Abstract
Purpose. The establishment of the role of water and electrolyte disorders in the pathogenesis postresuscitation hemo circulatory disorders after removal from the clinical death caused by acute myocardial infarction. Materials and methods. In experiments with 158 dogs studied under Nembutal anesthesia recovery processes of life after 5 minutes of clinical death caused by myocardial infarction. Results. It is found that dogs in the early postresuscitative after myocardial infarction occurs movement of sodium ions in the red blood cells, which is accompanied by gipoosmiey blood plasma and interstitial fluid. This causes the movement of water in the cell sector, which leads to the development of hypovolemia and drop in cardiac output. Movement of potassium and calcium ions from cell sector into the extracellular defines violation of myocardial, vascular tone, and increases the risk of arrhythmia postresuscitation myocardial infarction. Сonclusion. In postresuscitative in dogs undergoing clinical death with acute myocardial infarction, there is a redistribution of electrolytes sector body. During the first 9 hours after resuscitation sodium and calcium concentration in the cell sector increase and decrease in the extracellular. Changes in the potassium content of the opposite. By the end of 1st day recovery period increases plasma sodium concentration, and the corresponding potassium and calcium indicators reduced. The osmolarity of the extracellular space is reduced by 5 min postresuscitative period and increases toward the end of 1 day. It is associated with similar changes in sodium concentration. sodium retention in the cell movement causes the space portion therein, and development of extracellular fluid volume depletion, which leads to a decrease in venous return and cardiac output drop. In the interval of 9–24 hours after resuscitation begins a long period of stabilization of the circulatory system. This is due to the normalization of the water distribution sector, which leads to the restoration of intravascular volume and resolution of hemodynamic disturbances.
Highlights
Перемещение ионов калия и кальция из клеточного сектора во внеклеточный определяет нарушение сократимости миокарда, сосудистого тонуса и увеличивает риск развития аритмии в постреанимационном периоде инфаркта миокарда
The establishment of the role of water and electrolyte disorders in the pathogenesis postresuscitation hemo circulatory disorders after removal from the clinical death caused by acute myocardial infarction
In experiments with 158 dogs studied under Nembutal anesthesia recovery processes of life after 5 minutes of clinical death caused by myocardial infarction
Summary
ВОДНО-ЭЛЕКТРОЛИТНЫЕ НАРУШЕНИЯ В ПОСТРЕАНИМАЦИОННОМ ПЕРИОДЕ ОСТРОГО ИНФАРКТА МИОКАРДА. Установление роли водно-электролитных расстройств в патогенезе постреанимационных гемоциркуляторных нарушений после остановки сердца, вызванной острым инфарктом миокарда. Установлено, что у собак в раннем постреанимационном периоде после инфаркта миокарда происходит перемещение ионов натрия в эритроциты, что сопровождается гипоосмией плазмы крови и интерстициальной жидкости. Это обусловливает перемещение воды в клеточный сектор, что приводит к развитию гиповолемии и падению сердечного выброса. Закономерности острых расстройств водно-электролитного баланса в постреанимационном периоде у экспериментальных животных, перенесших клиническую смерть на фоне острого инфаркта миокарда, характеризуются периодичностью смещения натрия, калия и воды с фазностью клеточной гипергидратации, сменяющейся внеклеточной. Задержка натрия в клеточном пространстве обусловливает перемещение в него части внеклеточной жидкости и развитие гиповолемии, которая приводит к уменьшению венозного возврата и падению сердечного выброса. The establishment of the role of water and electrolyte disorders in the pathogenesis postresuscitation hemo circulatory disorders after removal from the clinical death caused by acute myocardial infarction
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