Dept. of Coronary Heart Disease, Skane University Hospital, Lund University, S-22185, Lund, Sweden.
Resuscitation. 2010 Sep;81(9):1190-6. doi: 10.1016/j.resuscitation.2010.04.033. Epub 2010 Jun 2.
Cardiogenic shock is the main cause of death in patients hospitalized due to an acute myocardial infarction. Mild hypothermia reduces metabolism and could offer protective effects for this condition. The aim of our study was to investigate if mild therapeutic hypothermia would improve outcome and hemodynamic parameters in an ischemic cardiogenic shock pig model.
Twenty-five pigs (40-50 kg) were anesthetized and a normothermic temperature of 38 degrees C was established utilising an endovascular cooling catheter in a closed-chest model. A Swan-Ganz catheter was placed in the pulmonary artery. Hemodynamic parameters were continuously monitored and blood gases were sampled every 30 min. Ischemia was induced by inflation of a PCI balloon in proximal LAD for 40 min. Sixteen pigs that have fulfilled predefined shock criteria were randomized to hypothermia (n=8), or normothermia (n=8). Hypothermia (33 degrees C) was induced after onset of reperfusion by using an endovascular temperature modulating catheter and was maintained until termination of the experiment.
The pigs in the hypothermia group were cooled to <34 degrees C in approximately 45 min. 5/8 pigs in the normothermia group died while all pigs in the hypothermia group survived (p<0.01). Stroke volume and blood pressure were significantly higher in the hypothermia group (p<0.05), whereas heart rate was significantly lower in the hypothermia group (p=0.01). Cardiac output did not differ among the groups (p=0.13). Blood gas analysis revealed higher mixed venous oxygen saturation, pH, and base excess in the hypothermia group indicating less development of metabolic acidosis (p<0.05).
In this pig model, mild therapeutic hypothermia reduces acute mortality in cardiogenic shock, improves hemodynamic parameters and reduces metabolic acidosis. These findings suggest a possible clinical benefit of therapeutic hypothermia for patients with acute cardiogenic shock.
心原性休克是因急性心肌梗死住院患者死亡的主要原因。轻度低温可降低代谢，并可能对这种情况提供保护作用。我们的研究目的是探讨轻度治疗性低温是否会改善缺血性心原性休克猪模型的预后和血液动力学参数。
25 头猪（40-50 公斤）被麻醉，并使用血管内冷却导管在闭胸模型中建立正常体温 38 度。肺动脉内放置 Swan-Ganz 导管。连续监测血液动力学参数，并每 30 分钟取样血气。通过在近端 LAD 中充气 PCI 球囊诱导缺血 40 分钟。满足预定休克标准的 16 头猪被随机分为低温组（n=8）或常温组（n=8）。在再灌注开始后，通过使用血管内温度调节导管将低温（33 度）诱导，并持续到实验结束。
低温组的猪在大约 45 分钟内冷却至<34 度。常温组的 5/8 头猪死亡，而低温组的所有猪均存活（p<0.01）。低温组的每搏量和血压明显较高（p<0.05），而低温组的心率明显较低（p=0.01）。心输出量在各组之间无差异（p=0.13）。血气分析显示低温组混合静脉血氧饱和度、pH 值和碱剩余较高，表明代谢性酸中毒的发展程度较低（p<0.05）。
在该猪模型中，轻度治疗性低温可降低心原性休克的急性死亡率，改善血液动力学参数，并减少代谢性酸中毒。这些发现提示治疗性低温对急性心原性休克患者可能有临床益处。
