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  • Title: Inhaled nitric oxide does not improve cardiac or pulmonary function in patients with an exacerbation of chronic obstructive pulmonary disease.
    Author: Baigorri F, Joseph D, Artigas A, Blanch L.
    Journal: Crit Care Med; 1999 Oct; 27(10):2153-8. PubMed ID: 10548198.
    Abstract:
    OBJECTIVE: To determine whether inhaled nitric oxide (NO) improves right ventricular function in mechanically ventilated patients with severe chronic obstructive pulmonary disease (COPD). DESIGN: Open, prospective, controlled trial. SETTING: General intensive care unit of a community hospital. PATIENTS: Twelve patients with acute respiratory failure caused by acute exacerbation of COPD requiring mechanical ventilation. INTERVENTIONS: Insertion of a pulmonary artery catheter modified with a rapid response thermistor and a radial arterial catheter. Nitric oxide was then administered to the patient via a T piece placed between the Y piece of the ventilator and the endotracheal tube. MEASUREMENTS AND MAIN RESULTS: Hemodynamic and gasometric variables were recorded before NO inhalation, during administration of inhaled NO (20 ppm, 20 mins), and 20 mins after NO discontinuation. Inhaled NO reduced pulmonary artery pressure from 26 +/- 6 to 22 +/- 5 mm Hg (p = .0004), but arterial oxygenation, cardiac output, and right ventricular ejection fraction remained unmodified (41% +/- 9% vs. 41% +/- 8%; not significant). Calculated pulmonary vascular resistance decreased from 453 +/- 233 to 348 +/- 108 dyne x sec/cm5 x m2 (p = .02), and right ventricular volumes did not change. Subsequently, right ventricular end-systolic pressure/volume ratio decreased from 0.52 +/- 0.22 to 0.44 +/- 0.19 mm Hg/mL/m2 (p = .01). No significant correlation was observed between the changes of pulmonary artery pressure (or pulmonary vascular resistance) and changes of right ventricular ejection fraction. CONCLUSION: Inhalation of NO does not seem to improve either right ventricular function or arterial oxygenation in patients with acute respiratory failure caused by acute exacerbation of COPD.
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