Recently the analysis of breathing during sleep has attracted increasing attention. Disordered breathing and oxygen desaturation are recognized in patients with chronic obstructive lung disease as well as in patients with sleep apnea syndrome. Previous studies by several investigators have demonstrated a close correlationship between alveolar hypoxia and elevated pulmonary artery pressure. Continuous measurement of arterial oxygen tension is necessary to analyse the effects of nocturnal hypoxia on pulmonary hemodynamics. We measured trans-cutaneous oxygen tension continuously by a heated electrode and studied the effects of nocturnal hypoxia on pulmonary hemodynamics.
Ten patients including 5 with old pulmonary tuberculosis with thoracoplasty (Thoracoplasty), 3 with chronic pulmonary emphysema (CPE), 1 with COLD with bronchial asthma (BA) and 1 with pulmonary fibrosis were studied using right side cardiac catheterization. Trans-cutaneous oxygen tension (P
TCO
2) was measured by a heated electrode (Trasoxode, Hellige) on the anterior chest wall. Pulmonary artery pressure by a Swann-Ganz catheter placed in the pulmonary trunk, tidal volume by impedance pneumography and P
TCO
2 were simultaneously recorded all night in these 10 patients.
A preliminary study concerning the trans-cutaneous electrode showed that the correlation between P
TCO
2 and PaO
2 was statistically significant (P
TCO
2=0.8×PaO
2+7.6, N=40, r=0.95, p<0.001). During exercise, the change of P
TCO
2 followed that of PaO
2 with some delay. These results proved the usefullness of P
TCO
2 for continuous analysis of PaO
2.
In 6 patients, including 4 with Thoracoplasty, 1 with CPE and 1 with BA, decreased P
TCO
2 corresponded to the decrease of ventilation. Furthermore the fall of P
TCO
2 accompanied the elevation of pulmonary artery pressure in all 6 patients (P
TCO
2: from 60.7±6.5 TORR to 34.7±4.2 TORR, PAm: from 21.0±5.0mmHg to 58.7±6.5mmHg). The change of P
TCO
2 was mirror image of the change of PAm and they moved reciprocally. Cardiac output measured in 2 patients during hypoxemia increased slightly compared with the elevation of PAm. The elevation of pulmonary artery pressure was considered to be hypoxic pulmonary vasoconstriction. Cardiopulmonary functions were compared between the 6 patients with nocturnal hypoxemia (NH(+)) and the 4 patients without nocturnal hypoxemia (NH(-)). The differences in %VC and FEV1% between 2 groups were not statistically significant, but %VC in NH(+) was lower. Patients with small VC might have poor ventilatory reserve and may be greatly influenced by depressed activity of the respiratory center during sleep. PaCO
2 was significantly higher in NH(+). It was thought to be due to low responsiveness of the respiratory center to CO
2 in these patients. PaO
2 in NH(+) was significantly lower compared with NH(-). Though the difference of PAm between NH(+) and NH(-) was not significant, the cardiac index was lower in NH(+). Pulmonary artery mean pressure during nocturnal hypoxia was higher than during sub-maximal excrcise in 5 patients studied.
We concluded that nocturnal hypoxia had significant effects on the pulmonary vasopressor response, which might contribute to the establishment of chronic cor pulmonale.
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