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Anatomy and Physiology of Left Ventricular Suction Induced by Rotary Blood Pumps

机译:旋转式血泵诱发左心室吸气的解剖生理

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This study in five large greyhound dogs implanted with a VentrAssist left ventricular assist device focused on identification of the precise site and physiological changes induced by or underlying the complication of left ventricular suction. Pressure sensors were placed in left and right atria, proximal and distal left ventricle, and proximal aorta while dual perivascular and tubing ultrasonic flow meters measured blood flow in the aortic root and pump outlet cannula. When suction occurred, end-systolic pressure gradients between proximal and distal regions of the left ventricle on the order of 40-160mmHg indicated an occlusive process of variable intensity in the distal ventricle. A variable negative flow difference between end systole and end diastole (0.5-3.4L/min) was observed. This was presumably mediated by variable apposition of the free and septal walls of the ventricle at the pump inlet cannula orifice which lasted approximately 100ms. This apposition, by inducing an end-systolic flow deficit, terminated the suction process by relieving the imbalance between pump requirement and delivery from the right ventricle. Immediately preceding this event, however, unnaturally low end-systolic pressures occurred in the left atrium and proximal left ventricle which in four dogs lasted for 80-120ms. In one dog, however, this collapse progressed to a new level and remained at approximately -5mmHg across four heart beats at which point suction was relieved by manual reduction in pump speed. Because these pressures were associated with a pulmonary capillary wedge pressure of -5mmHg as well, they indicate total collapse of the entire pulmonary venous system, left atrium, and left ventricle which persisted until pump flow requirement was relieved by reducing pump speed. We suggest that this collapse caused the whole vascular region from pulmonary capillaries to distal left ventricle to behave as a Starling resistance which further reduced right ventricular output thus contributing to a major reduction in pump flow. We contend that similar complications of manual speed control also occur in the human subject and remain a major unsolved problem in the clinical management of patients implanted with rotary blood pumps.
机译:这项研究在五只植入了VentrAssist左心室辅助装置的大型灵缇犬中进行,旨在确定由左心室吸引引起的并发症或潜在并发症的确切部位和生理变化。压力传感器分别放置在左,右心房,左心室近端和远端以及主动脉近端,而双血管周和管道超声流量计则测量主动脉根和泵出口套管中的血流量。当发生吸力时,左心室近端和远端区域之间的收缩末期压力梯度约为40-160mmHg,表明远端心室的闭塞过程强度可变。观察到收缩末期和舒张末期之间的可变负流量差(0.5-3.4L / min)。据推测,这是由持续约100ms的泵入口套管孔处的心室自由壁和间隔壁的并置介导的。通过诱发收缩末期流量不足,这种缓解通过减轻泵需求和右心室输送之间的不平衡而终止了抽吸过程。然而,紧接此事件之前,左心房和左心室近端发生了异常低的收缩末期压力,四只狗持续了80-120ms。然而,在一只狗中,这种塌陷发展到了一个新的水平,并且在四个心跳中保持在-5mmHg左右,此时通过手动降低泵速来减轻吸力。因为这些压力也与-5mmHg的肺毛细血管楔压相关,所以它们表明整个肺静脉系统,左心房和左心室完全塌陷,一直持续到通过降低泵速来缓解泵流量需求为止。我们认为,这种塌陷导致从肺毛细血管到左心室远端的整个血管区域表现为Starling阻力,从而进一步降低了右心室的输出,从而导致泵流量的大幅减少。我们认为,类似的手动速度控制并发症也发生在人类受试者中,并且在植入旋转式血泵的患者的临床管理中仍然是未解决的主要问题。

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