Wemmelund Kristian Borup, Ringgård Viktor Kromann, Vistisen Simon Tilma, Hyldebrandt Janus Adler, Sloth Erik, Juhl-Olsen Peter
Department of Anaesthesiology and Intensive Care, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.
Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 82, 8200, Aarhus N, Denmark.
Intensive Care Med Exp. 2017 Sep 11;5(1):42. doi: 10.1186/s40635-017-0158-x.
Pleural effusion (PLE) may lead to low blood pressure and reduced cardiac output. Low blood pressure and reduced cardiac output are often treated with fluid loading and vasopressors. This study aimed to determine the impact of fluid loading and norepinephrine infusion on physiologic determinants of cardiac function obtained by ultrasonography during PLE.
In this randomised, blinded, controlled laboratory study, 30 piglets (21.9 ± 1.3 kg) had bilateral PLE (75 mL/kg) induced. Subsequently, the piglets were randomised to intervention as follows: fluid loading (80 mL/kg/h for 1.5 h, n = 12), norepinephrine infusion (0.01, 0.03, 0.05, 0.1, 0.2 and 0.3 μg/kg/min (15 min each, n = 12)) or control (n = 6). Main outcome was left ventricular preload measured as left ventricular end-diastolic area. Secondary endpoints included contractility and afterload as well as global measures of circulation. All endpoints were assessed with echocardiography and invasive pressure-flow measurements.
PLE decreased left ventricular end-diastolic area, mean arterial pressure and cardiac output (p values < 0.001), but fluid loading (20 mL/kg) and norepinephrine infusion (0.05 μg/kg/min) restored these values (p values > 0.05) to baseline. Left ventricular contractility increased with norepinephrine infusion (p = 0.002), but was not affected by fluid loading (p = 0.903). Afterload increased in both active groups (p values > 0.001). Overall, inferior vena cava distensibility remained unchanged during intervention (p values ≥ 0.085). Evacuation of PLE caused numerical increases in left ventricular end-diastolic area, but only significantly so in controls (p = 0.006).
PLE significantly reduced left ventricular preload. Both fluid and norepinephrine treatment reverted this effect and normalised global haemodynamic parameters. Inferior vena cava distensibility remained unchanged. The haemodynamic significance of PLE may be underestimated during fluid or norepinephrine administration, potentially masking the presence of PLE.
胸腔积液（PLE）可能导致低血压和心输出量降低。低血压和心输出量降低通常采用补液和血管升压药进行治疗。本研究旨在确定补液和去甲肾上腺素输注对胸腔积液期间通过超声心动图获得的心脏功能生理决定因素的影响。
在这项随机、双盲、对照实验室研究中，30只仔猪（21.9±1.3千克）诱导产生双侧胸腔积液（75毫升/千克）。随后，将仔猪随机分为以下干预组：补液（80毫升/千克/小时，持续1.5小时，n = 12）、去甲肾上腺素输注（0.01、0.03、0.05、0.1、0.2和0.3微克/千克/分钟（各15分钟，n = 12））或对照组（n = 6）。主要结局是以左心室舒张末期面积测量的左心室前负荷。次要终点包括收缩性和后负荷以及整体循环指标。所有终点均通过超声心动图和有创压力-流量测量进行评估。
胸腔积液降低了左心室舒张末期面积、平均动脉压和心输出量（p值<0.001），但补液（20毫升/千克）和去甲肾上腺素输注（0.05微克/千克/分钟）使这些值恢复（p值>0.05）至基线水平。去甲肾上腺素输注使左心室收缩性增加（p = 0.002），但不受补液影响（p = 0.903）。两个干预组的后负荷均增加（p值>0.001）。总体而言，干预期间下腔静脉扩张性保持不变（p值≥0.085）。胸腔积液的排出使左心室舒张末期面积出现数值增加，但仅在对照组中显著增加（p = 0.006）。
胸腔积液显著降低左心室前负荷。补液和去甲肾上腺素治疗均能逆转这种效应并使整体血流动力学参数恢复正常。下腔静脉扩张性保持不变。在补液或去甲肾上腺素给药期间，胸腔积液的血流动力学意义可能被低估，这可能掩盖了胸腔积液的存在。
