Pulmonary haemodynamics in obstructive sleep apnoea: time course and associated factors

Abstract

Pulmonary hypertension is a potential complication of obstructive sleep apnoea. Most recent studies agree on a 15-20% prevalence [1]. The development of pulmonary hypertension is strongly linked to an obstructive ventilatory pattern, daytime hypoxaemia and hypercapnia, whereas the severity of obstructive sleep apnoea plays only a minor role [2]. However, some patients develop pulmonary hypertension despite normal waking arterial oxygen tension (Pa,O 2 ) levels [3]. In this group of patients, the nocturnal breathing disorder may be crucial for the development of pulmonary hypertension, since it has been hypothesized that episodic and recurrent hypertension, due to repeated apnoeas, could lead to permanent pulmonary hypertension [4].Transient and repetitive elevations in pulmonary artery pressure, with reference to atmospheric pressure, have been described [5]. While intravascular pulmonary artery pressure decreases during apnoea and increases at the resumption of breathing, transmural pulmonary artery pressure (Ppa,tm) (i.e. corrected for intrathoracic pressure swings) shows a trend toward a progressive increase throughout an apnoea and toward a decrease once ventilation has been resumed [6]. Several factors and mechanisms, mainly mechanical events or hypoxic vasoconstriction, have been proposed as contributing to the changes in the pulmonary artery pressure (Ppa,tm) within an apnoea cycle. Mechanical events are caused preferably by intrathoracic pressure swings [7]. Limitation of left ventricular filling and emptying at low intrathoracic pressure could contribute to an increase in pulmonary vascular resistance by increasing the pulmonary venous pressure and blood volume [8]. On the other hand, several studies have indicated an association between changes in oxygen saturation and changes in pulmonary artery pressure during an obstructive apnoea [4,9,10]. MARRONE et al. [11] showed that hypoxia is a major determinant of the slow changes in the transmural pulmonary artery pressure over the whole course of an apnoea. In addition, they found rapid changes in the Ppa,tm that was synchronous with intrathoracic pressure changes breathby-breath.The purpose of our study was to examine which factors contribute to the increase of the Ppa,tm in an apnoea. ABSTRACT: Changes in pulmonary artery pressure within an obstructive apnoea and elevations of transmural pulmonary artery pressure (Ppa,tm) towards the end of apnoea are well known. The purpose of our study was to examine which factors contribute to the increase of Ppa,tm in an apnoea. In addition, the time course of Ppa,tm and associated factors during a sleep study was investigated.We analysed the association of changes in arterial oxygen saturation (Sa,O 2 ), oesophageal pressure (Poes) to estimate intrathoracic pressure, systolic blood pressure (BPsys) to estimate left ventricular afterload, apnoea duration and the change in Ppa,tm (∆Ppa,tm) during the course of obstructive apnoeas. Consecutive apnoeas in nonrapid eye movement (NREM)-sleep at the beginning, the middle ...

P-wave duration and dispersion in patients with obstructive sleep apnea

“…It is plausible to speculate that factors directly related to OSA, such as repetitive hypoxemia, autonomic nervous system imbalance, systemic inflammation, fluctuations in intrathoracic hemodynamic, and diastolic dysfunction may lead to prolongation of inta-atrial and inter-atrial conduction time and provoke inhomogeneous propogation of sinus impulses reflected as increased Pmax and Pd, thereby serve as a trigger for atrial fibrillation and may favor the perpetuation of the atrial arrhythmia by altering the atrial substrate [13][14][15]18,[21][22][23][24].…”

PFO and Right-to-Left Shunting in Patients with Obstructive Sleep Apnea

“…23 Moreover, complete resolution of symptoms in a patient with OSA and desaturations during exercise has been described. 24 It is not yet clear whether OSA, by virtue of increased mean transmural pulmonary artery pressure during apneic episodes, 25 may allow an interatrial communication (PFO) that otherwise would be unrecognized, whether the PFO is a substantial contributor in the pathogenesis of OSA, or whether both apply.…”

Sleep Apnea in Patients with and without a Right-to-Left Shunt

“…8,25 Hypoxemia increases pulmonary vasoconstriction leading to pulmonary hypertension. 26 Even without RLS, episodes of apnea induce hypoxemia, which can result in an increase in Spencer grade is used to assess degree of shunting. Increase in grade correlates with more severe shunting.…”