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Work of Breathing and Mechanical Ventilation in Acute Lung Injury

2014-07-23 21:13:36 | BioPortfolio

Summary

The primary goal of this study is to measure changes in biological markers of inflammation in critically-ill patients with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) while they are treated with different styles of lung-protective, artificial breathing assistance.

Secondary goals are to measure the breathing effort of patients using different artificial breathing patterns from the breathing machine.

The primary hypothesis is that volume-targeted artificial patterns will produce less inflammation. The secondary hypothesis is that volume-targeted artificial patterns will increase breathing effort compared to pressure-targeted artificial patterns.

Description

Ventilator-induced lung injury contributes to the progression of ALI/ARDS,1 and is thought to occur partly from the unequal distribution of a super-normal tidal volume to normal areas of the lung.2 Alveolar overdistension causes alveolar-capillary membrane damage,3 increased-permeability pulmonary edema4 and hyaline membrane formation.5 Therefore, it is recommended that tidal volume should be reduced to 6-7 mL/kg, and that the peak alveolar pressure, or the end-inspiratory plateau pressure (PPLAT), should be limited to < 30 cm H2O.6 The National Heart Lung and Blood Institute's ARDS Network demonstrated a 22% reduction in mortality using a "lung-protective" (low tidal volume) ventilation strategy in patients with ALI/ARDS.7 High tidal volume ventilation causes a rapid and substantial increase plasma levels of proinflammatory mediators which decrease in response to lung protective ventilation.8,9 A consequence of lung-protective ventilation is dyspnea and increased work of breathing.10 Our recent study11 on work of breathing during lung-protective ventilation found that inspiratory pleural pressure changes were extraordinarily high, averaging 15-17 cm H2O. Whereas tidal volume was well controlled during volume ventilation, in contrast, it exceeded target levels in 40% of patients during pressure control ventilation.

High tidal volume-high negative pressure ventilation causes acute lung injury in animal models.12,13 Thus ventilator-induced lung injury results from excessive stress across lung tissue created by high transpulmonary (airway-pleural).pressure.14 This suggests the possibility that despite pressure control ventilation being set with a low positive airway pressure, "occult" high tidal volume-high transpulmonary pressure ventilation still may occur.11 However, during spontaneous breathing diaphragmatic contractions cause ventilation to be distributed preferentially to dorsal:caudal aspects of the lungs.15 Therefore, high transpulmonary pressures created by large negative swings in pleural pressure theoretically may not cause regional lung over-distension and ventilator-induced lung injury if tidal ventilation is preferentially distributed to dorsocaudal lung regions. However, a study16 examining the effects of diaphragmatic breathing during Pressure Control Ventilation found that dorsocaudal distribution of tidal volume was not necessarily improved compared to passive ventilation, as the amount of tidal ventilation distributed to areas of high ventilation/perfusion was unaltered. Regardless, during a recent conference on respiratory controversies in the critical care setting, it was noted that the effects of ventilator modes such as volume control, pressure control and airway pressure-release ventilation on proinflammatory cytokine expression during lung-protective ventilation has not been studied in humans.17 Thus it is unknown whether or not differences in transpulmonary pressure and tidal volume between these modes has a direct impact on lung inflammation.

Study Design

Allocation: Randomized, Control: Uncontrolled, Intervention Model: Crossover Assignment, Masking: Open Label, Primary Purpose: Supportive Care

Conditions

Acute Lung Injury

Intervention

Volume Control Ventilation, Pressure Control Ventilation

Status

Withdrawn

Source

University of California, San Francisco

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-07-23T21:13:36-0400

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Medical and Biotech [MESH] Definitions

Techniques for effecting the transition of the respiratory-failure patient from mechanical ventilation to spontaneous ventilation, while meeting the criteria that tidal volume be above a given threshold (greater than 5 ml/kg), respiratory frequency be below a given count (less than 30 breaths/min), and oxygen partial pressure be above a given threshold (PaO2 greater than 50mm Hg). Weaning studies focus on finding methods to monitor and predict the outcome of mechanical ventilator weaning as well as finding ventilatory support techniques which will facilitate successful weaning. Present methods include intermittent mandatory ventilation, intermittent positive pressure ventilation, and mandatory minute volume ventilation.

Ventilatory support system using frequencies from 60-900 cycles/min or more. Three types of systems have been distinguished on the basis of rates, volumes, and the system used. They are high frequency positive-pressure ventilation (HFPPV); HIGH-FREQUENCY JET VENTILATION; (HFJV); and high-frequency oscillation (HFO).

The ratio of alveolar ventilation to simultaneous alveolar capillary blood flow in any part of the lung. (Stedman, 25th ed)

A method of mechanical ventilation in which pressure is maintained to increase the volume of gas remaining in the lungs at the end of expiration, thus reducing the shunting of blood through the lungs and improving gas exchange.

A state in which the environs of hospitals, laboratories, domestic and animal housing, work places, spacecraft, and other surroundings are under technological control with regard to air conditioning, heating, lighting, humidity, ventilation, and other ambient features. The concept includes control of atmospheric composition. (From Jane's Aerospace Dictionary, 3d ed)

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