Aim: To compare the safety and efficacy of dexmedetomidine and haloperidol in patients with delirium and acute respiratory failure in non-invasive mask lung ventilation. Materials and methods. We carried out a retrospective analysis of data on patients with somatogenic delirium and acute respiratory failure (57 men, 4 women) experienced noninvasive ventilation (NIV) in the intensive care unit of the Botkin State Clinical Hospital in 2017–2018. Depending on the type of sedation the patients were divided into two groups: those on dexmedetomidine ( n =31) and those receiving haloperidol ( n =30). Dexmedetomidine was administered as a continuous infusion at a rate of 0.2–1.4 µg/kg/h while controlling the level of consciousness; haloperidol was administered by intravenous bolus injections until a sufficient level of sedation was reached in a dose of 2.5 mg 2–3 times a day. Results. The efficiency of sedation to achieve the required level of cooperation and possibility of NIV was 87.1% (27 patients) and 66.6% (20 patients) in dexmedetomidine and haloperidol groups. When estimating sedation in patients of both groups according to the RASS scale the scores did not differ significantly and were equal on the average to 1.7±0.3 (eye contact to voice). In haloperidol group in 10 out of 30 (33.3%) patients a sufficient level of sedation was not achieved, which required immediate tracheal intubation and invasive lung ventilation. Mortality in this group was 20% (6 patients), while in dexmedetomidine group it was 6.4% (2 patients). Conclusion. The use of dexmedetomidine, despite greater variability of hemodynamic parameters, allows to perform NIV with sufficient cooperation with the patient, reduces the frequency of tracheal intubation, risk of complications and mortality.

Aim: To compare the safety and efficacy of dexmedetomidine and haloperidol in patients with delirium and acute respiratory failure in non-invasive mask lung ventilation.Materials and methods. We carried out a retrospective analysis of data on patients with somatogenic delirium and acute respiratory failure (57 men, 4 women) experienced noninvasive ventilation (NIV) in the intensive care unit of the Botkin State Clinical Hospital in 2017–2018. Depending on the type of sedation the patients were divided into two groups: those on dexmedetomidine (n=31) and those receiving haloperidol (n=30). Dexmedetomidine was administered as a continuous infusion at a rate of 0.2–1.4 µg/kg/h while controlling the level of consciousness; haloperidol was administered by intravenous bolus injections until a sufficient level of sedation was reached in a dose of 2.5 mg 2–3 times a day.Results. The efficiency of sedation to achieve the required level of cooperation and possibility of NIV was 87.1% (27 patients) and 66.6% (20 patients) in dexmedetomidine and haloperidol groups. When estimating sedation in patients of both groups according to the RASS scale the scores did not differ significantly and were equal on the average to 1.7±0.3 (eye contact to voice). In haloperidol group in 10 out of 30 (33.3%) patients a sufficient level of sedation was not achieved, which required immediate tracheal intubation and invasive lung ventilation. Mortality in this group was 20% (6 patients), while in dexmedetomidine group it was 6.4% (2 patients).Conclusion. The use of dexmedetomidine, despite greater variability of hemodynamic parameters, allows to perform NIV with sufficient cooperation with the patient, reduces the frequency of tracheal intubation, risk of complications and mortality.

The researcher's opinions about myocardial and brain anesthetic preconditioning efficiency are yet contradictive. In addition, the anesthetic neuroprotection phenomenon is poorly investigated. In this study the authors attempted to evaluate the efficiency of myocardial and central nervous system (CNS) protection by using a modified method of volatile induction and maintenance of anesthesia (VIMA) based on pulse-like sevoflurane dosing that excludes propofol usage. Ninety CABG patients aged 45-75 years were included in the study group (VIMA) and underwent volatile induction with sevoflurane and anesthetic preconditioning (2 MAC) for 10 min before aortic cross-clamping, with ataralgesia used during CPB. The control group patients (TIVA) received propofol and fentanyl, no inhalation anesthetics were applied. Preoperative concentrations of NTpro-BNP were comparable. There was no significant rise of NTpro-BNP concentration in the VIMA group during the postoperative period. In the TIVA group NTpro-BNP concentrations were 3.8 and 4.8 times as much as the baseline values at 24 and 48 postoperative hours respectively (р<0.05). 17 patients in the VIMA group needed dopamine infusion during 24 postoperative hours, this number was 1.7 times less than that in the TIVA group (23 patients) (р<0.05). VIMA patients had 2-fold lower troponin T concentration in 24 hours after surgery (р<0.01). Significant differences in protein S100B concentrations were observed only during the postoperative period. No significant differences in cognitive functions of the patients from both groups were identified before surgery. On postoperative day 2 MMSE scale count was significantly lower in TIVA patients (20.843.73) in comparison with VI-MA patients (23.364.34) (р<0.05). Thus, the modified VIMA technique with sevoflurane has a greater neuroprotective potential during CABG with CPB and provides better preservation of myocardium structural integrity and cardiac performance than fentanyl/4propofol-based TIVA would do.

