scholarly journals Pulmonary haemodynamics in patients with OSAS or an overlap syndrome

2004 ◽  
Vol 61 (3) ◽  
Author(s):  
I. Hawrylkiewicz ◽  
P. Sliwinski ◽  
D. Górecka ◽  
R. Plywaczewski ◽  
J. Zielinski

Background. Alveolar hypoxia is the most important mechanism leading to pulmonary arterial vasoconstriction, remodelling and pulmonary hypertension. Patients with Obstructive Sleep Apnoea Syndrome (OSAS) experience multiple short periods of alveolar hypoxia during apnoeic episodes. However, the question as to whether these hypoxic episodes are responsible for the development of permanent pulmonary hypertension is still debatable. We aimed to investigate the relationship between the episodes of nocturnal desaturation and pulmonary haemodynamics in two distinct group patients: with pure OSAS or an overlap syndrome. Methods: We studied 67 patients with severe OSAS (means: age 45±8 years, AHI 62±22, FEV1 3.6±0.8 L = 97±16% of predicted PaO2 72±10 mmHg, PaCO2 40±4 mmHg) and 17 patients with an overlap syndrome (OS), means: age 51±5 years, AHI 64±19, FEV1 1.5±0.7 = 43±16% of predicted PaO2 57±9 mmHg). All subjects underwent pulmonary artery catheterisation with pressure and flow recordings and an overnight full sleep study. Results. On average patients with OSAS had nocturnal desaturation (mean overnight SaO2 = 87±5%) and normal PPA (15.8±4.6 mmHg). Only 11 out of 67 subjects (16%) presented with pulmonary hypertension. Patients with OS had nocturnal desaturation (mean overnight SaO2 = 80.2±8.5%) and mild pulmonary hypertension (PPA 24.2±7.4 mmHg). Only three out of 17 patients had normal pulmonary arterial pressure. Conclusions. In patients with severe OSAS, pulmonary hypertension is rare (16%) and is related best to the severity of the disease and to obesity. In OS patients diurnal pulmonary hypertension is frequent but does not correlate with the severity of nocturnal desaturation.

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Precek ◽  
K Vykoupil ◽  
F Kovacik ◽  
M Hutyra

Abstract Introduction Sleep disordered breathing (SDB) is a group of ventilatory disorders during sleep which includes obstructive sleep apnea (OSA), central sleep apnea (CSA), and sleep related hypoventilation. In patients with SDB, the prevalence of pulmonary hypertension (PH) ranges from 17% to 52%. While SDB is prevalent in the general population with recent estimates of 20% to 30%, in those with cardiovascular disease, particularly left ventricular failure, there is a higher reported prevalence of 47%. Aims The aims of this study were to determine the prevalence and prognostic relevance of sleep apnea in a cohort of patients with newly diagnosed pulmonary arterial hypertension (ESC/WHO Group 1 pulmonary hypertension). Methods We evaluated prospectively 76 patients with the pulmonary arterial hypertension (mean age 54±16 years; 45% male). All patients underwent right heart catheterisation, clinical assessments, sleep study, standard laboratory testing and evaluation of subjective sleepiness by the Epworth Sleepiness Scale. Sleep test was provided with an ApneaLink Plus, consisting of nasal pressure sensor, respiratory effort band, and pulse oximeter worn on the finger. Subjects previously treated for or diagnosed with SDB were excluded from the study. Results Sleep apnea (SA) – defined as apnea-hypopnea index (AHI) ≥5/h – was found in 59 (77.6%) of the pulmonary arterial hypertension (PAH) patients. Mean AHI in the cohort of PAH patients with SA was 26.1±16.6/h. Mean follow-up was 24 months, during which 15 (19.7%) patients died. Characteristics of parameters related to SA in groups of survivors and deceased are in table 1. From the sleep apnea-related parameters, only time with O2Sat <90% – T90 was significantly associated with mortality (AUC 0.856; 95% CI 0.693 – 1.019; p<0.001). Conclusions The presence of sleep apnea in pulmonary arterial hypertension patients is high. The prevalence of sleep apnea is higher in PAH patients than in the general population. The presence of sleep apnea in patients with PAH was not associated with worse prognosis, but noctural hypoxemia (time with O2Sat <90%) was related to poor prognosis. Sleep apnea in patients with PAH should be screened for systematically. Funding Acknowledgement Type of funding source: None


