The cardiovascular effects of obstructive sleep apnoeas: analysis of pathogenic mechanisms

Cardiorespiratory consequences of sleep apnoea syndrome in patients with massive obesity

“…Nocturnal apnoeas may lead to paroxysmic peaks of systemic blood pressure [4], but evidence for a causal association between nocturnal apnoeas and daytime arterial hypertension is still lacking because obesity as a confounding factor has not been assessed adequately in most studies [6,21]. In the present study concerning patients with massive obesity, the prevalence of daytime arterial hypertension was high, but did not differ significantly in apnoeic versus nonapnoeic patients.…”

“…The arousal frequency was not routinely computed at the time that the sleep studies were performed. Although arousals are recognized to be important correlates of rises in sympathetic activity that occur with abnormal respiratory events during sleep [4], the specific role of arousals in the cardiorespiratory complications of SAS is not yet fully understood and should be studied prospectively. Some patients in the SAS-group exhibited moderate nocturnal desaturation.…”

“…Sleep apnoea syndrome (SAS) has been reported to be associated with excess mortality [1,2] and a wide range of cardiac and respiratory sequelae [3][4][5]: daytime alveolar hypoventilation, pulmonary arterial hypertension, systemic arterial hypertension, left ventricular hypertrophy and dysfunction, cardiac arrhythmias and ischaemic heart disease. However, conflicting data have been published on the cardiorespiratory consequences of SAS.…”

Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs

“…In addition, mechanoreceptor afferents carried via the vagus could increase sympathetically mediated responses through an arousal mechanism (11,14). On the other hand, parasympathetic efferent signals carried via the vagus nerve could modulate sympathetic activation by decreasing heart rate and lowering blood pressure (3). Thus the vagus could play an important role in mediating the cardiovascular apneic response through both efferent and afferent mechanisms.…”

“…HR increases after apnea termination are related, at least in part, to nonvagally mediated reflexes. apnea; vagus; hemodynamics OBSTRUCTIVE SLEEP APNEA is a relatively common clinical condition in which upper airway collapse and cessation of airflow produce an acute cardiovascular response, including elevations in blood pressure as well as changes in heart rate and ventricular function (3,24,26). In general, cardiovascular variables fluctuate during the apnea-interapnea periods because of mechanical alterations and reflex changes in autonomic tone.…”