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Exacerbation of Acute Pulmonary Edema During Assisted Mechanical Ventilation Using a Low-Tidal Volume, Lung-Protective Ventilator Strategy*

Richard H. Kallet, MS, RRT; James A. Alonso, RRT; John M. Luce, MD, FCCP; Michael A. Matthay, MD, FCCP
Author and Funding Information

*From the Departments of Anesthesia (Drs. Luce and Matthay, Mr. Kallet, and Mr. Alonso) and Medicine (Drs. Luce and Matthay), University of California, San Francisco, at San Francisco General Hospital, San Francisco, CA; and Cardiovascular Research Insitute (Mr. Kallet, Mr. Alonso, and Dr. Matthay), University of California, San Francisco, San Francisco, CA.

Correspondence to: Richard H. Kallet, MS, RRT, Clinical Research Coordinator, Department of Anesthesia, San Francisco General Hospital Room NH:GA-2, 1001 Potrero Ave, San Francisco, CA 94110; e-mail: rkallet@sfghsom.ucsf.edu



Chest. 1999;116(6):1826-1832. doi:10.1378/chest.116.6.1826
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Study objectives: To assess the magnitude of negative intrathoracic pressure development in a patient whose pulmonary edema acutely worsened immediately following the institution of a low-tidal volume (Vt) strategy.

Design: Mechanical lung modeling of patient-ventilator interactions based on data from a case report.

Setting: Medical ICU and laboratory.

Patient: A patient with suspected ARDS and frank pulmonary edema.

Interventions: The patient’s pulmonary mechanics and spontaneous breathing pattern were measured. Samples of arterial blood and pulmonary edema fluid were obtained.

Measurements: A standard work-of-breathing lung model was used to mimic the ventilator settings, pulmonary mechanics, and spontaneous breathing pattern observed when pulmonary edema worsened. Comparison of the pulmonary edema fluid-to-plasma total protein concentration ratio was made.

Results: The patient’s spontaneous Vt demand was greater than preset. The lung model revealed simulated intrathoracic pressure changes consistent with levels believed necessary to produce pulmonary edema during obstructed breathing. A high degree of imposed circuit-resistive work was found. The pulmonary edema fluid-to-plasma total protein concentration ratio was 0.47, which suggested a hydrostatic mechanism.

Conclusion: Ventilator adjustments that greatly increase negative intrathoracic pressure during the acute phase of ARDS may worsen pulmonary edema by increasing the transvascular pressure gradient. Therefore, whenever sedation cannot adequately suppress spontaneous breathing (and muscle relaxants are contraindicated), a low-Vt strategy should be modified by using a pressure-regulated mode of ventilation, so that imposed circuit-resistive work does not contribute to the deterioration of the patient’s hemodynamic and respiratory status.

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