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[心律失常及抗心律失常治疗期间血流动力学的临床观点]

[Clinical viewpoints of hemodynamics in cardiac arrhythmias and during anti-arrhythmia treatment].

作者信息

Thormann J

机构信息

Kerchoff-Klinik der Max-Planck-Gesellschaft, Bad Nauheim.

出版信息

Z Kardiol. 1988;77 Suppl 5:121-36.

PMID:3066034
Abstract
  1. Hemodynamics during cardiac arrhythmias: Cardiac syncopes can be caused by bradycardia (temporary asystole) or by tachycardia. However, tachycardia might be tolerated without causing such symptoms. The necessary compensatory mechanisms (as initiated from the heart, the circulatory system, and the metabolism) are incompletely understood in man. The tolerance of tachycardia depends on the underlying cardiac disease, heart rate, and duration of tachycardia, as well as on the efficiency of compensatory mechanisms. The aspects of tachycardia tolerance, presented here by hemodynamic analysis, include: atrial transport, ventricular tachycardia (arterial pressure, coronary flow, coronary reserve, extravascular resistance), syncopal ventricular tachycardia, supraventricular tachycardia, tachycardia in aortic valvular stenosis, the AFORMED phenomenon, arrhythmia effects on valvular heart disease, and perfusion of organic systems. 2. Hemodynamics during antiarrhythmic therapy: The cardiodepressive side effects inherent in virtually all antiarrhythmic (AA) drugs are complex, variable, and cannot be accurately differentiated as to their components by using conventional hemodynamic parameters. As a rule, this cardiodepression is effective only in cases of impaired myocardial function and/or increased vagal tone. These unwanted hemodynamic effects might influence LV-pump function directly (myocardium: negative inotrope) and indirectly (vasoactive, neurohumoral-reflectory: changes of pre and/or afterload, and of heart rate). The identification of the potentially participating negative inotropic action of the AA-induced cardiodepression, therefore, was accomplished using the elaborate method of analyzing the endsystolic pressure-volume relationship (conductance-catheter technique). The temporary balloon occlusion in the vena cava inferior was used to establish the equation of the isometric maxima. AA-induced alterations of the diastolic ventricular function used echocardiographic data for analysis.
摘要
  1. 心律失常时的血流动力学:心源性晕厥可由心动过缓(暂时性心搏停止)或心动过速引起。然而,心动过速可能被耐受而不引起此类症状。人体中必要的代偿机制(由心脏、循环系统和代谢启动)尚未完全明确。心动过速的耐受性取决于潜在的心脏疾病、心率、心动过速持续时间以及代偿机制的效率。通过血流动力学分析呈现的心动过速耐受性方面包括:心房运输、室性心动过速(动脉压、冠状动脉血流、冠状动脉储备、血管外阻力)、晕厥性室性心动过速、室上性心动过速、主动脉瓣狭窄时的心动过速、AFORMED现象、心律失常对瓣膜性心脏病的影响以及机体各系统的灌注。2. 抗心律失常治疗时的血流动力学:几乎所有抗心律失常(AA)药物固有的心脏抑制副作用都很复杂且多变,使用传统血流动力学参数无法准确区分其组成部分。通常,这种心脏抑制仅在心肌功能受损和/或迷走神经张力增加的情况下才有效。这些不良血流动力学效应可能直接影响左心室泵功能(心肌:负性肌力作用),也可能间接影响(血管活性、神经体液反射性:前负荷和/或后负荷以及心率的变化)。因此,通过分析收缩末期压力 - 容积关系的精细方法(电导导管技术)来识别AA诱导的心脏抑制中潜在的负性肌力作用。利用下腔静脉临时球囊阻塞来建立等容最大值方程。AA诱导的舒张期心室功能改变则使用超声心动图数据进行分析。

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