Intramuscular lidocaine in the therapy of ventricular arrhythmias

Bellet, Samuel; Roman, Laurian; Kostis, John B.; Fleischmann, D.

doi:10.1016/0002-9149(71)90305-5

Cited by 38 publications

(7 citation statements)

References 17 publications

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“…They showed that these premature beats could be completely abolished a t lidocaine concentrations of 6-7 pg/ml. Intramuscular administration of lidocaine to human patients in another study resulted in abolition of premature ventricular contractions in eight patients and reduced their frequency in two others (Bellet et al, 1971). These effects were noted when patient serum lidocaine concentrations ranged from 2.4 to 2.8 pglml.…”

Section: Lidocaine Effectmentioning

confidence: 91%

Determination of lidocaine concentrations producing therapeutic and toxic effects in dogs

Wilcke

Davis

Neff-Davis

1983

Vet Pharm & Therapeutics

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Lidocaine was infused at a fixed zero-order rate to eight healthy mongrel dogs until tonic extension (n = 5) and cortical seizures (n = 7) were produced. Lidocaine concentrations determined at 5-min intervals were used to calculate concentrations at which these effects occurred. The tonic extension phase occurred at a mean lidocaine concentration of 8.21 +/- 1.69 micrograms/ml. After a 1-month rest period, the same dogs were anaesthetized and ventricular tachycardia was produced by administering ouabain. Lidocaine was again infused at a fixed zero-order rate until all beats of ventricular origin were abolished. This occurred at a mean lidocaine concentration of 6.25 +/- 1.49 micrograms/ml.

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Section: Lidocaine Effectmentioning

confidence: 91%

Determination of lidocaine concentrations producing therapeutic and toxic effects in dogs

Wilcke

Davis

Neff-Davis

1983

Vet Pharm & Therapeutics

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“…Absorption from Intramuscular Sites Intramuscular administration of lignocaine results in rapid and effective antiarrhythmic action (Bellet et al 1971;Bernstein et al 1972;Cohen et al 1972;Fehmers & Dunning 1972;Ryden et al 1973). After intramuscular injection of lignocaine 200 to 300mg, peak concentrations averaging 2.2 to 3.2 mg/L are observed after 10 to 15 minutes, and plasma concentrations remain in the therapeutic range for 1 to 2 hours (Cohen et al 1972;Oltmanns et al 1982;Singh & Kocot 1976).…”

Section: Absorptionmentioning

confidence: 99%

“…Gianelly et al (1967) measured whole blood lignocaine concentrations in patients with acute MI, and quoted a therapeutic range of 2 to 5 mg/L, but provided no reference or data on which this range was based. Reappearance of arrhythmia after intramuscular lignocaine was noted at an average concentration of 2 mg/L in plasma (Bellet et al 1971;Fehmers & Dunning 1972) or whole blood (Schwartz et al 1974). Singh and Kocot (1976) observed recurrence of arrhythmia at a median whole blood lignocaine concentration of 1.3 mg/L, while Sheridan et al (1977) observed arrhythmia return at a plasma concentration of 1.8 mg/L.…”

mentioning

confidence: 97%

The Pharmacokinetics of Lignocaine and β-Adrenoceptor Antagonists in Patients with Acute Myocardial Infarction