1995 ◽  
Vol 109 (4) ◽  
pp. 308-312 ◽  
Author(s):  
Shao-Jung Lu ◽  
Shyue-Yih Chang ◽  
Guang-Ming Shiao

AbstractFor a long time uvulopalatopharyngoplasty (UPPP) has been used to treat the obstructive sleep apnoea syndrome (OSAS). The diverse surgical effects, the inadequate understanding of operation effect consistency, the possibility of disease progression, and the few reported papers for long-term evaluation after UPPP aroused our interest in designing this study. Fifteen OSAS patients who had undergone UPPP with pre-operative, initial post-operative and long-term post-operative polysomnographic studies were included in this study. Long-term post-operative polysomnography was undertaken more than five years after surgery. The polysomnographic evaluations included respiratory disturbance index (RD I), duration of saturation SaO2 <85 per cent (DOS), and the lowest O2 saturation (LOS). Amongst them, 10 patients with initial post-operative RDI reduction > 50 per cent were considered responders. In these responders, the long-term follow-up results of all three parameters showed improvement compared to the preoperative data. In a comparison between the initial and long-term post-operative sleep study results, LOS and DOS showed no significant difference. However, the long-term post-operative RDI result became significantly worse. More than 80 per cent of all cases had subjective symptomatic improvement in the long-term post-operative evaluation. The subjective improvement after operation is not adequately correlated to the polysomnographic result. We suggest that long-term follow-up for patients after UPPP is necessary.


2020 ◽  
Vol 57 (1) ◽  
pp. 2002258
Author(s):  
Yochai Adir ◽  
Marc Humbert ◽  
Ari Chaouat

Sleep-related breathing disorders (SBDs) include obstructive apnoea, central apnoea and sleep-related hypoventilation. These nocturnal events have the potential to increase pulmonary arterial pressure (PAP) during sleep but also in the waking state. “Pure” obstructive sleep apnoea syndrome (OSAS) is responsible for a small increase in PAP whose clinical impact has not been demonstrated. By contrast, in obesity hypoventilation syndrome (OHS) or overlap syndrome (the association of chronic obstructive pulmonary disease (COPD) with obstructive sleep apnoea (OSA)), nocturnal respiratory events contribute to the development of pulmonary hypertension (PH), which is often severe. In the latter circumstances, treatment of SBDs is essential in order to improve pulmonary haemodynamics.Patients with pulmonary arterial hypertension (PAH) or chronic thromboembolic pulmonary hypertension (CTEPH) are at risk of developing SBDs. Obstructive and central apnoea, as well as a worsening of ventilation–perfusion mismatch, can be observed during sleep. There should be a strong suspicion of SBDs in such a patient population; however, the precise indications for sleep studies and the type of recording remain to be specified. The diagnosis of OSAS in patients with PAH or CTEPH should encourage treatment with continuous positive airway pressure (CPAP). The presence of isolated nocturnal hypoxaemia should also prompt the initiation of long-term oxygen therapy. These treatments are likely to avoid worsening of PH; however, it is prudent not to treat central apnoea and Cheyne–Stokes respiration (CSR) with adaptive servo-ventilation in patients with chronic right-heart failure because of a potential risk of serious adverse effects from such treatment.In this review we will consider the current knowledge of the consequences of SBDs on pulmonary haemodynamics in patients with and without chronic respiratory disease (group 3 of the clinical classification of PH) and the effect of treatments of respiratory events during sleep on PH. The prevalence and consequences of SBDs in PAH and CTEPH (groups 1 and 4 of the clinical classification of PH, respectively), as well as therapeutic options, will also be discussed.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A405-A406
Author(s):  
W A Youngren ◽  
K Miller

