This report describes an unusual ca...

This report describes an unusual case of stiff obstructive sleep apnea and alveolar hypoventilation leading to hypersomnolence and cor pulmonale, which were corrected at tracheostomy. Four years later, after a 225-kg weight gain, nocturnal apneas of similar commonness duration, and depth of desaturation reappeared moreover were totally central in origin. The central apneas were eliminated with domestic circle nocturnal positive-pressure ventilation via beated tracheostomy tube. Each time the patient's apneas were corrected (obstructive: tracheostomy; central: mechanical ventilation), daytime alveolar hypoventilation disappeared rapidly. Yearly right heart catheterizations and radionuclide ejection fractions documented pulmonary hypertension and right heart failure, with resolution following tracheostomy and return after appearance of central apneas. The changes in hemodynamic status corresponded to the patient's weight, demeanor of apnea, daytime alveolar hypoventilation, and treatment of nocturnal oxyhemoglobin desaturation. This case illustrates the theory of a belonging to all etiology of both central and obstructive apnea by the and of abnormal respiratory controller gain and points to several parts obesity may play in apnea. (Chest 1989; 95:205-09)

Monographs and work chapters describing sleep apnea typically define obstructive and central apnea as etiologically unrelated ends In reality, it is universal for both central and obstructive adventures to appear together in the same individual during rest suggesting a common etiology. novel studies have addressed possible central respiratory bridle factors in the etiology of the pair "central" and "obstructive" apneas.[1-4] Hypoxia has been shown to play a pivotal part in periodic breathing, whether induced from hypoxic gas mixtures or ascent to altitude.[5,6] The hypocapnia induced from compensatory hyperventilation in this setting may model the drive to breathe (apneic [COsub2] threshold) creating central pauses in respiration.[3,7] The changes in central drive could alter neuromuscular tone of the upper airway, increasing pharngeal resistance and predisposing to obstructive apnea.[6,8]

This report describes a patient with unadorned obesity in whom obstructive apnea and hypoventilation created simple hemodynamic abnormalities corrected by tracheostomy. Four years later, corresponding to a substantial increase in weight and despite a patent tracheostomy, touching apneic desaturation and right heart failure reappeared. The transaction of obstructive apnea followed at severe central apnea suggests a relationship between apnea etiologies.

Case Report

The patient first quick in emergenciesed in February, 1984 with dyspnea, harsh daytime hypersomnolence, morbid obesity, shortness of breath, and ankle swelling for three years. attack of symptoms corresponded to a 45-kg weight gain. He had a lifelong history of heavy snoring and smok single pack of cigarettes per day for 40 years. He exhibited many signs of right heart failure, including elevated jugular venous pulsation 'P' pulmonale on lead 2 of the ECG cardiomegaly onward chest roentgenogram, and leg edema. His admission weight was 1912 kg which decreased to 1534 kg after diuresis. Following stabilization (Table 1 February, 1984) gated radionuclide cogitation documented a reduced right ventricular ejection fraction (RVEF) and right heart catheterization confirmed elevation of pulmonary artery constraining force (Ppa). Spirometric study conclusions Showed no obvious expiratory airflow obstruction, moreover this was suggested by a marked elevation of residual tome (199 percent predicted). Polysomnography revealed 500 to 650 obstructive apneas by night (apnea index = 114/h) with waste in oxyhemoglobin saturation ([SaO.sub.2]) to around 30 percent during rapid judgment movement (REM) sleep (Fig 1 panel A). There were no central apneas, and fewer than 5 percent of apneas had any mixed component part which was always less than 10 s in duration. Tracheostomy was performed February, 1984 Polysomnography then showed no apneic desaturation, if it were not that during REM sleep, longer periods of desaturation previously described in patients with lung disease[9-11] were observ (Fig 1 panel B) These were ameliorated with 4L/min supplemental oxygen across the tracheostomy stoma (Fig 1 panel C) and the patient was discharged hearth with nocturnal supplemental oxygen and diuretics.

During the nearest two years, the patient remained symptom unrestrained and two subsequent right heart catheterizations and radionuclide studies (March/85, May/86) showed normalization of the Ppa and RVEF (Table 1) Arterial line gas values improved with resolution of alveolar hypoventilation, if it were not that a widened alveolar-arterial oxygen gradient, P([A-aO.sub.2]) persisted. At the extremity of the second year after tracheostomy (May, 1986) the patient's weight was noted to have increased (dietary counseling was of no avail). At the last of the third year following tracheostomy, (May/87) the patient complained of a get back of daytime hypersomnolence and peripheral edema, and he showed evidence of alveolar hypoventilation through blood gas analysis, and his weight had increased (162 + kg outvieed clinic scale limit). Patency of the tracheostomy tube was ascertained by the agency of fiberoptic visualization. The patient was again urg to squander weight. One year later (May, 1988) at a weight of 16425 kg the patient's vital current gas values had deteriorated. sustained by edema was treated with diuretics. Ppa and RVEF had again deteriorated (Table 1 June/88) Polysomnography (May, 1988) with the tracheostomy explain and unobstructed showed apnea desaturation of duration and nadir [SaO.sub.2] (apnea index = 50/h) similar to his original subject of attention of February/84 (Fig 1, panel D) However, all apneas were central in that no chest wall or abdominal activity was at hand (Fig 2). The ventilatory rejoinder to hyperoxic hypercarbia was virtually flat. Supplemental oxygen did little to ameliorate the apneic fall in [SaO.sub.2]. His metal tracheostomy was changed to a slaped plastic tube and he received ventilation with a constraining force cycle ventilator at night ([FIo.sub.2] = 021 percent) to achieve adequate oxygenation (Fig 1 panel E) Following single and three weeks of abode nocturnal ventilator use (June/88[unkeyable], June/88[unkeyable]), his daytime arterial [PaCO.sub.2] had decreased from 58 to 45 to 34 mm Hg and his [PaO.sub.2] had increased from 49 to 59 to 64 mm Hg (confirmed by the agency of multiple blood gas analyses). Repeated polysomnography during spontaneous respiration after three weeks of nocturnal ventilator use showed no central apneas, a non-REM [SaO.sub.2] of 88 to 90 percent and nonapneic REM desaturation to 78 percent (similar to Fig 1 B) Following weight los to 1377 kg nocturnal mechanical ventilation was discontinued (after three months) and after nocturnal oximetry during spontaneous respiration showed continued resolution of apneic desaturation. The RVEF and arterial posterity gas values likewise improved (September, 1988)