Factors influencing cardiopulmonary effects of inhaled nitric oxide in acute respiratory failure
| Autor: | Thomas E. Stewart, E. Mourgeon, Qin Lu, Jean-Jacques Rouby, Philippe Cluzel, C. Devilliers, J.D. Law-Koune, Z Souhil, S Roche, Louis Puybasset |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Male
Pulmonary and Respiratory Medicine Pulmonary Circulation Hemodynamics Lung injury Nitric Oxide Critical Care and Intensive Care Medicine Intermittent Positive-Pressure Ventilation Positive-Pressure Respiration Administration Inhalation medicine Humans Prospective Studies Hypoxia Lung Positive end-expiratory pressure Respiratory Distress Syndrome Pulmonary Gas Exchange business.industry Respiratory disease Oxygenation Middle Aged respiratory system medicine.disease respiratory tract diseases medicine.anatomical_structure Anesthesia Vascular resistance Pulmonary shunt Female medicine.symptom Tomography X-Ray Computed business circulatory and respiratory physiology |
| Zdroj: | American Journal of Respiratory and Critical Care Medicine. 152:318-328 |
| ISSN: | 1535-4970 1073-449X |
| DOI: | 10.1164/ajrccm.152.1.7599840 |
| Popis: | 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. Twenty-one hypoxemic patients with acute respiratory failure (PaO2 = 127 +/- 69 mm Hg during intermittent positive pressure ventilation, FiO2 = 1), were mechanically ventilated with 2 ppm NO and pure oxygen. The effect of positive end-expiratory pressure (PEEP) on alveolar recruitment was assessed on an anatomic basis using a high-resolution and spiral thoracic computed tomographic (CT) scan. Four conditions were studied in random order: zero end-expiratory pressure (ZEEP), ZEEP + 2 ppm 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/QT), and alveolar dead space (VDA/VT) and significantly increased PaO2 (p < 0.01). During ZEEP, NO-induced decreases in PVRI (delta PVRI) and 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 MPAP = -0.28 MPAP + 4.8, r = 0.69, p < 0.05). These changes were not potentiated by PEEP-induced alveolar recruitment. The NO-induced increase in PaO2 (delta PaO2) was not significantly correlated with baseline PaO2 but was correlated with baseline PVRI (delta PaO2 = 0.11 PVRI + 30, r = 0.67, p < 0.05). In patients in whom PEEP was associated with alveolar recruitment, NO increased PaO2 by 66 +/- 24 mm Hg during ZEEP 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 PaO2 was similar during ZEEP and PEEP conditions (+70 +/- 15 mm Hg versus +76 +/- 12 mm Hg, NS). In patients with adult respiratory distress syndrome, factors determining NO-induced improvement in arterial oxygenation and pulmonary vascular effects are PEEP-induced alveolar recruitment and the baseline level of pulmonary vascular resistance. |
| Databáze: | OpenAIRE |
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