h-Ang-(1–12) immunoneutralization in controlling the elevated blood pressure and reversing hypertension-induced target organ damage. Acute delivery of the h-Ang-(1–12) mAb (30 mg/Kg, i.v.) in anesthetized hypertensive transgenic rats induced a prompt arterial pressure fall (M ± SE: -18 ± 6/-16 ± 3 mm Hg, n=7; p&lt; 0.001) in the absence of corresponding heart rate changes. The antihypertensive effect of the h-Ang-(1-12) mAb triggered a rise in plasma renin concentrations (from 107 ± 24 to 381 ± 260 ng/mL/h) that was inversely correlated with the fall in mean arterial pressure (r= -0.92, p&lt; 0.001). Prior intravenous delivery of aliskiren fumarate (3-5 mg/Kg, i.v.) while inducing a fall in arterial pressure did not mask the antihypertensive action of the h-Ang-(1-12) mAb. Extension of these acute effects of the h-Ang-(1-12) mAb to awake instrumented transgenic hypertensive rats given consecutive daily doses of the mAb (30 mg/Kg, i.m. x 4 -5 days, n=7) documented a trend for significant statistical drops in daytime blood pressure and no changes in heart rate. We conclude that Ang-(1–12) is an endogenous Ang II forming substrate participating in the control of arterial pressure in a humanized model of high blood pressure and that selective immunoneutralization of this alternate substrate is a promising and novel therapeutic approach to treat hypertension and prevent its adverse cardiovascular sequelae.

Effect of supraglottic airway devices versus endotracheal intubation general anesthesia on outcomes in patients undergoing mechanical thrombectomy: A prospective randomized clinical trial.

Background:There are still controversies about the optimal anesthesia protocol for patients with acute ischemic stroke (AIS) undergoing mechanical thrombectomy (MT). The aim of this study was to explore the effect of supraglottic airway device (SAD) versus endotracheal intubation (EI) general anesthesia on clinical and angiographic outcomes in patients with AIS undergoing MT.Methods:One hundred sixteen patients with large-vessel occlusion stroke were randomized to receive either SAD or EI general anesthesia. The primary outcome was the rate of occurrence of >20% fall in mean arterial pressure (MAP). Secondary outcomes included hemodynamics, successful recanalization, time metrics, satisfaction score of neurointerventionalist, number of passes performed, the conversion rate from SAD to EI, the National Institutes of Health Stroke Scale score, and Alberta Stroke Program Early CT Score before and 24 hours after surgery, length of stay in the stroke unit and hospital, complications and functional independence at discharge, and 90 days after stroke.Results:Both the lowest systolic blood pressure and lowest diastolic blood pressure were significantly lower in the EI group (P = .001). The consumption of vasoactive agents, the occurrence of >20% reduction in MAP and time spent with >20% fall in MAP were significantly higher in the EI group (P < .05). Compared with the EI group, the time for door-to-puncture was significantly shorter in the SAD group (P = .015). There were no significant differences with respect to puncture-to-reperfusion time, number of passes performed, rates of successful recanalization, National Institutes of Health Stroke Scale score, and Alberta Stroke Program Early CT Score 24 hours after surgery. The satisfaction score of neurointerventionalist was significantly lower in the EI group (P = .043). Conversion rate from SAD to EI was 7.41%. There were no significant differences with respect to complications, mortality, and mean Modified Rankin Scale scores both at discharge and 90-day after stroke. However, length of stroke unit and hospital stays were significantly shorter in the SAD group (P < .05).Conclusion:AIS patients undergoing MT with SAD general anesthesia led to more stable hemodynamics, higher satisfaction score of neurointerventionalist, shorter door-to-puncture time, length of stroke unit, and hospital stay. However, there were no significant differences between the 2 groups on the angiographic and functional outcomes both at discharge and 90 days after stroke.

Baroreflex Activation Contributes to the Progression of the Systemic Inflammatory Response in Unanesthetized Rats

