CONTROL OF BREATHING IN PATIENTS WITH SEVERE HYPOTHYROIDISM

PURPOSE: Hypothyroid patients have been reported to have a blunted ven tilatory response to carbon dioxide stimulation. However, previous dat a did not clarify the localization of abnormalities responsible for th at disorder. The present investigation was aimed at evaluating to what extent central (neural) and/or peripheral (muscular) factors are invo lved in the abnormalities of the ventilatory control system in hypothy roid patients. PATIENTS AND METHODS: We studied 13 patients with sever e hypothyroidism before and after 6 to 9 months of replacement therapy , 7 age- and sex-matched normal subjects were also studied as a contro l. In each subject, we assessed (1) inspiratory muscle strength by mea suring maximal inspiratory pressure (MIP), and (2) respiratory control system during a carbon dioxide rebreathing test by measuring minute v entilation (VE), tidal volume (VT), mean inspiratory flow (VT/TI), and electromyographic (EMG) activity of the diaphragm (E(di)) and interco stal (E(int)) muscles. RESULTS: Compared with the normal control group (Group C), patients exhibited similar MIP, and similar VE and EMG res ponse slopes to carbon dioxide. However, evaluating individual VE resp onse slopes, we were able to identify two subsets of patients: Group A (six patients) with low VE response (less than mean - SD . 1.65 of Gr oup C) and Group B (seven patients) with normal VE response. Compared with both Groups B and C, Group A exhibited significantly lower VT/TI, E(di), and E(int) response slopes; the difference between Groups B an d C was not significant. Six patients (two from Group A and four from Group B) exhibited low MIP values compared with that in Group C. After replacement therapy, (1) VE, VT/TI, and E(di) response slopes increas ed significantly in Group A; and (2) MIP increased, but not significan tly in patients with low MIP. CONCLUSIONS. We conclude that: (1) In pa tients with severe hypothyroidism the ventilatory control system may b e altered at the neural level, as indicated by a blunted chemosensitiv ity, (2) Impaired respiratory muscle function does not seem to play a major role in the decreased ventilatory response to carbon dioxide sti mulation; (3) Replacement therapy appears to normalize the response to hypercapnic stimulation, but not respiratory muscle strength.