title: [Variations of left ventricular-arterial coupling in septic shock].
abstract: OBJECTIVE
  To explore the variations of left ventricular-arterial coupling and elucidate its mechanisms in septic shock.
  
  
  METHODS
  Septic shock rabbits were established by an intravenous injection of endotoxin. A total of 12 rabbits were divided randomly into sham operation group (S, n = 6) and endotoxin injection group (E, n = 6). Ultrasonic echocardiography and hemodynamic monitoring were conducted at 0h (30-min post-operation), 2h (1-hour after endotoxin or saline injection) and 4h (3-hour after endotoxin or saline injection) and the relative hemodynamic indices were recorded.
  
  
  RESULTS
  (1) In E group, end-systolic elastance (Ees) at 2h was lower than that at 0h (75.72 ± 5.16 vs 90.77 ± 7.17 mm Hg/ml) and Ees at 4h was lower than that at 2h (58.45 ± 3.63 vs 75.72 ± 5.16 mm Hg/ml, P < 0.05); (2) In E group, left ventricular diastolic volume (LVDV) at 2h and 4h were both lower than that at 0h (3.26 ± 0.21 vs 3.58 ± 0.25 ml, 3.27 ± 0.19 vs 3.58 ± 0.25 ml). And left ventricular end diastolic compliance (Ced) at 4h were lower than that at 0h and 2h (0.61 ± 0.05 vs 0.74 ± 0.07 ml/mm Hg, 0.61 ± 0.05 vs 0.75 ± 0.08 ml/mm Hg, P < 0.05); (3) In E group, Ea at 2h and 4h was lower than that at 0h (41.35 ± 2.87 vs 50.46 ± 3.22 mm Hg/ml, 40.13 ± 2.68 vs 50.46 ± 3.22 mm Hg/ml, P < 0.05); (4) In E group, Ea/Ees at 4h was higher than that at 0h and 4h (0.70 ± 0.07 vs 0.57 ± 0.06, 0.70 ± 0.07 vs 0.56 ± 0.05, P < 0.05). And Ea/Ees at 2h had no significant difference with that at 0h (0.56 ± 0.05 vs 0.57 ± 0.06, P < 0.05).
  
  
  CONCLUSIONS
  During compensatory stage of septic shock, left ventricular-arterial coupling shows no significant variation. However, during decompensatory stage of septic shock, there is significant left ventricular-arterial decoupling. The main reason for decoupling lies in that the decrease of left myocardial contractility is more significant than that of left ventricular afterload. And ventricular diastolic dysfunction may also participate.
authors.affiliation: Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing 100730, China.
authors.forename: Su-wei
authors.initials: SW
authors.lastname: Li
authors.affiliation: Email: dwliu@medmail.com.cn.
authors.forename: Da-wei
authors.initials: DW
authors.lastname: Liu
authors.forename: Xiao-ting
authors.initials: XT
authors.lastname: Wang
authors.forename: Bin
authors.initials: B
authors.lastname: Zhang
authors.forename: Xiu-kai
authors.initials: XK
authors.lastname: Chen
authors.forename: Wen-zhao
authors.initials: WZ
authors.lastname: Chai
authors.forename: Hong-min
authors.initials: HM
authors.lastname: Zhang
authors.forename: Qan-hui
authors.initials: QH
authors.lastname: Yang
authors.forename: Huai-wu
authors.initials: HW
authors.lastname: He
mesh_terms: D000818:Animals; D001158:Arteries / Q000503:physiopathology*; D004195:Disease Models, Animal; D006352:Heart Ventricles; D008297:Male; D011817:Rabbits; D012772:Shock, Septic / Q000503:physiopathology*; D016277:Ventricular Function, Left