Drugs
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Alterations in serum electrolytes may frequently accompany ischaemic heart disease. Many of these patients are hypertensive and receive diuretic therapy which results in chronic lowering of serum potassium and magnesium. In addition, acute catecholamine-induced shifts of potassium into cells may also occur in the setting of acute myocardial ischaemia. ⋯ Diuretic-induced magnesium deficiency may be yet another factor favouring the emergence of ventricular arrhythmias in patients with ischaemic heart disease. While such electrolyte disturbances do not account for all of the ventricular irritability seen in patients with ischaemic heart disease, they represent easily identifiable and treatable risk factors. Primary prevention of these electrolyte disturbances in patients at risk for coronary ischaemia is recommended.
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Review Clinical Trial
Lorcainide. A preliminary review of its pharmacodynamic properties and therapeutic efficacy.
Lorcainide is a type I antiarrhythmic drug of the local anesthetic type. It can be given either intravenously or orally, and its pharmacokinetic properties allow relatively long (12 hours) dosing intervals with oral administration. A slowly eliminated metabolite, norlorcainide, probably contributes to the effects of orally administered lorcainide in chronically treated patients. ⋯ The most frequent side effect is disturbed sleep during the initiation of oral treatment, which may occur in the majority of patients but usually responds to treatment with a benzodiazepine and subsides with time. Thus, lorcainide appears useful against a variety of arrhythmias. With its convenient dosage schedule and apparently low incidence of serious side effects it should become a useful addition to the antiarrhythmic agents available, although longer term studies are needed to confirm its continued efficacy and lack of unexpected side effects when used for long periods.
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The judicious use of local anaesthetic agents requires knowledge of the pharmacological properties of the various drugs, technical skill in the performance of the different nerve blocks, and a thorough evaluation of the patient's clinical status. Regional anaesthesia may be classified anatomically as follows: (a) infiltration anaesthesia (extravascular or intravascular); (b) peripheral nerve blockade (minor or major nerve block); and (c) central neural blockade (epidural or subarachnoid block). Anaesthetic potency, onset time and duration of action are the most important clinical properties of any local anaesthetic agent. ⋯ The local anaesthetic agents commonly employed for regional anaesthesia may be classified according to their relative potency and duration of activity into: (1) agents of low potency and short duration, e.g. procaine and chloroprocaine; (2) agents of moderate potency and duration, e.g. lignocaine (lidocaine), mepivacaine and prilocaine; and (3) agents of high potency and long duration, e.g. amethocaine (tetracaine), bupivacaine and etidocaine. In general, the onset, duration and quality of regional anaesthesia are enhanced by an increase in dose achieved by either an increase in concentration or in the volume of anaesthetic solution, and by the concomitant use of a vasoconstrictor drug, adrenaline (epinephrine). However, the local anaesthetic properties of the intrinsically more potent and longer acting agents are influenced less by the addition of adrenaline, particularly when such agents are employed for central neural blockade of the epidural type.
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Several compounds of the chemical class arylethanolamines have been shown to possess combined alpha- or vasodilator and beta-adrenoceptor blocking properties. The first drug was labetalol (AH5158)[5-(1-hydroxy-2)1-methyl-3-phenylpropyl(amino)-ethyl (salicylamide)]. Others include medroxalol, bucindolol and YM-09538, which differ from labetalol either by the nature of the substitution on the primary benzene ring and/or on the terminal nitrogen. ⋯ It is particularly valuable in allowing a reduction in the number of drugs required for adequate blood pressure control. The early theoretical prediction that postural hypotension would occur with high doses is now acknowledged to be labetalol's major dose-limiting side effect. Most of the available pharmacokinetic data on labetalol were derived from studies which utilised a fluorimetric assay.(ABSTRACT TRUNCATED AT 400 WORDS)