The Upper Airway Resistance Syndrome: Hypertension

The Upper Airway Resistance Syndrome: HypertensionGuilleminault et al reported similar results in 110 patients known to have UARS. In these patients, systolic and diastolic BP increased during the breaths associated with the arousal when compared to the BP measures that directly preceded the arousal. The systolic and diastolic BP also increased significantly during segments of labored breathing without the arousal Pes nadir (more negative than —30 cm H2O) in a subset of seven patients. Echocardiography demonstrated a leftward shift of the interventricular septum during segments with the most negative Pes nadirs (more negative than —35 cm H2O). Pulsus paradoxus was also demonstrated during these segments. Also shown were significant decreases in the average systolic and diastolic daytime BP as well as the average nocturnal diastolic BP in six patients with borderline hypertension who were treated with nCPAP for 1 month. Of note, one patient who was not compliant with nCPAP did not show these changes.
It is likely that both sympathetic activation from arousal and hemodynamic factors, such as changes in intrathoracic pressure and ventricular interdependence, cause BP changes during IUAR events. Reasonable evidence exists to support both mechanisms, and there are no data to exclude either one of the mechanisms read more flovent inhaler.
Silverberg and Oksenberg concluded, in an extensive review of the literature regarding hypertension and sleep-disordered breathing, that most cases of “essential hypertension” are caused by IUAR during sleep from either OSAS or UARS. They quoted a 30% to 40% incidence of OSAS and a 30% to 75% incidence of nonapneic snoring in hypertensive patients, gleaned from data published within the previous 5 to 6 years. They also hypothesized that the epidemiologic, physiologic, hereditary, clinical, and laboratory similarities between the populations with essential hypertension and the populations with sleep-disordered breathing were the result of a causal relationship, and that treatment of sleep-disordered breathing may be central to the management of essential hypertension. This is an interesting, but not well-substantiated, proposal.

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