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.
