Cardiorespiratory effects of automatic tube compensation during airway pressure release ventilation in patients with acute lung injury

Citation
H. Wrigge et al., Cardiorespiratory effects of automatic tube compensation during airway pressure release ventilation in patients with acute lung injury, ANESTHESIOL, 95(2), 2001, pp. 382-389
Citations number
32
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
ANESTHESIOLOGY
ISSN journal
00033022 → ACNP
Volume
95
Issue
2
Year of publication
2001
Pages
382 - 389
Database
ISI
SICI code
0003-3022(200108)95:2<382:CEOATC>2.0.ZU;2-X
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 pres sure during inspiration and lowering airway pressure during expiration, the reby compensating for resistance of the artificial airway. The authors stud ied 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 spontaneou sly during APRV with or without automatic tube compensation in random order . Airway pressure, esophageal and abdominal pressure, and gas flow were con tinuously measured, and tracheal pressure was estimated. Transdiaphragmatic pressure time product was calculated. End-expiratory lung volume was deter mined by nitrogen washout. The validity of the tracheal pressure calculatio n 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) w hile decreasing trans-diaphragmatic pressure time product from 45 +/- 27 to 27 +/- 15 cm H2O.s(-1).min(-1) (P < 0.05), whereas tracheal pressure ampli tude 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 cardiovas cular function. End-expiratory lung volume increased from 2,806 +/- 991 to 3,009 +/- 994 ml (P < 0.05). Analysis of tracheal pressure-time curves indi cated nonideal regulation of the dynamic pressure support during automatic tube compensation as provided by a standard ventilator. Conclusion. In the studied patients with acute lung injury, automatic tube compensation markedly unloaded the inspiratory muscles and increased alveol ar ventilation without compromising cardiorespiratory function and end-expi ratory lung volume.