American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Jul 1995
Randomized Controlled Trial Comparative Study Clinical TrialFactors 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. 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. ⋯ 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.
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Am. J. Respir. Crit. Care Med. · Jul 1995
Comparative StudyTitration of tidal volume and induced hypercapnia in acute respiratory distress syndrome.
Mechanical ventilation may promote overdistension-induced pulmonary lesions in patients with acute respiratory distress syndrome (ARDS). The static pressure-volume (P-V) curve of the respiratory system can be used to determine the lung volume and corresponding static airway pressure at which lung compliance begins to diminish (the upper inflection point, or UIP). This fall in compliance may indicate overdistension of lung units. ⋯ The end-inspiratory plateau pressure (Pplat) was compared to the UIP, and VT was lowered when the Pplat was above the UIP. In the range of lung volume studied on the P-V curves (up to 1600 ml), a UIP could be shown in only one control patient (at 23 cm H2O). By contrast, a UIP was present on the P-V curve obtained from all patients with ARDS, corresponding to a mean airway pressure of 26 +/- 6 cm H2O, a lung volume of 850 +/- 200 ml above functional residual capacity and 610 +/- 235 ml above PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)
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Am. J. Respir. Crit. Care Med. · Jul 1995
A dual-binding antibody to E- and L-selectin attenuates sepsis-induced lung injury.
Many studies indicate a pivotal role for neutrophil adhesion in sepsis-associated lung injury. Neutrophil adhesion to endothelium depends on activation and expression of selectin and integrin adhesion receptors. We studied the effects of pretreatment with a dual-binding porcine anti-E- and anti-L-selectin monoclonal antibody (EL-246) on a porcine model of sepsis-induced lung injury. ⋯ There was no significant difference in pulmonary and systemic hemodynamics between Groups 2 and 3. Group 4 animals exhibited a transient neutropenia, but otherwise no other differences in measured parameters were found compared with Group 1 control animals. In conclusion, EL-246 significantly reduced neutrophil accumulation in lung and attenuated sepsis-induced lung injury, but failed to attenuate deranged pulmonary and systemic hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)
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Am. J. Respir. Crit. Care Med. · Jul 1995
Arterial oxygenation time after an FIO2 increase in mechanically ventilated patients.
The time for arterial PO2 to reach equilibrium after a 0.2 increase in the fraction of inspired oxygen (FIO2) was studied, using arterial blood gases measured at 1, 2, 3, 4, 5, 7, 9, and 11 min in 30 stable, mechanically ventilated medical intensive care unit (ICU) patients. Eight patients also underwent a 0.4 increase in FIO2. Each patient's rise in PO2 over time [PO2(t)] was fit to the following exponential equation: PO2(t) = PO2i + (PO2f-PO2i) (1-e-kt), where t refers to time, PO2i and PO2f refer to the initial and final equilibrated PO2. ⋯ The mean t90% (+/- SD) was 6.0 (+/- 3.4) min for all patients (range 1.7 to 14.3 min); 7.1 +/- 2.1 min for 18 patients with chronic obstructive pulmonary disease (COPD) and 4.4 +/- 2.0 min for 12 patients without COPD (p < 0.05). In the subgroup of patients undergoing both an FIO2 increase of 0.2 and 0.4, there was no significant difference in the mean t90%'s for the two FIO2 changes (7.7 versus 7.7 min). We conclude that after a 0.2 or 0.4 increase of FIO3, a 15-min equilibration time period is adequate for 90% of the increase in PO2 to occur, in stable, mechanically ventilated medical ICU patients.