The four subjects averaged 36 years of age. Prior to weight loss, their mean body weight was 231 kg, or 341 percent of ideal body weight, derived from standard tables. At the time of restudy, their mean weight was 123 kg, or 176 percent of ideal body weight. The average weight loss was 108 kg (range 53-155 kg).
Prior to surgery, the two heaviest subjects (patients 1 and 2 in Table 1) were symptomatic with daytime somnolence, loud snoring, and peripheral edema. Both of these men had hypercapnia and moderate hypoxemia on awake arterial blood gas analysis. The two remaining subjects (patients 4 and 5) were asymptomatic. At the time of restudy, all patients were asymptomatic. Repeat arterial blood gas analysis and pulmonary function tests in patients 1 and 2 were now within normal limits.
In all subjects, weight loss was accompanied by a reduction in the number of episodes per hour of sleep-disordered breathing. The mean number of episodes of sleep-disordered breathing per hour of sleep period time was 78 preoperatively and 1.4 after weight loss. In three of the four subjects, there was improvement in the severity of desaturation accompanying episodes of disordered breathing. This was most dramatic in the two previously symptomatic subjects whose lowest oxygen saturation during sleep was less than 50 percent prior to surgery, and 90 percent and 87 percent at restudy.
Analysis of the sleep characteristics of these subjects after weight loss (Table 2) showed a change in the direction toward deeper sleep with fewer awakenings. Sleep quality was, thus, improved.
This study shows that massive weight loss in morbidly obese men with sleep apnea results in a marked reduction in the incidence of sleep-disordered breathing events. This is in agreement with other findings,’ but is in contrast to the findings of Lugaresi et al that even though patients were symptomatically improved after weight loss, sleep apnea persisted. Since the amount of weight loss is not noted by some authors, it is possible that the degree of weight loss is the critical factor. In any case, our results suggest that obesity is primary, rather than secondary, in the development of the obesity-related sleep apnea syndrome.
A simple hypothesis to explain our findings is that fat in the upper airway physically causes obstruction which is then removed when weight loss occurs. While thickening of the soft palate and posterior pharyngeal wall may play a minor role, the major mechanism for upper airway obstruction during sleep appears to be central, with decreased firing of the nerves affecting the genioglossus and other muscles. Obstruction then results from periodic relaxation of these muscles with resultant collapse of the posterior pharynx and relaxation of the tongue.
If the mechanism is central, how does weight reduction effect an improvement in the syndrome? Two possibilities are that this occurs because of improvement in oxygenation and/or lessening of the mass load on the chest wall and abdomen with resultant improvement in respiratory muscle function. Chronic hypoxemia and mass loading have both been shown to have a detrimental effect on central ventilatory drives. That massive obesity almost invariably causes chronic hypoxemia has been shown by many studies» and is thought to be due to ventilation-perfusion mismatch. Prolonged hypoxemia in subjects at altitude or with cyanotic congenital heart disease has been shown to result in a blunted hypoxemic ventilatory response. Worsening hypoxemia may result in even further diminution of ventilation. Weight loss might thus alleviate sleep apnea by improvement in oxygenation and, thus, improvement in hypoxemic ventilatory response. The problems with this explanation are several. While the severity of hypoxemia does appear to correlate with whether a patient with obesity-related sleep apnea is symptomatic with daytime somnolence, the presence of a blunted hypoxic ventilatory response has not been looked for. Thus, the relationship of hypoxic ventilatory response to sleep apnea is not known. In addition, several studies have not found the blunted hypoxic response to be reversible with correction of hypoxemia. Finally, patient studies on the effect of obesity on ventilatory drives have not demonstrated a change with weight reduction, with a few exceptions. The relevance of those studies to our patients is uncertain, however. For example, the patients reported by Kronenberg et al with normal hypoxic and hypercapnic ventilatory responses before and after weight loss were all asymptomatic women. My Canadian Pharmacy may help to achieve weight loss. The remedies suggested by our online pharmacy are suitable for people of all ages. You will definitely find remedy exactly for you.
The mechanical effects of massive obesity include diminished thoracic compliance and increased work of breathing. Evidence of a respiratory-loading effect on central ventilatory drives comes from the work of Milic-Emili and Tyler, who demonstrated a diminished ventilatory response to hyper-capnia secondary to resistive loading during inspiration. Recently, Lopata and co-workers demonstrated that obese patients with sleep apnea had a significantly diminished occlusion pressure response to CO2 rebreathing, compared to non-obese control subjects and obese subjects without sleep apnea. This indicated impaired generation of respiratory muscle output in the sleep apnea group. They also found that obese patients without sleep apnea had a greater than normal diaphragmatic EMG response to CO2, suggesting a compensatory response to mass loading which obese sleep apnea and obesity hypoventilation patients did not mount Lopata et al suggest that sleep fragmentation and hypoxemia in patients with sleep apnea eventually lead to impaired mass load compensation and chronic hypoventilation.
Since sleep apnea does improve with weight reduction, it seems appropriate to try weight reduction in sufficiently motivated patients with obesity-sleep apnea prior to recommending tracheostomy if the clinical situation allows the time delay. The degree of weight reduction needed to produce resolution needs further study.
Table 1—Dieordered Breathing and Desaturation Before and After Weight Lou
|Patient*||Weight(Kg)||Sleep Period Time (Hours)||Total No. Episodes per hour||Desaturations fper hour||Hypopneas per hour||Apneas per hour||Low Sat (%)|
|p (based on means)||.063||.063||.375||–||.063||0.125|
Table 2—Sleep Characteristics
|%0||of T 1||Ime i 2||in Ej 3||Eich 1 4||StageREM|
|After weight loss||247||8||6||45||7||24||10|