Cheyne-Stokes ventilation is ofttimes found in conjunction with heart failaure.

Cheyne-Stokes ventilation is ofttimes found in conjunction with heart failaure. The pathogenesis is multifactorial and upper airway instability has been insinuateed to play a role. This report documents the conversion of Cheyne-Stokes ventilation during rest to obstructive apnea after heart transplantation.

The relationship between cardiac disease and sleep-disordered breathing has lately received considerable attention in the medical literature. Obstructive doze apnea (OSA) and Cheyne-Stokes ventilation (CSV) have been rest in many patients with cardiac disease. Treatment with nasal CPAP has been shown to improve both[12] suggesting that upper airway instability, known to cause OSA, may also play a part in the pathogenesis of CSV In this report, we describe a patient who was set up to have a severe form of CSV following rejection of his first heart transplant and then "developed" OSA after retransplantation occurred

CASE REPORT

A 48-year-old white man underwent orthotopic heart transplantation for idiopathic cardiomyopathy in November 1989 In July 1990 a multiple gated acquisition sean showed left ventricular ejection fraction had fallen from 49 percent to 29 percent and the was treated for rejection without improvement. He exhibited worsening congestive heart failure and was hospitalized in September 1990

At the time of hospital admission, he complained of daytime sleepiness, orthopnea, and increasing pedal edema. He was noted to have apneic periods while sleeping and bedside oximetry revealed oxygen desaturation. Overnight polysomnography was performed. Apneas were scored as cessation of airflow for [greater than or equal to] 10 s; hypopneas were a diminution in airflow associated with [greater than or equal to] 4 percent oxygen desaturation.

The patient demonstrated CSV with postponeed central apneas (Fig 1). During the initial 85 min of lie in the grave he had 57 apneas lasting 30 to 45 s Oxygen saturation consistently malign to 60 percent and application of nasal cannula oxygen at 2 L/min neither improved oxygen desaturation nor changed the longitudinal dimensions or number of apneas. Nasal CPAP at 7 cm [Hsub2]O press with 4 L/min oxygen produc no significant change in the character, number, or severity of apneas; a higher influence was not tolerated.

The patient underwent a trial with nasal BiPAP (Respironics, Monroeville, Pa). BiPAP is a ventilatory assist device that allows independent adjustment of inspiratory and expiratory airway constraining forces The pressures were titrated to inspiratory positive airway urgency of 10 cm [H.sub.2]O and expiratory positive airway hurry of 6 cm [H.sub.2]O without significant change in respiratory issues The addition of timed breaths was also bootless The patient was again unable to tolerate higher settings.

Ventilation was attempted during drowse with a cuirass. Negative influence was titrated to 50 cm [Hsub2]O with 12 breaths/min. The patient did not tolerate the cuirass well and although oxygen saturation improved slightly, there was no consistent improvement in the CSV

The patient was placed forward a regimen of acetazolamide, 250 mg orally each 6 h that decreased the serum bicarbonate even from 25 mmol/L to 17 mmol/L He was restudied with oxygen and continued to have periodic breathing with central apneas, still events were shorter and oxygenation was improved: at 4 L/min, oxygen saturation remained [greater than]85d percent He was subsequently discharged from the hospital in succession a regimen of oxygen therapy and acetazolamide, 250mg orally each 12 h.

He underwent retransplantation in November 1990 His postoperative course was complicated unless he was ultimately discharged from the hospital in stable condition.

He was readmitted to the hospital in February 1991 for treatment of mild rejection. Repeated polysomnography continued to demonstrate sleep-disordered breathing nevertheless now events were predominantly obstructive (Fig 2) His apnea-hypopnea index was 45 consequences per hour and the lowest oxygen saturation was 83 percent A repeated nasal CPAP attempt was not tolerated. As the patient was essentially asympotomatic (no daytime sleepiness) and his physical condition was unstable, observation alone was decided. He subsequently has refused further doze evaluations.

DISCUSSION

Cheyne-Stokes ventilation is a form of periodic breathing whose pathophysiology is consideration to be from an instability in the respiratory ascendency center. In patients wth heart failure, a variety of factors may have a destablizing influence forward the respiratory control center, including chemoreceptor circulatory delay, augmented chemoreceptor gain becoming to hypoxia, and reduced FRC leading to reasonable lung [O.sub.2] and [CO.sub.2] reservoirs.[3] Upper airway instability may also play a part as it has been shown that upper airway collapse meet the eyes in some patients during the decrescendo and the crescendo ventilatory phases of CSV[4] Further support of upper airway involvement is glance ated by studies showing nasal CPAP improves CSV and central apnea.[2,5] The mechanism of effectiveness of nasal CPAP in this situation may be to be ascribed to its ability to act as a pneumatic splint stabilizing the upper airway.

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