• Su-wei Li, Da-wei Liu, Xiao-ting Wang, Bin Zhang, Xiu-kai Chen, Wen-zhao Chai, Hong-min Zhang, Qan-hui Yang, and Huai-wu He.
• Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing 100730, China.
• Zhonghua Yi Xue Za Zhi. 2013 Sep 17;93(35):2782-5.

ObjectiveTo explore the variations of left ventricular-arterial coupling and elucidate its mechanisms in septic shock.MethodsSeptic 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).ConclusionDuring 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.

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