Time course of pulmonary artery pressure during sleep in sleep apnoea syndrome: role of recurrent apnoeas

Abstract

The increase in pulmonary arterial pressure (Ppa) during acute hypoxia is mainly related to alveolar hypoxaemia inducing vasoconstriction of precapillary pulmonary arterioles [1,2] whereas during chronic hypoxia, mechanical and hormonal factors make the vessels adapt to hypoxia and modify their response to chemical stimulus [3]. Furthermore, the temporal profile of the hypoxaemic stimulus may have a substantial effect on the pulmonary vascular response [4] as suggested by experimental studies allowing that repeated exposure to intermittent hypoxaemia [5] enhances the pulmonary hypoxic pressor response.Previous studies [6] in obstructive sleep apnoea (OSAS) patients have shown that repeated desaturations from obstructive apnoeas induce a transient increase in Ppa that, together with daytime hypoxaemia, is considered to be the key factor responsible for daytime pulmonary hypertension [7,8]. Recent evidence in animals [9][10][11] has demonstrated that repetitive hypoxic stimuli, simulating the chemical changes produced by apnoeas lead to systemic hypertension either during the exposure or during the recovery period. A more direct approach to the pulmonary vascular effects of repetitive hypoxaemia has been used by IWASE et al. [12]. Using a canine model they have demonstrated a progressive increase in systemic and pulmonary arterial pressure during repetitive hypoxaemic exposure. On the basis of these latter findings a trend in the pulmonary arterial pressure response to repetitive hypoxaemia similar to the one produced experimentally may occur in patients with OSAS.The two aims of the present study were: 1) to ascertain whether recurrent apnoea-related oxygen desaturations are associated with a progressive rise in Ppa during the night in OSAS patients; 2) if there was a rise in the expected direction, to determine whether diurnal and nocturnal variables would predict the degree of progressive nocturnal increase in Ppa. Patients and methods PatientsThirty five consecutive patients referred to the sleep laboratory for habitual snoring and possible sleep apnoea We have, therefore, examined the nocturnal trend of Ppa in seven obstructive sleep apnoea syndrome (OSAS) patients and in five snorers. Mean Ppa was measured before, at the start, at the end and after the selected apnoeas. The analysis was performed for each 1 h period for at least 7 h throughout the night on at least 10 randomly selected apnoeas per hour. In snorers, 100 randomly chosen values were measured during every hour of the night. In the morning after the nocturnal study, the Ppa responses to acute hypoxia and hypercapnia were measured.No Ppa changes throughout the 7 h were found during sleep in snorers (Ppa slope:-0.002±0.10 mmHg·h -1 ). In OSAS patients a small but significant increase in Ppa throughout the night was noted, affecting the values before (Ppa slope: 0.7±0.16 mm Hg·h -1 ), at the start of apnoea (Ppa slope: 0.53±0.1 mmHg·h -1 ) as well as at the end (Ppa slope: 0.44±0.08 mmHg·h -1 ) and in the postapnoeic period (Ppa slope: 0.55±0.1 mmHg...

Hypoxic Pulmonary Vasoconstriction

“…Whereas normal subjects exhibited only slight changes in P PA (4)(5) with no variation during the different stages of sleep (998), patients with OSA exhibited large swings in P PA during apneic events, and a generally progressive increase in P PA overnight (232,1185,1534,1751) with systolic P PA often reaching 50 -60 mmHg (232,1388,1909). Although some studies found no correlation between sleep stage and severity of pulmonary hypertension (1751), most found that extreme increases in P PA tended to occur during periods of rapid-eye-movement (REM) sleep (321,1388,1720,1841), probably because airway obstruction and arterial O 2 desaturation were most severe during this time (321,1186,1720).…”

Obstructive sleep apnea and heart failure

“…The mean increase in pulmonary artery pressure was about 10 mm Hg, observed toward the end of an apneic episode, although no evidence of a progressively increased pulmonary artery pressure throughout the night was seen. However, other researchers have reported a small increase in pulmonary artery pressure throughout the night of about 0.5 mm Hg/hour of sleep in patients with OSA [51] (class III). Taken together, these studies suggest that elevated pulmonary artery pressure in the setting of OSA likely is the result of a combination of mechanical effects, a short-term hypoxic vasoconstrictive effect, and perhaps subacute effects leading to progressively higher pulmonary artery pressures.…”

Use of Pulmonary Arterial Hypertension–Specific Therapy in Overweight or Obese Patients with Obstructive Sleep Apnea and Pulmonary Hypertension

“…The mPAP in our study was ∼40 mmHg, whereas it is usually in the 20s in patients with PH secondary to OSA. [3][4][5][6][7][8][9] Severe PH (mPAP > 40 mmHg) is rare in patients with OSA. A recent study of patients with OSA reported severe PH in 8 (44%) of the 18 patients with PAH in that study.…”