Voluntary hyperventilation in obesity hypoventilation.

  title={Voluntary hyperventilation in obesity hypoventilation.},
  author={Judith Leech and Erg{\"u}n Onal and Robert M. Aronson and Melvin Lopata},
  volume={100 5},
Arterial blood gas analysis was performed before and after 60 to 90 s of voluntary hyperventilation in 27 consecutive patients with occlusive sleep apnea syndrome (OSA) and daytime hypercapnia. The percentage of fall in PaCO2 from baseline was examined in relationship to age, body mass index, sleep-disordered breathing indices, and pulmonary function variables. In 14 subjects without airflow obstruction, only one individual could not voluntarily hyperventilate into the normal range, whereas 6… 

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Ventilatory responses to hypercapnia and hypoxia in relatives of patients with the obesity hypoventilation syndrome

There is no evidence of impaired ventilatory chemoresponsiveness in first degree relatives of patients with OHS compared with age and BMI matched control subjects.

Obesity hypoventilation syndrome: bicarbonate concentration and acetazolamide.

In patients with OHS, hypercapnia occurs despite the ability of most patients to voluntarily normalize their PaCO2, and the ventilatory response tohypercapnia is reduced further than in those with simple obesity.

Obesity hypoventilation syndrome

Both continuous positive airway pressure (CPAP) and noninvasive ventilation (NIV) improve clinical symptoms, quality of life, gas exchange, and sleep disordered breathing in OHS patients and are considered the first-line treatment modality for OHS phenotype with concomitant severe obstructive sleep apnoea.

Obesity Hypoventilation Syndrome

Alternative methods of positive airway pressure treatment, such as average volume-assured pressure support or surgical interventions such as bariatic surgery or tracheostomy can be offered to patients who are refractory to CPAP or BIPAP.

Treatment effects on carbon dioxide retention in patients with obstructive sleep apnea-hypopnea syndrome.

Depressed chemoresponsiveness plays a role that is independent of obesity in the development of CO(2) retention in some OSAHS patients, and it may be a response to sleep-disordered breathing.

Clinical Heterogeneity among Patients with Obesity Hypoventilation Syndrome: Therapeutic Implications

Nocturnal/diurnal oximetries should be made to assess treatment efficacy in stable OHS patients who fail to achieve good control withCPAP and those controlled with CPAP have better spirometry and a significantly higher apnea-hypopnea index.

Obesity hypoventilation syndrome.

The concept is that chronic sustained hypercapnia occurs when the disorder of ventilation that produces acutehypercapnia interacts with inadequate compensation (both during sleep and during the periods of wakefulness); neither alone is sufficient to fully explain the final result.



Determinants of hypercapnia in occlusive sleep apnea syndrome.

It is suggested that daytime hypoxemia, mechanical impairment of the respiratory system due to obesity or obstructive airway disease (or both), and the severity of sleep-induced respiratory abnormalities as assessed by AHI contribute toThe severity of carbon dioxide retention in patients with occlusive sleep apnea in a multifactorial fashion.

Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnea.

The findings suggest that OSA alone does not produce daytime hypercapnia even in obese patients, and that the presence of diffuse airway obstruction is an important predisposing factor to the development of chronic CO2 retention in such patients.

Mass loading, sleep apnea, and the pathogenesis of obesity hypoventilation.

  • M. LopataE. Onal
  • Medicine, Biology
    The American review of respiratory disease
  • 1982
It is concluded that both OSA and OH patients were equally unable to develop the expected increase in respiratory muscle drive and output and the presence of sleep apnea may result in impaired mass load compensation and predispose obese patients to develop hypercapnia.

Relationship between pulmonary function and sleep-induced respiratory abnormalities.

It is suggested that decreased pulmonary volume and increased Raw contribute to the severity of sleep-induced respiratory abnormalities in patients with sleep apnea syndrome regardless of the degree of obesity.

Elevated pulse flow resistance in awake obese subjects with obstructive sleep apnea.

Transpulmonary and total transrespiratory system pulse flow resistance (RI and Rtot) were highly correlated with desaturation index and the elevated pulse flow airway resistance in patients may be caused by upper airway narrowing because of compression by fat, by lax tone in pharyngeal muscles, or by both.

Diaphragm activity in obesity.

The results suggest that an incapacity to increase the activity in the respiratory muscles, to levels necessary to overcome the load caused by obesity, plays a major role in the genesis of respiratory failure in obese subjects.

Maximal respiratory pressures: normal values and relationship to age and sex.

The normal range of values for the maximal inspiratory and expiratory pressures in males and females from 20 to 74 years of age was determined and there was no significant regression of Pi max or Pe max with age in subjects younger than 55 years.

[Sleep apnea syndromes].

  • J. Krieger
  • Medicine
    Comptes rendus des seances de la Societe de biologie et de ses filiales
  • 1989
The predominant clinical signs are snoring and daytime somnolence due to sleep fragmentation and the treatment is based upon the use of continuous positive airway pressure (CPAP) during sleep.

Idiopathic alveolar hypoventilation: clinical spectrum.

Abstract Seven patients had varying degrees of impaired pulmonary function but in other respects resembled patients with idiopathic alveolar hypoventilation. These patients were characterized by ch...