End-tidal CO2 levels lower in subclinical and overt hypothyroidism than healthy controls; no relationship to thyroid function tests

BACKGROUND Hypoventilation is a frequently suspected complication of hypothyroidism. OBJECTIVE In this study we examined the hypothesis that changes in alveolar ventilation, as measured by end-tidal carbon dioxide (Et-CO(2)), differ between patients with mild (subclinical) and overt (clinical) thyroid hormone deficiency, and both differ from healthy control subjects. METHODS A total of 95 subjects, including 33 with subclinical hypothyroidism (an elevated thyroid-stimulating hormone (TSH) level and a normal thyroxin (fT(4)) level), 31 with overt hypothyroidism (elevated TSH and decreased fT(4)), and 31 healthy controls. All subjects were female and were evaluated clinically by an endocrinologist for evidence of thyroid disease and categorized on the basis of thyroid hormone levels. Et-CO(2) was measured using a capnograph. Et-CO(2) levels were measured three times and the mean value was considered as the mean level for the individual. RESULTS Mean Et-CO(2) values of the subclinical hypothyroidism group were significantly lower than those of the healthy controls (31.79 ± 2.75 vs 33.81 ± 2.38; P = 0.01). Moreover, mean Et-CO(2) values for the overt hypothyroidism group were significantly lower than those for healthy controls (32.13 ± 3.07 vs 33.81 ± 2.38; P = 0.04). There was a significant correlation between Et-CO(2) values and TSH levels (r = -0.24; P = 0.01). However, Et-CO(2) values were not correlated with fT(4) levels (r = 0.13; P = 0.20). CONCLUSIONS Alveolar ventilation, as inferred from lower Et-CO(2) levels, is higher in subjects with subclinical hypothyroidism and overt hypothyroidism (lower Et-CO(2)) than in healthy controls. Furthermore, Et-CO(2) levels have no relationship to the levels of TSH or fT(4). The lower Et-CO(2) in these patients with hypothyroidism, particularly at the subclinical stage, suggests presence of hyperventilation, which may be related to direct effect of TRH on respiratory center or to local changes within the lung.