Diaphragmatic Contribution to Ventilation in Patients with Ankylosing Spondylitis

Abstract

Part I reports pulmonary function and clinical measurements of 222 patients with ankylosing spondylitis, before and after physical therapy, to quantify thoracic impairment and to evaluate therapeutic effect. Vital capacity and forced expiratory volume remained virtually unchanged; cervical extensibility, lumbar flexibility, and chest expansion improved significantly. Part II reports findings in 25 patients and 25 age-matched normal subjects. The linear momentum of breathing was measured, from which the respiratory muscle balance (rib-cage vs. abdominal breathing) was derived. During normal breathing in supine position the mean diaphragmatic contribution to a tidal volume was 84.8 ± 3.3% SE in the patients and 68.4 ± 1.5% in the normal subjects. In 3 patients with severe ankylosis of cervical and thoracic vertebrae there was paradoxical movement of the chest, resulting in a diaphragmatic contribution of > 100%. An understanding of respiratory muscle function is essential to the formulation of rational physical therapy for patients with such conditions.

Acute clinical benefits of chest wall-stretching exercise on expired tidal volume, dyspnea and chest expansion in a patient with chronic obstructive pulmonary disease: A single case study

“…The reduction of chest wall compliance, in particular the expansion of the rib cage, leads to atrophy of the intercostal muscles, as well as the diaphragm (Josenhans et al, 1971;Hauge, 1973). This in turn leads to rib cage immobility, dyspnea, and insufficiency of spontaneous breathing (Elliott et al, 1985).…”

Chest wall kinematics and respiratory muscle action in ankylosing spondylitis patients

“…The pathological process of ankylosing spondylitis may involve fusion of costovertebral and sternoclavicular joints, along with intercostal muscle atrophy [1], resulting in limited motion of the chest wall [2][3][4][5]. With the reduction in expansion of the ribcage, ventilation becomes increasingly dependent on the diaphragm, which largely compensates for ribcage immobility during hyperventilation [4,6].…”

Restrictive Chest Wall Disorders

“…167 The same group in a second study found less difference between MIP and MEP values of normal controls and patients with either early or late AS, although MVV was low in late AS. 165 It was recognized early by Josenhans et al, who used supine ballistography, 168,169 and confirmed later by Grimby et al applying magnetometry in upright patients, 170 and by Ferrigno and Carnevali by their optoelectronic method, 171 that increased diaphragmatic movements compensate for reduced rib cage mobility in AS, especially during hyperventilation. Increased abdominal wall contribution was also demonstrated by Romagnoli et al and by Ragnarsdottir et al 172,173 In exercise tolerance, Elliott et al reported a decrease in AS patients, explained by deconditioning or cardiovascular disease but not ventilatory limitation.…”