Objective. To study the effect of nitric oxyde (NO) inhalation on right ventricular function of patients with acute severe respiratory failure. Methods. Nine patients with acute severe respiratory failure were prospectively studied. All patients were under sedation and paralysis and were ventilated with an assisted-controlled volume, a constant inspiratory flow and a positive end-expiratory pressure (PEEP) adjusted according to the pressure-volume curve. Blood gases and hemodynamic measurements from pulmonary and systemic arteries were performed before (baseline) and 30 minutes after (with NO) the inhalation of 5 parts per million (ppm) of NO. The right ventricular ejection fraction (RVEF) was assessed with a rapid-response thermodilution catheter. The doses of NO administered were monitored continuously with a chemoluminiscence analyzer. Analysis of the variance and simple linear correlation tests were used for the statistical analysis. Results. After inhalation of 5 ppm of NO, the RVEF increased from 35.8% = 5.7% to 42.1% ± 4.9% (p = 0.002). The right ventricular telediastolic volume index declined from 129 = 18 ml/m 2 to 112 = 22 ml/m 2 (p = 0.003). The telediastolic volume index was 82 ± 13 ml/m 2 at the baseline and after the inhalation of NO, it declined to 65 ± 14 ml/m 2 (p = 0.01). The mean pulmonary artery pressure (MPAP) was 31.1 ± 6.4 at the baseline and 27-5.1 with NO (p = 0.001). The PaO 2/FiO 2, at the baseline was 107 ± 66 mmHg and increased to 135 ± 66 (p = 0.005) after the administration of NO. The intrapulmonary shunt decreased from 42% ± 13% at the baseline to 34% ± 10% with NO (p = 0.05). No changes were observed in the systemic and pulmonary vascular resistance indexes (PVRI), mean arterial pressure, pulmonary capillary pressure, cardiac index (CI) or PaCO 2. A simple lineal correlation test between the change observed in the RVEF and in the PVRI after the inhalation of NO yielded an r 2 = 0.56 with a p < 0.02. Conclusions. The inhalation of 5 ppm of nitric oxyde increases the RVEF in patients with acute severe respiratory failure through a declining in the right ventricular afterload; it also improves the oxygenation and decreases the intrapulmonary shunt and the MPAP as well and these effects can not be attributed to changes in the CI.
|Publication status||Published - 1 Feb 1997|
- Acute respiratory distress syndrome
- Acute respiratory failure
- Ejection fraction
- Nitric oxyde (NO)
- Right ventricle