Resumption Of Breathing Research Articles

Corticoperipheral neuromuscular disconnection in obstructive sleep apnoea.

The roles of central nervous mechanisms and cortical output in obstructive sleep apnoea remain unclear. We addressed corticomuscular coupling between cortical sensorimotor areas and lower facial motor units as a mechanistic pathway and as a possible surrogate marker of corticoperipheral motor control in obstructive sleep apnoea. In this exploratory cross-sectional retrospective study, we analysed EEG (C3 and C4 leads) and chin EMG from polysomnography recordings in 86 participants (22 females; age range: 26–81 years): 27 with mild (respiratory disturbance index = 5–15 events/h), 21 with moderate (15–30 events/h) and 23 with severe obstructive sleep apnoea (>30 events/h) and 15 control subjects (<5 events/h). By computing C3-/C4-EEG–chin EMG coherence of signal dynamics in time and frequency domains, we investigated corticomuscular coupling between cortical sensorimotor areas and lower facial motor units with increasing obstructive sleep apnoea severity during the entire sleeping time, during different sleep stages and during obstructive respiratory events, including 5 s before (stable breathing) and after events (breathing resumption). In addition, we studied a possible influence of body mass index and autonomic nervous system activation. We found that both average and respiratory event-specific corticomuscular coupling between cortical sensorimotor areas and lower facial motor units weakened significantly with increasing obstructive sleep apnoea severity, was strongest during N3 and weakened in N1, N2 and rapid eye movement stages (in decreasing order). Coupling increases significantly during the obstructive respiratory events compared with coupling just before and following them. Results were independent of body mass index or autonomic nervous system activation. We conclude that obstructive respiratory events in obstructive sleep apnoea are very strongly associated both quantitatively and temporally with the degree of disconnection within the cortical sensorimotor areas—lower facial motor units pathway. This quite coordinated activity pattern suggests a cortical sensorimotor area-driven obstructive respiratory event pattern generator and a central motor output disorder in obstructive sleep apnoea.

The Effect of Chin-Down Position and Bolus Volume on Swallow-Induced Respiratory Measures in Young Healthy Adults

Though head positioning strategies are widely used in the rehabilitation of swallowing dysfunction, little is yet known about its effect on the respiratory-swallow interaction. We hypothesised that a chin-down positioning would alter the respiratory behaviour in healthy young individuals. In a within-group study, we compared the characteristics of nasal airflow and its coordination with swallow events before, after, and during the swallow of liquid in a group of 30 young healthy individuals. The measures were obtained with simultaneous recording of surface electromyography, nasal airflow, and swallow sound recording during spontaneous drinking of 5, 15, and 20 ml water. Duration of swallowing apnoea (SAD) and the slope (Spre & Spost), duration (Dpre & Dpost), and direction (Expiration/Inspiration) of respiratory phases surrounding the apnoea were obtained. The statistical comparisons revealed that chin-down position significantly prolonged breathing arrest (SAD) and pharyngeal transit time (event interval) during swallow. The Dpost of large volume swallows were shorter indicating a quick resumption of breathing, indicating high post-swallow respiratory demand. The other statistically significant differences in various event intervals suggested the influence of chin-down position and bolus volume on the oral and pharyngeal transit time. Also, there was an increase in the incidence of inspiratory swallows in the chin-down position with large bolus volumes. We conclude that the chin-down position can provide longer airway decoupling but may increase the respiratory demand during swallows. Use of smaller bolus volumes should be recommended for chin-down swallows in persons with respiratory distress and dysphagia.

Physiological instability after respiratory pauses in preterm infants.

