title: [Effects of the β-blockers on cardiac protection and hemodynamics in patients with septic shock: a prospective study].
abstract: OBJECTIVE
  To investigate the effects of β-blockers on cardiac protection and hemodynamic in patients with septic shock.
  
  
  METHODS
  A prospective randomized controlled trial was conducted. Forty-one patients with septic shock in accordance with early goal directed treatment and met the target within 6 hours, and admitted to intensive care unit (ICU) of Affiliated Huxi Hospital of Jining Medical College from January 2012 to January 2014 were enrolled. The patients were divided into treatment group (n=21) and control group (n=20) by random number table. The patients in both groups were given the standard treatment, esmolol was giving to patients in treatment group in order to control the heart rate(HR) below 100 bpm within 2 hours, and the patients in control group only received standard treatment. The changes in hemodynamic parameters [mean arterial pressure (MAP), central venous pressure (CVP), HR, cardiac index (CI), stroke volume index (SVI), systemic vascular resistance (SVRI), global end diastolic volume index (GEDVI)], biochemistry metabolic of tissue [central venous oxygen saturation (ScvO₂), lactic acid (Lac)], and cardiac markers [troponin I (cTnI)] before and 12, 24, 48, 72 hours after the treatment were recorded.
  
  
  RESULTS
  (1) Before treatment, the hemodynamic parameters, tissue metabolism index and cTnI had no significant differences in both groups (all P>0.05). (2) The hemodynamic parameters after treatment in the control group showed no significant difference compared with that before treatment. HR and CI in the treatment group were gradually declined after treatment, SVRI and GEDVI were gradually increased. There were significant differences in HR, CI, SVRI, and GEDVI between treatment group and control group from 12 hours on [HR (bpm): 93 ± 4 vs. 118 ± 13, CI (L × min⁻¹ × m⁻²): 3.3 ± 0.8 vs. 4.5 ± 0.6, SVRI (kPa×s × L⁻¹ × m⁻²): 159.2 ± 27.4 vs. 130.5 ± 24.2, GEDVI (mL/m²): 668 ± 148 vs. 588 ± 103, P<0.05 or P<0.01]. MAP, CVP and SVI in the treatment group showed no significant changes. (3) Lac after treatment in both groups was decreased slowly, Lac (mmol/L) at 12 hours after treatment was significantly decreased compared with that before treatment (control group: 8.8 ± 3.2 vs. 9.8 ± 3.4, treatment group: 9.5 ± 3.1 vs. 10.5 ± 4.1, both P<0.05). The Lac of control group and treatment group were 2.5 ± 1.2 and 2.7 ± 1.1 at 72 hours after treatment, and there was no significant difference between two groups (all P>0.05). The ScvO₂was not decreased in both groups. (4) Compared with before treatment, cTnI in the control group was gradually increased, peaked at 72 hours, and that in the treatment group was gradually increased, peaked at 24 hours and then gradually declined. Compared with control group, the cTnI (μg/L) in the treatment group was decreased significantly at 24, 48, 72 hours (1.15 ± 0.57 vs. 1.74 ± 0.77, 0.93 ± 0.52 vs. 2.15 ± 1.23, 0.52 ± 0.36 vs. 2.39 ± 1.17, all P<0.01).
  
  
  CONCLUSIONS
  β-blockers (esmolol) can improve cardiac function and myocardial compliance, reduce the myocardial injury in patients with sepsis shock. Although β-blockers can decrease cardiac output, it has no influence on the circulation function and tissue perfusion.
authors.affiliation: Department of Intensive Care Unit, Affiliated Huxi Hospital of Jining Medical College (Shanxian Central Hospital), Shanxian 274300, Shandong, China, Corresponding author: Shi Qibiao, Email: shixinzhong3698@163.com.
authors.forename: Shengqiang
authors.initials: S
authors.lastname: Yang
authors.forename: Zhen
authors.initials: Z
authors.lastname: Liu
authors.forename: Wenbao
authors.initials: W
authors.lastname: Yang
authors.forename: Guizhen
authors.initials: G
authors.lastname: Zhang
authors.forename: Baojun
authors.initials: B
authors.lastname: Hou
authors.forename: Jihua
authors.initials: J
authors.lastname: Liu
authors.forename: Qibiao
authors.initials: Q
authors.lastname: Shi
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D062186:Arterial Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D002496:Central Venous Pressure / Q000187:drug effects; D006331:Heart Diseases / Q000517:prevention & control*; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D011412:Propanolamines / Q000494:pharmacology*; D011446:Prospective Studies; D012772:Shock, Septic / Q000188:drug therapy* / Q000503:physiopathology; D013318:Stroke Volume / Q000187:drug effects; D016896:Treatment Outcome
chemical_list: D000319:Adrenergic beta-Antagonists; D011412:Propanolamines; C036604:esmolol