Slow and fast changes in transmural pulmonary artery pressure in obstructive sleep apnoea

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 ...

Section: Discussionsupporting

confidence: 82%

mentioning

confidence: 99%

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

Schäfer¹,

Hasper²,

Ewig³

et al. 1998

“…It has been demonstrated experimentally [3][4][5]12] that pulmonary vascular responsiveness depends on the intensity, the duration and the repetition of the hypoxic stimulus applied. MARRONE et al [17] found that transmural systolic Ppa progressively increased during repetitive apnoeas in four OSAS patients only when the falls in Sa,O 2 became greater and in REM sleep. In our analysis, we first included values during NREM and REM sleep so that changes in Ppa would reflect the time course during the night.…”

Section: Discussionmentioning

confidence: 99%

Time course of pulmonary artery pressure during sleep in sleep apnoea syndrome: role of recurrent apnoeas

Sforza

Laks²,

Grunstein³

et al. 1998

The increase in pulmonary arterial pressure (Ppa) during acute hypoxia is mainly related to alveolar hypoxaemia inducing vasoconstriction of precapillary pulmonary arterioles [1,2] whereas during chronic hypoxia, mechanical and hormonal factors make the vessels adapt to hypoxia and modify their response to chemical stimulus [3]. Furthermore, the temporal profile of the hypoxaemic stimulus may have a substantial effect on the pulmonary vascular response [4] as suggested by experimental studies allowing that repeated exposure to intermittent hypoxaemia [5] enhances the pulmonary hypoxic pressor response.Previous studies [6] in obstructive sleep apnoea (OSAS) patients have shown that repeated desaturations from obstructive apnoeas induce a transient increase in Ppa that, together with daytime hypoxaemia, is considered to be the key factor responsible for daytime pulmonary hypertension [7,8]. Recent evidence in animals [9][10][11] has demonstrated that repetitive hypoxic stimuli, simulating the chemical changes produced by apnoeas lead to systemic hypertension either during the exposure or during the recovery period. A more direct approach to the pulmonary vascular effects of repetitive hypoxaemia has been used by IWASE et al. [12]. Using a canine model they have demonstrated a progressive increase in systemic and pulmonary arterial pressure during repetitive hypoxaemic exposure. On the basis of these latter findings a trend in the pulmonary arterial pressure response to repetitive hypoxaemia similar to the one produced experimentally may occur in patients with OSAS.The two aims of the present study were: 1) to ascertain whether recurrent apnoea-related oxygen desaturations are associated with a progressive rise in Ppa during the night in OSAS patients; 2) if there was a rise in the expected direction, to determine whether diurnal and nocturnal variables would predict the degree of progressive nocturnal increase in Ppa. Patients and methods PatientsThirty five consecutive patients referred to the sleep laboratory for habitual snoring and possible sleep apnoea We have, therefore, examined the nocturnal trend of Ppa in seven obstructive sleep apnoea syndrome (OSAS) patients and in five snorers. Mean Ppa was measured before, at the start, at the end and after the selected apnoeas. The analysis was performed for each 1 h period for at least 7 h throughout the night on at least 10 randomly selected apnoeas per hour. In snorers, 100 randomly chosen values were measured during every hour of the night. In the morning after the nocturnal study, the Ppa responses to acute hypoxia and hypercapnia were measured.No Ppa changes throughout the 7 h were found during sleep in snorers (Ppa slope:-0.002±0.10 mmHg·h -1 ). In OSAS patients a small but significant increase in Ppa throughout the night was noted, affecting the values before (Ppa slope: 0.7±0.16 mm Hg·h -1 ), at the start of apnoea (Ppa slope: 0.53±0.1 mmHg·h -1 ) as well as at the end (Ppa slope: 0.44±0.08 mmHg·h -1 ) and in the postapnoeic period (Ppa slope: 0.55±0.1 mmHg...

“…In patients with OSA, large swings of intrathoracic pressure during apnoea greatly affect intravascular PAP. To assess HPV during apnoeic episodes, true transmural PAP has to be measured [71]. HPV is resolved at the resumption of breathing [72].…”

Section: Intermittent Hypoxia In Copd Patients On Long-term Oxygen Trmentioning

confidence: 99%

Effects of intermittent hypoxia on pulmonary haemodynamics: animal modelsversusstudies in humans

Zieliński¹

2005

The aim of this review was to analyse the effects of intermittent hypoxia (IH) on pulmonary haemodynamics, comparing results of animal experiments with results of clinical studies.In animal investigations even short hypoxic exposure, continuously or in short repeated episodes mimicking obstructive sleep apnoea (OSA), leads to pulmonary artery remodelling and to pulmonary hypertension (PH). Results of investigations on effects of nocturnal IH on pulmonary haemodynamics in patients with chronic obstructive pulmonary disease (COPD) are discordant. Earlier studies reported the development of mild PH in subjects desaturating during sleep, while more recent investigations did not confirm those findings.Alveolar IH developing during apnoeic episodes during sleep in OSA patients is a diseaseinduced model to study its effects on pulmonary haemodynamics. In the majority of studies in OSA patients pulmonary arterial pressure remained within normal values. PH was found in patients with OSA accompanied by COPD and/or extreme obesity.People commuting between lowland and high altitude due to their employment, are also repeatedly exposed to IH. Results of clinical investigations suggest that it did not lead to the development of permanent PH.The mechanisms of discrepancies between effects of intermittent hypoxia in animal models and in humans remain to be studied.