Abstract Introduction The enigmatic nature of Posttrauma Nightmares (PTNs) has left research without an agreed upon operational definition. This is partially due to PTNs often containing well remembered content that is similar to the triggering trauma, but also manifesting as severe nighttime awakenings without a concise or remembered dream narrative. Given that recent research has linked episodes of Obstructive Sleep Apnea (OSA) to PTNs, this study aimed to examine if OSA could explain why some distressed awakenings occur without memory of nightmare content. Methods Participants included 36 trauma survivors who reported experiencing PTNs, recruited from a clinical referral or at a Veterans Affairs Hospital. Presence of OSA was captured from self-reports of previous polysomnography-based sleep study results. PTNs were measured via a self-report measure that assessed past month nightmare frequency and if the content was remembered upon awakening. Analysis included descriptive statistics and chi-square tests. Results Out of the group with a reported diagnosis of OSA (N = 8), 75% (n = 6) reported they did not remember the content of their nightmares upon awakening, whereas out of the group without a reported OSA diagnosis (N = 28), only 4% of participants (n = 1) reported not remembering the content of their nightmares. There was a significant difference between OSA diagnosis and remembering nightmare content (X2 = 57.83, p &lt; 0.001). Conclusion Individuals with diagnosed OSA commonly experienced nightmares that were often not remembered upon awakening, while the group without OSA most often remembered the content of their nightmares. Due to this relationship, it is possible that some PTNs experienced by the OSA group may instead be misinterpreted respiratory events. Understanding the relationship between OSA and PTNs is crucial for developing the most effective treatment course. Support None.


2021 ◽  
Vol 30 (161) ◽  
pp. 210053
Author(s):  
Ashraful Haque ◽  
David G. Kiely ◽  
Gabor Kovacs ◽  
A.A. Roger Thompson ◽  
Robin Condliffe

Pulmonary hypertension (PH) commonly affects patients with systemic sclerosis (SSc) and is associated with significant morbidity and increased mortality. PH is a heterogenous condition and several different forms can be associated with SSc, including pulmonary arterial hypertension (PAH) resulting from a pulmonary arterial vasculopathy, PH due to left heart disease and PH due to interstitial lung disease. The incidence of pulmonary veno-occlusive disease is also increased. Accurate and early diagnosis to allow optimal treatment is, therefore, essential. Recent changes to diagnostic haemodynamic criteria at the 6th World Symposium on Pulmonary Hypertension have resulted in therapeutic uncertainty regarding patients with borderline pulmonary haemodynamics. Furthermore, the optimal pulmonary vascular resistance threshold for diagnosing PAH and the role of exercise in identifying early disease require further elucidation. In this article we review the epidemiology, diagnosis, outcomes and treatment of the spectrum of pulmonary vascular phenotypes associated with SSc.


1998 ◽  
Vol 274 (5) ◽  
pp. L775-L785 ◽  
Author(s):  
C. S. Packer ◽  
J. E. Roepke ◽  
N. H. Oberlies ◽  
R. A. Rhoades

The principal stimulus that evokes pulmonary hypertension is chronic alveolar hypoxia. Pulmonary hypertension is associated with remodeling of the vessel walls, involving hypertrophy and hyperplasia of pulmonary arterial smooth muscle (PASM) and a concomitant increase in the deposition of connective tissue, resulting in increased wall thickness. The purpose of the present study was to determine the effect of hypoxia-induced hypertension on the structure and function of PASM. Experiments were designed to determine whether hypoxia-induced pulmonary hypertension is associated with alterations in PASM: 1) reactivity to a variety of agonists, 2) contractile protein proportions and isoforms, and 3) structural properties. Young adult male rats were made hypoxic by lowering the fraction of inspired O2 (10%) for 14 days. Pulmonary arterial segments were isolated and dose-response curves to various agonists (high K+, norepinephrine, serotonin, angiotensin II, and adenosine) were generated. Gel electrophoresis was used to measure changes in the relative amounts of actin or myosin and of myosin heavy chain (MHC) isoforms. Structural changes were correlated with the pharmacological and biochemical data. Hypoxia-induced pulmonary hypertension caused a general decreased reactivity, an increase in the proportion of nonmuscle to muscle MHC isoforms in PASM, and an increase in arterial wall thickness with PASM hypertrophy or hyperplasia.


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