A A s si im mp pl le e m me et th ho od d t to o d de et te ec ct t e ex xp pi ir ra at to or ry y f fl lo ow w l li im mi it ta at ti io on n d du ur ri in ng g s sp po on nt ta an ne eo ou us s b br re ea at th hi in ng g N.G. Koulouris*, P. Valta*, A. Lavoie*, C. Corbeil**, M. Chassé**, J. Braidy**, J. Milic-Emili*A simple method to detect expiratory flow limitation during spontaneous breathing. N.G. Koulouris, P. Valta, A. Lavoie, C. Corbeil, M. Chassé, J. Braidy, J. Milic-Emili. ERS Journals Ltd 1995. ABSTRACT: Patients with severe chronic obstructive pulmonary disease (COPD) often exhale along the same flow-volume curve during quiet breathing as during a forced expiratory vital capacity manoeuvre, and this has been taken as indicating flow limitation at rest. To obtain such curves, a body plethysmograph and the patient's co-operation are required. We propose a simple technique which does not entail these requirements. It consists in applying negative pressure at the mouth during a tidal expiration (NEP). Patients in whom NEP elicits an increase in flow throughout the expiration are not flow-limited. In contrast, patients in whom application of NEP does not elicit an increase in flow during most or part of the tidal expiration are considered as flowlimited. Using this technique, 26 stable COPD patients were studied sitting and supine.Eleven patients were flow-limited both seated and supine, eight were flow-limited only when supine, and seven were not flow-limited either seated or supine. Only 5 of 19 patients who were flow-limited seated and/or supine had severe ventilatory impairment (forced expiratory volume in one second (FEV 1 ) <40% predicted).We conclude that the NEP technique provides a simple, rapid, and reliable method for detection of expiratory flow limitation in spontaneously breathing subjects, which does not require the patient's co-operation, and can be applied in different body positions both at rest and during muscular exercise. Our results also indicate a high prevalence of flow limitation in COPD patients at rest, particularly when supine. Eur Respir J., 1995, 8, 306-313 It has long been suggested that patients with severe chronic obstructive pulmonary disease (COPD) may exhibit expiratory flow limitation at rest, as reflected by the fact that they breathe tidally along or above their maximum expiratory flow-volume curves [1][2][3]. The effects of expiratory flow limitation may be partly compensated by breathing at lung volumes higher than the relaxation volume of the respiratory system [3]. The latter condition, which is termed dynamic pulmonary hyperinflation, is associated with intrinsic positive endexpiratory pressure (PEEPi) [4]. The combined effects of increased flow resistance, dynamic hyperinflation and PEEPi place a severe burden on the inspiratory muscles of COPD patients [5][6][7], and may also contribute to dyspnoea [8].Though dynamic hyperinflation is the hallmark of expiratory flow limitation, the prevalence and clinical significance of this phenomenon have not been adequa...

Two new methods, application of negative pressure at the airway opening during expiration (NEP) and reduction of flow resistance by bypassing the expiratory line of the ventilator by exhaling into the atmosphere (ATM), were used to detect expiratory flow limitation in 12 semirecumbent (45 degree) mechanically ventilated patients, seven with chronic airway obstruction (CAO). An increase of expiratory flow with NEP or ATM, relative to the preceding control breath, was taken as indicating absence of expiratory flow limitation. By contrast, the portion of the tidal expiration over which there was no change in flow with NEP or ATM was considered as flow-limited. With NEP, nine patients exhibited flow limitation, six (all with CAO) were flow-limited over most of the tidal expiration (> 70% VT), and three at < 60% VT. Although the results with NEP and ATM were in general in good agreement, in the three non-flow-limited patients the ATM method gave erroneous results. Six patients were also studied supine, including two who were not flow-limited when semirecumbent: both became flow-limited when supine. We conclude that NEP provides a simple method to detect flow limitation in mechanically ventilated patients. The supine position enhances flow limitation.

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In CF, early insulin secretion defect but also IR contribute to glucose intolerance. Early in the course of the disease, increased glucose AUC and reduced early insulin secretion are more closely associated with a worse clinical status than conventional glucose tolerance categories.

Inhaled nitric oxide (iNO), a selective pulmonary vasodilator, has been shown to decrease pulmonary artery pressures but not increase cardiac output in hemodynamically stable patients with a variety of causes of pulmonary hypertension. The response to iNO in hemodynamically unstable patients with acute right heart syndrome has not been previously described. We determined the response to iNO in 26 critically ill adult patients with acute right heart failure defined by echocardiographic criteria. Patients received iNO through the inspiratory limb of the ventilator in increments of 10 ppm with hemodynamic and gas-exchange measurements made before and after each level. When maximal effect was seen, iNO was discontinued to compare parameters with baseline. iNO significantly increased cardiac output (5.5 +/- 3 to 6.4 +/- 4 L/min), stroke volume (54 +/- 27 to 65 +/- 38 ml), and mixed-venous oxygen saturation (69 +/- 8 to 73 +/- 10%), all p < 0.01. With discontinuation of iNO, all parameters returned immediately to baseline. These parameters of improved perfusion were related to a decrease in pulmonary vascular pressures and resistance. In a subset of approximately 50% of patients, these changes were substantial (> 20%) and in approximately 25% of all patients, the improvement in hemodynamic measures permitted a decrease in other vasoactive drug administration. The mean concentration of iNO required to achieve these effects was 35 ppm, and 85% of patients exhibiting a substantial improvement in hemodynamics did so at a concentration of iNO of less than or equal to 40 ppm. Underlying causes of right heart failure and baseline hemodynamics did not predict response to iNO, but the use of alpha-agonist catecholamines did. We conclude iNO improves hemodynamics in patients with respiratory failure, shock, and right ventricular dysfunction. Although mortality was not a key end point in this pilot study, it was high for both responders and nonresponders to this therapy. Further evaluation of the role of iNO in this patient population is supported by these data.