[Diagnostic criteria for obstructive sleep apnea syndrome in adolescent]. / Critères diagnostiques des troubles respiratoires obstructifs du sommeil de l'adolescent.

The obstructive sleep apnoea syndrome (OSAS) affects 1-4% of adolescents. It represents a transitional stage between paediatric and adult OSA and is characterized by specific symptoms. BACKGROUND: The persistence of childhood OSAS during adolescence is not frequent. Risk factors are male sex, obesity and a history of tonsillectomy or adenoidectomy. Symptoms may be misleading such as tiredness and depressive disorders. In adolescence, untreated OSAS may result in neuro-behavioural and cognitive deficits, systemic inflammation, cardiovascular and metabolic disorders. The French Society of Research and Sleep Medicine organized a meeting on OSAS in adolescents. A multidisciplinary group of specialists (pulmonologists, pediatricians, ENT and maxillo-facial surgeons, dentofacial orthopedists/orthodontists, myofunctional therapists and sleep specialists) exchanged their experience, discussed publications and drew up a consensus document on the diagnosis and polysomnographic criteria for OSAS in adolescents. They proposed a practical diagnostic guideline and follow-up for these adolescents. OUTLOOK AND CONCLUSION: A good knowledge of the particularities of this pathology by the physician will lead to an early diagnosis, propose adapted multifactorial treatments and avoid the deleterious consequences of this pathology at adult age.

[Telemonitoring in continuous positive airway pressure-treated patients with obstructive sleep apnoea syndrome: An algorithm proposal]. / Télésuivi des patients traités par pression positive continue pour un syndrome d'apnées/hypopnées obstructives du sommeil : proposition d'un arbre décisionnel.

Most of the continuous positive airway pressure (CPAP) devices currently in use allow telemonitoring of observance, leaks and the apnoea-hypopnoea index (AHI). La Société française de recherche et de médecine du sommeil (SFRMS) and La Société de pneumologie de langue française (SPLF) workgroup offer to CPAP prescribers and to home care providers a scientific document which has the following purposes: to underline the relevance of the telemonitoring of leaks and the AHI, to define alert thresholds, to describe the principal mechanisms generating excessive leaks and high AHI, and to propose a diagnostic algorithm.

A new model of chronic intermittent hypoxia in humans: effect on ventilation, sleep, and blood pressure.

Obstructive sleep apnea is characterized by repetitive nocturnal upper airway obstructions that are associated with sleep disruption and cyclic intermittent hypoxia (CIH) The cyclic oscillations in O(2) saturation are thought to contribute to cardiovascular and other morbidity, but animal and patient studies of the pathogenic link between CIH and these diseases have been complicated by species differences and by the effects of confounding factors such as obesity, hypertension, and impaired glucose metabolism. To minimize these limitations, we set up a model of nocturnal CIH in healthy humans. We delivered O(2) for 15 s every 2 min during sleep while subjects breathed 13% O(2) in a hypoxic tent to create 30 cycles/h of cyclic desaturation-reoxygenation [saturation of peripheral O(2) (Sp(O(2))) range: 95-85%]. We exposed subjects overnight for 8-9 h/day for 2 wk (10 subjects) and 4 wk (8 subjects). CIH exposure induced respiratory disturbances (central apnea hypopnea index: 3.0 +/- 1.9 to 31.1 +/- 9.6 events/h of sleep at 2 wk). Exposure to CIH for 14 days induced an increase in slopes of hypoxic and hypercapnic ventilatory responses (1.5 +/- 0.6 to 3.1 +/- 1.2 l.min(-1).% drop in Sp(O(2)) and 2.2 +/- 1.0 to 3.3 +/- 0.9 l.min(-1).mmHg CO(2)(-1), respectively), consistent with hypoxic acclimatization. Waking normoxic arterial pressure increased significantly at 2 wk at systolic (114 +/- 2 to 122 +/- 2 mmHg) and for diastolic at 4 wk (71 +/- 1.3 to 74 +/- 1.7 mmHg). We propose this model as a new technique to study the cardiovascular and metabolic consequences of CIH in human volunteers.

