Daytime hypoventilation in obstructive sleep apnoea syndrome

doi:10.1016/S1087-0792(99)90015-1

Sleep Medicine Reviews

Volume 3, Issue 1, March 1999, Pages 79-93

https://doi.org/10.1016/S1087-0792(99)90015-1 Get rights and content

Abstract

Chronic alveolar hypoventilation is a classic feature of the “pickwickian syndrome” (i.e. obesity-hypoventilation syndrome) but in fact hypercapnia is observed in a minority of obstructive sleep apnoea syndrome (OSAS) patients. Most recent studies having included large numbers of unselected, consecutive OSAS patients agree on a prevalence of 10–20% of alveolar hypoventilation. The mechanisms of hypercapnia in OSAS are not fully understood but the determining factors of daytime respiratory insufficiency are probably the presence of a marked obesity, leading to the obesity hypoventilation syndrome and, principally, the association of OSAS with chronic obstructive pulmonary disease. This association (the so-called “overlap syndrome”) is observed in >10% of OSAS patients. Bronchial obstruction is generally mild to moderate and may be asymptomatic. The severity of the nocturnal events (apnoeas, hypopnoeas) and a (possible) diminished chemosensitivity to hypercapnic and hypoxic stimuli do not appear to be determining factors of hypercapnia. The most important consequence of chronic alveolar hypoventilation is pulmonary hypertension which is only observed in patients with daytime arterial blood gases disturbances, and which can lead to right heart failure. When nasal continuous positive airway pressure fails to correct sleep-related hypoxaemia, supplementary O, must be given or another way of assisted ventilation (BIPAP) must be considered. In the most severe patients (diurnal PaO₂ <55 mmHg) conventional O₂ therapy ( $≥ 16h 24h$ ) is required in addition to nocturnal ventilation.

References (45)

R. Jung et al.
Neurophysiological studies of abnormal night sleep and the Pickwickian syndrome
S. Redline et al.
Recognition and consequences of obstructive sleep apnoea-hypopnoea syndrome
Clin Chest Med
(1998)
D.F. Rochester et al.
Current concepts in the pathogenesis of the obesity-hypoventilation syndrome
Am J Med
(1974)
J. Krieger et al.
Pulmonary hypertension, hypoxemia and hypercapnia in obstructive sleep apnoea patients
Chest
(1989)
J.A. Leech et al.
Determinants of hypercapnia in occlusive sleep apnoea syndrome
Chest
(1987)
A. Chaouat et al.
Pulmonary hemodynamics in the obstructive sleep apnoea syndrome: results in 220 consecutive patients
Chest
(1996)
D.M. Rapoport et al.
Hypercapnia in the obstructive sleep apnoea syndrome: a re-evaluation of the Pickwickian syndrome
Chest
(1986)
D.C. Flenley
Sleep in chronic obstructive lung disease
Clin Chest Med
(1985)
J. Widimsky et al.
Intermittent high altitude hypoxia
Chest
(1980)
O. Marrone et al.
Transmural pressure measurements: importance in the assessment of pulmonary hypertension in obstructive sleep apnoeas
Chest
(1989)

E. Weitzenblum et al.

Pulmonary hemodynamics in patients with chronic obstructive pulmonaire disease before and during an episode of peripheral edema

Chest

(1994)

C.E. Sullivan et al.

Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares

lancet

(1981)

H. Gastaut et al.

Etude polygraphique des manifestations épisodiques (hypniques et respiratoires) du syndrome de Pickwick

Rev Neurol (Paris)

(1965)

C.S. Burwell et al.

Extreme obesity associated with alveolar hypoventilation: a Pickwickian syndrome

Am J Med

(1956)

J.H. Auchincloss et al.

Clinical and physiological aspects of a case of obesity, polycythemia, and alveolar hypoventilation

J Clin Invest

(1995)

M.H. Weil

Polycythemia associated with obesity

JAMA

(1955)

C. Guilleminault et al.

The sleep apnoea syndromes

Ann Rev Med

(1976)

R. Kessler et al.

The obesity-hypoventilation syndrome revised. A series of 34 patients

Eur Respir J

(1998)

ATS Statement

Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease

Am J Respir Crit Care Med

(1995)

E. Weitzenblum et al.

Pulmonary hypertension due to chronic hypoxic lung disease

T.D. Bradley et al.

Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnoea syndrome

Am Rev Respir Dis

(1985)

T.D. Bradley et al.

Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnoea

Am Rev Respir Dis

(1986)

Cited by (32)

A bio-based, sweat-resistant and markedly sensitive iontronic skin for advancing central sleep apnea monitoring
2024, Chemical Engineering Journal
Central Sleep Apnea (CSA) is characterized by respiratory pauses during sleep, posing risks like cardiovascular diseases, stroke and sudden death. The challenges in managing it arise from the current monitoring tools, which are often complicated and inaccurate. Furthermore, respiratory pauses leading to decreased blood oxygen can induce profuse sweating, further affecting accuracy. Herein, we have synthesized a bio-based, biocompatible and sweat-resistant polyurethane. By utilizing it as the matrix, we incorporated [BMIM]⁺[PF₆]⁻ to fabricate a markedly sensitive dielectric material, termed i-DFPU. The fluorine groups in i-DFPU contributed to a trap-release effect for migratable ions, while the alkyl side chains provided smooth ion migration channels, endowing i-DFPU with exceptional sensitivity. In combination with a stress concentration layer and serpentine-shaped electrodes, the resultant iontronic skin exhibited a remarkable sensitivity up to 132.2 kPa⁻¹, operational stability and portability. Consequently, it could accurately monitor various respiratory states in CSA, potentially preventing complications such as sudden death.
Effectiveness of CPAP vs. Noninvasive Ventilation Based on Disease Severity in Obesity Hypoventilation Syndrome and Concomitant Severe Obstructive Sleep Apnea
2022, Archivos de Bronconeumologia
Citation Excerpt :
Roughly 90% of patients with OHS have concomitant obstructive sleep apnea (OSA),2 with 73% having severe OSA.3 Compared with eucapnic OSA4,5 and eucapnic obese,6,7 patients with OHS have a higher prevalence of cardiovascular and respiratory morbidity resulting in increased hospitalization risk, greater healthcare resource utilization, and augmented mortality.7–16 Ambulatory patients with OHS are typically treated with nocturnal positive airway pressure (PAP) therapy during sleep such as noninvasive ventilation (NIV), usually with bilevel pressure settings, or continuous positive airway pressure (CPAP).
Obesity hypoventilation syndrome (OHS) with concomitant severe obstructive sleep apnea (OSA) is treated with CPAP or noninvasive ventilation (NIV) during sleep. NIV is costlier, but may be advantageous because it provides ventilatory support. However, there are no long-term trials comparing these treatment modalities based on OHS severity.
To determine if CPAP have similar effectiveness when compared to NIV according to OHS severity subgroups.
Post hoc analysis of the Pickwick randomized clinical trial in which 215 ambulatory patients with untreated OHS and concomitant severe OSA, defined as apnoea-hypopnea index (AHI) ≥ 30 events/h, were allocated to NIV or CPAP. In the present analysis, the Pickwick cohort was divided in severity subgroups based on the degree of baseline daytime hypercapnia (PaCO₂ of 45–49.9 or ≥50 mmHg). Repeated measures of PaCO₂ and PaO₂ during the subsequent 3 years were compared between CPAP and NIV in the two severity subgroups. Statistical analysis was performed using linear mixed-effects model.
204 patients, 97 in the NIV group and 107 in the CPAP group were analyzed. The longitudinal improvements of PaCO₂ and PaO₂ were similar between CPAP and NIV based on the PaCO₂ severity subgroups.
In ambulatory patients with OHS and concomitant severe OSA who were treated with NIV or CPAP, long-term NIV therapy was similar to CPAP in improving awake hypercapnia, regardless of the severity of baseline hypercapnia. Therefore, in this patient population, the decision to prescribe CPAP or NIV cannot be solely based on the presenting level of PaCO₂.
El síndrome de hipoventilación-obesidad (SHO) con apnea obstructiva del sueño (AOS) grave concomitante se trata con CPAPo ventilación no invasiva (VNI) durante el sueño. La VNI es más costosa, pero puede ser beneficiosa porque proporciona soporte ventilatorio; sin embargo, no existen estudios a largo plazo que comparen estas modalidades de tratamiento basándose en la gravedad del SHO.
Determinar si la CPAP tiene una eficacia similar a la VNI según los subgrupos de gravedad del SHO.
Análisis a posteriori del ensayo clínico aleatorizado Pickwick en el que 215 pacientes ambulatorios con SHO sin tratar y con AOS grave concomitante (definida como un índice de apnea-hipopnea [IAH] ≥ 30 episodios/hora) recibieron tratamiento con VNI o CPAP. En el presente análisis, la cohorte Pickwick se dividió en subgrupos según la gravedad basándose en el grado de hipercapnia diurna al inicio del estudio (PaCO₂ de 45-49.9 mm Hg o ≥ 50 mm Hg). Se compararon las mediciones periódicas de PaCO₂ y PaO₂ durante los 3 años siguientes entre la CPAP y la VNI entre los dos subgrupos de gravedad. Se realizó un análisis estadístico utilizando un modelo lineal mixto.
Se analizaron 204 pacientes, 97 en el grupo de VNI y 107 en el grupo de CPAP. Las mejoras lineales de PaCO₂ y PaO₂ fueron similares entre la CPAP y la NIV según los subgrupos de gravedad en función de la PaCO₂.
En los pacientes ambulatorios con SHO y AOS grave concomitante a los que se trató con VNI o CPAP, el tratamiento a largo plazo con VNI resultó similar a la CPAP, en cuanto a la mejora de la hipercapnia en vigilia, independientemente de la gravedad de la hipercapnia de inicio. Por lo tanto, en esta población de pacientes la decisión de prescribir CPAP o VNI no puede basarse exclusivamente en el nivel de partida de PaCO₂.
Pulmonary Hypertension in Parenchymal Lung Disease
