Le Tulzo Y, Seguin P, Gacouin A, Camus C, Suprin E, Jouannic I, Thomas R
Service de Réanimation Médicale et Maladies Infectieuses, CHRU de Rennes, Hôpital Pontchaillou, Rennes, France.
Intensive Care Med. 1997 Jun;23(6):664-70. doi: 10.1007/s001340050391.
To recognize patients with unresponsive septic shock and right ventricular (RV) failure and to evaluate the effects of epinephrine on RV performance in these patients.
Prospective descriptive study.
Medical intensive care unit.
14 consecutive patients in septic shock unresponsive to fluid loading, dopamine, and dobutamine.
Evaluation of RV function by thermodilution with a pulmonary artery catheter equipped with a rapid-response thermistor. Measurements were obtained before and during epinephrine infusion to achieve a systolic arterial pressure > or = 90 mmHg or a mean arterial pressure (MAP) > or = 70 mmHg.
At the time of inclusion in the study the hemodynamic pattern in the 14 patients was as follows: (MAP) 58 +/- 14 mmHg, systemic vascular resistance (SVR) 1046 +/- 437 dyne.s.cm-5.m-2, pulmonary artery occlusion pressure (PAOP) 14 +/- 4 mmHg, mean pulmonary artery pressure (MPAP) 24 +/- 4 mmHg, right arterial pressure (RAP) 11 +/- 4 mmHg, cardiac index (CI) 4 +/- 1.7 l/min per m2. During epinephrine infusion, MAP, CI and stroke volume index (SVI) were increased (27%, p < 0.01; 20%, p < 0.01; 15%, p < 0.05, respectively). There was no change in PAOP, SVR or heart rate. Seven patients (group A) had marked RV failure defined by both RV dilation [RV end-diastolic volume index (RVEDVI) > 92 ml/m2] and low RV ejection factor (RVEF) (< 52%) and 7 did not (group B). Group A had a lower baseline RVEF than group B (24 +/- 7 vs 45 +/- 9%, p < 0.05), a higher RVEDVI (134 +/- 28 vs 79 +/- 17 ml/ m2, p < 0.01), and a higher RVES (systolic) VI (103 +/- 30 vs 43 +/- 11 ml/ m2, p < 0.01). The other hemodynamics, especially RAP and RV stroke work index (RVSWI) were no different in the two groups and did not predict RV dysfunction. In group A, epinephrine infusion improved RVEF (25%, p < 0.05) by a reduction in RVESVI (-8%, p < 0.05) without any change in RVEDVI or in RAP, in spite of a rise in MPAP (11%, p < 0.05). A rise in RVSWI (76%, p < 0.05), SVI (23%, p < 0.05), and CI (24%, p < 0.05) was also achieved. An upward vertical shift of the Frank-Starling relationship RVSWI/ RVEDVI and an upward shift to the left of the pressure volume relationship pulmonary artery peak pressure/RVESVI was observed only in the group with RV failure following treatment with epinephrine. In group B (without RV failure), RV parameters were not modified by epinephrine.
In patients with severe septic shock, RV dysfunction was identified by the use of an RVEF pulmonary artery catheter and was improved by epinephrine by means of an improvement in RV contractility.
识别无反应性感染性休克和右心室（RV）衰竭患者，并评估肾上腺素对这些患者右心室功能的影响。
前瞻性描述性研究。
医学重症监护病房。
14例对液体负荷、多巴胺和多巴酚丁胺无反应的感染性休克患者。
使用配备快速响应热敏电阻的肺动脉导管通过热稀释法评估右心室功能。在肾上腺素输注前及输注过程中进行测量，以使收缩压≥90 mmHg或平均动脉压（MAP）≥70 mmHg。
纳入研究时，14例患者的血流动力学模式如下：MAP为58±14 mmHg，全身血管阻力（SVR）为1046±437达因·秒·厘米⁻⁵·米⁻²，肺动脉闭塞压（PAOP）为14±4 mmHg，平均肺动脉压（MPAP）为24±4 mmHg，右心房压（RAP）为11±4 mmHg，心脏指数（CI）为4±1.7升/分钟·平方米。在肾上腺素输注期间，MAP、CI和每搏量指数（SVI）升高（分别升高27%，p<0.01；20%，p<0.01；15%，p<0.05）。PAOP、SVR或心率无变化。7例患者（A组）因右心室扩张[右心室舒张末期容积指数（RVEDVI）>92毫升/平方米]和低右心室射血分数（RVEF）（<52%）而有明显的右心室衰竭，另7例患者无右心室衰竭（B组）。A组的基线RVEF低于B组（24±7%对45±9%，p<0.05），RVEDVI更高（134±28对79±17毫升/平方米，p<0.01），右心室收缩末期容积指数（RVESVI）更高（103±30对43±11毫升/平方米，p<0.01）。两组的其他血流动力学指标，尤其是RAP和右心室每搏功指数（RVSWI）无差异，也不能预测右心室功能障碍。在A组中，肾上腺素输注通过降低RVESVI（-8%，p<0.05）改善了RVEF（25%，p<0.05），而RVEDVI或RAP无变化，尽管MPAP升高（1l%，p<0.05）。RVSWI（76%，p<0.05）、SVI（23%，p<0.05）和CI（24%，p<0.05）也升高。仅在肾上腺素治疗后右心室衰竭的组中观察到Frank-Starling关系RVSWI/RVEDVI的向上垂直移位以及压力-容积关系肺动脉峰值压力/RVESVI向左上方移位。在B组（无右心室衰竭）中，肾上腺素未改变右心室参数。
在严重感染性休克患者中，使用RVEF肺动脉导管可识别右心室功能障碍，肾上腺素可通过改善右心室收缩力来改善右心室功能障碍。