Nattel

Gagne

Pineau

1987

Clinical Pharmacokinetics

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Lignocaine (lidocaine) and beta-adrenoceptor antagonists are widely used after acute myocardial infarction. The therapeutic value of these agents depends on the achievement and maintenance of safe and effective plasma concentrations. Lignocaine pharmacokinetics after acute myocardial infarction (MI) are controlled by a number of variables. The single most important is left ventricular function, which affects both volume of distribution and plasma clearance. Other major factors include bodyweight, age, hepatic function, the presence of obesity, and concomitant drug therapy. Lignocaine is extensively bound to alpha 1-acid glycoprotein, a plasma protein which is also an acute phase reactant. Increases in alpha 1-acid glycoprotein concentration occur after an acute MI, decreasing the free fraction of lignocaine in the plasma and consequently decreasing total plasma lignocaine clearance without altering the clearance of non-protein-bound lignocaine. Complex changes in lignocaine disposition occur with long term infusions, and therefore early discontinuation of lignocaine infusions (within 24 hours) should be undertaken whenever possible. Because the risk of ventricular tachyarrhythmia declines rapidly after the onset of an acute MI, lignocaine therapy can be rationally discontinued within 24 hours in most patients. Lignocaine has a narrow toxic/therapeutic index, so that pharmacokinetic factors are critical in dose selection. In contrast, beta-adrenoceptor antagonists' adverse effects are more related to the presence of predisposing conditions (such as asthma, heart failure, bradyarrhythmias, etc.) than to plasma concentration. The pharmacokinetics of beta-adrenoceptor antagonists are important to help assure therapeutic efficacy, to provide information about the anticipated time course of drug action, and to predict the possible role of ancillary drug effects (such as direct membrane action) and loss of cardioselectivity. Lipid solubility is the main determinant of the pharmacokinetic properties of a beta-adrenoceptor antagonist. Lipid-soluble agents like propranolol and metoprolol are well absorbed orally, and undergo rapid hepatic metabolism, with important presystemic clearance and a short plasma half-life. Water-soluble drugs like sotalol, atenolol, and nadolol are less well absorbed, and are eliminated more slowly by renal excretion. Clinical assessment of beta-adrenoceptor antagonism is more valuable than plasma concentration determinations in evaluating the adequacy of the dose of a particular beta-adrenoceptor antagonist.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…This concentration can be achieved by injecting about 300 mg lignocaine intramuscularly (Scott et al, I968;Meyer and Zelechowski, 197I;Cohen et al, I972;Ryden et al, 1972;Zener et al, I973). Some studies claim effectiveness of intramuscular lignocaine on ventricular tachyarrhythmia (Bellet et al, 197I;Bernstein et al, 1972;Fehmers and Dunning, I972). However, those studies were not controlled, and except for the investigation by Fehmers and Dunning (1972), the aetiology of ventricular tachyarrhythmia was heterogeneous with only some of the patients suffering from acute myocardial infarction.…”

Section: Resultsmentioning

confidence: 99%

Comparison between effectiveness of intramuscular and intravenous lignocaine on ventricular arrhythmia complicating acute myocardial infarction.

Rydén¹,

Waldenström²,

Ehn³

et al. 1973

Heart

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Forty-three patients with acute myocardial infarction were treated with lignocaine after developing certain ventricular tachyarrhythmias.Eighteen patients received intravenous treatment: 75 mg as an intravenous bolus immediately followed by an infusion of 2 mg/min, and 25 per cent solution given into the lateral vastus muscle should be investigated for its clinical effect. With this amount of the drug, satisfactory blood levels were achieved from between io to I5 minutes after the injection for up to go to I20 minutes. In the present study intramuscularly administered lignocaine has been compared with intravenously administered lignocaine in patients with ventricular tachyarrhythmia complicating acute myocardial infarction. Subjects and methodsPatients admitted to the coronary care unit because of proven or suspected acute myocardial infarction were taken into the study if they developed ventricular tachyarrhythmia of one or more of the following types: i) _ 5 ventricular ectopic beats/min; 2) paired ventricular ectopic beats; 3) multifocal ventricular ectopic beats; 4) R on T ventricular ectopic beats; and 5) ventricular tachycardia defined as 3 or more ventricular ectopic beats in sequence.

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Intramuscular lidocaine in the therapy of ventricular arrhythmias

Cited by 38 publications

References 17 publications

Determination of lidocaine concentrations producing therapeutic and toxic effects in dogs

Determination of lidocaine concentrations producing therapeutic and toxic effects in dogs

The Pharmacokinetics of Lignocaine and β-Adrenoceptor Antagonists in Patients with Acute Myocardial Infarction

Comparison between effectiveness of intramuscular and intravenous lignocaine on ventricular arrhythmia complicating acute myocardial infarction.

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