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Transmural Pressure Measurements: Importance in the Assessment of Pulmonary Hypertension in Obstructive Sleep Apneas
Section snippets
PATIENTS AND METHODS
Seven patients, three men and four women, affected by OSAS, previously diagnosed by means of nocturnal polysomnography, were studied; they showed normal or mildly altered blood gas tensions during wakefulness, normal spirometric values, and a variable degree of weight excess (Table 1). All patients gave informed consent to the following studies.
A Swan-Ganz catheter was introduced into the pulmonary artery through an antecubital or femoral vein and connected to a pressure transducer; mean PAP
RESULTS
All patients were shown to be affected by severe OSAS, as demonstrated by a high frequency of apneas (AI = 89.9 ± 15.2 SD) of variable duration (26 ± 9.6 s), which accounted for a high AT/TST percentage (65.3 ±15.6 percent). Only NREM sleep was recorded. The selected apneas were characterized by comparable duration (26.9 ±8.3 s), resulting in marked falls in SaO2 (lowest SaO2, 77.3 ±4.2 percent; SaO2 fall, 12.1 ±4.5 percent) (Table 2).
Periodic oscillations corresponding to the apneaventilation
DISCUSSION
Evaluation of pulmonary hemodynamics during sleep-induced obstructive apneas clearly demonstrated that these events were associated with a progressive increase in PAP. Although this phenomenon had already been hypothesized,5, 6, 7 a reliable account of its actual relationship with mechanical and chemical variables throughout the apnea has never been reported, since all previous investigations have had major limitations. In fact, the only investigation1 dealing with hemodynamic follow-up in the
ACKNOWLEDGMENTS
the authors are indebted to Professor Carlo Giuntini and Professor Mario Morpurgo for their helpful advice.
REFERENCES (15)
- et al.
Pulmonary hypertension: individual and species variability relative to vascular reactivity (Editorial).
Am Heart J
(1963) - et al.
Aspects hemodynamiques et respiratoires du syndrome pickwickien.
Bull Physiopath Resp
(1972) - et al.
Continuous recording of the pulmonary and systolic arterial pressure during sleep in syndromes of hypersomnia with periodic breathing.
Bull Physiopath Resp
(1972) - et al.
Hemodynamics in sleep-induced apnea.
Studies during wakefulness and sleep. Ann Intern Med
(1976) - et al.
Hemodynamic studies in sleep apnea.
Sleep apnea syndromes.
(1978) Gas exchange and hemodynamics during sleep.
Med Clin NA
(1985)- et al.
Nocturnal hemodynamics in patients with sleep apnea.
Eur J Respir Dis
(1986)
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Manuscript received February 25; revision accepted June 8.