Talmor Daniel, Sarge Todd, O'Donnell Carl R, Ritz Ray, Malhotra Atul, Lisbon Alan, Loring Stephen H
Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, USA.
Crit Care Med. 2006 May;34(5):1389-94. doi: 10.1097/01.CCM.0000215515.49001.A2.
Pressure inflating the lung during mechanical ventilation is the difference between pressure applied at the airway opening (Pao) and pleural pressure (Ppl). Depending on the chest wall's contribution to respiratory mechanics, a given positive end-expiratory and/or end-inspiratory plateau pressure may be appropriate for one patient but inadequate or potentially injurious for another. Thus, failure to account for chest wall mechanics may affect results in clinical trials of mechanical ventilation strategies in acute respiratory distress syndrome. By measuring esophageal pressure (Pes), we sought to characterize influence of the chest wall on Ppl and transpulmonary pressure (PL) in patients with acute respiratory failure.
Prospective observational study.
Medical and surgical intensive care units at Beth Israel Deaconess Medical Center.
Seventy patients with acute respiratory failure.
Placement of esophageal balloon-catheters.
Airway, esophageal, and gastric pressures recorded at end-exhalation and end-inflation Pes averaged 17.5 +/- 5.7 cm H2O at end-expiration and 21.2 +/- 7.7 cm H2O at end-inflation and were not significantly correlated with body mass index or chest wall elastance. Estimated PL was 1.5 +/- 6.3 cm H2O at end-expiration, 21.4 +/- 9.3 cm H2O at end-inflation, and 18.4 +/- 10.2 cm H2O (n = 40) during an end-inspiratory hold (plateau). Although PL at end-expiration was significantly correlated with positive end-expiratory pressure (p < .0001), only 24% of the variance in PL was explained by Pao (R = .243), and 52% was due to variation in Pes.
In patients in acute respiratory failure, elevated esophageal pressures suggest that chest wall mechanical properties often contribute substantially and unpredictably to total respiratory impedance, and therefore Pao may not adequately predict PL or lung distention. Systematic use of esophageal manometry has the potential to improve ventilator management in acute respiratory failure by providing more direct assessment of lung distending pressure.
机械通气期间对肺进行压力充气是气道开口处施加的压力（Pao）与胸膜压力（Ppl）之间的差值。根据胸壁对呼吸力学的影响，给定的呼气末正压和/或吸气末平台压对一名患者可能是合适的，但对另一名患者可能不足或有潜在伤害。因此，未能考虑胸壁力学可能会影响急性呼吸窘迫综合征机械通气策略的临床试验结果。通过测量食管压力（Pes），我们试图描述胸壁对急性呼吸衰竭患者Ppl和跨肺压（PL）的影响。
前瞻性观察性研究。
贝斯以色列女执事医疗中心的内科和外科重症监护病房。
70例急性呼吸衰竭患者。
放置食管球囊导管。
呼气末和吸气末记录的气道、食管和胃内压力。呼气末Pes平均为17.5±5.7 cmH₂O，吸气末为21.2±7.7 cmH₂O，与体重指数或胸壁弹性无显著相关性。呼气末估计的PL为1.5±6.3 cmH₂O，吸气末为21.4±9.3 cmH₂O，吸气末屏气（平台期）时为18.4±10.2 cmH₂O（n = 40）。虽然呼气末PL与呼气末正压显著相关（p <.0001），但PL中只有24%的变异可由Pao解释（R =.243），52%是由于Pes的变化。
在急性呼吸衰竭患者中，食管压力升高表明胸壁机械特性通常对总呼吸阻抗有很大且不可预测的影响，因此Pao可能无法充分预测PL或肺扩张情况。系统使用食管测压法有可能通过更直接地评估肺扩张压力来改善急性呼吸衰竭患者的呼吸机管理。