Our laboratory showed that electrical activation of the baroreflex could modulate the immune system by controlling the inflammatory response in rats. However, no study has investigated whether physiological reflex activation of the baroreflex also has an anti‐inflammatory effect. Therefore, the objective of the present study was to investigate the effect of physiological activation of the baroreflex in unanesthetized rats, through abdominal aortic coarctation (AAC), on the systemic inflammatory response elicited by lipopolysaccharide (LPS) administration. Sprague‐Dawley male rats (250‐300g) were anesthetized for placing, surgically, a cuff around the abdominal aorta and catheters into the carotid artery and femoral vein. On the next day, the hemodynamic parameters were recorded in the unanesthetized animals. Subsequently, the AAC was carried out for 2 min, followed by the administration of LPS (1.5 mg/kg, i.v.) or saline in the control subjects. After 90 min, blood and spleen samples were collected for subsequent cytokine analysis. As expected, compared to baseline, AAC increased systolic (122 ± 5 vs. 173 ± 10 mmHg), diastolic (90 ± 3 vs. 105 ± 4 mmHg), and mean arterial pressure (106 ± 4 vs. 131 ± 6 mmHg), and reduced heart rate (365 ± 25 vs. 306 ± 17 bpm), confirming the reflex activation of the baroreflex. However, the administration of LPS promoted an increase in heart rate (361 ± 11 vs. 428 ± 21 bpm) over time. Of note, the AAC group associated with LPS administration exhibited, 90 min after LPS administration, a fall in mean arterial pressure (98 ± 7 vs. 88 ± 7 mmHg), combined with an increase in heart rate (362 ± 15 vs. 470 ± 16 bpm). Moreover, compared to the group which received only LPS, the AAC associated with LPS increased the levels of cytokines (IL‐6 and IL‐10) in plasma (IL‐6: 4505 ± 1294 vs. 8782 ± 520 pg/mL; IL‐10: 5 ± 5 vs. 1079 ± 232 pg/mL) and spleen (IL‐6: 3 ± 1 vs. 20 ± 3 pg/mg of tissue; IL‐10: 0.1 ± 0.04 vs. 2 ± 0.4 pg/mg of tissue); potentiating, therefore, the release of cytokines after the induction of the inflammatory process. In conclusion, physiological baroreflex activation elicits a modulatory effect of the immune response during the systemic inflammation elicited by LPS, facilitating the inflammatory process and potentiating the hemodynamic responses promoted by the administration of LPS. Thus, this study showed for the first time that physiological baroreflex activation, through AAC, plays a role in the progression of the inflammatory process.

A COMPARATIVE STUDY ON THE TOTAL DOSE REQUIREMENTS AND HEMODYNAMIC ALTERATIONS WITH AND WITHOUT THE APPLICATION OF PRIMING PRINCIPLE AMONG PATIENTS INDUCED WITH PROPOFOL

Background:- Propofol given at standard induction dose, is known to produce haemodynamic instability, especially hypotension. Application of “priming principle” helps to reduce the total dose of propofol. Objectives:- To study the total dose requirements of propofol and peri-intubation haemodynamic stability in patients undergoing surgery under GACV when priming principle is applied. Methodology:- This was an observational study among 54 ASA I and II patients undergoing surgery under GACV, who were randomly divided into three groups of 18 patients each. All patients received fentanyl 1 mcg/kg over 30 seconds followed by propofol. Group 1 patients received the total (100%) calculated dose of propofol. Group 2 and 3 patients received 20% and 40% of the dose respectively as priming dose, and the remaining was given 30 seconds later, until there was loss of eyelash reex. The total dose of propofol given, the heart rate, systolic and diastolic blood pressures, mean arterial pressures at various time intervals before, during and after induction and intubation, and complications observed were compared and statistically analysed using SPSS 2.0. Results:- The mean induction dose of propofol was signicantly lower in the priming groups (71.7 ± 17.2mg in group 2 and 80.0 ± 17.1mg in group 3) compared to group1 (107.9 ± 8.0mg). The fall in mean arterial pressure was signicantly lower in groups 2 and 3 (p&lt;0.05) compared to group1 at one minute post-induction. Conclusion:-Application of priming principle reduces the induction dose of propofol and is associated with better peri-intubation haemodynamic stability.

Intravascular Administration of Isotonic Saline versus Polymerised Gelatin in the Prevention of Spinal Induced Hypotension: A Randomised Clinical Trial

Introduction: Hypotension remains one of the most common problems associated with subarachnoid blockade. A number of strategies have been developed for its prevention, of which administration of fluids prior to subarachnoid block holds the importance. Gelatin is a colloidal plasma volume expander obtained from degraded gelatine. It is as effective as albumin solution in the treatment of spinal induced hypotension. Aim: To compare the incidence and frequency of hypotension after subarachnoid block in patients receiving colloid (polymerised gelatin) or crystalloid (0.9% normal saline) as prehydration and compare side-effects of colloid and crystalloid prehydration. Materials and Methods: A total of 60 patients scheduled for elective Transurethral Resection of Prostate (TURP) surgery were selected to participate in this prospective randomised double-blind study for a period of two years from April 2006 to April 2008. Patients were randomly allocated into two groups of 30 patients each. Group H received 500 mL of polymerised gelatine (Haemaccel) solution and group N received 1000 mL of 0.9% normal saline15 minutes prior to subarachnoid block. Intraoperative monitoring includes SBP, DBP, MAP and HR for 30 minutes. Incidence of hypotension and number of mephentermine boluses were noted.Statistical analysis of data was determined with Mann-Whitney U test and analysis of variance for repeated measures (ANOVA). Chi-square test was used to find out possible associations. Result: After spinal anaesthesia mean systolic blood pressure decreased in both the groups and was lower in group N compared to group H (97±18.9 vs 102±9.26 mmHg). There was fall in diastolic blood pressure in both the groups and was maximum at 20th minute in group N and group H (66.37±5.47 vs 64.67±10.30). There was highly significant (p&lt;0.01) fall in mean arterial pressure in group N. The change in the heart rate was highly significant (p&lt;0.01) at different time interval in both the groups. Vasopressor was required in 90% and 60% patients in group N and group H, respectively. No statistical difference in the incidence of nausea and vomiting in both the groups. Conclusion: The present study showed that preloading of fluids either with colloids or crystalloids prior to subarachnoid block reduces the incidence of hypotension but not completely eliminating it, also showed that colloids offset hypovolemia and hypotension more effectively than crystalloids in patients undergoing TURP surgery.

