An Unusual Cause Of Bimodal Pattern Of Nocturnal Hypoxemia In An Obstructive Sleep Apnea Patient.

Background. Venous return and right atrial pressure are increased by clinostatism and by the intrathoracic negative pressure during obstructive sleep apneas. In presence of a interatrial defect this may results in right-to-left shunt. Case report. A 51-yrs obese male was admitted to the cardiology department of our hospital for evaluation of arrhythmias and exertional dyspnoea. He was also referred to the Respiratory unit because of dry mouth and sore throat upon awakening, daytime sleepiness and fatigue, snoring, restlessness during sleep, with a story of wheezing and recurrent bronchitis for years. He had a history of former smoking (20pack/yrs) and a prolonged occupational exposure to wheat. Lung function tests documented a mild chronic obstructive pulmonary disease and high values of the carbon monoxide transfer coefficient. Arterial blood gas analysis in ambient air and in spontaneous breathing was normal. A nocturnal cardiorespiratory polygraphy (CRP) documented a severe pattern of obstructive sleep apnoea syndrome (OSAS) (AHI=83/h, ODI=71/h), with hypoxemia (time with SpO2<90%=89%, <80%=53%). There were different fasis of severe prolonged hypoxemia with superimposed typical apnoeic desaturations (Fig.1). After a short awakening in standing position the hypoxemia recurred after about 1 hour of sleep. The deepest desaturations occurred in both right and left lateral positions. The number of hypo-apnoeic episodes was similar in both normoxemic and hypoxemic phases. The distribution of hypoxemia showed a bimodal pattern (Fig.2). A chest TC scan showed signs of COPD and air trapping during the expiratory phase, with no abnormal findings in the pulmonary circulation. A transthoracic ecocardiography documented a suspected interatrial right-to-left shunt with normal values of pulmonary artery systolic pressure (20 mmHg). A transesophageal ecocardiography confirmed the presence of an interatrial right-to-left shunt which occurred only during deep inspirations. After a 4 days progressive pressure titration, we prescribed the application of a continuous positive airway pressure (CPAP) of 13cmH2O with an oronasal mask during sleep. After 6 days a CRP with CPAP documented a marked improvement: AHI=9.3/h, ODI=8.1/h, time with SpO2<90%=7.6%, SpO2<80%=0%, with the usual unimodal pattern. A significant subjective improvement was reported. Conclusion. Our observation confirms the efficacy of CPAP therapy in reducing intermittent right-to-left shunt in interatrial defects in presence of OSAS. In our case sustained but inconstant hypoxemia was not explained by supine position or number of apnoeas and was temporarily reversed by a short standing period. Variable right-to-left shunt is a possible cause of a bimodal pattern of SpO2 distribution.