The factors influencing the severity of apnea-related hypoxemia and bradycardia are incompletely characterized, especially in infants receiving noninvasive respiratory support. To identify the frequency and predictors of physiological instability (hypoxemia-oxygen saturation (SpO2 ) <80%, or bradycardia-heart rate (HR) < 100 bpm) following respiratory pauses in infants receiving noninvasive respiratory support. Respiratory pause duration, derived from capsule pneumography, was measured in 30 preterm infants of gestation 30 (24-32) weeks [median (interquartile range)] receiving noninvasive respiratory support and supplemental oxygen. For identified pauses of 5 to 29 seconds duration, we measured the magnitude and duration of SpO2 and HR reductions over a period starting at the pause onset and ending 60 seconds after resumption of breathing. Temporally clustered pauses (<60 seconds separation) were analyzed separately. The relative contribution of respiratory pauses to overall physiological instability was determined, and predictors of instability were sought in regression analysis, including demographic, clinical and situational variables as inputs. In total, 17 105 isolated and 9180 clustered pauses were identified. Hypoxemia and bradycardia were more likely after longer duration and temporally-clustered pauses. However, the majority of such episodes occurred after 5 to 9 second pauses given their numerical preponderance, and short-lived pauses made a substantial contribution to physiological instability overall. Birth gestation, hemoglobin concentration, form of respiratory support, caffeine treatment, respiratory pause duration and temporal clustering were identified as predictors of instability. Brief respiratory pauses, especially when clustered, contribute substantially to hypoxemia and bradycardia in preterm infants.

EFFECT OF BETA BLOCKERS ON NOCTURNAL ARRHYTHMIAS AND HEART RATE VARIABILITY IN OBSTRUCTIVE SLEEP APNOEA PATIENTS

Objective: To explore the effects of BB on nocturnal peri-apnoeic heart rate variability (HRV) and on arrhythmias in OSA patients. Design and method: Arrhythmias and increased cardiovascular V are highly prevalent in patients with obstructive sleep apneas (OSA), possibly resulting in fatal events, as showed by the significant increase of sudden cardiac death and arrhythmias during sleep in OSA patients. Data concerning drug effects on this phenomenon are scarce and the use of beta blockers (BB) has been limited by the concern that they might lead to bradyarrhythmias. However, recent evidence suggests that BB mostly reduce rhythm accelerations with trivial influence on decelerations. We enrolled 166 OSA patients (78 BB-treated and 88 BB-naïve), who performed cardiorespiratory polysomnography (PSG) between 2013 and 2015. Patients on antiarrhythmic therapy were excluded. We analysed PSG-derived ECG traces for the assessment of arrhythmias. Moreover, through an ad hoc developed software, we performed a specific analysis of HRV associated with apnoeic events. We considered HR decelerations occurring during the apnoeic phase and accelerations during the post-apnoeic phase (the first five seconds after the resumption of breathing). Statistical analysis was performed with Mann-Whitney U test. Results: We did not find any difference between BB-treated and BB-naïve groups concerning prevalence of nocturnal arrhythmias. HRV analysis showed a reduction of HR accelerations, expressed as RR length, during post-apnoeic phase in BB group (940.7 ± 121.4msec BB-treated vs 897.8 ± 122.5msec BB-naïve; P = 0.040). Moreover, BB-treated patients showed a smaller delta between HR decelerations/accelerations and mean HR during apnoeic phase (58.5 ± 28.5 vs 74.6 ± 40.2msec; P = 0.010 and75.0 ± 42.4 vs 96.7 ± 55.5msec; P = 0.018, respectively). Finally, the delta between HR accelerations and decelerations was smaller in BB-treated group (133.5 ± 63.8 vs 171.3 ± 87.7msec; P = 0.010). Conclusions: BB therapy does not worsen apnoea-induced HR decelerations nor increase the risk of bradyarrhythmias, while reducing the frequency and magnitude of apnoea-induced HR acceleration. Therefore, our study suggests that BB are safe and possibly advantageous in OSA patients, although further studies are needed to establish if in the long term they may have a role in reducing fatal events.

