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Impaired arterial oxygenation, ranging from increased alImpaired arterial oxygenation, ranging from increased alveolar-arterial oxygen gradient (AaDo 2 ) to hypoxemia, is veolar-arterial oxygen gradient (AaDo 2 ) to hypoxemia, is comcommonly reported in patients with cirrhosis. 1 In the absence monly present in patients with cirrhosis. Nitric oxide (NO), of overt mechanical dysfunction of the lung, it has been through pulmonary vasodilatation, may play a major role in suggested that oxygenation abnormalities of cirrhotic pathe oxygen abnormalities of cirrhosis. Our aim was to study tients may be a consequence of ventilation/perfusion misthe relationship between NO production and O 2 abnormalities match and intrapulmonary shunting. 2-4 Intrapulmonary vasin 45 nonsmoking patients with cirrhosis and without major cular dilatations and artero-venous communications are cardiovascular and respiratory diseases. Intrapulmonary thought to be the pathological bases of the physiological shunting was detected by contrast-enhanced (CE) echocardimechanisms of oxygenation abnormalities. 5,6 ography. Lung volumes and diffusion, arterial blood gas analy-The vascular dilatations can result in severe hypoxemia, sis, serum NO 0 2 /NO 0 3 , NO output in the exhaled air, and which, at variance from that caused by intrapulmonary cardiac index by the echocardiographic method were detershunts, may respond normally to supplemental oxygen. mined in all patients. Twenty-seven (60%) patients had anIncreased circulation of a pulmonary vasodilator seems abnormally increased (ú15 mm Hg) AaDo 2 . The mean values to be the favored mechanism for intrapulmonary vascular of exhaled NO output and serum NO 0 2 /NO 0 3 were significantly dilatations in cirrhosis, and nitric oxide (NO) has recently higher in cirrhotic patients than in controls (252 { 117 vs.ascended to the top of the list of possible substances. 6,7 75.2 { 19 nL/min/m 2 , P õ .0001; and 47.5 { 29.4 vs. 32.9NO is a powerful local vasodilator of endothelial origin, { 10.1 mmol/L, P õ .02, respectively). In all patients, there which contributes to the normally low pulmonary vascular was a significant correlation between exhaled NO and AaDo 2 tone. 8 NO has been shown to play an important role in regulat-(r Å .78, P õ .0001). Twelve patients (26.6%) were found to ing the vasomotor tone in experimental cirrhosis. 9,10 It is now have CE-echocardiographic evidence of intrapulmonary possible to measure NO produced in the lung by measuring its shunting (positive CE-echo). Nine patients were considered concentration in exhaled air. 11,12 Recently, increased NO output to have hepatopulmonary syndrome (HPS) on the basis of an in exhaled air has been reported in patients with advanced AaDo 2 ú 15 mm Hg and positive CE-echo. These 9 patients cirrhosis, in whom exhaled NO was associated with systemic had a mean value of exhaled NO significantly higher than circulatory disturbances. 13 Exhaled NO was reported to be patients without HPS (331 { 73.2 vs. 223 { 118.4 nL/min/ raised almost threefold in t...

Oligoanalgesia in Emergency Departments (ED) is known to be common. The aim of our study is to determine how often patients in pain desire and receive analgesics while in the ED. Four main outcomes have been considered: desire of analgesics, administration of analgesics in the ED, correlation between initial analgesic administration and triage priority scores, patients' satisfaction at discharge during the ED visit. Pain severity was evaluated by a 10-point numerical rating scale (0 = no pain, 10 = worst possible pain) A total of 393 patients were enrolled in the study. The majority were non-Hispanic whites with a median age of 62 years. Of the 393 patients, 202 expressed desire for analgesics, but only 146 received a treatment. Among patients refusing analgesics (48.6%), the most common reasons were to diagnose pain causes and pain tolerance. In multivariate analysis, pain score severity was significant factor that predicted wanting analgesics, whereas desiring analgesics was predictive factor to receive them. On the other hand, patients with pain localized in lower extremities and in nose or ear less probably received analgesia. In conclusion, the underuse of analgesics in the ED continues to represent a problem and our study demonstrates that half of all ED patients in pain desire analgesics and that only half of those wanting analgesics receive them. Patients that desired and received analgesic treatment represented the group with a higher degree of satisfaction.

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Inspiratory resistance (RINSP) and reactance (XINSP) were measured for 7 min at 5 Hz in 10 subjects with mild asymptomatic asthma and 9 healthy subjects to assess the effects of airway smooth muscle (ASM) activation by methacholine (MCh) and unloading by chest wall strapping (CWS) on the variability of lung function and the effects of deep inspiration (DI). Subjects were studied at control conditions, after MCh, with CWS, and after MCh with CWS. In all experimental conditions XINSP was significantly more negative in subjects with asthma than in healthy subjects, suggesting greater inhomogeneity in the former. However, the variability in both RINSP and XINSP was increased by either ASM activation or CWS, without significant difference between groups. DI significantly reversed MCh-induced changes in RINSP both in subjects with asthma and healthy subjects, but XINSP in the former only. This effect was impaired by CWS more in subjects with asthma than in healthy subjects. The velocity of RINSP and XINSP recovery after DI was faster in subjects with asthma than healthy subjects. In conclusion, these results support the opinion that the short-term variability in respiratory impedance is related to ASM tone or operating length, rather than to the disease. Nevertheless, ASM in individuals with asthma differs from that in healthy individuals in an increased velocity of shortening and a reduced sensitivity to mechanical stress when strain is reduced.