INCOMPLETE FILLING AND INCOORDINATE CONTRACTION AS MECHANISMS OF HYPOTENSION DURING VENTRICULAR-TACHYCARDIA IN MAN
INCOMPLETE FILLING AND INCOORDINATE CONTRACTION AS MECHANISMS OF HYPOTENSION DURING VENTRICULAR-TACHYCARDIA IN MAN
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DOI：
10.1161/01.cir.68.5.928
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发表时间：
1983-01-01
期刊：
影响因子：
37.8
通讯作者：
TRAILL, TA
中科院分区：
文献类型：
--
作者：
LIMA, JAC;WEISS, JL;TRAILL, TA
为探讨人室性心动过速（VT）时心输出量减少和低血压的发生机制，对20例患者在诱发室性心动过速（VT）前、中、末进行二维和M型超声心动图及微压导管左室压力测定。根据电生理检查前血管造影射血分数（EF）评估的窦性心律下左心室功能将患者分为2组。第1组（n = 8）血管造影EF ≥。正常窦性心律50%，第2组（n = 12）EF ≤。百分之四十在VT期间，左心室腔容积（以短轴和长轴2维舒张末期腔面积为指标）在组1中从19.7 ± 0.5显著减少。2至8.6 .+-。2cm ~ 2（P < 0.001），从32.0 ±. 8到22.5 .+-。7 cm 2（P < 0.001），但在第2组中仅从34.1 ± 0.7cm 2略微降低。6到31.5 .+-。7 cm ~ 2（P = 0.044），从45.0 ±. 8到49.4 .+-。7cm 2（P = NS）。相反，VT期间的左心室收缩功能（以二维短轴和长轴区域的分数减少为指标）在组2中从25.6 ± 0.01显著降低。6%至4.2 .+-。4%（P = 0.005），从13.7 . ±. 3%至1.8 .+-。0.8%（P < 0.001），但在组1中仍保持在对照水平。第1组的左心室舒张末压从11.8 ±增加。2至27.7 .+-。8 mm Hg（P = 0.005），组2在VT期间无变化。从左心室压力和M模式超声心动图确定的腔尺寸从VT发作结束时产生的压力-尺寸环显示，舒张压-尺寸关系恢复到对照水平，第1组患者的第一个舒张间期延长，表明不完全舒张是这些患者VT期间心输出量减少的机制。收缩和松弛的协调性（由压力-尺寸环面积与刚好包围环的矩形面积的百分比表示）从37 ± 10降低。11%至16 .+-。组2患者在VT期间为13%（P = 0.013），但组1患者保持在对照水平。因此，在VT期间，窦性心律下左心室功能受损的患者（第2组）出现严重的不协调，功能正常或接近正常的患者（第1组）出现不完全舒张，以解释每搏输出量恶化和低血压。
Mechanisms were sought for decrease of cardiac output and for hypotension during ventricular tachycardia (VT) in man. Two-dimensional and M mode echocardiograms and left ventricular pressure from micromanometer-tipped catheters were obtained in 20 patients before, during, and at the end of induced hypotensive VT. Patients were divided into 2 groups according to left ventricular function in sinus rhythm as assessed by angiographic ejection fraction (EF) before electrophysiologic study. Group 1 (n = 8) had angiographic EF .gtoreq. 50% in normal sinus rhythm, and group 2 (n = 12) had EF .ltoreq. 40%. During VT, left ventricular cavity volume (as indexed by short- and long-axis 2-dimensional end-diastolic cavity areas) as markedly reduced in group 1, from 19.7 .+-. 2 to 8.6 .+-. 2 cm2 (P < 0.001) and from 32.0 .+-. 8 to 22.5 .+-. 7 cm2 (P < 0.001), respectively, but was only slightly reduced in group 2, from 34.1 .+-. 6 to 31.5 .+-. 7 cm2 (P = 0.044) and from 45.0 .+-. 8 to 49.4 .+-. 7 cm2 (P = NS), respectively. Conversely, left ventricular systolic function during VT (as indexed by fractional reduction in 2-dimensional short- and long-axis areas) was markedly depressed in group 2, from 25.6 .+-. 6% to 4.2 .+-. 4% (P = 0.005) and from 13.7 .+-. 3% to 1.8 .+-. 0.8% (P < 0.001), respectively, but remained at control levels in group 1. Left ventricular end-diastolic pressures increased in group 1, from 11.8 .+-. 2 to 27.7 .+-. 8 mm Hg (P = 0.005) and did not change in group 2 during VT. Pressure-dimension loops from left ventricular pressure and M mode echocardiographically determined cavity dimensions generated from the end of the VT episodes showed that diastolic pressure-dimension relationships returned to control levels with the first prolonged diastolic interval in group 1 patients, indicating that incomplete relaxation was the mechanism responsible for reduction of cardiac output during VT in these patients. Coordination of contraction and relaxation (indicated by the percent ratio of the pressure-dimension loop area to the area of the rectangle just enclosing the loop) decreased from 37 .+-. 11% to 16 .+-. 13% in group 2 patients during VT (P = 0.013) but remained at control levels in group 1 patients. Thus, during VT patients with impaired left ventricular function in sinus rhythm (group 2) developed severe discoordination, and patients with normal or near-normal function (group 1) developed incomplete relaxation to account for stroke volume deterioration and hypotension.