Inhibition of augmented muscle vasoconstrictor drive following asphyxic apnoea in awake human subjects is not affected by relief of chemical drive

Progressive asphyxia, produced by a prolonged voluntary breath hold (end-expiratory apnoea), evokes large bursts of muscle sympathetic nerve activity (MSNA). These bursts increase in amplitude until the asphyxic break point is reached, at which point the bursts are inhibited. We tested the hypothesis that lung inflation, rather than relief from hypoxia and hypercapnia, is responsible for the inhibition of MSNA. Multiunit MSNA was recorded from motor fascicles of the common peroneal nerve in 11 subjects. Following a period of quiet breathing, subjects were instructed to behave as follows: (i) to hold their breath in expiration for as long as they could (mean duration 32.3 ± 1.9 s); (ii) to take a single breath of room air, 100% N(2) or 10% CO(2) + 90% N(2) at the asphyxic break point; (iii) to exhale and continue the apnoea until the next break point; and then (iv) to resume breathing. All subjects reported relief during inhalation of any gas, and could continue holding their breath for a further 30.7 ± 2.8 s with room air, 18.6 ± 1.7 s with N(2) and 11.8 ± 1.8 s with 10% CO(2) + 90% N(2). Despite the exaggerated chemoreceptor drive in the latter two conditions (hence the significantly shorter latencies to the subsequent asphyxic break point), the inhibition still occurred; moreover, there was no significant difference in duration of the inhibition of MSNA following the single breath of room air (7.6 ± 0.7 s), N(2) (6.2 ± 0.6 s) or 10% CO(2) + 90% N(2) (5.5 ± 0.4 s). Following the resumption of breathing, however, the duration of MSNA inhibition (11.0 ± 1.0 s) was significantly longer than that following a single breath. To investigate the involvement of chemoreceptors in the respiratory modulation of MSNA further, the same gases were used during an inspiratory-capacity apnoea, which causes a brief inhibition of MSNA during the inflation phase and a sustained increase during the hold phase. The duration of the apnoea was shortest after a breath of 10% O(2) + 90% N(2), but the latency until the bursts resumed after the inspiratory breath hold were similar for all gases, which suggests that there is no chemoreceptor involvement during the sympathetic silence seen during the inflation phase of inspiratory-capacity apnoeas. We conclude that neither peripheral nor central chemoreceptors are responsible for the inhibition of muscle vasoconstrictor drive following an end-expiratory apnoea or an end-inspiratory apnoea. Rather, we suggest that the inhibition is evoked by stretch receptors in the lungs and/or chest wall, which may also contribute to the longer inhibition associated with the hyperventilation following the subsequent resumption of rhythmic breathing.

Loss of brainstem serotonergic neurons impairs autoresuscitation in neonate rats: is this relevant to the sudden infant death syndrome?

Loss of brainstem serotonergic neurons impairs autoresuscitation in neonate rats: is this relevant to the sudden infant death syndrome?

Cardiovascular time courses during prolonged immersed static apnoea

To define the dynamics of cardiovascular adjustments to apnoea during immersion, beat-to-beat heart rate (HR) and systolic (SBP) and diastolic (DBP) blood pressures were recorded in six divers during and after prolonged apnoeas while resting fully immersed in 27 degrees C water. Apnoeas lasted 215 +/- 35 s. Compared to control values, HR decreased by 20 beats min(-1) and SBP and DBP increased by 23 and 17 mmHg, respectively, in the initial 20 +/- 3 s (phase I). Both HR and BP remained stable during the following 92 +/- 15 s (phase II). Subsequently, during the final 103 +/- 29 s, SBP and DBP increased linearly to values about 60% higher than control, whereas HR remained unchanged (phase III). Cardiac output (Q') decreased by 35% in phase I and did not further change in phases II and III. Compared to control, total peripheral resistances were twice and three times higher than control, respectively, at the end of phases I and III. After resumption of breathing, HR and BP returned to control values in 5 and 30 s, respectively. The time courses of cardiovascular adjustments to immersed breath-holding indicated that cardiac response took place only at the beginning of apnoea. In contrast, vascular responses showed two distinct adjustments. This pattern suggests that the chronotropic control via the baroreflex is modified during apnoea. These cardiovascular changes during immersed static apnoea are in agreement with those already reported for static dry apnoeas.

Impact of Sleeping Angle on the Upper Airway and Pathogenesis of Cheyne Stokes Respiration

Impact of Sleeping Angle on the Upper Airway and Pathogenesis of Cheyne Stokes Respiration

Role of sensory input from the lungs in control of muscle sympathetic nerve activity during and after apnea in humans.

