Geissler H J, Allen S J, Mehlhorn U, Davis K L, de Vivie E R, Kurusz M, Butler B D
Department of Anesthesiology, University of Texas-Houston Medical School 77030, USA.
Ann Thorac Surg. 1997 Jul;64(1):100-4. doi: 10.1016/s0003-4975(97)82824-x.
Previous studies demonstrated gas emboli formation during rewarming from hypothermia on cardiopulmonary bypass when the temperature gradient exceeded a critical threshold. It also has been suggested that formation of arterial gas emboli may occur during cooling on cardiopulmonary bypass when cooled oxygenated blood exiting the heat exchanger is warmed on mixture with the patient's blood. The purpose of this study was to determine under what circumstances gas emboli formation would occur during cooling on cardio-pulmonary bypass.
Eight anesthetized mongreal dogs were placed on cardiopulmonary bypass using a roller pump, membrane oxygenator, and arterial line filter. For emboli detection, we positioned a transesophageal echocardiographic probe at the aortic arch distal to the aortic cannula and Doppler probes at the common carotid artery and the arterial line. Cooling gradients between normothermic blood and cooled arterial perfusate of 5 degrees, 10 degrees, 15 degrees, 20 degrees, and 0 degree C (isothermal controls) were investigated. In addition to preestablished temperature gradients, we investigated the effect of rapid cooling (maximal flow through the heat exchanger at a water bath temperature of 4 degrees C) after the initiation of normothermic cardiopulmonary bypass.
Minimal gas emboli were detected at the aortic arch at gradients of 10 degrees C or greater. The incidence of emboli was related directly to the magnitude of the temperature gradient (p < 0.01). No emboli were detected at the carotid artery. During rapid cooling, no emboli were observed either at the aorta or at the carotid artery.
Cooling gradients of 10 degrees C or greater may be associated with gas emboli formation, but they may be of limited clinical significance because no emboli were detected distal to the aortic arch. During the application of rapid cooling, no emboli formation was observed.
先前的研究表明,在体外循环中体温过低复温期间,当温度梯度超过临界阈值时会形成气体栓子。也有人提出,当离开热交换器的冷却氧合血与患者血液混合时被加热,在体外循环冷却期间可能会发生动脉气体栓子形成。本研究的目的是确定在体外循环冷却期间气体栓子形成会在何种情况下发生。
将八只麻醉的杂种狗置于使用滚压泵、膜式氧合器和动脉滤器的体外循环中。为了检测栓子,我们将经食管超声心动图探头置于主动脉插管远端的主动脉弓处,并将多普勒探头置于颈总动脉和动脉管道处。研究了正常体温血液与冷却动脉灌注液之间5℃、10℃、15℃、20℃和0℃(等温对照)的冷却梯度。除了预先设定的温度梯度外,我们还研究了在正常体温体外循环开始后快速冷却(在水浴温度为4℃时通过热交换器的最大流量)的影响。
在10℃或更高的梯度下,在主动脉弓处检测到极少的气体栓子。栓子的发生率与温度梯度的大小直接相关(p<0.01)。在颈动脉处未检测到栓子。在快速冷却期间,在主动脉或颈动脉处均未观察到栓子。
10℃或更高的冷却梯度可能与气体栓子形成有关,但它们的临床意义可能有限,因为在主动脉弓远端未检测到栓子。在应用快速冷却期间,未观察到栓子形成。