THE STATE OF HEMODYNAMICS IN THE CARRYING OUT THERAPEUTIC HYPOTHERMIA IN THE OF INTENSIVE CARE OF SEVERY TRAUMA BRAIN INJURY

Tsarev A. V.

CLINICAL AND EXPERIMENTAL MEDICINE

Scentific article

The aim of the studywas to study changes in hemodynamic parameters in patients with severe trauma brain injury (TBI) in therapeutic hypothermia in the intensive care compared with the control group. Object and methods. The patients were divided into 2 groups were examined: Group 1 (n=12) – patients with standard intensive care, according to the “Guidelines for the Management of Severe Traumatic Brain Injury 4th Edition, 2016” in the treatment of the ICU; Group 2 (n=12) – with the therapeutic hypothermia “Blanketrol II” (CSZ) with the use of non-invasive technology to achieve the target core body temperature (Tco) of 34.5 0 C. Induction of therapeutic hypothermia was performed by intravenous drip as fast as possible infusion of 4 0 C with a saline at a dose of 30 ml/kg, followed by maintenance of therapeutic hypothermia with the hypotherm “Blanketrol-II” through blankets with circulating cold water. In the induction phase, an analgesia and pharmacological prevention of cold shiver development. Induction, maintenance of therapeutic hypothermia, and warming of patients, the body core temperature was continuously measured by means of an esophageal temperature sensor connected to the “Blanketrol-II”. Criteria for the inclusion of patients in the study: the first 24 hours from the moment of receiving severe TBI (both with the carrying out without an operative neurosurgical intervention), the initial level of neurological deficit, which was assessed on the Glasgow Coma Scale (GCS), in the range of 5-7 points. Exclusion criteria were: age ≤18 years, neurological status on the GCS ≥8 and ≤4 points at the time of the study, pregnancy, refractory arterial hypotension using high doses of vasopressors. Patients of both groups were mechanically ventilated. Results.At the time of inclusion of patients in the study, we did not find reliable intergroup differences in the baseline level of neurological deficit, the level of MAP, heart rate and Tco. In the analysis of changes in the heart rate in Group 2 of patients, a significant decrease in this indicator was observed: 61±5,50; 56,5±4,83 and 66,83±4,77 at 12, 24 and 36 hours, respectively, compared with patients in the Group 1 (83,58±15,90; 84,66±14,95; 90,16±13,10 beats per minute) (p <0.05).The development of bradycardia in the Group 2 of patients, more pronounced at the 24 hour study, was due to induction and subsequent maintenance of therapeutic hypothermia and a physiological reaction to cooling. At a stage of 48 hours in the group of patients with the use of therapeutic hypothermia, a significant decrease in diastolic blood pressure (75±5,0 vs 80,0±4,08 mm Hg) (p<0.05) and decrease in the mean arterial pressure (89,95±4,51 vs 93,58±5,35 mm Hg, P 0.05) compared to the Group 1. Conclusions. The development of bradycardia in the second group of patients was due to induction and subsequent maintenance of therapeutic hypothermia and was a physiological reaction to cooling. At the same time, it must be emphasized that there was no clinically significant bradycardia in patients with therapeutic hypothermia. There was a significant decrease in the diastolic blood pressure index and a trend towards a decrease in the mean blood pressure at the warming and restoration stage of normothermia, the latter being due to a change in the vascular tone in response to the attainment of normothermia. The revealed hemodynamic changes in the group of patients using therapeutic hypothermia were reversible.

trauma brain injury, therapeutic hypothermia, hemodynamics, intensive care

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«Bulletin of problems biology and medicine» Issue 1 Part 1 (142), 2018 year, 213-217 pages, index UDK 617.51-001.4

10.29254/2077-4214-2018-1-1-142-213-217