Chronic intermittent hypoxia increases infarction in the isolated rat heart.

Coronary heart disease is frequently associated with obstructive sleep apnea syndrome and treating obstructive sleep apnea appears to significantly improve the outcome in coronary heart disease. Thus we have developed a rat model of chronic intermittent hypoxia (IH) to study the influence of this condition on myocardial ischemia-reperfusion tolerance and on functional vascular reactivity. Wistar male rats were divided in three experimental groups (n = 12 each) subjected to chronic IH (IH group), normoxia (N group), or control conditions (control group). IH consisted of repetitive cycles of 1 min (40 s with inspired O(2) fraction 5% followed by 20 s normoxia) and was applied for 8 h during daytime, for 35 days. Normoxic cycles were applied in the same conditions, inspired O(2) fraction remaining constant at 21%. On day 36, mean arterial blood pressure (MABP) was measured before isolated hearts were submitted to an ischemia-reperfusion protocol. The thoracic aorta and left carotid artery were also excised for functional reactivity studies. MABP was not significantly different between the three experimental groups. Infarct sizes (in percent of ventricles) were significantly higher in IH group (46.9 +/- 3.6%) compared with N (26.1 +/- 2.8%) and control (21.7 +/- 2.1%) groups. Vascular smooth muscle function was similar in aorta and carotid arteries from all groups. The endothelium-dependent relaxation in response to acetylcholine was also similar in aorta and carotid arteries from all groups. Chronic IH increased heart sensitivity to infarction, independently of a significant increase in MABP, and did not affect vascular reactivity of aorta and carotid arteries.

Peripheral vascular resistance increases after termination of obstructive apneas.

The mechanisms by which obstructive apneas produce intermittent surges in arterial pressure remain poorly defined. To determine whether termination of obstructive apneas produce peripheral vasoconstriction, we assessed forearm blood flow during and after obstructive events in sleeping patients experiencing spontaneous upper airway obstructions. In all subjects, heart rate was monitored with an electrocardiogram and blood pressure was monitored continuously with digital plethysmography. In 10 patients (protocol 1), we used forearm plethysmography to assess forearm blood flow, from which we calculated forearm vascular resistance by performing venous occlusions during and after obstructive episodes. In an additional four subjects, we used simultaneous Doppler and B-mode images of the brachial artery to measure blood velocity and arterial diameter, from which we calculated brachial flow continuously during spontaneous apneas (protocol 2). In protocol 1, forearm vascular resistance increased 71% after apnea termination (29.3 +/- 15.4 to 49.8 +/- 26.5 resistance units, P < 0.05) with all patients showing an increase in resistance. In protocol 2, brachial resistance increased at apnea termination in all subjects (219.8 +/- 22.2 to 358.3 +/- 46.1 mmHg x l(-1) x min; P = 0.01). We conclude that termination of obstructive apneas is associated with peripheral vasoconstriction.

Cardiovascular responses to nonrespiratory and respiratory arousals in a porcine model.

Spontaneous and provoked nonrespiratory arousals can be accompanied by a patterned hemodynamic response. To investigate whether a patterned response is also elicited by respiratory arousals, we compared nonrespiratory arousals (NRA) to respiratory arousals (RA) induced by airway occlusion during non-rapid eye movement sleep. We monitored mean arterial blood pressure (MAP), heart rate, iliac and renal blood flow, and sleep stage in 7 pigs during natural sleep. Iliac and renal vascular resistance were calculated. Airway occlusions were obtained by manually inflating a chronically implanted tracheal balloon during sleep. The balloon was quickly deflated as soon as electroencephalogram arousal occurred. As previously reported, NRA generally elicited iliac vasodilation, renal vasoconstriction, little change in MAP, and tachycardia. In contrast, RA generally elicited iliac and renal vasoconstriction, an increase in MAP and tachycardia. The frequent occurrence of iliac vasoconstriction and arterial pressure elevation following RA but not NRA suggests that sleep state change alone does not account for the hemodynamic response to airway occlusion during sleep.

