Showing papers on "Cardiac arrhythmia published in 1982"

Studies on South African cardiac glycosides. II. Observations on the clinical and haemodynamic effects of cotyledoside

Abstract: In guinea-pigs, the oral and subcutaneous LD50 values were very similar (cf. 0,173 mg/kg over 48 h with 0,116 mg/kg over 24 and 48 h). When dosed subcutaneously, a cumulative effect was observed. Intravenous administration of cotyledoside to anaesthetized guinea-pigs resulted in: dyspnoea, increased heart rates and blood pressures, and electrocardiagraphic changes typical of cardiac glycoside poisoning. A positive cardiac inotropic effect was succeeded by a positive chronotropic one. In sheep, acute and subacute intoxication resulted in ruminal, respiratory and cardiac changes. The signs included ruminal stasis, cyanosis, cardiac arrhythmia, ectopic foci and AV dissociation, followed by hypotension and progressive respiratory and cardiac failure. The skeletal muscles were affected in only 1 sheep vide infra. In chronically intoxicated sheep typical clinical signs of "krimpsiekte" developed, e.g. weakness, reluctance to stand, unsteadiness on feet, tremor and paresis of hindquarter muscles, paresis of the neck, arching of the back and standing with the feet close together. Respiratory function was affected in all 3 cases; ruminal stasis, with concomitant loss of appetite occurring in one, and a transient change in heart function in another. The syndrome induced by acute cotyledoside poisoning is similar to that of other cardiac glycosides, but the paretic signs of chronic intoxication resemble "krimpsiekte", a disease associated only with intoxication with the plants of the family Crassulaceae.

Hyperkalaemic cardiac arrhythmia caused by potassium citrate mixture.

Abstract: cases (1, 3, and 4) were the highest values of 1,25(OH)2D (during the summer months) over 200 pmol/l (80 pg/ml). The fluctuations in the other subjects were within the above-mentioned normal range of 50-180 pmol/l. The range of 1,25-(OH)2D levels in normal subjects as indicated by Chesney et al,5 in a paper to which Dr Tjellesen and others refer, is even larger-that is, 26-266 pmol/l. Therefore we do not agree that our serum levels of 1,25-(OH)2D would on average be double those found by others. On the question of the reliability of the determination of metabolites of vitamin D in human serum we would like to refer also to an interlaboratory study which was undertaken in the Netherlands, in which we participated and the results of which were presented at the 16th European Symposium on Calcified Tissue.6 With regard to the explanation put forward by Dr Tjellesen and others to account for the discrepancy between our data and theirs, we previously excluded a possible interference of high concentrations of 25-OHD and 24,25-(OH)2D with the assay of 1,25-(OH)2D, as indicated in table II of our article. As to 25,26-(OH)2D we did not add this substance to a standard serum for evaluation of possible interference with the 1,25-(OH)2D assay, but we found (like others7) that with high-pressure liquid chromatography using a Radial Pack B Column eluted with hexane/isopropranolol (90/10, v/v) at a flowrate of 1-8 ml/min and UV detection at 254 nm an excellent separation of all the vitamin D metabolites that have been mentioned is obtained, including 25,26-(OH)2D, which comes off the column in the 8-10-minute fractions while 1,25(OH)2D appears after 13-15 minutes. So in our hands no interference of 25,26-(OH)2D with the radioimmunoassay of 1,25-(OH)2D is to be expected.

Effect of alinidine on experimental cardiac arrhythmias.

Abstract: Summary Alinidine (2.9 ± 0.7 mg/kg) prevented an adrenaline-induced ventricular arrhythmia in dogs respired with halothane. In ouabain-induced ventricular tachycardia, a cumulative dose of alinidine (15.5 mg/kg) reduced the number of ventricular beats by 91.6 ± 1.9%. The drug was much less effective in abolishing the ventricular tachycardia 24 h after ligation of a coronary artery, with only a 36 ± 15% reduction in ventricular ectopic beats after 15.5 mg/kg. The administration of alinidine (0.5–1.0 mg/kg) to anaesthetized dogs with no cardiac arrhythmia reduced sinus node rate with little effect on the response of the node to vagal stimulation.

Cardiac arrhythmia in basilar migraine.

Abstract: SYNOPSIS Basilar migraine may produce temporary change in brainstem function resulting in impairment of activity of medullary autonomic nuclei A case of basilar migraine with transient cardiac arrhythmia is described and it is suggested that abnormalities in cardiac rhythm may be detected by cardiographic monitoring in some cases of basilar migraine This report emphasizes the occasional occurrence of serious complications during a migraine attack

Incidence of post-anaesthetic arrhythmias in the dog

Abstract: A total of 50 dogs, judged to be free of cardiovascular disease on the basis of physical and electrocardiographic (ECG) examination, underwent ECG monitoring during recovery from general anaesthesia. Fifteen of these dogs (30 per cent) developed some form of cardiac arrhythmia during the recovery period. The arrhythmias most frequently observed were premature ventricular contractions and atrioventricular conduction defects of varying degrees of severity. The observed arrhythmias had ceased by the end of the observation period and did not require specific therapy. There was no apparent correlation between the duration of anaesthesia, the type of medical or surgical procedure and the development of arrhythmias. However, the dogs developing arrhythmias were older than those that did not. The relatively high frequency of occurrence of cardiac arrhythmias must be considered in the evaluation of ECG data from dogs being monitored during recovery from anaesthesia.

Method of treating cardiac arrhythmia

Abstract: The 3-(5'-adenylate) of lincomycin- and clindamycin-type compounds in which the propyl hygric acid moiety has been replaced by different cyclic amino acids can be used to treat cardiac arrhythmia in humans and animals.

A new manifestation of thrombocytopenia: myocardial haemorrhage with symptomatic arrhythmia.

Abstract: We describe a patient with thrombocytopenia who developed episodes of dyspnoea due to recurrent cardiac arrhythmia. Necropsy revealed that the apparent mechanism was extensive myocardial haemorrhage.

Cardiac arrhythmia detector and recorder

Abstract: Cardiac arrhythmias are detected by measuring the duration of the first derivative of the QRS component signal of a cardiac rhythm and comparing such duration to a running average duration, and/or by measuring the duration of the R-R interval and comparing such interval to a running average interval. A cassette recorder is activated in response to an arrhythmia detected by either one of the above techniques. The cardiac rhythm signal is fed to the recorder through a delay network such that the recorded signal brackets the detected arrhythmia. A manual record switch is also provided for separate wearer actuation to record what he considers to be unusual heart activity. -o-

Holter Monitoring — How should It be Performed?

Abstract: Essential to the diagnosis and management of paroxysmal episodes of cardiac arrhythmia and ischaemia is electrocardiographic documentation. Continuous 24 hour ECG recording or a similar continuously available telemetric or transtelephonic ECG recording satisfies this need.

Methods useful in the treatment of cardiac arrhythmia using 4-substituted-2-iminoimidazolidine compounds

Abstract: This invention provides a novel class of 2-iminoimidazolidines which include 4-substituted derivatives such as 4-(2-chloroethyl)-1-methyl-2-methylimino-3-phenyl imidazolidine fumarate: ##STR1## This illustrated 4-substituted 2-iminoimidazolidine compound exhibits cardiovascular hypotensive, hypoglycemic (glucose tolerance, and sugar cataract) and anti-inflammatory (pleural effusion) pharmacological activities in test animals.