Discharge readiness after minor gynaecological surgeries comparing dexmedetomidine and ketamine premedication in bispectral index (BIS) guided propofol-based anaesthesia

Background and Aims:Dexmedetomidine and ketamine are commonly used pre-medicants to propofol. Previous literature shows a delay in recovery with their use without any clarity on discharge. This study was planned to find out whether adding these premedicants to Bispectral index (BIS) guided propofol anaesthesia led to delayed discharge in minor gynaecological surgeries.Methods:Totally, 120 adult females belonging to American Society of Anesthesiologists (ASA) physical status I and II undergoing minor gynaecological surgeries under general anaesthesia were randomly allocated to receive 1 μg/kg dexmedetomidine (Group D), 0.5 mg/kg ketamine (Group K) and normal saline (Group P) as premedication. Propofol 1% was used for induction and maintenance of anaesthesia keeping BIS between 55 and 70. After the procedure, patients were assessed primarily for discharge readiness using Modified Post Anaesthesia Discharge Scoring System (MPADSS).The secondary outcomes were Modified Aldrete Score (MAS), total dose of propofol used and haemodynamics.Results:The percentage of patients ready for discharge were 22.5%, 30% and 15%at 1 hour in group D, K and P, respectively (p = 0.275). Median MAS was 5, 4 and 6 respectively for group D, K and P immediately post-surgery (p = 0.000). The mean dose of propofol used was 69.75 ± 12.56 mg in group D and 135.25 ± 9.2 mg in group P (p = 0.001). There were significant haemodynamic variations in group D (16.4% fall in heart rate at 5 minutes and 24.18% fall in mean arterial pressure at 15 minutes).Conclusion:Premedication with dexmedetomidine and ketamine in propofol anaesthesia does not delay discharge. However, stable haemodynamics and good analgesia with ketamine make it a better option.

Evaluation of safety and efficacy with propofol and etomidate for induction of Anaesthesia in dilatation and curettage

Introduction and Aims: We compared the safety, efficacy, hemodynamic variation, recovery duration and adverse effects of propofol and etomidate, with or without fentanyl, in patients undergoing dilatation and curettage for incomplete abortions. Materials and Methods: One hundred patients, ASA status I & II, aged 20-50 years, undergoing dilatation and curettage, were randomly divided into four groups of 25 patients each. Group P received propofol 2 mg/kg + normal saline 2 ml for anesthesia induction. Group PF received propofol 2 mg/kg +fentanyl 1mcg/kg to make volume 2 ml for anesthesia induction. Group E received etomidate 0.2 mg/kg + normal saline 2 ml for anesthesia induction and Group EF received etomidate 0.2 mg/kg + fentanyl 1 mcg/kg to make volume 2 ml for anesthesia induction. Heart rate, arterial pressure and SpO2 were recorded at different time intervals. The recovery time, pain on injection, myoclonus and postoperative nausea vomiting were also recorded. Results: During induction, mean arterial pressure fall significantly in both propofol groups. Amongst four groups, there was no significant difference observed in recovery time after anesthesia. The incidence of pain on injection was lower in etomidate groups. Myoclonus and Postoperative nausea and vomiting were significantly higher in etomidate groups. Conclusion: This study demonstrates that etomidate is superior in term of hemodynamic stability and less incidence of pain on injection. Etomidate combined with low dose fentanyl is more favourable than etomidate alone for attenuating myoclonus. Keywords: Etomidate, Dilatation and curettage, Propofol.

