Antiarrhythmic drugs. Part VII. Lidocaine as an antiarrhythmic agent

Frieden, Julian

doi:10.1016/0002-8703(65)90399-6

Cited by 55 publications

(12 citation statements)

References 5 publications

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“…After studying the effects produced by a wide range of lidocaine concentrations, we feel that the effects seen at 1 X 10-mole/liter (2.34 tig/ml) correspond to the effects produced by therapeutic concentrations (2)(3)(4)(5) ,ug/ml) in man (6). Certainly, the concentration corresponding to therapeutic levels in man must be less than 1 x 10' mole/liter since this concentration had effects which would produce widening of the QRS complex of the electrocardiogram in vivo; full antiarrhythmic doses of lidocaine do not cause widening of the QRS complex in man (13).…”

Section: Effects Of Lidocaine On Automaticity In Purkinje Fibersmentioning

confidence: 97%

“…Lidocaine hydrochloride has been used sporadically as a cardiac antiarrhythmic drug since 1950 (1) and in the past few years, has been frequently used to treat ventricular arrhythmias which occur during and after cardiac surgery (2)(3)(4)(5) and myocardial infarction (6)(7)(8)(9). The antiarrhythmic and electrophysiological properties of lidocaine were assumed to be similar to those of procaine amide.…”

Section: Introductionmentioning

confidence: 99%

“…This assumption is not unreasonable when one considers the similarity of structure and of local anesthetic properties shared by these two drugs. Indeed, the strongest arguments made for the clinical use of lidocaine in the treatment of arrhythmias rather than procaine amide or quinidine usually have been related to either the pronounced differences in its mode and rate of metabolism (4)(5)(6)(7)(8) or to differences between the effects of lidocaine and these two drugs on blood pressure, cardiac output, and myocardial contractility (9)(10)(11)(12). Differences in electrophysiological properties or antiarrhythmic spectrum usually have been neglected in such discussions.…”

Section: Introductionmentioning

confidence: 99%

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Effect of lidocaine on the electrophysiological properties of ventricular muscle and Purkinje fibers

Jt¹,

Wj²

1970

J. Clin. Invest.

249

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A B S T R A C T Preparations of right ventricular papillary muscle and false tendon (Purkinje fiber) were obtained from dog hearts, placed in a bath perfused with Tyrode solution, and observed both under control conditions and during exposure to lidocaine in concentrations from 1 X 10-7 to 5 X 10-' mole/liter. Transmembrane voltages were recorded from both ventricular muscle (VM) and Purkinje fibers (PF) of spontaneously beating and electrically driven preparations. Low concentrations (1 X 10' and 1 X 10' mole/liter) attenuated or abolished phase 4 (diastolic) depolarization and spontaneous firing in PF without decreasing their diastolic excitability. Concentrations of 1 X 10' mole/ liter produced maximal shortening of both action potential duration (APD) and effective refractory period (ERP) and made the ERP long relative to APD; the latter alteration was more prominent in VM. At concentrations < 1 X 10' mole/liter, lidocaine either caused a slight increase or no change in peak maximum rate of phase 0 depolarization (Vrax) and membrane responsiveness, the relationship between transmembrane activation voltage (MAV)

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Section: Effects Of Lidocaine On Automaticity In Purkinje Fibersmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of lidocaine on the electrophysiological properties of ventricular muscle and Purkinje fibers

Jt¹,

Wj²

1970

J. Clin. Invest.

249

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“…In all experiments in which a 2 mg/kg lidocaine bolus was injected, the effect of the drug was seen within 30 sec of the injection, reached maximum within 1-2 min, persisted for 4-8 min, and almost completely disappeared within [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] min.…”

Section: Effect Of Lidocaine On Re-entrant Ventricular Tachycardiasmentioning

confidence: 99%

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 4. Mechanism of action of lidocaine.

El‐Sherif¹,

Scherlag²,

Lazzara³

et al. 1977

Circulation

114

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SUMMARY The effect of lidocaine on re-entrant ventricular arrhythmias (RVA) was studied in dogs 3-7 days following ligation of the anterior descending coronary artery; direct recordings were made of the re-entrant pathway (RP) from the epicardial surface of the infarction zone (IZ). Lidocaine in a therapeutic dose consistently prolonged refractoriness of potentially RP(s) in the IZ and produced a higher degree of conduction block at a constant heart rate. Conduction in the adjacent normal zone was not affected.

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“…This drug acts very rapidly, its onset of action beginning 15 to 90 seconds after an intravenous injection (33)(34)(35). The blood level of lidocaine at first falls rap- idly (the plasma half-life of the distribution phase being around 17 minutes) (36), so that a therapeutic blood level is best maintained by following the ini tial injection with a continuous infusion of between 1-4 mg/min.…”

Section: Antiarrhythmic Drugsmentioning

confidence: 99%

Treatment of Ventricular Extrasystoles and Tachyarrhythmias in Acute Myocardial Infarction

Selzer¹,

Cohn²

1970

Annu. Rev. Med.

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Two developments at the beginning of this decade exerted a profound influence upon clinical management of acute myocardial infarction: the in troduction of closed-chest resuscitation with electric shock therapy for ven tricular fibrillation, and the availability of continuous monitoring of the electrocardiogram by means of the cathode-ray oscilloscope. As a result of this, the coronary care unit has become a standard facility for the treatment of myocardial infarction. I t should be recognized that the concept of thera peutic centers for patients with myocardial infarction encompasses a broad range of facilities available in such units (1). On the one end of the spectrum, one can place the comprehensive cardiology center, equipped to treat all as pects and complications of myocardial infarction, including the use of emer gency surgery and artificial pump-support. On the other end, is the small area in a hospital in which nurses can observe the patient's rhythm displayed upon the monitoring oscilloscope. The great majority of coronary care units ap proach the latter end of the spectrum-based primarily on the availability of electrocardiographic monitoring units. Thus, the role of such units is the identification, early recognition, treatment, and prevention of dangerous arrhythmias. The most common arrhythmias that are potentially life-threat ening are related to increased "irritability" of the ventricular myocardium. The purpose of this review is to examine the rationale for the therapy of ventricular arrhythmias in acute myocardial infarction-both the fundamen tal and practical considerations. INCIDENCE OF ARRHYTHMIASDuring the earlier era, when the diagnosis of arrhythmias was based on their occurrence during routine examination of the patient or during record ing of an electrocardiographic tracing, the incidence of arrhythmias was es timated to range between 9 and 27 percent, with an average of 18 percent

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Antiarrhythmic drugs. Part VII. Lidocaine as an antiarrhythmic agent

Cited by 55 publications

References 5 publications

Effect of lidocaine on the electrophysiological properties of ventricular muscle and Purkinje fibers

Effect of lidocaine on the electrophysiological properties of ventricular muscle and Purkinje fibers

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 4. Mechanism of action of lidocaine.

Treatment of Ventricular Extrasystoles and Tachyarrhythmias in Acute Myocardial Infarction

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