Drug-induced arterial pressure elevation is associated with arousal from NREM sleep in normal volunteers.

Abrupt changes in arterial pressure produce arousal in sleeping animals. To determine whether arterial pressure elevations can cause arousal from sleep in humans, we studied five healthy individuals without sleep complaints or cardiac abnormalities. Monitoring included electroencephalogram, electrooculogram, and electromyogram to determine stage sleep; finger cuff to measure arterial pressure; and electrocardiogram to measure heart rate. We administered intravenous bolus doses of either phenylephrine or saline after performing a dose-response curve to establish the amount of phenylephrine that produced a 20-mmHg increase in mean arterial pressure. Ten boluses of phenylephrine and ten boluses of saline were then administered in random order during stable non-rapid-eye-movement sleep. An observer blinded to the order of drug administration identified arousals using a standard definition. Arousals were five times more likely to occur after phenylephrine than after saline (58 vs. 12%; P = 0.0071). Phenylephrine administration produced heart rate slowing, indicative of baroreflex stimulation. We conclude that pharmacologically induced arterial pressure elevation is associated with arousal from sleep in normal volunteers.

Patients with obstructive sleep apnea have an abnormal peripheral vascular response to hypoxia.

Patients with obstructive sleep apnea (OSA) have been reported to have an augmented pressor response to hypoxic rebreathing. To assess the contribution of the peripheral vasculature to this hemodynamic response, we measured heart rate, mean arterial pressure (MAP), and forearm blood flow by venous occlusion plethysmography in 13 patients with OSA and in 6 nonapneic control subjects at arterial oxygen saturations (Sa(O(2))) of 90, 85, and 80% during progressive isocapnic hypoxia. Measurements were also performed during recovery from 5 min of forearm ischemia induced with cuff occlusion. MAP increased similarly in both groups during hypoxia (mean increase at 80% Sa(O(2)): OSA patients, 9 +/- 11 mmHg; controls, 12 +/- 7 mmHg). Forearm vascular resistance, calculated from forearm blood flow and MAP, decreased in controls (mean change -37 +/- 19% at Sa(O(2)) 80%) but not in patients (mean change -4 +/- 16% at 80% Sa(O(2))). Both groups decreased forearm vascular resistance similarly after forearm ischemia (maximum change from baseline -85%). We conclude that OSA patients have an abnormal peripheral vascular response to isocapnic hypoxia.

Cardiovascular morbidity in obstructive sleep apnea.

The repetitive respiratory events that characterize obstructive sleep apnea (OSA) are each followed by abrupt increases in heart rate and in pulmonary and systemic artery pressure and by sudden decreases in right and left ventricular stroke volume. The changes in systemic pressure may be profound, with patients who are normotensive while awake having systolic pressures approaching 300 mm Hg after apnea termination. Because of these dramatic hemodynamic oscillations during sleep, many clinicians and investigators have postulated a connection between sleep-disordered breathing and cardiovascular morbidity and even mortality. This review critically examines the evidence for such a causal relationship. We begin, however, by reviewing the normal hemodynamic changes that occur during sleep. We then describe the acute hemodynamic events associated with OSA. Finally, we summarize the evidence for and against a causal connection between sleep apnea and cardiovascular morbidity.

[Intensive care and respiratory sleep disorders]. / Réanimation et troubles respiratoires du sommeil.

