• M J Carmona and J O Auler.
• Department of Anesthesiology and Intensive Care, Heart Institute of the University of São Paulo-Hospital das Clinicas, Brazil.
• J. Cardiothorac. Vasc. Anesth. 1998 Apr 1;12(2):157-61.

ObjectiveTo evaluate the hemodynamic and respiratory effects of inhaled nitric oxide (NO) in postoperative cardiac patients.DesignA prospective evaluation.SettingA university hospital intensive care unit.ParticipantsFourteen adults with pulmonary hypertension, studied postoperatively.Interventions60 minutes of NO inhalation (20 ppm).Measurements And Main ResultsRespiratory mechanics were analyzed by inflating the relaxed respiratory system with constant flow, followed by rapid airway occlusion at end-inflation, which was maintained until a plateau in tracheal pressure was obtained. Gas exchange and hemodynamics were evaluated by conventional means. The data were studied using the analysis of variance for repeated measures. Minimum airway resistance (Rmin) increased significantly from 8.87+/-3.24 cm H2O/L x s to 9.69 +/-3.22 cm H2O/L x s at the end of NO inhalation and remained elevated after NO was discontinued. A selective vasodilator effect on pulmonary vasculature was observed in the pulmonary-systemic vascular resistance ratio, which decreased from 0.18+/-0.11 to 0.13+/-0.08 at the end of inhalation and returned to baseline values after gas suspension. No significant alterations in oxygenation were observed.ConclusionThe effects of NO as a powerful and useful vasodilator agent were confirmed. However, it is important to be aware that the effects observed on respiratory mechanics may interfere with the final response of the respiratory system to NO.

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