Determinants of Right Ventricular Performance in Severe Acute Pulmonary Embolism

Zachary D. Demertzis DO, Terry R. Bowers MD, James A. Goldstein MD
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引用次数: 0

Abstract

Background

Severe acute pulmonary embolism (PE) induces hemodynamic compromise due to a failing right ventricle (RV) and a “dry” hyperdynamic left ventricle (LV). RV systolic dysfunction is the key parameter to determine acute PE risk stratification, clinical management, and prognosis. The present study delineates the determinants of RV performance in acute PE resulting in RV dysfunction.

Methods

This was a single-center, retrospective analysis of a high-volume PE response team database of patients with intermediate-high-risk or high-risk PE with an echocardiogram prior to escalation of care.

Results

The RV free wall motion (total RVFW motion score = 8.1 ± 2.8) was correlated with the magnitude of RV systolic depression (RV fractional area change [FAC] = 29 ± 13%, tricuspid annular planar systolic excursion = 1.57 ± 0.49 cm, and S′ velocity = 10.57 ± 3.14 cm/s). LV preload and stroke volume were markedly reduced (LV end diastolic size = 4.04 ± 0.68 cm and volume = 73.6 ± 25.8 mL; LV stroke volume = 46.2 ± 16.6 mL). LV preload deprivation was correlated with the severity of RV systolic dysfunction (total RVFW motion score, r = −0.11, P = .39; FAC, r = 0.25, P = .04; S′ velocity, r = 0.27, P = .03). RV overload induced reversed interventricular septal curvature reflected by LV end diastolic eccentricity index = 1.21 ± 0.21, which correlated with RV systolic dysfunction (total RVFW motion score, r = 0.47, P < .001; FAC, r = −0.35, P < .005; S′ velocity, r = −0.43, P < .001) and RV dilation.

Conclusions

Afterload strain imposed by PE may induce severe RV systolic dysfunction attributable to marked RVFW dysfunction. RV systolic pressure generation and transpulmonary flow are generated through systolic ventricular interactions mediated by primary septal contraction and paradoxical septal motion.
严重急性肺栓塞患者右心室功能的决定因素
严重急性肺栓塞(PE)导致右心室(RV)衰竭和左心室(LV)“干”高动力导致血流动力学损害。右心室收缩功能障碍是决定急性肺动脉栓塞风险分层、临床处理和预后的关键参数。本研究描述了急性PE导致右心室功能障碍时右心室功能的决定因素。方法:本研究是一项单中心、回顾性分析中高风险或高风险PE患者的大容量PE反应团队数据库,这些患者在治疗升级前进行了超声心动图检查。结果右心室自由壁运动(总RVFW运动评分为8.1±2.8)与右心室收缩抑制程度相关(右心室分数面积变化[FAC] = 29±13%,三尖瓣环形平面收缩偏移= 1.57±0.49 cm, S '速度= 10.57±3.14 cm/ S)。左室预负荷和卒中容积明显降低(左室舒张末期尺寸= 4.04±0.68 cm,容积= 73.6±25.8 mL;左室卒中容积= 46.2±16.6 mL)。左室预负荷剥夺与左室收缩功能障碍严重程度相关(RVFW总运动评分,r = - 0.11, P = 0.39; FAC, r = 0.25, P = 0.04; S’velocity, r = 0.27, P = 0.03)。右心室负荷引起的左室舒张末期偏心率指数反映的室间隔扭转曲率= 1.21±0.21,与右室收缩功能障碍(RVFW总运动评分r = 0.47, P < 0.001; FAC, r = - 0.35, P < 0.001; S ' velocity, r = - 0.43, P < 0.001)和右室扩张相关。结论肺动脉高压可引起严重的右心室收缩功能障碍,引起明显的右心室收缩功能障碍。右心室收缩压的产生和跨肺流动是通过初级间隔收缩和矛盾间隔运动介导的收缩心室相互作用产生的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
1.40
自引率
0.00%
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审稿时长
48 days
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