We reasoned that, if the lung inflation reflex contributes importantly to apnea-induced sympathetic activation, such activation would be attenuated in bilateral lung transplant recipients (LTX). We measured muscle sympathetic nerve activity (MSNA; intraneural electrodes), heart rate, mean arterial pressure, tidal volume, end-tidal Pco(2), and arterial oxygen saturation in seven LTX and seven healthy control subjects (Con) before, during, and after 20-s end-expiratory breath holds. Our evidence for denervation in LTX was 1) greatly attenuated respiratory sinus arrhythmia and 2) absence of cough reflex below the level of the carina. During apnea, the temporal pattern and the peak increase in MSNA were virtually identical in LTX and Con (347 +/- 99 and 359 +/- 46% of baseline, respectively; P > 0.05). In contrast, the amount of MSNA present in the first 5 s after resumption of breathing was greater in LTX vs. Con (101 +/- 4 vs. 38 +/- 7% of baseline, respectively; P < 0.05). There were no between-group differences in apnea-induced hypoxemia or hypercapnia, hemodynamic, or ventilatory responses. Thus cessation of the rhythmic sympathoinhibitory feedback that normally accompanies eupneic breathing does not contribute importantly to sympathetic excitation during apnea. In contrast, vagal afferent input elicited by hyperventilation-induced lung stretch plays an important role in the profound, rapid sympathetic inhibition that occurs after resumption of breathing after apnea.

Topographical distribution of pulmonary perfusion and ventilation, assessed by PET in supine and prone humans.

Using positron emission tomography (PET) and intravenously injected (13)N(2), we assessed the topographical distribution of pulmonary perfusion (Q) and ventilation (V) in six healthy, spontaneously breathing subjects in the supine and prone position. In this technique, the intrapulmonary distribution of (13)N(2), measured during a short apnea, is proportional to regional Q. After resumption of breathing, regional specific alveolar V (sVA, ventilation per unit of alveolar gas volume) can be calculated from the tracer washout rate. The PET scanner imaged 15 contiguous, 6-mm-thick, slices of lung. Vertical gradients of Q and sVA were computed by linear regression, and spatial heterogeneity was assessed from the squared coefficient of variation (CV(2)). Both CV and CV were corrected for the estimated contribution of random imaging noise. We found that 1) both Q and V had vertical gradients favoring dependent lung regions, 2) vertical gradients were similar in the supine and prone position and explained, on average, 24% of Q heterogeneity and 8% of V heterogeneity, 3) CV was similar in the supine and prone position, and 4) CV was lower in the prone position. We conclude that, in recumbent, spontaneously breathing humans, 1) vertical gradients favoring dependent lung regions explain a significant fraction of heterogeneity, especially of Q, and 2) although Q does not seem to be systematically more homogeneous in the prone position, differences in individual behaviors may make the prone position advantageous, in terms of V-to-Q matching, in selected subjects.

Hypoxia augments apnea-induced peripheral vasoconstriction in humans.

Obstructive apnea and voluntary breath holding are associated with transient increases in muscle sympathetic nerve activity (MSNA) and arterial pressure. The contribution of changes in blood flow relative to the contribution of changes in vascular resistance to the apnea-induced transient rise in arterial pressure is unclear. We measured heart rate, mean arterial blood pressure (MAP), MSNA (peroneal microneurography), and femoral artery blood velocity (V(FA), Doppler) in humans during voluntary end-expiratory apnea while they were exposed to room air, hypoxia (10.5% inspiratory fraction of O2), and hyperoxia (100% inspiratory fraction of O2). Changes from baseline of leg blood flow (Q) and vascular resistance (R) were estimated from the following relationships: Q proportional to V(FA), corrected for the heart rate, and R proportional to MAP/Q. During apnea, MSNA rose; this rise in MSNA was followed by a rise in MAP, which peaked a few seconds after resumption of breathing. Responses of MSNA and MAP to apnea were greatest during hypoxia and smallest during hyperoxia (P < 0.05 for both compared with room air breathing). Similarly, apnea was associated with a decrease in Q and an increase in R. The decrease in Q was greatest during hypoxia and smallest during hyperoxia (-25 +/- 3 vs. -6 +/- 4%, P < 0.05), and the increase in R was the greatest during hypoxia and the least during hyperoxia (60 +/- 8 vs. 21 +/- 6%, P < 0.05). Thus voluntary apnea is associated with vasoconstriction, which is in part mediated by the sympathetic nervous system. Because apnea-induced vasoconstriction is most intense during hypoxia and attenuated during hyperoxia, it appears to depend at least in part on stimulation of arterial chemoreceptors.

