The artificial noses cause unfavorable mechanical effects by increasing inspiratory resistance, ventilation requirements, and dynamic intrinsic PEEP. Clinicians should consider these effects when setting mechanical ventilation and when assessing patients' ability to breathe spontaneously.

The LSF method allows non-invasive evaluation of respiratory mechanics during PSV, provided that a near-relaxation condition is obtained by means of an adequately increased pressure support level. The measurement of P0.1 may be helpful for titrating the pressure support in order to obtain the condition of near-relaxation.

Right ventricular failure after left ventricular assist device placement is the major concern on weaning from cardiopulmonary bypass and it is one of the most serious complications in the postoperative period. This complication has a poor prognosis and is generally unpredictable. The identification of pre-operative risk factor for this serious complication is incomplete yet. In order to determine pre-operative risk for severe right ventricular failure after left ventricular assist device support we analyzed preoperative hemodynamics, laboratory data and characteristics of 48 patients who received Novacor (World Heart Corp., Ottawa, ON, Canada). We compared the data from the patients who developed right ventricular failure and the patients who did not. Right ventricular failure occurred in 16% of the patients. There was no significant difference between the groups in demographic characteristics. We identified as preoperative risk factors the pre-operative low mean pulmonary artery and the impairment of hepatic and renal function on laboratory data. Our results confirm in part the findings of the few previous studies. This information may be useful for the patient selection for isolated left ventricular assist device implantation, but other studies are necessary before establishing criteria for patient selection for univentricular support universally accepted.

In patients with adult respiratory distress syndrome (ARDS), inhaled nitric oxide (NO) may both reduce pulmonary hypertension and improve arterial oxygenation [1,2]. The NO-induced decrease in pulmonary artery pressure depends on the selective pulmonary vasodilating effect of inhaled NO [3], while the NO-induced increase in arterial oxygenation is related to the redistribution of pulmonary blood flow to well-ventilated lung areas, which results in improved ventilation to perfusion matching [1,4]. Although potentially beneficial, inhaled NO is a toxic compound, and its toxicity is increased by the oxidation of NO to NO 2 , which occurs during administration of inhaled NO, especially when the inhaled oxygen concentration is high [5]. In order to minimize the risks of toxicity, inhaled NO should be administered at the lowest effective concentration to achieve maximal therapeutic effects [6,7].There is conflicting information on the NO dose for optimal treatment of pulmonary hypertension and hypoxaemia in ARDS. It has been shown that very low NO doses (<1 parts per million (ppm)) may have a measurable effect both on pulmonary circulation and on arterial oxygenation in ARDS patients [8][9][10]. Published data indicate that low NO doses, between 1-5 ppm, achieve maximal haemodynamic and oxygenation responses [9][10][11][12]. However, other studies in ARDS patients indicate that higher NO doses may induce an additional reduction in pulmonary hypertension and hypoxaemia. In a study by GERLACH et al. [13], a dose of NO as high as 100 ppm was required to achieve maximal pulmonary vasodilation, while the impro-vement in arterial oxygen tension (Pa,O 2 ) was maximal at 1 ppm. In contrast, a study on septic ARDS patients rep-orted a dose-dependent increase in Pa,O 2 in the range 0.1-150 ppm and a plateau effect in pulmonary pressure at 5 ppm [14]. A recent study showed that the optimum NO dose to improve Pa,O 2 may vary widely between individuals, ranging 0.1-100 ppm [15]. In that same study, however, the effect on pulmonary haemodynamics was negligible.The aim of this study was to evaluate the dose-response effect of inhaled NO (0.5-100 ppm) on gas exchange and haemodynamics in ARDS patients treated with conventional mechanical ventilation. Materials and methods PatientsDuring a 10-month period, 19 consecutive patients who were mechanically ventilated for severe ARDS were screen- Olivei, A. Palo, C. Galbusera, R. Veronesi, A. Braschi. ©ERS Journals Ltd 1998. ABSTRACT: This study evaluated the dose-response effect of inhaled nitric oxide (NO) on gas exchange, haemodynamics, and respiratory mechanics in patients with adult respiratory distress syndrome (ARDS). Acute effects of inhaled nitric oxide in adult respiratory distress syndrome. G.A. Iotti, M.C.Of 19 consecutive ARDS patients on mechanical ventilation, eight (42%) responded to a test of 10 parts per million (ppm) NO inhalation with a 25% increase in arterial oxygen tension (Pa,O 2 ) over the baseline value. The eight NO-responders were extensively studied during admin...