Respiratory response during arm elevation in isolated diaphragm weakness

Upper extremity exercise is associated with a significant metabolic and ven tilatory cost that is particularly evident in patients with severe chronic airflow obstruction. In these patients abnormal ventilatory muscle recruitm ent has been hypothesized to relate to impaired diaphragm function resultin g from hyperinflation. Similar data have never been reported in patients wi th isolated diaphragm weakness but without airflow obstruction or hyperinfl ation, a group that would ideally define the role of diaphragm function dur ing arm elevation (AE). We prospectively studied 15 patients with isolated diaphragm weakness of varying severity (Pdi(sniff), 31.74 +/- 3.75 cm H2O) as contrasted with eight normal subjects (Pdi(sniff), 111.77 +/- 13.35 cm H 2O) of similar age. Patients with diaphragm weakness demonstrated significa nt lung volume restriction with normal DLCo/VA There was no difference in r esting oxygen consumption ((V) over dot O-2), carbon dioxide production ((V ) over dot CO2), minute ventilation ((V) over dot E), and tidal volume (VT) between the two groups; however, a borderline difference in resting breath ing frequency (f(b)) (p = 0.056) was evident. Both groups demonstrated a ri se in (V) over dot O-2, (V) over dot CO2, and (V) over dot E during 2 min o f AE anteriorly. Normal subjects demonstrated a statistically significant r ise in VT but a statistically insignificant rise in fb during AE. In contra st, patients with diaphragm weakness demonstrated a statistically significa nt rise in fb during AE but a statistically insignificant rise in Vr. In pa tients the observed rise in VT directly correlated with baseline Pdi(sniff) (r = 0.59, p = 0.02) and Pdi(max) (r = 0.81, p = 0.002). Both groups demon strated a rise in Pdi during AE. The rise in Pdi during AE directly correla ted to Pdi(sniff) in the patients (r = 0.69, p = 0.004). Observed end-expir atory Ppl rose during arm elevation in both the patient group and in the no rmal control group, but no evidence of a differential response to AE was fo und. In those patients with greater diaphragm weakness (Pdi(sniff) < 30 cm H2O), abnormal respiratory muscle function (lesser rise in Pdi) and a lesse r increase in VT during AE were more evident. These data highlight the impo rtance of diaphragm function in determining the metabolic and respiratory m uscle response to arm elevation.