Li Jia, Zhang Gencheng, Holtby Helen, Guerguerian Anne-Marie, Cai Sally, Humpl Tilman, Caldarone Christopher A, Redington Andrew N, Van Arsdell Glen S
Heart Center, the Hospital for Sick Children, Toronto, Ontario, Canada.
J Thorac Cardiovasc Surg. 2008 Jan;135(1):83-90, 90.e1-2. doi: 10.1016/j.jtcvs.2007.07.036.
Ischemic brain injury is an important morbidity in neonates after the Norwood procedure. Its relationship to systemic hemodynamic oxygen transport is poorly understood.
Sixteen neonates undergoing the Norwood procedure were studied. Continuous cerebral oxygen saturation was measured by near-infrared spectroscopy. Continuous oxygen consumption was measured by respiratory mass spectrometry. Pulmonary and systemic blood flow, systemic vascular resistance, oxygen delivery, and oxygen extraction ratio were derived with measurements of arterial, and superior vena cava and pulmonary venous gases and pressures at 2- to 4-hour intervals during the first 72 hours in the intensive care unit.
Mean cerebral oxygen saturation was 66% +/- 12% before the operation, reduced to 51% +/- 13% on arrival in the intensive care unit, and remained low during the first 8 hours; it increased to 56% +/- 9% at 72 hours, still significantly lower than the preoperative level (P < .05). Postoperatively, cerebral oxygen saturation was closely and positively correlated with systemic arterial pressure, arterial oxygen saturation, and arterial oxygen tension and negatively with oxygen extraction ratio (P < .0001 for all). Cerebral oxygen saturation was moderately and positively correlated with systemic blood flow and oxygen delivery (P < .0001 for both). It was weakly and positively correlated with pulmonary blood flow (P = .001) and hemoglobin (P = .02) and negatively correlated with systemic vascular resistance (P = .003). It was not correlated with oxygen consumption (P > .05).
Cerebral oxygen saturation decreased significantly in neonates during the early postoperative period after the Norwood procedure and was significantly influenced by systemic hemodynamic and metabolic events. As such, hemodynamic interventions to modify systemic oxygen transport may provide further opportunities to reduce the risk of cerebral ischemia and improve neurodevelopmental outcomes.
缺血性脑损伤是诺伍德手术后新生儿的一种重要发病情况。其与全身血流动力学氧输送的关系尚不清楚。
对16例接受诺伍德手术的新生儿进行研究。通过近红外光谱法测量连续脑氧饱和度。通过呼吸质谱法测量连续氧消耗。在重症监护病房的头72小时内，每隔2至4小时测量动脉、上腔静脉和肺静脉气体及压力，从而得出肺和全身血流量、全身血管阻力、氧输送和氧摄取率。
术前平均脑氧饱和度为66%±12%，进入重症监护病房时降至51%±13%，并在最初8小时内保持较低水平；72小时时升至56%±9%，仍显著低于术前水平（P<.05）。术后，脑氧饱和度与全身动脉压、动脉血氧饱和度和动脉血氧分压密切正相关，与氧摄取率呈负相关（所有P<.0001）。脑氧饱和度与全身血流量和氧输送呈中度正相关（两者P<.0001）。它与肺血流量（P=.001）和血红蛋白（P=.02）呈弱正相关，与全身血管阻力呈负相关（P=.003）。它与氧消耗无相关性（P>.05）。
诺伍德手术后新生儿术后早期脑氧饱和度显著下降，并受到全身血流动力学和代谢事件的显著影响。因此，改变全身氧输送的血流动力学干预措施可能为降低脑缺血风险和改善神经发育结局提供更多机会。
