Prevention of sudden coronary death.

Czechoslovak medicine Pub Date : 1991-01-01
Z Fejfar, M Vrána, L Hess, Z Vránová, Z Blazek
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Abstract

The following results were obtained in an experimental study in the dogs in general pentobarbital anaesthesia: Lidocaine type antiarrhythmics (lidocaine, Xylocaine ASTRA, Ethmozin USSR) administered shortly before artery ligation have a pro-fibrillation effect. This effect is indirectly proportional to the ischaemic focus development. A 3rd-generation beta blocker with intrinsic sympathetic activity (celiprolol, Selectol Chemie-Linz) had the same electrostabilizing effect on the ventricles in the acute phase of ischaemia as a 1st-generation beta blocker (metipranolol, Trimepranol SPOFA). The 3rd-generation blocker, however, stopped short of provoking a drop in the heart rate invariably associated with the 1st-generation beta blocker. The analgesic fentanyl (G. Richter) in combination with benzodiazepine (m,idazolam, Dormicum Hoffmann-La Roche) inducs analgosedation. In this way the dose of the analgetic can be reduced and yet the analgesia and electrostability of the heart remain the same. Due to the lower dose of the analgesic there is a lesser decrease in the heart rate and blood pressure. Analgosedation can be discontinued by administering an antagonist-agonist of benzodiazepines (flumazenil, Anexate Hoffmann-La Roche) or an antagonist of potent analgesics (butorphanol, Beforal SPOFA) without the risk of eliminating, at the same time, the electrostabilizing effect of analgosedation on the ischaemically damaged ventricles of the heart. For the prevention of sudden coronary death due to ventricular fibrillation in the acute phase of local myocardial ischaemia we can, on the basis of our experimental results, recommend analgosedation and the use of beta blockers with intristic sympathetic action. The use of lidocaine antiarrhythmics may lead to a reduction in the electric stability of the heart ventricles the ischaemic focus is developing under a certain "critical" blood level of the antiarrhythmics.

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预防冠状动脉猝死。
在戊巴比妥全身麻醉犬的实验研究中得到以下结果:在动脉结扎前不久给予利多卡因型抗心律失常药(利多卡因,Xylocaine ASTRA, Ethmozin USSR)具有促纤作用。这种效应与局部缺血灶的发育成正比。具有内在交感神经活性的第三代β受体阻滞剂(塞利洛尔,Selectol chemine - linz)在缺血急性期对心室的电稳定作用与第一代β受体阻滞剂(美普萘洛尔,曲美萘洛尔SPOFA)相同。然而,第三代受体阻滞剂并没有像第一代受体阻滞剂那样引起心率下降。镇痛药芬太尼(G. Richter)联合苯二氮卓类药物(m、咪唑仑、多米康)诱导镇痛镇静。通过这种方法,止痛剂的剂量可以减少,但心脏的镇痛作用和电稳定性保持不变。由于镇痛药的剂量较低,心率和血压的下降幅度较小。可以通过给予苯二氮卓类拮抗剂-激动剂(氟马西尼,Anexate Hoffmann-La Roche)或强效镇痛药拮抗剂(布托啡诺,befora)来停用镇痛镇静,同时,镇痛镇静对缺血性损伤的心脏心室的电稳定作用没有被消除的风险。为了预防局部心肌缺血急性期室性颤动引起的冠状动脉猝死,根据我们的实验结果,我们可以推荐镇痛镇静和使用具有内在交感作用的β受体阻滞剂。使用利多卡因抗心律失常药物可能导致心脏心室电稳定性降低,在抗心律失常药物的一定“临界”血药水平下,心肌缺血病灶正在形成。
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