Chest
Selected ReportsExacerbation of Acute Pulmonary Edema During Assisted Mechanical Ventilation Using a Low-Tidal Volume, Lung-Protective Ventilator Strategy
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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