Ventricular arterial (V-A) decoupling may persist in patients with septic shock. V-A decoupling can be exacerbated by increased afterload and by tachycardia. Decoupling is relevant as it can be associated with inefficiency and unfavourable myocardial energetics. Tachycardia also increases myocardial oxygen consumption and, by shortening diastolic relaxation time, may impair coronary perfusion
The use of an esmolol infusion in a tachycardic, fluid resuscitated, septic shock patient population was reported in this study (1). Esmolol induced decrease in heart rate (HR) was associated with improved haemodynamics and reductions in norepinephrine dosing and troponin levels. This improvement may be related, at least in part, to enhanced diastolic function and/or better V–A coupling. As arterial tone is a major determinant of V–A coupling (2), HR reduction may improve V–A coupling by decreasing static arterial elastance (Ea).
The purpose of this recent prospective observational study was to investigate the effects of HR reduction on Ea in tachycardic septic shock patients (2). The hypothesis stated that esmolol improves Ea by positively affecting the tone of arterial vessels and their responsiveness to HR-related changes in stroke volume.
After at least 24 h of haemodynamic optimisation, 45 septic shock patients, with an HR ≥95 bpm and requiring norepinephrine to maintain mean arterial pressure (MAP) ≥65 mmHg, received a titrated esmolol infusion to maintain HR between 80 and 94 bpm. Ea was calculated as MAP/SV. All measurements, including data from right heart catheterisation, echocardiography, arterial waveform analysis, and norepinephrine requirements, were obtained at baseline and at 4 h after commencing esmolol. Esmolol reduced HR in all patients and this was associated with a decrease in Ea (2.19 ± 0.77 vs. 1.72 ± 0.52 mmHg l−1), arterial dP/dtmax (1.08 ± 0.32 vs. 0.89 ± 0.29 mmHg ms−1), and a parallel increase in SV (48 ± 14 vs. 59 ± 18 ml), all p < 0.05. Cardiac output and ejection fraction remained unchanged, whereas norepinephrine requirements were reduced (0.7 ± 0.7 to 0.58 ± 0.5 μg kg−1 min−1, p < 0.05).
HR reduction with esmolol effectively improved Ea while allowing adequate systemic perfusion in patients with severe septic shock who remained tachycardic despite standard volume resuscitation. As Ea is a major determinant of V–A coupling, its reduction may contribute to improving cardiovascular efficiency in septic shock. In the presence of optimal V–A coupling, the cardiovascular system reaches its maximum efficiency; this implies that all the pulsating energy produced by the left ventricle is transmitted downstream to the peripheries with lower energy costs.
These findings confirm that, in the presence of an adequate preload, lowering HR allows better ventricular filling during diastole, hence increasing SV. The increase in SV was also the result of improved arterial loading as a consequence of a reduced Ea.
Taken together, these results suggest that reducing HR in tachycardic septic shock patients with a beta-blocker will have variable effects, in particular on V–A coupling. This reinforces the need to individualise patient treatment according to both myocardial performance as well as their haemodynamic status. The study lacks a control group so it cannot be certain that the findings are the consequence of the esmolol-induced reduction of HR rather than an independent evolution of the patient’s condition.
Article review was submitted by James Day on behalf of the ESICM Journal Review Club.
1. Morelli A, Ertmer C, Westphal M et al (2013). Effect of heart rate control with esmolol on hemodynamic and clinical outcomes in patients with septic shock: a randomized clinical trial. JAMA 310:1683–1691
2. Morelli A et al. (2016). Heart rate reduction with esmolol is associated with improved arterial elastance in patients with septic shock: a prospective observational study. Intensive Care Med DOI 10.1007/s00134-016-4351-2
3. Guarracino F, Ferro B, Morelli A, Bertini P, Baldassarri R, Pinsky MR (2014). Ventriculoarterial decoupling in human septic shock. Crit Care 18:R80