Shen I, Levy F H, Benak A M, Rothnie C L, O'Rourke P P, Duncan B W, Verrier E D
Department of Anesthesia, Children's Hospital and Medical Center, Seattle, Washington, USA.
Ann Thorac Surg. 2001 Mar;71(3):868-71. doi: 10.1016/s0003-4975(00)02281-5.
Perfusion of the coronary circulation with hypoxemic blood from the left ventricle has been postulated to cause myocardial dysfunction during venoarterial extracorporeal membrane oxygenation for respiratory support.
We investigated this hypothesis in 10 anesthetized open-chest piglets (7 to 9 kg) undergoing venoarterial extracorporeal membrane oxygenation after placement of minor-axis sonomicrometry crystals and left ventricular micromanometer. The left atrial partial pressure of oxygen was made hypoxemic (25 to 40 mm Hg) after initiation of extracorporeal membrane oxygenation by ventilation with a hypoxic gas mixture. Left ventricular contractile function, including peak LV pressure, shortening fraction, maximum rate of increase of left ventricular pressure, velocity of circumferential fiber shortening, end-systolic pressure-minor axis dimension relationship, and preload recruitable dimensional stroke work, was measured or calculated on extracorporeal membrane oxygenation before (baseline) and at 4 and 6 hours after rendering the left atrial blood hypoxemic.
Left ventricular shortening fraction and velocity of circumferential fiber shortening were significantly lower (p < 0.05) at 4 and 6 hours when compared with baseline. The slope of the end-systolic pressure-minor axis dimension relationship decreased but was not significantly different at 4 and 6 hours when compared with baseline owing to poor linear correlation (r = 0.30 to 0.93). The preload recruitable dimensional stroke work was more linear (r = 0.87 to 0.99), and the slope was significantly lower (p < 0.01) at 4 and 6 hours when compared with baseline.
Hypoxemic cardiac output from the left ventricle during venoarterial extracorporeal membrane oxygenation is associated with depression of left ventricular systolic function in this animal model. Current use of venoarterial extracorporeal membrane oxygenation for respiratory support may not provide adequate oxygen supply to the myocardium.
在静脉 - 动脉体外膜肺氧合用于呼吸支持期间,有人推测左心室的低氧血灌注会导致心肌功能障碍。
我们在10只麻醉开胸仔猪(7至9千克)中研究了这一假设,这些仔猪在植入短轴超声测微晶体和左心室微测压计后接受静脉 - 动脉体外膜肺氧合。在体外膜肺氧合开始后,通过用低氧气体混合物通气使左心房氧分压降低(25至40毫米汞柱)。在体外膜肺氧合前(基线)以及左心房血液低氧后4小时和6小时测量或计算左心室收缩功能,包括左心室峰值压力、缩短分数、左心室压力最大上升速率、圆周纤维缩短速度、收缩末期压力 - 短轴尺寸关系以及可招募前负荷的尺寸搏功。
与基线相比,4小时和6小时时左心室缩短分数和圆周纤维缩短速度显著降低(p < 0.05)。收缩末期压力 - 短轴尺寸关系的斜率降低,但由于线性相关性差(r = 0.30至0.93),与基线相比,4小时和6小时时无显著差异。可招募前负荷的尺寸搏功更具线性(r = 0.87至0.99),与基线相比,4小时和6小时时斜率显著降低(p < 0.01)。
在这个动物模型中,静脉 - 动脉体外膜肺氧合期间左心室的低氧心输出量与左心室收缩功能降低有关。目前使用静脉 - 动脉体外膜肺氧合进行呼吸支持可能无法为心肌提供足够的氧气供应。