Biomedical subjects
Publications and source records attributed to J M Deglin.
As the availability and use of drugs, both prescription and over-the-counter, increase, so increases the potential for interference by one drug with the action of another. This article reviews the types of interactions possible, spells out some of the most widely encountered interactions, and gives recommendations for their avoidance.
Eighty-four serum lidocaine determinations were made in 33 hospitalized patients with the use of a rapid enzyme innumoassay technique. Prediction of lidocaine concentration within broad categories based on clinical assessment alone was compared with actual measurements. When serum concentrations were not considered, most episodes of lidocaine toxic reactions were obscured by associated complex clinical problems. The rapid lidocaine enzyme immunoassay is a useful tool for assisting in the detection of lidocaine toxic reactions in the coronary care unit.
A wide variety of drugs may be associated with serious cardiovascular toxicity. Toxicity due to drugs primarily used for treating cardiovascular toxicity. Toxicity due to drugs primarily used for treating cardiac disorders is the most extensively documented, especially the arrhythmias due to digitalis glycosides. Various arrhythmias are also caused by toxic levels of many antiarrhythmic agents including quinidine, procainamide and phenytotin. Myocardial depression and heart failure are serious side-effects of beta-adrenoceptor blocking agents and myocardial ischaemia due to sympathominetic amines may result from both direct and indirect mechanisms. The many toxic reactions in the cardiovascular system due to non-cardiac drugs are less widely known and for the most part less clearly understood. Many remain controversial at the current time; for example, the diathesis toward thromboembolism in women taking oral contraceptives. Potential cardiac toxicity due to drugs used in the rapidly expanding sphere of anti-neoplastic chemotherapy is exemplified by the cardiomyopathy-like toxicities of doxorubicin and daunorubicin. Many of the psychotherapeutic drugs including phenothiazine antipsychotics and tricyclic antidepressants have arrhythmogenic potential.
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After a single 1-g intravenous dose of vancomycin, the mean peak concentration in the serum of 29 anephric patients was 48.3 micrograms/ml. An initial rapid decline to 15 micrograms/ml within 3-5 hr was followed by slow elimination, with 3.5 micrograms/ml present after 18 days. Intermittent dialysis had no appreciable effect on drug levels in serum. The biphasic decline in serum concentrations of vancomycin indicates at least two-compartment pharmacokinetics in both anephric and normal patients. In anephric patients the elimination half-life was 7.5 days and the elimination rate constant was 0.32; these values were 8 hr and 10.25, respectively, in normal patients. On the basis of these results, the vancomycin regimen recommended for anephric patients is an initial 1-g intravenous dose followed by 500 mg every eight days. With these dosages peak concentrations are 49 micrograms/ml (well below reported toxic levels) and trough concentrations are 7 micrograms/ml (well above the minimal inhibitory concentrations for susceptible pathogens causing shunt infections).