To assess the acute effects of nasal continuous positive airway pressure (CPAP) on the 24-hour blood pressure and the secretion of catecholamines in urine and plasma, we investigated the changes in the 24-hour blood pressure and urinary and plasma concentrations of epinephrine (E) and norepinephrine (NE) in 26 men with obstructive sleep apnea (OSA) with and without nasal CPAP. Nasal CPAPresulted in significant decreases in the daytime diastolic pressure (from 86 ± 16 mmHgto 83 ± 12 mmHg), the nighttime diastolic pressure (from 81 ± 12 mmHgto 77 ±9 mmHg) and the nighttime systolic pressures (from 125 ± 15 mmHgto 120 ± 10 mmHg). There was no significant difference between patients with and without CPAPin the daytime or nighttime urinary E level, but patients who received CPAPshowed a significant decrease in daytime urinary NElevel (from 156± 112 |ig/14h to 119 ± 101 |0g/14h) and nighttime urinary NE level (from 143 ±91 |ig/10h to 112 ± 65 |ig/10h). The morning plasma level of NE also decreased (from 371 ± 181 pg/ml to 273 ± 148 pg/ml) in patients who received nasal CPAP (p<0.02), but the plasma level of E remained unchanged. There were no correlations between PSGparameters and the reductions in blood pressure and the catecholamine levels induced by nasal CPAP.These findings suggest that OSA contributes, at least in part, to the development of systemic hypertension by increasing sympathetic nervous activity.
To evaluate the circadian pattern of blood pressure (BP) and the effects of nasal continuous positive airway pressure (CPAP) on patients with obstructive sleep apnea (OSA), we examined 24-hour BP in 38 male OSA patients with and without nasal CPAP. We measured the BP at 30-min intervals during daytime (800 to 2200) and nighttime (2200 to 800) hours. A "dipper" was defined as a patient who showed an average reduction of at least 10 mm Hg systolic and 5 mm Hg diastolic between daytime and nighttime values. The subjects were predominantly "non-dipper" (22 of 38 patients, 58%). Daytime hypertension (>160/95 mm Hg) was present in 11 of 38 patients (4 "dippers" and 7 "non-dippers"). After nasal CPAP treatment for 3 days, the average BP decreased significantly during the day and night in all subjects (p<0.05). Fifteen of 22 subjects who were "non-dippers" before treatment reversed to become "dippers." And daytime hypertension was detected in only 5 of these patients during nasal CPAP treatment (4 "dippers" and 1 "non-dipper"). These results showed that the "non-dipper" status was common in patients with OSA, and that nasal CPAP restored the normal circadian "dipper" pattern. We suggest that nasal CPAP may contribute to an improved prognosis in patients with OSA because of a reduction in cardiovascular risk factors in "non-dipper" with severe OSA.
Daytime blood pressure (BP) in 31 male patients with obstructive sleep apnea syndrome (OSAS) was measured and the effects of nasal continuous positive airway pressure (CPAP) treatment on daytime BP were studied. Subjects were 48±10 (mean+SD) years old and weighed 80±13 kg. The mean systolic BP and diastolic BP were 135+15 mmHgand 88±14 mmHg, respectively and daytime hypertension was present in 12 (38%) subjects. Apnea index (AI) and the lowest oxygen saturation during sleep were significantly more severe in the hypertensive (HT) than in the non-hypertensive (NHT) patients (p<0.05). AI was significantly correlated with diastolic BP (p<0.05) and the mean and lowest oxygen saturation during sleep were significantly correlated with both systolic (p<0.05) and diastolic BP (p<0.01). After nasal CPAPtreatment for two weeks, both systolic and diastolic BP were significantly reduced; the former from 135+15 mmHgto 126+10 mmHg(p<0.005) and the latter from 88+14 mmHgto 78±6 mmHg(p<0.001). These data form direct evidence that daytime hypertension is partially induced by OSASand is reversible with nasal CPAPtreatment. (Internal Medicine 34: 528-532, 1995)
We investigated the acute effects of nasal continuous positive airway pressure (CPAP) on pulmonary haemodynamics and tissue oxygenation in eight men with obstructive sleep apnoea (OSA) by means of right heart catheterization. They were tested at four dosage levels of nasal CPAP: 0, 5, 10, and 15 cmH2O. Nasal CPAP significantly reduced the cardiac index at the 10 and 15 cmH2O doses. The mean pulmonary artery pressure was significantly elevated with 10 and 15 cmH2O, and pulmonary capillary wedge pressure was significantly increased with 15 cmH2O of nasal CPAP. Pulmonary vascular resistance was significantly increased with 10 cmH2O of nasal CPAP. The 5 cmH2O dose of nasal CPAP did not affect significantly these parameters. Mixed venous oxygen tension was unchanged at any pressure. We conclude that tissue oxygenation was maintained in the OSA patients during administration of nasal CPAP, even though a high CPAP clearly affected pulmonary haemodynamics.
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