Царев, А.В. (2018) Состояние гемодинамики при проведении терапевтической гипотермии в комплексе интенсивной терапии тяжелой черепно-мозговой травмы. Вісник проблем біології і медицини, Вип.1 (т1(142). pp. 213-217. ISSN 2077-4214
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Abstract
В работе представлены результаты изучения изменений гемодинамики у пациентов с тяжелой ЧМТ при использовании терапевтической гипотермии (n=12) в комплексе интенсивной терапии с целевым значением температуры ядра тела – 34,50 С, в сравнении с группой контроля (n=12). В результате было выявлено достоверное снижение числа сердечных сокращений на 27%, 25,9% и 25,8% на этапе 12, 24 и 36 часов соответственно, по сравнению с пациентами контрольной группы (p>0,05). Отмечено достоверное снижение АД диастолического на 6,2% (p<0,05) и тенденция к снижению среднего артериального давления на 4% в группе пациентов с применением терапевтической гипотермии на этапе 48 часов по сравнению с контрольной группой. Выявленные гемодинамические сдвиги были обусловлены в первом случае реакцией на гипотермию, а во втором снижением общего периферического сопротивления сосудов, в ответ на контролируемое согревание пациентов с целью восстановления нормотермии. Указанные гемодинамические изменения носили обратимый характер. The aim of the study was 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 34.50C. Induction of therapeutic hypothermia was performed by intravenous drip as fast as possible infusion of 40C 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.
| Item Type: | Article |
|---|---|
| Additional Information: | DOI 10.29254/2077-4214-2018-1-1-142-213-217 |
| Uncontrolled Keywords: | черепно-мозговая травма, терапевтическая гипотермия, гемодинамика, интенсивная терапия. trauma brain injury, therapeutic hypothermia, hemodynamics, intensive care. |
| Subjects: | Anesthesiology and Intensive care |
| Divisions: | Departments > Department of Anaesthesiology and Intensive Care |
| Depositing User: | Анастасия Жигар |
| Date Deposited: | 24 Sep 2018 06:42 |
| Last Modified: | 24 Sep 2018 06:42 |
| URI: | http://repo.dma.dp.ua/id/eprint/3228 |
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