title: Control of breathing in patients with severe hypothyroidism.
abstract: OBJECTIVE
  Hypothyroid patients have been reported to have a blunted ventilatory response to carbon dioxide stimulation. However, previous data did not clarify the localization of abnormalities responsible for that disorder. The present investigation was aimed at evaluating to what extent central (neural) and/or peripheral (muscular) factors are involved in the abnormalities of the ventilatory control system in hypothyroid patients.
  
  
  METHODS
  We studied 13 patients with severe hypothyroidism before and after 6 to 9 months of replacement therapy; 7 age- and sex-matched normal subjects were also studied as a control. In each subject, we assessed (1) inspiratory muscle strength by measuring maximal inspiratory pressure (MIP), and (2) respiratory control system during a carbon dioxide rebreathing test by measuring minute ventilation (VE), tidal volume (VT), mean inspiratory flow (VT/TI), and electromyographic (EMG) activity of the diaphragm (Edi) and intercostal (Eint) muscles.
  
  
  RESULTS
  Compared with the normal control group (Group C), patients exhibited similar MIP, and similar VE and EMG response slopes to carbon dioxide. However, evaluating individual VE response 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 Group C) and Group B (seven patients) with normal VE response. Compared with both Groups B and C, Group A exhibited significantly lower VT/TI, Edi, and Eint response slopes; the difference between Groups B and 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 Edi response slopes increased significantly in Group A; and (2) MIP increased, but not significantly in patients with low MIP.
  
  
  CONCLUSIONS
  We conclude that: (1) In patients with severe hypothyroidism, the ventilatory control system may be altered at the neural level, as indicated by a blunted chemosensitivity; (2) Impaired respiratory muscle function does not seem to play a major role in the decreased ventilatory response to carbon dioxide stimulation; (3) Replacement therapy appears to normalize the response to hypercapnic stimulation, but not respiratory muscle strength.
authors.affiliation: Istituto di Clinica Medica III, Università degli Studi di Firenze, Florence, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Duranti
authors.forename: R G
authors.initials: RG
authors.lastname: Gheri
authors.forename: M
authors.initials: M
authors.lastname: Gorini
authors.forename: F
authors.initials: F
authors.lastname: Gigliotti
authors.forename: A
authors.initials: A
authors.lastname: Spinelli
authors.forename: A
authors.initials: A
authors.lastname: Fanelli
authors.forename: G
authors.initials: G
authors.lastname: Scano
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D005260:Female; D006801:Humans; D007037:Hypothyroidism / Q000188:drug therapy / Q000503:physiopathology*; D008875:Middle Aged; D009420:Nervous System / Q000503:physiopathology; D012119:Respiration / Q000502:physiology*; D012129:Respiratory Function Tests; D015656:Respiratory Mechanics; D012720:Severity of Illness Index; D013997:Time Factors