In 6 patients with early acute respiratory distress syndrome and highly responsive to inhaled nitrix oxide, the administration of intravenous almitrine at a concentration of 16 micrograms.kg-1.min-1 induced an additional increase in Pao2. Dose response of nitric oxide was not changed by the administration of almitrine and a plateau effect was observed at inspiratory nitric oxide concentrations of 1.5 ppm.

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.

Local anesthetic infiltration has been proposed to decrease postoperative pain. The aim of this study was to determine whether scalp infiltration with bupivacaine or ropivacaine would improve analgesia after supratentorial craniotomy for tumor resection. Eighty patients were recruited into a randomized double-blind study. Infiltration was performed after skin closure with 20 mL of saline 0.9% (placebo group, n = 40), of 0.375% bupivacaine with epinephrine 1:200,000 (bupivacaine group, n = 20), or of 0.75% ropivacaine (ropivacaine group, n = 20). Postoperative analgesia was provided with patient-controlled morphine IV analgesia (PCA). The study was continued until PACU discharge, which occurred early in the morning following surgery. Results are reported on 37 patients in the placebo group, 20 in the bupivacaine group, and 19 in the ropivacaine group because 4 patients experienced postoperative complications and were excluded from the study. Morphine titration at arrival in the postanesthesia care unit was necessary more often in the placebo group (62% of the patients) than in the 2 treated groups (19% in each, P = 0.02). The median quantity of morphine administered during the first 2 postoperative hours, including initial titration administered by a nurse and PCA-administered morphine, was lower in each treated group than in the placebo group (P < 0.01). The median morphine consumption up to the 16th postoperative hour was not significantly different among the 3 groups. There was no difference in the visual analogue scale scores among the 3 groups at any time. Scalp infiltration with either bupivacaine or ropivacaine had a statistically significant effect on morphine consumption during the first 2 postoperative hours.

Studies investigating the influence of muscle relaxants on the bispectral index have yielded contradictory results. In our prospective, randomized, double-blind experiments, patients received a fixed target concentration of remifentanil along with a target-controlled infusion of propofol, titrated until loss of consciousness. Two minutes after loss of consciousness, the study group received a bolus injection of atracurium, whereas the control group received a placebo. The following variables were recorded: bispectral index, spectral edge frequency, electromyographic activity, state entropy, and response entropy provided by the Datex-Ohmeda Entropy monitor. Similar values were obtained in both groups at loss of consciousness. Placebo administration induced a decrease in bispectral index (P < 0.002), spectral edge frequency (P < 0.05), electromyographic activity (P < 0.02), state entropy (P < 0.05), and response entropy (P < 0.01) compared with the values measured at loss of consciousness. Atracurium administration induced a decrease in bispectral index (P < 0.0001), spectral edge frequency (P < 0.01), electromyographic activity (P < 0.0001), state entropy (P < 0.0001), and response entropy (P < 0.0001) values. Decreases in bispectral index (P < 0.05), electromyographic activity (P < 0.0001), and response entropy (P < 0.01) were larger after atracurium than placebo injection. In lightly anesthetized patients, myorelaxant administration decreases bispectral index and response entropy, but not state entropy values.

This study was directed at assessing changes in bronchial cross-sectional surface areas (BCSA) and in respiratory resistance induced by endotracheal suctioning in nine anesthetized sheep. Cardiorespiratory parameters (Swan-Ganz catheter), respiratory resistance (inspiratory occlusion technique), BCSA, and lung aeration (computed tomography) were studied at baseline, during endotracheal suctioning, and after 20 consecutive hyperinflations. Measurements performed initially at an inspired oxygen fraction (FI(O(2))) of 0.3 were repeated at an FI(O(2)) of 1.0. At an FI(O(2)) of 0.3, endotracheal suctioning resulted in atelectasis, a reduction in BCSA of 29 +/- 23% (mean +/- SD), a decrease in arterial oxygen saturation from 95 +/- 3% to 87 +/- 12% (p = 0.02), an increase in venous admixture from 19 +/- 10% to 31 +/- 19% (p = 0. 006), and an increase in lung tissue resistance (DR(rs)) (p = 0. 0003). At an FI(O(2)) of 1.0, despite an extension of atelectasis and an increase in pulmonary shunt from 19 +/- 5% to 36 +/- 2% (p < 0.0001), arterial O(2) desaturation was prevented and BCSA decreased by only 7 +/- 32%. A recruitment maneuver after endotracheal suctioning entirely reversed the suctioning-induced increase in DR(rs) and atelectasis. In three lidocaine-pretreated sheep, the endotracheal suctioning-induced reduction of BCSA was entirely prevented. These data suggest that the endotracheal suctioning-induced decrease in BCSA is related to atelectasis and bronchoconstriction. Both effects can be reversed by hyperoxygenation maneuver before suctioning in combination with recruitment maneuver after suctioning.