FACTORS INFLUENCING CARDIOPULMONARY EFFECTS OF INHALED NITRIC-OXIDE IN ACUTE RESPIRATORY-FAILURE

The aim of this prospective study was to determine factors influencing effects of inhaled nitric oxide (NO) on the pulmonary circulation and on gas exchange in critically ill patients with acute lung injury. Tw enty-one hypoxemic patients with acute respiratory failure (Pa-o2 = 12 7 +/- 69 mm Hg during intermittent positive pressure ventilation, Fl(o 2) = 1), were mechanically ventilated with 2 ppm NO and pure oxygen. T he effect of positive end-expiratory pressure (PEEP) on alveolar recru itment was assessed on an anatomic basis using a high-resolution and s piral thoracic computed tomographic (CT) scan. Four conditions were st udied in random order: zero end-expiratory pressure (ZEEP), ZEEP + 2 p pm NO, 10 cm H2O PEEP, 10 cm H2O PEEP + 2 ppm NO. During ZEEP and PEEP , NO significantly decreased pulmonary vascular resistance index (PVRI ), mean pulmonary arterial pressure (MPAP), true pulmonary shunt (QS/Q T), and alveolar dead space (VDA/VT) and significantly increased Pa-o2 (p < 0.01). During 2EEP, NO-induced decreases in PVRI (Delta PVRI) an d MPAP (Delta MPAP) were significantly correlated to baseline PVRI and MPAP (Delta PVRI = -0.5 PVRI + 125, r = 0.97, p < 0.01 and Delta MPBP = -0.28 MPAP + 4.8, r = 0.69, p < 0.05). These changes were not poten tiated by PEEP-induced alveolar recruitment. The NO-induced increase i n Pa-o2 (Delta Pa-o2) zwas not significantly correlated with baseline Pa-o2 but was correlated with baseline PVRI (Delta Pa-o2 = 0.11 PVRI 30, r = 0.67, p < 0.05). In patients in whom PEEP was associated with alveolar recruitment, NO increased Pa-o2 by 66 +/- 24 mm Hg during ZE EP and by 104 +/- 26 mm Hg during PEEP (p < 0.01). In patients in whom PEEP did not induce alveolar recruitment, the NO-induced increase in Pa-o2 was similar during ZEEP and PEEP conditions (+70 +/- 15 mm Hg ve rsus +76 +/- 12 mm Hg, NS). In patients with adult respiratory distres s syndrome, factors determining NO-induced improvement in arterial oxy genation and pulmonary vascular effects are PEEP-induced alveolar recr uitment and the baseline level of pulmonary vascular resistance.