Putensen Christian, Wrigge Hermann, Hering Rudolf
Department of Anesthesiology and Intensive Care Medicine, University of Bonn, Bonn, Germany.
Curr Opin Crit Care. 2006 Apr;12(2):160-5. doi: 10.1097/01.ccx.0000216585.54502.eb.
Mechanical ventilation generates an increase in airway pressure and, therefore, in intrathoracic pressure, which may decrease systemic and intraabdominal organ perfusion. Critically ill patients rarely die of hypoxia and/or hypercarbia but commonly develop a systemic inflammatory response that culminates in multiple-organ dysfunction syndrome and death. In the pathogeneses of this syndrome the gastrointestinal tract and liver have received considerable attention.
Mechanical ventilation with high positive end-expiratory pressure has been found to decrease splanchnic perfusion. Hepatic arterial buffer response is preserved and an increased hepatic arterial blood flow will compensate the decrease in portal blood flow. Despite an increased cardiac output with an acute moderate increase in arterial PCO2 during protective ventilation it cannot be expected that splanchnic and gut perfusion is improved. In the absence of a significant rise in intraabdominal pressure without impairment in cardiovascular function, splanchnic and gastrointestinal function remained unchanged during short periods of prone positioning. Spontaneous breathing during ventilator support improves systemic blood flow and gastrointestinal and splanchnic perfusion.
In critically ill patients mechanical ventilation should be adjusted to avoid conditions known to be associated with decreased gastrointestinal and splanchnic perfusion.
机械通气会使气道压力升高，进而导致胸内压升高，这可能会降低全身和腹腔内器官的灌注。危重症患者很少死于缺氧和/或高碳酸血症，而是通常会引发全身炎症反应，最终导致多器官功能障碍综合征和死亡。在该综合征的发病机制中，胃肠道和肝脏受到了相当多的关注。
已发现高呼气末正压通气会降低内脏灌注。肝动脉缓冲反应得以保留，肝动脉血流增加会补偿门静脉血流的减少。尽管在保护性通气期间动脉PCO₂急性适度升高会使心输出量增加，但内脏和肠道灌注并不会因此得到改善。在腹内压无显著升高且心血管功能未受损的情况下，短时间俯卧位期间内脏和胃肠功能保持不变。通气支持期间的自主呼吸可改善全身血流以及胃肠道和内脏灌注。
对于危重症患者，应调整机械通气以避免出现已知与胃肠道和内脏灌注减少相关的情况。