The study of respiratory sleep disorders in intensive care is a developing field. Indeed sleep pathology concerns not only pneumologists and neurophysiologists but also numerous specialties including medicosurgical resuscitation. The advent of "portable" appliances should facilitate access to polysomnography (PSG) for diagnosis of sleep respiratory disorders (RDS) in the intensive care unit. This examination can be appropriate in two separate circumstances. RDS in life-threatening situations (generally respiratory and/or cardiac failure) or when RDS is worsened by the specific conditions of intensive care units: "intensive care-induced RDS". In both cases, easy diagnosis of RDS by PSG allows adjustment of the treatment (corrections of iatrogenic factors, continuous positive airway pressure [CPAP], noninvasive ventilation [NIV], oxygen [O2]. A specific treatment of the well documented RDS is most desirable, as the patients are considered to be at high risk for endotracheal intubation. If diagnosis of RDS is not made during the acute phase, the intensive care physician should be informed of the clinical and paraclinical elements leading to prescription of a delayed polysomnography in order to reduce the risk of further vital distress.

Patterned cardiovascular responses to sleep and nonrespiratory arousals in a porcine model.

Patients with obstructive sleep apnea experience marked cardiovascular changes with apnea termination. Based on this observation, we hypothesized that sudden sleep disruption is accompanied by a specific, patterned hemodynamic response, similar to the cardiovascular defense reaction. To test this hypothesis, we recorded mean arterial blood pressure, heart rate, iliac blood flow and vascular resistance, and renal blood flow and vascular resistance in five pigs instrumented with chronic sleep electrodes. Cardiovascular parameters were recorded during quiet wakefulness, during non-rapid-eye-movement and rapid-eye-movement sleep, and during spontaneous and induced arousals. Iliac vasodilation (iliac vascular resistance decreased by -29.6 +/- 4.1% of baseline) associated with renal vasoconstriction (renal vascular resistance increased by 10.3 +/- 4.0%), tachycardia (heart rate increase: +23.8 +/- 3.1%), and minimal changes in mean arterial blood pressure were the most common pattern of arousal response, but other hemodynamic patterns were observed. Similar findings were obtained in rapid-eye-movement sleep and for acoustic and tactile arousals. In conclusion, spontaneous and induced arousals from sleep may be associated with simultaneous visceral vasoconstriction and hindlimb vasodilation, but the response is variable.

Respiratory function of velopharyngeal constrictor muscles during wakefulness in normal adults.

The levator veli palatini (LVP) and the superior pharyngeal constrictor (SPC) influence velopharyngeal patency and soft palate position, but their behavior during respiration is incompletely characterized. To further clarify their respiratory function, we recorded electromyographic activity (EMG) in the LVP and the SPC in awake normal subjects breathing orally. EMG data were obtained in six subjects for the LVP and in nine subjects for the SPC. EMG activity and timing and ventilation were measured during isocapnic hypoxia and hyperoxic hypercapnia. Phasic EMG activity was inconsistently present during unstimulated oral breathing. Timing of EMG phasic activity was variable for both muscles. Peak LVP activity was mainly or exclusively expiratory in three of six subjects. Peak SPC activity was mainly or exclusively expiratory in five of nine subjects. With chemostimulation, recruitment of phasic activity was observed in the LVP and in four of six subjects and in the SPC in five of nine subjects. Tonic activity increased in four of six subjects for the LVP and in three of nine subjects for the SPC. However, the response was alinear, and intersubject as well as breath-to-breath variability was substantial. In conclusion, LVP and SPC are characterized by the higher inter- and intrasubject variability of EMG activity, timing of activation, and response to chemostimulation.

Relationship between velopharyngeal dimensions and palatal EMG during progressive hypercapnia.

To examine the contribution of specific palatal muscles to velopharyngeal dimensions, we recorded electromyographic (EMG) activity in the levator veli palatini, the tensor veli palatini, and the palatoglossus while examining the velopharynx (VP) with videoendoscopy in eight awake normal adults. Simultaneous display of VP images and airflow provided precise timing of events. Video images and EMG signals were recorded during progressive hypercapnia. Every tenth breath was analyzed. For each selected breath, VP area, anteroposterior and lateral diameters, and EMG activity were determined at five points: beginning, middle, and end of inspiration and middle and end of expiration. VP measurements changed significantly during the respiratory cycle. Although maximum area was measured at end inspiration or middle expiration and minimum area at the beginning or end of the breath, respiratory-related changes in VP measurements and EMG activity were characterized by substantial inter- and intrasubject variability. This variability is similar to velopharyngeal behavior during nonrespiratory tasks and suggests that upper airway patency is determined by multiple factors.

