Sganzerla P, Fabbiocchi F, Grazi S, Cipolla C, Moruzzi P, Guazzi M D
Istituto di Cardiologia, University of Milan, Italy.
Eur Heart J. 1989 Jan;10(1):32-9. doi: 10.1093/oxfordjournals.eurheartj.a059378.
In 16 subjects with paroxysmal supraventricular tachycardia (SVT) we sought a relationship between haemodynamic changes associated with artificially induced arrhythmias and the electrophysiological properties of the related atrioventricular (AV) nodal reentry circuit. In 10 patients (group 1) induced SVT was typical (long AH) and caused a significant fall in cardiac output (-1.720 ml min-1) and arterial systolic pressure (-18 mmHg). In six subjects (group 2), induced SVT was atypical (long HA) and did not significantly alter the output of the heart and systolic pressure, despite the elicitation of similar tachycardia. The opposite AV nodal reciprocation pattern which resulted in a substantial increase in AH/HH in group 1 and in a slight rise of the same variable in group 2, may explain these haemodynamic differences. In fact, atrial and ventricular systoles occurred simultaneously and impeded the ventricular filling in the former group, while a regular subsequence of contraction was maintained in the latter group. In group 2, systolic arterial pressure and cardiac output fell to the same level as in group 1 when right atrial pacing, at a similar rate of SVT, determined an increase of AH/HH similar to that observed during typical tachycardia. Thus, the haemodynamic response to SVT differs significantly between the two types of reciprocating tachycardia, particularly as regards cardiac output and blood pressure, and is mainly influenced by the temporal relationship between atrial and ventricular systole, independent of the rate of contraction. The different conduction velocities of the reciprocating circuit limbs and their interrelation seem to be major determinants of the haemodynamic pattern of SVT.
在16例阵发性室上性心动过速（SVT）患者中，我们探寻了与人工诱发心律失常相关的血流动力学变化与相关房室（AV）结折返环路电生理特性之间的关系。在10例患者（第1组）中，诱发的SVT为典型性（AH间期长），导致心输出量显著下降（-1720 ml/min）和动脉收缩压下降（-18 mmHg）。在6例受试者（第2组）中，诱发的SVT为非典型性（HA间期长），尽管诱发了相似的心动过速，但并未显著改变心脏输出量和收缩压。第1组中导致AH/HH大幅增加而第2组中该变量略有上升的相反房室结折返模式，可能解释了这些血流动力学差异。事实上，在第1组中，心房和心室收缩同时发生，阻碍了心室充盈，而在第2组中则维持了有规律的收缩顺序。在第2组中，当以与SVT相似的速率进行右心房起搏，使AH/HH增加至与典型心动过速时观察到的情况相似时，收缩期动脉压和心输出量降至与第1组相同的水平。因此，两种类型的折返性心动过速对SVT的血流动力学反应存在显著差异，尤其是在心输出量和血压方面，并且主要受心房和心室收缩之间的时间关系影响，与收缩速率无关。折返环路分支的不同传导速度及其相互关系似乎是SVT血流动力学模式的主要决定因素。
