Pulmonary Hemodynamics in the Obstructive Sleep Apnea Syndrome
It has long been recognized that the occurrence of apneas during sleep is accompanied by an increase in the pulmonary arterial pressure. However, early data were obtained by measuring the intravascular arterial pressure, while changes in the transmural pulmonary arterial pressure (PAPtm), the parameter which conditions right heart afterload, received less attention. Our results have been obtained by electronically subtracting the intravascular pressure (esophageal balloon) from the intravascular arterial pressure (Swan-Ganz catheter) obtained during standard polysomnographic recordings in three patients. PAPtm decreased slightly durig the initial part of obstructive apneas and increased during the final part. On breathing resumption there was often a further increase in PAPtm. The changes in PAPtm were found to correlate to varying degrees with the esophageal pressure, SaO2, and heart rate.
In order to elucidate the mechanisms of daytime pulmonary hypertension in obstructive sleep apnea patients, we studied 114 consecutive patients who underwent polysomnography and pulmonary function tests including right heart catheterization. Nineteen (19%) had resting pulmonary hypertension (PAP ≥ 20 mm Hg). Fourteen were hypoxemic and five were hypercapnic. Patients with pulmonary hypertension differed from the other patients in having a lower PaO2, higher PaCO2, and lower total lung capacity (TLC), forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and FEV1/FVC ratio. They also had higher apnea and hypopnea + apnea indices as well as lower SaO2 during sleep. Multiple regression analysis showed that FEV1 and PaO2 (both with a negative coefficient) and PaCO2 (with a positive coefficient) significantly contributed to the pulmonary arterial pressure.
These data suggest that the sleep-apnea-related increase in PAPtm could be due to various combinations of intrathoracic pressure changes, hypoxic vasoconstriction, and changes in cardiac output. The development of permanent pulmonary hypertension seems to be related to permanent hypoxemia and hypercapnia, which themselves depend on multiple factors including diffuse airway obstruction, the severity of sleep apneas, and the chemosensitivity to CO2.
KeywordsObesity Catheter Respiration Neurol Cardiol
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