den Uil Corstiaan A, Lagrand Wim K, van der Ent Martin, Nieman Koen, Struijs Ard, Jewbali Lucia S D, Constantinescu Alina A, Spronk Peter E, Simoons Maarten L
Thoraxcenter, Erasmus Medical Center, Departments of Cardiology and Intensive Care Medicine, Rotterdam, the Netherlands.
Academic Medical Center, Department of Intensive Care Medicine, Amsterdam, the Netherlands.
PLoS One. 2014 Aug 1;9(8):e103978. doi: 10.1371/journal.pone.0103978. eCollection 2014.
To investigate the effects of inotropic agents on parameters of tissue perfusion in patients with cardiogenic shock.
Thirty patients with cardiogenic shock were included. Patients received dobutamine, enoximone, or norepinephrine. We performed hemodynamic measurements at baseline and after titration of the inotropic agent until cardiac index (CI) ≥ 2.5 L.min-1.m(-2) or mixed-venous oxygen saturation (SvO2) ≥ 70% (dobutamine or enoximone), and mean arterial pressure (MAP) ≥ 70 mmHg (norepinephrine). As parameters of tissue perfusion, we measured central-peripheral temperature gradient (delta-T) and sublingual perfused capillary density (PCD). All patients reached predefined therapeutic targets. The inotropes did not significantly change delta-T. Dobutamine did not change PCD. Enoximone increased PCD (9.1 [8.9-10.2] vs. 11.4 [8.4-13.9] mm.mm(-2); p<0.05), and norepinephrine tended to decrease PCD (9.8 [8.5-11.9] vs. 8.8 [8.2-9.6] mm.mm-2, p = 0.08). Fifteen patients (50%) died within 30 days after admission. Patients who had low final PCD (≤ 10.3 mm.mm-2; 64%) were more likely to die than patients who had preserved PCD (>10.3 mm.mm(-2); mortality 72% vs. 17%, p = 0.003).
This study demonstrates the effects of commonly used inotropic agents on parameters of tissue perfusion in patients with cardiogenic shock. Despite hemodynamic optimization, tissue perfusion was not sufficiently restored in most patients. In these patients, mortality was high. Interventions directed at improving microcirculation may eventually help bridging the gap between improved hemodynamics and dismal patient outcome in cardiogenic shock.
研究强心药物对心源性休克患者组织灌注参数的影响。
纳入30例心源性休克患者。患者接受多巴酚丁胺、依诺昔酮或去甲肾上腺素治疗。我们在基线时以及在滴定强心药物后进行血流动力学测量,直至心脏指数(CI)≥2.5L·min⁻¹·m⁻²或混合静脉血氧饱和度(SvO₂)≥70%(多巴酚丁胺或依诺昔酮),以及平均动脉压(MAP)≥70mmHg(去甲肾上腺素)。作为组织灌注参数,我们测量了中心-外周温度梯度(ΔT)和舌下灌注毛细血管密度(PCD)。所有患者均达到预定治疗目标。强心药物未显著改变ΔT。多巴酚丁胺未改变PCD。依诺昔酮增加了PCD(9.1[8.9 - 10.2]对11.4[8.4 - 13.9]mm·mm⁻²;p<0.05),而去甲肾上腺素倾向于降低PCD(9.8[8.5 - 11.9]对8.8[8.2 - 9.6]mm·mm⁻²,p = 0.08)。15例患者(50%)在入院后30天内死亡。最终PCD较低(≤10.3mm·mm⁻²;64%)的患者比PCD正常(>10.3mm·mm⁻²)的患者死亡可能性更高(死亡率72%对17%,p = 0.003)。
本研究证明了常用强心药物对心源性休克患者组织灌注参数的影响。尽管进行了血流动力学优化,但大多数患者的组织灌注仍未充分恢复。在这些患者中,死亡率很高。针对改善微循环的干预措施最终可能有助于弥合心源性休克患者血流动力学改善与不良预后之间的差距。