Bradley Scott M, Simsic Janet M, Mulvihill Denise M
Division of Cardiothoracic Surgery, Medical University of South Carolina, 96 Jonathan Lucas St., Charleston, SC 29425, USA.
J Thorac Cardiovasc Surg. 2003 Oct;126(4):1033-9. doi: 10.1016/s0022-5223(03)00203-4.
Bidirectional superior cavopulmonary connection may be complicated by systemic hypoxemia. Previous work has shown that hyperventilation worsens systemic oxygenation in patients after bidirectional superior cavopulmonary connection. The likely mechanism is that hyperventilation-induced hypocarbia decreases cerebral, superior vena caval, and pulmonary blood flow. The aim of the current study was to determine whether the converse approach, hypoventilation, improves oxygenation after bidirectional superior cavopulmonary connection.
This is a prospective, patient-controlled study of 15 patients (median age 8.0 months, range 4.7-15.5) who underwent bidirectional superior cavopulmonary connection. Patients were studied in the intensive care unit, within 8 hours of surgery, while sedated, paralyzed, and mechanically ventilated. To avoid acidosis during hypoventilation, sodium bicarbonate was administered before hypoventilation. Cerebral blood flow velocity was measured by transcranial Doppler sonography of the middle cerebral artery.
Hypoventilation following administration of sodium bicarbonate (pH-buffered hypoventilation) produced hypercarbia (mean Pco(2) = 58 mm Hg versus 42 mm Hg at baseline). During hypoventilation, there were significant increases in both mean arterial Po(2) (from 50 mm Hg at baseline to 61 mm Hg; P <.05) and mean systemic oxygen saturation (from 86% at baseline to 90%; P <.05). These increases occurred despite accompanying, small increases in pulmonary artery pressure and transpulmonary gradient. Hypoventilation also produced an increase in mean cerebral blood flow velocity (from 37 cm/s at baseline to 55 cm/s; P <.05) and a decrease in the arteriovenous oxygen saturation difference across the upper body (from 33% at baseline to 23%; P <.05), consistent with increased cerebral blood flow.
This study demonstrates that hypoventilation improves systemic oxygenation in patients after bidirectional superior cavopulmonary connection. The likely mechanism for this effect is that hypoventilation-induced hypercarbia decreases cerebral vascular resistance, thus increasing cerebral, superior vena caval, and pulmonary blood flow. Hypoventilation may be a useful clinical strategy in patients who are hypoxemic in the early postoperative period after bidirectional superior cavopulmonary connection.
双向腔肺连接可能并发全身性低氧血症。既往研究表明，双向腔肺连接术后患者过度通气会使全身氧合恶化。可能的机制是过度通气诱发的低碳酸血症会减少脑、上腔静脉和肺的血流量。本研究的目的是确定相反的方法，即低通气，是否能改善双向腔肺连接术后的氧合。
这是一项前瞻性、患者对照研究，纳入了15例接受双向腔肺连接手术的患者（中位年龄8.0个月，范围4.7 - 15.5个月）。患者在重症监护病房接受研究，于术后8小时内，在镇静、麻痹和机械通气状态下进行。为避免低通气期间出现酸中毒，在低通气前给予碳酸氢钠。通过经颅多普勒超声测量大脑中动脉的脑血流速度。
给予碳酸氢钠后的低通气（pH缓冲低通气）导致高碳酸血症（平均Pco₂ = 58 mmHg，而基线时为42 mmHg）。在低通气期间，平均动脉血氧分压（从基线时的50 mmHg升至61 mmHg；P <.05）和平均全身氧饱和度（从基线时的86%升至90%；P <.05）均显著增加。尽管肺动脉压和跨肺压梯度略有增加，但这些增加仍出现。低通气还使平均脑血流速度增加（从基线时的37 cm/s升至55 cm/s；P <.05），上半身动静脉氧饱和度差减小（从基线时的33%降至23%；P <.05），这与脑血流量增加一致。
本研究表明，低通气可改善双向腔肺连接术后患者的全身氧合。这种效应的可能机制是低通气诱发的高碳酸血症降低了脑血管阻力，从而增加了脑、上腔静脉和肺的血流量。对于双向腔肺连接术后早期低氧血症患者，低通气可能是一种有用的临床策略。
