Physiology and Experimental Medicine, Hospital for Sick Children, Toronto, Ontario, Canada.
Crit Care Med. 2012 Jun;40(6):1864-72. doi: 10.1097/CCM.0b013e318246bd6a.
In acute lung injury, atelectasis is common and frequently develops in the dependent and diaphragmatic regions. Attempts to recruit lung with positive pressure constitute a major aim in the management of acute respiratory distress syndrome but are associated with overdistension and injury in nonatelectatic regions.
To test the hypothesis that continuous negative abdominal pressure using an iron lung would augment positive end-expiratory pressure in recruiting atelectatic lung.
An in vivo rabbit model of ventilator-induced lung injury was used in which a recruitment maneuver followed by positive end-expiratory pressure (110 cm H2O) had no effect on oxygenation. Addition of sustained continuous negative abdominal pressure (-5 cm H2O) to the positive end-expiratory pressure significantly increased the end-expired lung volume and PaO2 but impaired ventricular preload and cardiac output (suggested by echocardiography). Addition of transient (15 mins) continuous negative abdominal pressure resulted in comparable and lasting (60 mins) increases in PaO2. Sustained, but not transient, continuous negative abdominal pressure was associated with hemodynamic depression and lactic acidosis, which appeared (illustrative echocardiography, n = 2) to be caused by decreased cardiac preload. Computerized tomography (n = 2) suggested that continuous negative abdominal pressure was an effective adjunct to positive end-expiratory pressure for recruiting atelectasis in dependent and diaphragmatic regions. In surfactant-depleted but noninjured lungs, sustained continuous negative abdominal pressure augmented lung recruitment and oxygenation in the setting of higher (but not lower) levels of positive end-expiratory pressure and reduced central venous oxygenation.
Continuous negative abdominal pressure may be a potential adjunct to positive end-expiratory pressure in the recruitment of diaphragmatic atelectasis. The approach ultimately might be useful when ceilings exist on the level of desired positive end-expiratory pressure.
在急性肺损伤中,肺不张很常见,且常发生于肺的下垂部位和膈肌部位。用正压复张肺是急性呼吸窘迫综合征治疗的主要目标之一,但与非肺不张区域的过度膨胀和损伤相关。
检验这样一个假设,即使用铁肺施加持续的负压会增加正呼气末压在复张肺不张肺中的效果。
在一个兔的呼吸机所致肺损伤模型中,复张操作后给予正呼气末压(110cmH2O),但对氧合没有影响。在正呼气末压的基础上施加持续的负压(-5cmH2O),显著增加了呼气末肺容积和 PaO2,但降低了心室前负荷和心输出量(超声心动图提示)。给予短暂(15 分钟)的持续负压,会导致相当的、持久的(60 分钟)PaO2 升高。持续的负压,而不是短暂的负压,与血流动力学抑制和乳酸酸中毒相关,这似乎(通过超声心动图,n=2)是由前负荷减少引起的。计算机断层扫描(n=2)提示,持续的负压是正呼气末压复张肺下垂部位和膈肌部位肺不张的有效辅助手段。在表面活性物质耗竭但无损伤的肺中,持续的负压增加了肺复张和氧合,而呼气末正压水平较高(但不是较低),中心静脉氧饱和度降低。
持续的负压可能是正呼气末压复张膈肌肺不张的一个潜在辅助手段。当所需的呼气末正压水平存在上限时,这种方法最终可能是有用的。