[Does nocturnal hypoxia relate to acute exacerbation of chronic respiratory failure with right heart failure in late sequelae of pulmonary tuberculosis?].

Thirty-eight patients with late sequelae of pulmonary tuberculosis (TB seq.) were studied to clarify whether or not nocturnal oxyhemoglobin desaturation (NOD) could relate to acute exacerbation of chronic respiratory failure (AE). All patients had been untreated with home oxygen therapy, because they were not severely hypoxic. We performed sleep studies, pulmonary function tests and arterial blood gas analysis and investigated past history about AE in each patient. Twelve patients had experienced AE with right heart failure and they were classified as CHF (congestive heart failure) group. The rest was classified as Non-CHF group. These two groups were compared as for each variables examined. There was no difference between the two groups in age, body weight, %VC, FEV1.0%, and awake PaO2. Awake PaCO2 was significantly higher in CHF group. Although no difference was observed in baseline SaO2, the degree of NOD was significantly greater in CHF group when evaluated by lowest SaO2 during sleep and 85% desaturation time (total time spent with SaO2 less than 85%). Moreover, 21 of Non-CHF and 6 of CHF were studied for cardiac parameters using right side cardiac catherization. While the differences of mean pulmonary arterial pressure and cardiac output between the two groups were not significant, pulmonary arteriolar resistance was higher in CHF group. We concluded that NOD in TB seq. had a major role in AE with right heart failure. We speculated that AE might be caused, at least partly, by pulmonary vasopressor response to recurrent NOD.