Objective: to provide a rationale for the efficiency of sevoflurane-induced cardiac preconditioning (CPC), by assessing the pattern of recovery of heart rate and by estimating troponin I levels and changes in NT-proBNP concentrations in patients undergoing aortocoronary bypass surgery (ACBS) under extracorporeal circulation (EC). Subjects and methods. Sixty patients aged 60.6±8 years (M±&) were examined after elective ACBS using EC and divided into two groups of 30 patients each: 1) inhalation induction and maintenance of anesthesia (IIMA) with sevoflurane and fentanyl, with CPC being simulated; 2) total intravenous anesthesia (TIA) with propofol and fentanyl. Inhalation induction of sevoflurane anesthesia was performed in the IIMA group. Ten minutes before aortic ligation, the dose of the anesthetic was increased up to 2 MAC for CPC. Inhaled anesthetics were not used in the TIA group. The authors assessed the pattern of cardiac performance recovery and estimated the level of NT-proBNP 24 and 48 hours after tracheal intubation and that of troponin I following 24 hours of the intubation. Results. Defibrillation was required in one patient from the TIA group who developed ventricular fibrillation. The baseline levels of NT-proBNP were comparable in both groups. Following 24 hours, its level was more than thrice higher in the TIA group than that in the IIMA one (p<0.05). By the end of 2 days, the concentration of NT-proBNP continued to rise (up to 480% of the baseline level) in the TIA group and returned to the preoperative values in the IIMA group (p=0.05). Twenty-four hours after tracheal intubation the level of troponin I was insignificantly higher in the TIA group than that in the IIMA group (p=0.1). Conclusion. Sevoflurane has cardioprotective properties in preventing and/or reducing the degree of heart failure after ACBS using EC. There is a need to continue the study in increased cohort to provide evidence that sevoflurane-induced CPC can lower cardiomyocyte damage due to ischemia/perfusion. Key words: anesthetic preconditioning, sevoflurane, NT-proBNP, troponin I, heart failure.

The article describes current scientific views on the predictors of neurological complications caused by coronary artery bypass grafting (CABG) surgery. The authors present the results of the study clarifying the most important predictors of stroke and postoperative delirium. The predictive value of preoperative data of neuropsychological testing in the identification of risk factors for postoperative long-term cognitive decline in patients undergoing CABG has been shown.

Objective: to study the effect of sevoflurane on functional recovery in animals after clinical death. Materials and methods. Experiments were carried out on male albino rats. The cardiac vascular fascicle was ligated to simulate temporary circulatory arrest. Its time was 10 minutes. Clinical death was modeled in the animals anesthetized with sevoflurane or chloral hydrate. The functional state of resuscitated animals was evaluated from the time of recovery of effective cardiac performance, spontaneous breathing, corneal reflex, and neurological deficit scores. Their elevated plus-maze behavior was examined. Results. The rats anesthetized with chloral hydrate, unlike those anesthetized with sevoflurane, showed an earlier recovery of spontaneous external breathing and corneal reflex and, in succeeding 2 days following resuscitation, less neurological deficit scores. In addition to a prompter recovery of central nervous system functions on postresuscitation day 4, the sevoflurane-anesthetized rats had a greater gain in body weight for its value on the day of clinical death modeling than the chloral hydrate-anesthetized rats. A study of their behavioral activity showed that the resuscitated rats of both groups differed from false-operated ones in a trend towards reduced number of executions, which is indicative of the higher level of rat phobic state in the postresuscitation period. No differences were observed between the groups of the resuscitated animals in all the indicators examined. Conclusion. Ten-minute clinical death modeling in sevoflurane-anesthetized rats accelerates neurological recovery and improves their general state as compared to chloral hydrate-anesthetized rats. At the same time, both anesthesia modes stop the development of the higher level of phobic state seen in the rats in the postresuscitation period. The findings do not preclude the involvement of the preconditioning properties of sevoflurane in the postresuscitation processes of brain functional recovery. Key words: circulatory arrest, sevoflurane.