The value of hypotensive prediction index and dP/dtmax to predict and treat hypotension in a patient with a dilated cardiomyopathy

The Hypotension Prediction Index (HPi) is a new parameter, recently developed to predict the risk of a patient developing a hypotensive event, defined as a fall in mean arterial pressure below 65 mmHg. The calculated HPi value is displayed on a monitor as a number ranging from 1 to 100; where the first warning for the appearance of such event occurs when HPi values exceed 85. A secondary screen shows the stroke volume variation value; the dP/dt max; and the dynamic arterial elastance. We described a patient with a mild to moderately dilated cardiomyopathy that presented several episodes of hypotension after induction of anaesthesia and how by using HPi technology, these were successfully solved. We recommend the use of a HPi value >85 as a warning of intervention, and to use the secondary screen to determine the cause and the treatment. We consider that HPi technology may be a valid alternative for the anaesthetic management of patients with a dilated cardiomyopathy. El Índice de Predicción de la Hipotensión (iPH) es un nuevo parámetro diseñado para predecir el riesgo de aparición de un evento hipotensor, definido como una caída de la presión arterial media por debajo de 65 mmHg. El valor numérico del iPH se muestra en un monitor como un digito que va de 1 a 100, donde la primera alarma de aparición de la hipotensión ocurre cuando dicho valor excede de 85. Una pantalla secundaria muestra el volumen de variación sistólica; el dP/dtmax ; y la elastancia dinámica arterial. Describimos un caso de un paciente con una miocardiopatía dilatada moderada que presento varios episodios de hipotensión tras la inducción anestésica, y cómo usando la tecnología iPH éstos fueron resueltos. Recomendamos usar el valor de iPH > 85 como alarma de intervención, y utilizar la pantalla secundaria para determinar su causa y adecuar su tratamiento. Creemos que la tecnología iHP puede ser una alternativa válida en el manejo anestésico de los pacientes con una miocardiopatía dilatada.

Nitrate induced vasoplegia depletes cardiac energy reserves: a model for acute cardiomyopathy in septic shock?

Abstract Introduction The healthy heart is at its most efficient when contractile filaments are stretched with preload. To produce the same cardiac output, oxygen requirement rises are proportionally greater with increased inotropy or heart rate than with increased preload. We hypothesized that in vasoplegia, loss of preload (owing to dilation of capacitance veins) and compensatory rises in heart rate and contractility would compromise the efficiency of the heart. We speculated that this may be one factor impairing cardiac function in conditions of distributive shock such as sepsis and looked to model the effects. We used cardiac magnetic resonance imaging to capture changes in cardiac volumes and contractility and magnetic resonance spectroscopy to investigate changes in ATP metabolism within the myocardium in healthy volunteers given GTN as a vasodilator. Methods We recruited 7 healthy volunteers (mean age 40 years, range 28–62 years; mean BMI 21.9, range 18.5–24.5) and measured their baseline cardiac volumes and function, PCr/ATP ratio and Creatine Kinase first order rate constant (CKkf), using cardiac magnetic resonance imaging and magnetic resonance spectroscopy and saturation transfer at 3 Tesla. At the same visit, they received a glyceryl trinitrate (GTN) infusion to induce vasoplegia and the measurements were repeated. We targeted GTN infusion rate to a fall in mean arterial pressure of 15mmHg. Results The GTN infusion brought about a fall in mean arterial pressure (from a baseline of 79±7mmHg to 64±7 mmHg, p&amp;lt;0.0001) and a fall in LV end diastolic volume (169±57 ml vs 148±58 ml, p=0.003) indicating a reduction in preload. As expected, there was a compensatory rise in heart rate (61±7 bpm vs 69±10bpm, p=0.0005) and ejection fraction (62±3% vs 67±3%, p=0.001), however cardiac output remained unchanged (6.72±1.49 L/min vs 6.68±1.48 L/min, p=0.87). Cardiac work (calculated as stroke volume x MAP x heart rate) fell (477±123 vs 424±119 L.mmHg/min, p=0.03). There was a fall in PCr/ATP ratio on GTN (2.18±0.25 vs 1.91±0.2, p 0.03) while CKkf more than doubled (0.14±0.06 s-1 vs 0.23±0.08 s-1, p=0.02) and creatine kinase flux also showed a significant increase (1.65±0.78 μmol/g/s vs 2.28±0.71 μmol/g/s, p=0.05). Conclusions What is novel here is that we show a fall in PCr/ATP ratio: as ATP concentrations in the cell are strictly maintained, this suggests phosphocreatine pool depletion occurs when preload is lost and cardiac output is maintained by an increase in inotropy and chronotropy. The rise in CKkf and CK flux confirm the increased energy demand. Progressive energetic depletion during high demand may give rise to contractile dysfunction over time as the heart is unable to keep up with increased requirements for ATP, and progressively becomes more starved of energy. This could be a mechanism of cardiac dysfunction in septic shock and other vasoplegic states. Figure 1 Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation