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
Design: Mechanical lung
modeling of patient-ventilator interactions based on data from a case
Setting: Medical ICU and laboratory.
Patient: A patient with suspected ARDS and frank pulmonary
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.
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
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.