This paper is the second part of an overview dealing with experimental and clinical studies in ischemic and pharmacological preconditioning. It considers the possibilities of practically using the available knowledge on the mechanisms of preconditioning, the interaction of agents from different groups in exhibiting the protective effects of inhaled anesthetics in anesthesiology and resuscitation. Data are given on the efficacy of the discussed processes in different organs and tissues. The possibility of using opioids and other biologically active substances that are likely to have a protective effect against hypoxia is discussed separately. The problems of remote preconditioning and post-conditioning are touched upon. The available data on the impact of choosing an anesthetic mode on the course of immediate and long-term postoperative periods and mortality rates are analyzed; the problem of the old heart is discussed. It is concluded that studies dealing with the problems of pre- and postconditioning are urgent and of great scientific and practical value. Key words: ischemic preconditioning, pharmacological preconditioning, anesthetic preconditioning, postconditioning.

Objective: to investigate the activity of sevoflurane, dalargin, and lithium chloride in protecting the rat brain from total ischemia/reperfusion and to define whether the GSK=3^ deposphorylation contributes to the mechanism of pharmacological preconditioning. Materials and methods. Experiments were carried out on 80 male albino rats in which temporary circulatory arrest (CA) was simulated by ligating the cardiovascular fascicle for 10 and 20 minutes. The animals were revived by mechanical ventilation external cardiac massage, and the intratracheal injection of adrenaline (epinephrine, Moscow Endocrinology Plant) at a dose of 0.1 mg/kg. Animals were divided into 9 groups and sevorane (sevoflurane, Abbott Laboratories), dalargin (Microgen Research-and-Production Association), or lithium chloride (Sigma Chemical Co.) were separately given with and without CA. Brain tissue homogenate specimens were obtained from euthanized animals. The concentration of total glycogen synthase kinase-3^ (GSK-3^) was colorimetrically determined using a Hitachi-557 spectrophotometer (Hitachi Ltd., Japan). The content of phosphorylated GSK-3/3 (pGSK-3^) in brain homogenate was estimated by Western blotting. Results. The total level of GSK-3^ in each group was similar (80—90 relative units) and remained unchanged throughout each experiment. Twenty-minute ischemia maximally activated GSK-30 through dephosphorylation. Ten-minute ischemia elevated pGSK-3^ levels by more than 5 times as compared to the baseline value revealing the «training» effect. The quantity of pGSK-3^ was unchanged in the ischemia/perfusion group during sevoflurane insufflation and was decreased by 27% during dalargin administration. Conclusion. The experimental model of total ischemia provided evidence that the test drugs had a pharmacological preconditioning effect on brain neurons. According to their increasing effect, the drugs were arranged in the following order: dalargin < sevoflurane < lithium chloride. The data warranties further studies to reveal the clinical significance of dalargin, sevofluran and lithium for preconditioning to protect the brain. Key words: lithium, dalargin, sevofluran, preconditioning, brain.

The paper describes a rare case of successful surgical treatment for mitral insufficiency due to heart valvular apparatus damage in the acute period of severe concomitant injury. Prosthetic mitral valve replacement was done on day 3 after injury. The patient was switched to spontaneous breathing on day 7 postoperatively and transferred to a surgical unit on day 11. Timely diagnosis, a comprehensive therapeutic approach, active surgical policy, the availability of up-to-date medical equipment, and the presence of high-quality physicians allowed severe cardiopulmonary insufficiency to be eliminated and the patient was discharged from hospital in a satisfactory state on day 25 after injury. Key words: severe concomitant injury, blunt chest injury, mitral valve damage, cardiac surgery.