2012, Heart Failure Clinics
Citation Excerpt :
As above, the pathophysiology is hypoxia-induced vasoconstriction and subsequent vascular remodeling. Identifying and treating hypoxemia with oxygen supplementation improves PAP.76 As with sleep-disordered breathing, there is no data supporting pharmaceutical treatment of PH caused by hypoxemia.
Acute cardiopulmonary failure from sleep-disordered breathing
2012, Chest
Sleep-disordered breathing (SDB) comprises a diverse set of disorders marked by abnormal respiration during sleep. Clinicians should realize that SDB may present as acute cardiopulmonary failure in susceptible patients. In this review, we discuss three clinical phenotypes of acute cardiopulmonary failure from SDB: acute ventilatory failure, acute congestive heart failure, and sudden death. We review the pathophysiologic mechanisms and recommend general principles for management. Timely recognition of, and therapy for, SDB in the setting of acute cardiopulmonary failure may improve short- and long-term outcomes.
Short-term memory performances during sustained wakefulness in patients with obstructive sleep apnea-hypopnea syndrome
2011, Brain and Cognition
Both working and immediate memories were assessed every 4 h by specific short-term memory tasks over sustained wakefulness in 12 patients with obstructive sleep apnea and hypopnea syndrome (OSAHS) and 10 healthy controls. Results indicated that OSAHS patients exhibited lower working memory performances than controls on both backward digit span and complex Sternberg tasks. Speed and accuracy on Sternberg tasks were affected by memory load in both groups. However, immediate memory was not impaired in OSAHS patients. Diurnal and nocturnal SaO₂ were correlated with speed and accuracy high-speed memory scanning performance on Sternberg tasks in patients. These results suggest specific working memory deficits associated with OSAHS over sustained wakefulness with a possible deficiency in the central executive responsible for the higher information processing, in addition to a potentially insufficient storage capacity. Among OSAHS patients, working memory ability involved in high-speed memory scanning may be impaired by chronic hypoxemia.
Complex sleep apnea and obesity hypoventilation syndrome. Opposite ends of the spectrum of obstructive sleep apnea?
2009, Medical Hypotheses
In most cases, the application of continuous positive airway pressure (CPAP) during sleep in patients affected by obstructive sleep apnea (OSA) eliminates upper airway obstruction and makes breathing stable and regular. However, some OSA patients develop periodic breathing and central apneas during CPAP administration, a finding that has been labelled as “complex sleep apnea” (complex SA). Such breathing disorder may occur only acutely after CPAP treatment initiation or sometimes persist with chronic CPAP treatment. We hypothesize that complex SA may be the consequence of mechanisms analogous to those leading to obesity hypoventilation syndrome (OHS), but operating in an opposite direction.
Periodic breathing is one of the factors predisposing to OSA and is an essential factor for the recurrence of central apneas in normo or hypocapnic patients. A high ventilatory responsiveness to chemical stimuli enhances breathing periodicity. In subjects with periodic central apneas chemoresponsiveness is high, while in subjects with OSA it spans throughout a wide range, and is correlated to diurnal blood gas levels. In fact, sleep respiratory disorders may be responsible for either an augmentation in ventilatory responses to chemical stimuli consequent to chronic exposure to intermittent hypoxia, or for a decrease in ventilatory responses when prolonged exposure to hypercapnia is experienced. Among OSA subjects, those with OHS show very depressed hypercapnic responses. After chronic OSA treatment, ventilatory responses to chemical stimuli may either decrease, in previously hyperresponsive subjects, or increase, in previously hyporesponsive subjects. Most patients with OHS decrease daytime PCO₂ levels and increase their ventilatory responses after chronic CPAP treatment.
Complex SA could appear in those OSA subjects in whom chronic exposure to nocturnal respiratory disorders leads to the highest responsiveness to chemical stimuli, and could disappear after blunting of ventilatory responses following chronic CPAP treatment. Complex SA may be one extreme of evolutionary spectrum of OSA, the opposite end being represented by OHS.

View all citing articles on Scopus

View full text

Review articleDaytime hypoventilation in obstructive sleep apnoea syndrome

Abstract

Clin Chest Med

Am J Med

Chest

Chest

Chest

Chest

Clin Chest Med

Chest

Chest

Chest

lancet

Etude polygraphique des manifestations épisodiques (hypniques et respiratoires) du syndrome de Pickwick

Rev Neurol (Paris)

Extreme obesity associated with alveolar hypoventilation: a Pickwickian syndrome

Am J Med

Clinical and physiological aspects of a case of obesity, polycythemia, and alveolar hypoventilation

J Clin Invest

Polycythemia associated with obesity

JAMA

The sleep apnoea syndromes

Ann Rev Med

The obesity-hypoventilation syndrome revised. A series of 34 patients

Eur Respir J

Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease

Am J Respir Crit Care Med

Pulmonary hypertension due to chronic hypoxic lung disease

Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnoea syndrome

Am Rev Respir Dis

Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnoea

Am Rev Respir Dis

Review article
Daytime hypoventilation in obstructive sleep apnoea syndrome