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Biomedical subjects

A S Savina

Publications and source records attributed to A S Savina.

At least 19 recordsLinked to original sources
PubMed1992

[Acute heart failure and its treatment in cardiologic drug poisoning].

The causes of sudden cardiac arrest (SCA) and its associated early death were examined in 179 patients with acute intoxications due to amitriptyline, antiarrhythmic agents and cardiac glycosides. In the first hours of intoxication, various cardiac conduction disturbances were found to occur in 39.6% of the patients, among whom 11.7% died due to SCA predominantly in complete bundle-branch block. The cause of SCA was an acute (contractile) heart failure that had run as cardiogenic shock and been associated with the specific selective action of the agents in question on cardiomyocytes. Premodulation of acute heart failure with membrane protective agents (unithiol, alpha-tocopherol, hydrocortisone), pharmacological antagonists (novodrin, alupent, isoprenaline), and the cardiotonic agent dobutamine enabled acute heart failure to be effectively treated, hemosorption to be made in early periods and cardiac events to be abolished in 80% of the patients, SCA mortality rates decreased from 11.7 to 3.2%.

Adolescent↗
PubMed1990

[Acute klofelin poisoning].

Clofelin poisoning induced accidentally, criminally or suicidally was treated and followed up in 862 adults and 96 children admitted to specialized centers. The most common clinical symptoms were bradycardia and mental confusion due to SNC toxic affection. Specific cardiotoxic effect of the drug was not registered. Therapeutic measures included detoxication (gastric lavage, forced diuresis, ect.) and pharmacological correction of cardiac rhythm with atropine and metacine.

Acute Disease↗
PubMed1978

[Lesion of the heart in exotoxic shock].

The functional condition of the heart in exotoxic shock, the most severe complication in the early toxicogenic form of acute poisoning, was studied in 230 patients in whom shock had developed on the background of severe acute poisoning with fluid caustics, dichloroethane, organophosphoric insecticides or soporifics. The results of the studies show that in the phase of compensated shock the revealed disorders are mainly due to the compensatory intensification of the cardiac activity in response to the "chemical trauma". Affection of the contractile myocardium in this period of shock does not play any noticeable role in the development of hemodynamic disorders, the only exception are cases in which the preparation that had caused the poisoning possesses a specific cardiotoxic effect ("primary specific cardiotoxic effect"). The increase of the general phenomena of disorders of microcirculation and hypoxia leads to diminution of the enzyme control of metabolic processes in the myocardium and the development of secondary dystrophic changes in the myocardial fibre ("secondary nonspecific cardiotoxic effect").

Acetates↗
PubMed1976

[Exotoxic shock].

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Acetates↗
PubMed1975

[Pathogenesis of disorders of cardiac rhythm and conductivity in acute organophasphate insecticide poisoning].

A dynamic examination of ECG and K and Na level in plasma and erythrocyte was conducted in 73 patients during the acute period of poisoning with phosphorus-organic insecticides -- thiophos, chlorophos, carbophos. In 18.6% of the cases severe rhythm and conductivity disorders were revealed that caused cardiac arrest and death in 29 patients. Besides, a sharp increase in the electric systole on the ECG was noted in all the patients during the acute period of poisoning. A study of the electrolytes revealed hypokalemia, hypernatremia and an increased content of K and Na in the erythrocytes. The authors believe that the disturbances in the cardiac activity during acute poisonings with phosphorus-organic insecticides are due to the effect of the excessive acetylcholine upon the ion permeability towards increasing intracellular potassium.

Acute Disease↗