Central hemodynamics and 24-hour blood pressure in obstructive sleep apnea syndrome: Effects of corrective surgery

Abstract

Obstructive sleep apnea syndrome is associated with hypoxemia, respiratory acidosis, and frequent arousals during sleep that induce elevation of both the pulmonary and systemic arterial pressure [1,2]. The prevalence of chronic systemic hypertension in patients with sleep apnea syndrome has been reported to exceed 60% [3,4]. Conversely, the incidence of unrecognized sleep apnea in patients with essential hypertension may be as great as 25% to 35% [5-7]. Hemodynamic abnormalities in patients with obstructive sleep apnea appear to be greatest when there are vigorous inspiratory efforts performed against a closed airway during the apneic episodes [1]. Recently, there has been evidence that some of the hemodynamic derangements, notably casual blood pressure elevation, may improve in a few weeks following tracheostomy [4], specific drug therapy [7], and nasal continuous positive airway pressure [8]. In the report herein, we evaluated both noninvasively and invasively recorded hemodynamic parameters before and after uvulopalatopharyngoplasty in a hypertensive man with obstructive sleep apnea. METHODS Hemodynamic Studies Hemodynamic studies were performed as described previously [9]. The systemic arterial blood pressure was recorded intra-arterially by a thin polyethylene catheter introduced into the brachial artery and connected to a strain gauge manometer. The electrocardiogram and arterial pressures were recorded on a multichannel oscillographic recorder. The systolic, diastolic, and electrically integrated mean arterial pressures were recorded during several respiratory cycles, and 15-second intervals were hand-smoothed to blood pressure values. The cardiac output was recorded by the dye dilution method using a linearly responding monochromatic densitometer and recording continuously in arterial blood. Duplicate curves were plotted on semilogarithmic paper, and cardiac output was derived from the area under the curves by a research technician unaware of the clinical data. The cardiac output was indexed by the body surface area. The stroke index was calculated by dividing the cardiac index by the heart rate. The total peripheral resistance index was calculated by using the formula: mean arterial pressure × 80/cardiac index [9].