Relation between Plasma Lignocaine Levels and Induced Haemodynamic Changes

Binnion, Peter F.; Murtagh, Gillian; Pollock, Andrew; Fletcher, E.

doi:10.1136/bmj.3.5667.390

Cited by 37 publications

(7 citation statements)

References 7 publications

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“…When there is no identifiable cause empirical' therapy may be used, either with a pharmacological agent such as procainamide (Friedberg, 1966;Leading article, British Medical Journal, 1970a) or lignocaine (Friedberg, 1966;Binnion, Murtagh, Pollock, and Fletcher, 1969), or with a physical agent such as pacing (Harris et al, 1967). By capturing the cardiac rhythm, pacing may suppress the dysrhythmia, augment the rate, and increase the cardiac output (Harris et al, 1967;Litwak et al, 1968).…”

Section: Discussionmentioning

confidence: 99%

Atrial and ventricular pacing after open heart surgery

Wisheart

Wright

Rosenfeldt

et al. 1973

Thorax

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The effect of cardiac pacing, through a wide range of pacing rates, has been studied in 13 patients in stable sinus rhythm within 24 hours of operation. Using first atrial and then ventricular pacing, the cardiac rate was raised to 60% above control value. The effects of atrial and ventricular pacing were compared by observing the differences in the various parameters measured at corresponding paced heart rates. With atrial pacing there was no significant difference in the cardiac output, mean aortic pressure, mean left atrial pressure, or left ventricular work. During ventricular pacing there were significant falls in cardiac output (P<0-05), mean aortic pressure (P<0-01), and left ventricular work (P

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Section: Discussionmentioning

confidence: 99%

Atrial and ventricular pacing after open heart surgery

Wisheart

Wright

Rosenfeldt

et al. 1973

Thorax

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“…This block does not occur in a haphazard fashion, but rather in an orderly and sequential manner depending on fibre size and myelination. [12][13][14][15][16][17][18][19][20] Proprioception, soma tic motor sense BETA [5][6][7][8][9][10][11][12] Pressure GAMMA [3][4][5][6] Motor to muscle spindle post-ganglionic sYmEathetic Adapted from GANONG (42 ) 6.…”

Section: Chapter II Physiological and Pharmacological Considerationsmentioning

confidence: 99%

The Cardiorespiratory Effects of Thoracic Epidural Anaesthesia

Wahba¹,

Craig²,

Don³

et al. 1973

Survey of Anesthesiology

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The cardio-respiratory effects of a thoracic epidural anaesthetic as is given for pain relief following upper abdominal surgery were examined in thirteen surgical patients studied in the immediate pre-operative period.following an overnight fast and without premedication.The focus of interest was on its effects on FRC and on gas exchange (measured as A-aD02 and OS/OT%), waich have not been previously reported. AlI subjects were given 10 ml/Kg glucose in saline I.V. during the pre-epidural periode Lidocaine 1.5% was used in aIl cases, plain lidocaine for the first eight and lidocaine with epinephrine 1/200,.000 in the other five subjects. This agent was given to achieve a sensory block to both pin-prick and ice up to T4. Neither FRC nor gas exchange showed any consistent changes following the epidural anaesthetic. These findings are in keeping with what was anticipated from a consideration of the basic physiology and pharmacology concerned and with a review of the pertinent literature. following an overnight fast and without premedication.The focus of interest was on its effects on FRC and on gas exChange (measured as A-aD02 and OS/OT%), which have not been previously reported. All subjects were given 10 ml/Kg glucose in saline I.V. during the ~re-epidural periode Lidocaine 1.5%was used in all cases, plain lidocaine for the first eight and lidocaine with epinephrine 1/200~OOO in the other five subjects. This agent was given to achieve a sensory block to both pin-prick and ice up to T4. Neither FRC nor gas exchange showed any consistent Changes following the epidural anaesthetic. These findings are in keeping with what was anticipated from a consideration of the basic physiology and pharmacology concerned and with a rev~ew of the pertinentliterature.w. MELEIKA~WAHBA' M.Sc. Exp. Red.

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“…Lidocaine has narrow therapeutic index, with only small difference between therapeutic and potential toxic concentrations [22]. The serum concentration associated with the clinical side effects is considered greater than 6.0 μg/ml [23,24].…”

Section: Discussionmentioning

confidence: 99%

Effects of Lidocaine on Ischemia/Reperfusion Injury in In vivo Rabbit Hearts

Furuya¹,

Yui²

2012

J Anesthe Clinic Res

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Objective: The aim of this study was to investigate the cardioprotective effects of lidocaine administered at three different timings, as indexes of hemodynamics, infarct size, antiarrhythmic action, and changing activation time by electrocardiogram in in vivo rabbit hearts. Methods: Thirty two rabbits received regional ischemia by 30 min of left anterior descending coronary artery occlusion followed 3 hours of reperfusion under ketamine and xylazine anesthesia. The animals were randomly assigned to the following 4 treatment groups: a control group, a lidocaine-preconditioned group, a lidocainepostconditioned group, and a lidocaine-continuous administration group. Results: The ratio of areas at risk revealed no significant difference among all groups. Mean infarct size of the area at risk was significantly less in a lidocaine-continuous administration group than other 3 groups. The incidence of arrhythmias during myocardial ischemia was no significant difference between a control group and other 3 groups. The incidence of arrhythmias during reperfusion was no significant difference among all groups. However, lidocaine depressed the activation time which was prolonged by ischemia. Conclusions: It was suggested that lidocaine produced neither preconditioning nor post-conditioning benefits. Lidocaine did not have antiarrhythmic effects during ischemia/reperfusion injury. The clinical implications of this investigation are that lidocaine infusion is no longer recommended for the treatment of ventricular arrhythmias during acute coronary syndrome; however, continuous administration of lidocaine may be effective to make the infarct size small. The prolonged activation time during ischemia was depressed by lidocaine. Thus, it was also indicated that the activation time during ischemia and reperfusion can be normalized by lidocaine. J o u rn al of A n e s th es ia & C li n ic a l Resea rc h

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Relation between Plasma Lignocaine Levels and Induced Haemodynamic Changes

Cited by 37 publications

References 7 publications

Atrial and ventricular pacing after open heart surgery

Atrial and ventricular pacing after open heart surgery

The Cardiorespiratory Effects of Thoracic Epidural Anaesthesia

Effects of Lidocaine on Ischemia/Reperfusion Injury in In vivo Rabbit Hearts

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