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      Optoelectronic Plethysmography has Improved our Knowledge of Respiratory Physiology and Pathophysiology

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          It is well known that the methods actually used to track thoraco-abdominal volume displacement have several limitations. This review evaluates the clinical usefulness of measuring chest wall kinematics by optoelectronic plethysmography [OEP]. OEP provides direct measurements (both absolute and its variations) of the volume of the chest wall and its compartments, according to the model of Ward and Macklem, without requiring calibration or subject cooperation. The system is non invasive and does not require a mouthpiece or nose-clip which may modify the pattern of breathing, making the subject aware of his breathing. Also, the precise assessment of compartmental changes in chest wall volumes, combined with pressure measurements, provides a detailed description of the action and control of the different respiratory muscle groups and assessment of chest wall dynamics in a number of physiological and clinical experimental conditions.

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          Most cited references 99

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          Dyspnea. Mechanisms, assessment, and management: a consensus statement. American Thoracic Society.

           P Meek,  G. Adams (1998)
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            Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes?

            To assess the possible differences in respiratory mechanics between the acute respiratory distress syndrome (ARDS) originating from pulmonary disease (ARDSp) and that originating from extrapulmonary disease (ARDSexp) we measured the total respiratory system (Est,rs), chest wall (Est,w) and lung (Est,L) elastance, the intra-abdominal pressure (IAP), and the end-expiratory lung volume (EELV) at 0, 5, 10, and 15 cm H2O positive end-expiratory pressure (PEEP) in 12 patients with ARDSp and nine with ARDSexp. At zero end-expiratory pressure (ZEEP), Est,rs and EELV were similar in both groups of patients. The Est,L, however, was markedly higher in the ARDSp group than in the ARDSexp group (20.2 +/- 5.4 versus 13.8 +/- 5.0 cm H2O/L, p < 0.05), whereas Est,w was abnormally increased in the ARDSexp group (12.1 +/- 3.8 versus 5.2 +/- 1.9 cm H2O/L, p < 0.05). The IAP was higher in ARDSexp than in ARDSp (22.2 +/- 6.0 versus 8.5 +/- 2.9 cm H2O, p < 0.01), and it significantly correlated with Est,w (p < 0. 01). Increasing PEEP to 15 cm H2O caused an increase of Est,rs in ARDSp (from 25.4 +/- 6.2 to 31.2 +/- 11.3 cm H2O/L, p < 0.01) and a decrease in ARDSexp (from 25.9 +/- 5.4 to 21.4 +/- 55.5 cm H2O/L, p < 0.01). The estimated recruitment at 15 cm H2O PEEP was -0.031 +/- 0.092 versus 0.293 +/- 0.241 L in ARDSp and ARDSexp, respectively (p < 0.01). The different respiratory mechanics and response to PEEP observed are consistent with a prevalence of consolidation in ARDSp as opposed to prevalent edema and alveolar collapse in ARDSexp.
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              Muscle strength, symptom intensity, and exercise capacity in patients with cardiorespiratory disorders.

              The contribution of muscle strength to symptom intensity and work capacity was examined in normal individuals and patients with cardiorespiratory disorders. Respiratory muscle strengths (maximal inspiratory and expiratory pressures) and peripheral muscle strengths (leg extension, leg flexion, seated bench press, and seated row) were measured in 4,617 subjects referred for clinical exercise testing. Subjects then rated the intensity of leg effort, discomfort with breathing (dyspnea), and chest pain (Borg scale) during an incremental exercise task (100 kpm/min each minute) to capacity on a cycle ergometer. Subjects were classified into groups on the basis of pulmonary function, drug therapy for cardiac disorders, and the presence of chest pain during exercise with electrocardiographic changes indicative of myocardial ischemia. Respiratory and peripheral muscle strengths, normalized for differences in age, sex, and height, were significantly reduced in patients with cardiorespiratory disorders compared with normal individuals. Muscle strength was a significant contributor to symptom intensity and work capacity in both health and disease; a two-fold increase in muscle strength was associated with a 25 to 30% decrease in the intensity of both leg effort and dyspnea and a 1.4- to 1.6-fold increase in work capacity. These results emphasize the need for an integrative approach in the assessment and therapeutic management of exercise intolerance, which considers the contribution of muscle weakness to excessive symptoms and reduced work capacity, in addition to the contribution of ventilatory, gas exchange, and circulatory impairments.

                Author and article information

                Sensors (Basel)
                Sensors (Basel)
                Sensors (Basel, Switzerland)
                Molecular Diversity Preservation International (MDPI)
                December 2008
                05 December 2008
                : 8
                : 12
                : 7951-7972
                Don C. Gnocchi Foundation ONLUS, via Imprunetana 124, 50023 Pozzolatico, Florence, Italy; E-Mails: iromagnoli@ (I. R.); blanini@ (B. L.); babybin@ (B. B.); coccio7@ (R. B.); c.claud@ (C. C.); lstendardi@ (L. S.); fgigliotti@ (F. G.)
                Author notes
                [* ] Author to whom correspondence should be addressed; E-Mail: gscano@ ; Tel.: +39 055 2601296; Fax: +39-055-2601271
                © 2008 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.

                This article is an open-access article distributed under the terms and conditions of the CreativeCommons Attribution license (



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