Prescott L F, Adjepon-Yamoah K K, Talbot R G
Br Med J. 1976 Apr 17;1(6015):939-41. doi: 10.1136/bmj.1.6015.939.
Plasma concentrations of lignocaine were measured during and after infusion of lignocaine at 1.4 mg/min for 36-46 hours in 12 patients with myocardial infarction and one patient with cardiac failure due to uncontrolled ventricular tachycardia. In six patients without cardiac failure the plasma concentrations of lignocaine rose progressively during the infusion and the mean lignocaine half life was 4.3 hours compared with 1.4 hours in healthy subjects. Mean plasma lignocaine concentrations were significantly higher in seven patients with cardiac failure, and concentrations also rose during the infusion and the half life was considerably prolonged to 10.2 hours. Lignocaine concentrations rose rapidly to toxic levels when cardiogenic shock developed in one patient and did not fall when the infusion was stopped. The mean plasma antipyrine half life was moderately prolonged (19.4 hours) in a larger group of patients with myocardial infarction and cardiac failure but returned to normal during convalescence (13.2 hours). The metabolism of lignocaine is grossly abnormal in patients with cardiac failure and cardiogenic shock after myocardial infarction.
在12例心肌梗死患者和1例因室性心动过速控制不佳导致心力衰竭的患者中,以1.4mg/分钟的速度输注利多卡因36 - 46小时,期间及输注后测定血浆利多卡因浓度。在6例无心力衰竭的患者中,输注期间血浆利多卡因浓度逐渐升高,平均利多卡因半衰期为4.3小时,而健康受试者为1.4小时。7例心力衰竭患者的平均血浆利多卡因浓度显著更高,输注期间浓度也升高,半衰期大幅延长至10.2小时。1例患者发生心源性休克时,利多卡因浓度迅速升至中毒水平,停止输注后浓度未下降。在一大组心肌梗死和心力衰竭患者中,平均血浆安替比林半衰期中度延长(19.4小时),但在恢复期恢复正常(13.2小时)。心肌梗死后心力衰竭和心源性休克患者利多卡因的代谢严重异常。