Department of Internal Clinical, Anesthesiological and Cardiovascular Sciences, University of Rome, 'La Sapienza', Rome, Italy.
Department of Experimental and Clinical Medicine, Unit of Internal Medicine and Cardiology, University of Florence, Florence, Italy.
Br J Anaesth. 2020 Dec;125(6):1018-1024. doi: 10.1016/j.bja.2020.05.058. Epub 2020 Jul 18.
During sepsis, heart rate (HR) reduction could be a therapeutic target, but identification of responders (non-compensatory tachycardia) and non-responders (compensatory for 'fixed' stroke volume [SV]) is challenging. We tested the ability of the difference between systolic and dicrotic pressure (SDP), which reflects the coupling between myocardial contractility and a given afterload, in discriminating the origin of tachycardia.
In this post hoc analysis of 45 patients with septic shock with persistent tachycardia, we characterised features of haemodynamic response focusing on SDP, classifying patients according to variations in arterial dP/dt after 4 h of esmolol administration to maintain HR <95 beats min. A cut-off value of 0.9 mm Hg ms was used for group allocation.
After reducing HR, arterial dP/dt remained above the cut-off in 23 patients, whereas it decreased below the cut-off in 22 patients (from 0.99 [0.37] to 0.63 [0.16] mm Hg ms; mean [SD], P<0.001). At baseline, patients with decreased dP/dt after esmolol had lower SDP than those with higher dP/dt (40 [19] vs 53 [16] mm Hg, respectively; P=0.01). The SDP remained unchanged after esmolol in the higher dP/dt group (49 [16] mm Hg), whereas it decreased significantly in patients with lower dP/dt (29 [11] mm Hg; P<0.001). In the latter, the HR reduction resulted in a significant cardiac output reduction with unchanged SV, whereas in patients with higher dP/dt SV increased (from 48 [12] to 67 [14] ml; P<0.001) with maintained cardiac output.
A decrease in SDP could discriminate between compensatory and non-compensatory tachycardia, revealing a covert loss of myocardial contractility not detected by conventional echocardiographic parameters and deteriorating after HR reduction with esmolol.
NCT02188888.
在脓毒症中，心率（HR）降低可能是一个治疗目标，但识别反应者（非代偿性心动过速）和无反应者（“固定”心输出量的代偿性心动过速）具有挑战性。我们测试了收缩压和舒张压之间的差异（SDP）的能力，该差异反映了心肌收缩力与给定后负荷之间的耦合，以区分心动过速的起源。
在这项 45 例脓毒性休克持续心动过速患者的事后分析中，我们以 SDP 为特征，对血流动力学反应的特征进行了分类，根据艾司洛尔给药 4 小时后动脉 dp/dt 的变化，将患者分类，以维持 HR<95 次/分。使用 0.9mm Hg ms 的截断值进行分组分配。
在降低 HR 后，23 例患者的动脉 dp/dt 仍高于截断值，而 22 例患者的动脉 dp/dt 低于截断值（从 0.99 [0.37]降至 0.63 [0.16] mm Hg ms；平均值 [SD]，P<0.001）。在基线时，艾司洛尔后 dp/dt 降低的患者的 SDP 低于 dp/dt 较高的患者（分别为 40 [19]与 53 [16] mm Hg；P=0.01）。在 dp/dt 较高的组中，艾司洛尔后 SDP 保持不变（49 [16] mm Hg），而在 dp/dt 较低的患者中，SDP 显著下降（29 [11] mm Hg；P<0.001）。在后者中，HR 降低导致心输出量显著降低，而 SV 不变，而在 dp/dt 较高的患者中，SV 增加（从 48 [12]增加到 67 [14] ml；P<0.001），同时心输出量保持不变。
SDP 的降低可以区分代偿性和非代偿性心动过速，揭示了常规超声心动图参数无法检测到的心肌收缩力的隐性丧失，并在 HR 降低后恶化，用艾司洛尔治疗。
NCT02188888。
