Chest
Volume 116, Issue 6, December 1999, Pages 1826-1832
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Selected Reports
Exacerbation of Acute Pulmonary Edema During Assisted Mechanical Ventilation Using a Low-Tidal Volume, Lung-Protective Ventilator Strategy

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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.

Section snippets

Case Report

A 26-year-old man presented to the emergency department with severe tonsillitis and a temperature of 103°F. His previous medical history was significant only for adrenal insufficiency, for which he had been noncompliant with glucocorticoid therapy. The patient was in severe respiratory distress with a BP of 70/30 mm Hg (mean, 43 mm Hg). A chest radiograph revealed bilateral infiltrates. During emergent endotracheal intubation, the patient suffered cardiovascular collapse and required high doses

Pulmonary Edema Fluid Collection and Analysis

Once the patient's Spo2 had stabilized at a Vt of 600 mL, the airway was suctioned for pulmonary edema fluid using a previously described method.10 Arterial blood was obtained for comparison of pulmonary edema fluid protein concentration to plasma protein concentration. Measurement of the total protein in the pulmonary edema fluid and plasma samples was done by the biuret and bromcresol green dye-binding technique.11 Measurement of the total protein concentration in the edema fluid and the

Pulmonary Edema Fluid Analysis

The pulmonary edema fluid-to-plasma total protein concentration ratio was 0.47. Initial ratios < 0.65 are characteristic of hydrostatic pulmonary edema, whereas initial ratios between 0.75 and 1.0 are characteristic of increased-permeability pulmonary edema.12 The pulmonary edema fluid-to-plasma total protein ratio found in this case was in the range recently reported during postobstructive pulmonary edema.10

Lung Model

Re-creation of the patient-ventilator interactions with the lung model resulted in a

Discussion

We have reported a case in which exacerbation of acute pulmonary edema coincided with the institution of a lung-protective strategy. The fact that pulmonary edema quickly appeared and resolved with the institution and removal of a low-Vt ventilation strategy led us to suspect that vigorous inspiratory efforts were responsible for the sudden deterioration in the patient's cardiorespiratory status. This impression was supported by the fact that the patient had been consistently triggering the

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