[Hiccups in adults]. / Le hoquet de l'adulte.

Hiccoughs are an involuntary spasmodic and coordinated contractions of the inspiratory muscles associated with a delayed and sudden closure of the glottis which is responsible for the characteristic noise. The pathophysiology of hiccoughs have not been elucidated. There have only been a few observations describing the sequence of inspiratory muscle activation and these suggest that the control of hiccoughs is within the central nervous system. The clinical circumstances associated with acute benign hiccoughs are both numerous and disparate. In these cases, when they stop spontaneously or as a result of simple physical manoeuvres hiccoughs do not require any particular medical attention. Chronic hiccoughs, defined as hiccoughs persisting for more than 24 hours or recurring as repetitive attacks are a rare phenomenon. The causes cover the whole of organic pathology. Systematic protocols of complementary examinations most often enable an underlying organic cause to be found. Amongst these, particular attention should be paid to oesophageal causes by the reason of their being the most frequent. An important place should be reserved for the aetiological treatment as is frequently enables a remission of chronic hiccough.

Pharyngeal narrowing and closing pressures in patients with obstructive sleep apnea.

Based on previous studies, we hypothesized that the pharynx collapses at multiple sites in most patients with obstructive sleep apnea (OSA). The purpose of this study was to document, in a population of apneic subjects, the site(s) of narrowing and closing pressure of the hypotonic pharynx. We endoscopically examined the pharynx in 45 OSA patients during sleep while they received nasal continuous positive airway pressure (CPAP), which produces hypotonia of pharyngeal muscles. Intrapharyngeal images and pressures were obtained at the end of expiration during single-breath tests (SBT). The fractional narrowing (FN) of each pharyngeal segment (nasopharynx, oropharynx, and hypopharynx) was calculated as the relative change in area when nasal airway pressure was reduced from a pressure that held the pharynx fully distended to the pressure at which the airway closed. The frequency distribution of FN for the nasopharynx was skewed toward larger values, and the frequency was relatively evenly distributed for the oropharynx and hypopharynx. A site having FN greater than 0.75 was defined as a site of primary narrowing, and a site showing FN 0.25 to 0.75 was defined as a site of secondary narrowing. The nasopharynx was a site of primary narrowing in 80% of patients, and two or more sites of narrowing were commonly observed (82%). Four categories of combined narrowing were identified: (1) primary narrowing only at the nasopharynx (18%); (2) primary narrowing at the nasopharynx plus other sites of secondary narrowing (40%); (3) primary narrowing at the nasopharynx plus other sites of primary narrowing (22%); and (4) other patterns (20%).(ABSTRACT TRUNCATED AT 250 WORDS)

Static mechanics of the velopharynx of patients with obstructive sleep apnea.

The static mechanics of the hypotonic pharynx were endoscopically evaluated in nine sleeping patients with obstructive sleep apnea, having a primary narrowing only at the velopharynx. The velopharynx closed completely at a mean pressure of 0.18 +/- 1.21 cmH2O, and the mean half-dilation pressure was 1.93 cmH2O above closing pressure. The dependence of area on pressure was distinctly curvilinear, being steep near closing pressure and asymptotically approaching maximum area (mean = 1.32 cm2). The data for each patient were satisfactorily fitted by an exponential function (mean R2 = 0.98), and a single exponential relationship usefully represented the dependence of relative area on pressure above closing pressure for the population (R2 = 0.85). During the test inspiration, flow limitation was consistently observed when mask pressure exceeded closing pressure by 0.5-3.0 cmH2O. In summary, the static mechanics of the hypotonic velopharynx of patients with obstructive sleep apnea can be described by an exponential pressure-area relationship, with a closing pressure near atmospheric pressure and a high compliance in the range of airway pressure 0-3 cmH2O above closing pressure.