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Cardiorespiratory Effects of Automatic Tube Compensation during Airway Pressure Release Ventilation in Patients with Acute Lung Injury
Authors:Wrigge, Hermann M.D.   Zinserling, J  rg M.Sc.&#x     Hering, Rudolf M.D.   Schwalfenberg, Nico&#x     Stü  ber, Frank M.D.      von Spiegel, Tilman M.D.   Schroeder, Stefan M.D.   Hedenstierna, G  ran M.D.&#x  &#x     Putensen, Christian M.D.#
Affiliation:Wrigge, Hermann M.D.*; Zinserling, Jörg M.Sc.†; Hering, Rudolf M.D.*; Schwalfenberg, Nico‡; Stüber, Frank M.D.§; von Spiegel, Tilman M.D.*; Schroeder, Stefan M.D.*; Hedenstierna, Göran M.D.‖‖; Putensen, Christian M.D.#
Abstract:Background: Spontaneous breaths during airway pressure release ventilation (APRV) have to overcome the resistance of the artificial airway. Automatic tube compensation provides ventilatory assistance by increasing airway pressure during inspiration and lowering airway pressure during expiration, thereby compensating for resistance of the artificial airway. The authors studied if APRV with automatic tube compensation reduces the inspiratory effort without compromising cardiovascular function, end-expiratory lung volume, and gas exchange in patients with acute lung injury.

Methods: Fourteen patients with acute lung injury were breathing spontaneously during APRV with or without automatic tube compensation in random order. Airway pressure, esophageal and abdominal pressure, and gas flow were continuously measured, and tracheal pressure was estimated. Trans-diaphragmatic pressure time product was calculated. End-expiratory lung volume was determined by nitrogen washout. The validity of the tracheal pressure calculation was investigated in seven healthy ventilated pigs.

Results: Automatic tube compensation during APRV increased airway pressure amplitude from 7.7 +/- 1.9 to 11.3 +/- 3.1 cm H2O (mean +/- SD;P < 0.05) while decreasing trans-diaphragmatic pressure time product from 45 +/- 27 to 27 +/- 15 cm H2O [middle dot] s-1 [middle dot] min-1 (P < 0.05), whereas tracheal pressure am-plitude remained essentially unchanged (10.3 +/- 3.5 vs. 10.1 +/- 3.5 cm H2O). Minute ventilation increased from 10.4 +/- 1.6 to 11.4 +/- 1.5 l/min (P < 0.001), decreasing arterial carbon dioxide tension from 52 +/- 9 to 47 +/- 6 mmHg (P < 0.05) without affecting arterial blood oxygenation or cardiovascular function. End-expiratory lung volume increased from 2,806 +/- 991 to 3,009 +/- 994 ml (P < 0.05). Analysis of tracheal pressure-time curves indicated nonideal regulation of the dynamic pressure support during automatic tube compensation as provided by a standard ventilator.

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