THE DYNAMICS OF PULSUS ALTERNANS: ALTERNATING END-DIASTOLIC FIBER LENGTH AS A CAUSATIVE FACTOR.
THE DYNAMICS OF PULSUS ALTERNANS: ALTERNATING END-DIASTOLIC FIBER LENGTH AS A CAUSATIVE FACTOR.
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交替脉的动力学：交替舒张末期纤维长度作为致病因素。
DOI：
10.1172/jci104696
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发表时间：
1963
期刊：
影响因子：
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通讯作者：
E. Sonnenblick
中科院分区：
文献类型：
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作者：
J. H. Mitchell;S. Sarnoff;E. Sonnenblick
交替脉，首先由Traube于1872年描述（1），其特征是心室收缩强弱交替，节律规则（2-4）。心电图通常正常，但可能存在电交替（3，5）。临床上，交替脉最常发生在心肌疾病的情况下（3，6），但也可在无任何明显心肌异常的自发性心动过速中观察到（2，7）。关于这种现象的机制，已经提出了各种理论。Wenckelach认为，影响心室充盈程度的心外因素以及舒张末期压和容积是交替的主要决定因素，弱搏动是从较低的压力和较小的容积开始的（8，9）。Straub的实验使研究人员相信，弱搏动是从较小的体积但较高的压力开始的，这是由于先前强搏动的代谢恢复不完全所致（10）。第三种观点（11-15）认为某些心肌节段存在交替的收缩失败，这一观点仍然是当前的观点（16，17）。这份来文的目的是提出似乎与文克巴赫和斯特劳布的观点相一致的证据。我们将证明，弱搏动可以从较低的、相同的或较高的舒张末期压开始，但在我们的实验条件下，共同点似乎是弱搏动发生在收缩元件的较短舒张末期长度。尽管这些发现并不排除某些心肌节段交替收缩失败的可能性，
Pulsus alternans, first described by Traube in 1872 (1), is characterized by an alternation between weak and strong ventricular systoles with a regular rhythm (2-4). The electrocardiogram is usually normal but electrical alternans may be present (3, 5). Clinically, pulsus alternans most frequently occurs in the presence of myocardial disease (3, 6), but may also be seen in spontaneous tachycardia without any apparent myocardial abnormality (2, 7). Various theories regarding the mechanism of this phenomenon have been postulated. Wenckelach believed that extracardiac factors influencing the degree of ventricular filling and therefore enddiastolic pressure and volume were the major determinants of alternation, the weak beat being initiated from a lower pressure and a smaller volume (8, 9). Straub's experiments led that investigator to believe that the weak beat is initiated from a smaller volume but a higher pressure and that this was attributable to incomplete metabolic recovery from the previous strong beat (10). A third view (11-15) holds that there is an alternate failure of contraction of certain myocardial segments, a view which is still current (16, 17). The obj ect of this communication is to present evidence which appears to reconcile the views of Wenckebach and Straub. It will be shown that the weak beat can be initiated from either a lower, the same, or a higher end-diastolic pressure but that, under the conditions of our experiments, the common denominator appears to be that the weak beat occurs from a shorter end-diastolic length of the contractile element. Although these findings do not rule out the possibility that an alternate failure of contraction of certain myocardial seg-