Ventricular-arterial (V-A) decoupling decreases myocardial efficiency and is exacerbated by tachycardia that increases static arterial elastance (Ea). We thus investigated the effects of heart rate (HR) reduction on Ea in septic shock patients using the beta-blocker esmolol. We hypothesized that esmolol improves Ea by positively affecting the tone of arterial vessels and their responsiveness to HR-related changes in stroke volume (SV). After at least 24 h of hemodynamic optimization, 45 septic shock patients, with an HR aeyen95 bpm and requiring norepinephrine to maintain mean arterial pressure (MAP) aeyen65 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 catheterization, 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 +/- A 0.77 vs. 1.72 +/- A 0.52 mmHg l(-1)), arterial dP/dt (max) (1.08 +/- A 0.32 vs. 0.89 +/- A 0.29 mmHg ms(-1)), and a parallel increase in SV (48 +/- A 14 vs. 59 +/- A 18 ml), all p < 0.05. Cardiac output and ejection fraction remained unchanged, whereas norepinephrine requirements were reduced (0.7 +/- A 0.7 to 0.58 +/- A 0.5 A mu g 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.
Heart rate reduction with esmolol is associated with improved arterial elastance in patients with septic shock. A prospective observational study
MASCIA, LUCIANA
2016-01-01
Abstract
Ventricular-arterial (V-A) decoupling decreases myocardial efficiency and is exacerbated by tachycardia that increases static arterial elastance (Ea). We thus investigated the effects of heart rate (HR) reduction on Ea in septic shock patients using the beta-blocker esmolol. We hypothesized that esmolol improves Ea by positively affecting the tone of arterial vessels and their responsiveness to HR-related changes in stroke volume (SV). After at least 24 h of hemodynamic optimization, 45 septic shock patients, with an HR aeyen95 bpm and requiring norepinephrine to maintain mean arterial pressure (MAP) aeyen65 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 catheterization, 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 +/- A 0.77 vs. 1.72 +/- A 0.52 mmHg l(-1)), arterial dP/dt (max) (1.08 +/- A 0.32 vs. 0.89 +/- A 0.29 mmHg ms(-1)), and a parallel increase in SV (48 +/- A 14 vs. 59 +/- A 18 ml), all p < 0.05. Cardiac output and ejection fraction remained unchanged, whereas norepinephrine requirements were reduced (0.7 +/- A 0.7 to 0.58 +/- A 0.5 A mu g 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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