Heart failure and central respiratory dysregulation. Cheyne-Stokes respiration during sleep in advanced left heart failure

Central sleep apnoea, especially Cheyne-Stokes respiration, is found in 45 to 66% of patients with congestive heart failure (CHF) in functional classes NYHA II to IV. Cheyne-Stokes breathing cycles are characterised by central apnoeas, followed by a crescendo--like increase of tidal volume into hyperventilation and a subsequent decline of tidal volume, ending in another central apnoea. Cheyne-Stokes respiration has been shown to be a poor prognostic factor for patients with CHF. Apnoeas and hypopnoeas cause marked oxygen desaturation and rises of carbon dioxide concentrations in the blood. The resumption of breathing is frequently associated with arousals, which might cause daytime symptoms like fatigue and sleepiness as well as persistent activation of the sympathetic nervous system. Elevated concentrations of catecholamines increase cardiac work, adversely affecting cardiac function. Serum catecholamines are known to augment the chemoreceptor susceptibility for carbon dioxide. This might be one reason for the permanent mild hyperventilation found in these patients during wakefulness. Increased chemoreceptor responsiveness destabilises the feedback control of breathing, and hyperventilation below the apnoeic threshold grows more likely. Other contributing factors for the development of Cheyne-Stokes respiration include alterations in the control of breathing during sleep and the increased circulation time between the lung and chemoreceptors in CHF patients. The feedback regulation of breathing might be less dampened since carbon dioxide levels are reduced in these patients. Treatment includes nCPAP, but in many cases this is poorly tolerated in patients with central sleep apnoea. Future approaches to Cheyne-Stokes respiration might focus on improving ventilatory pattern and pharmacological manipulation of carbon dioxide receptor susceptibility.

OBSTRUCTIVE SLEEP APNOEA CAUSES TRANSIENT AND SUSTAINED SYSTEMIC HYPERTENSION

SUMMARYApnoea with associated fall in arterial oxygen tension results in increased blood pressure and a striking surge in sympathetic activity, which can be measured as high catecholamine levels or increase in muscle sympathetic nerve activity. Following the termination of apnoea with resumption of breathing, sympathetic nerve activity decreases and blood pressure returns to lower values. Sympathetic mediated alternations in peripheral vascular resistance best explain these findings. Hypertension during wakefulness in untreated patients with apnoea is also associated with high sympathetic nervous system activity. Nasal continuous positive airway pressure (CPAP) has been shown to lower blood pressure in some hypertensive obstructive sleep apnoea (OSA) patients. Recently, previously untreated OSA patients exhibiting awake sympathetic hyperexcitation demonstrated striking attentuation of the response following initiation of effective CRAP therapy. Accordingly, the common problem of systemic hypertension found in untreated OSA appears to be mediated by sympathetic excitation and responds to effective CRAP therapy.

Hippocampal activity during transient respiratory events in the freely behaving cat.

We measured dorsal hippocampal activity accompanying sighs and apnea using reflectance imaging and electrophysiologic measures in freely behaving cats. Reflected 660-nm light from a 1-mm2 area of CA1 was captured during sighs and apnea at 25 Hz through a coherent image conduit coupled to a charge coupled device camera. Sighs and apnea frequently coincided with state transitions. Thus, state transitions without apnea or sighs were separately assessed to control for state-related activity changes. All dorsal hippocampal sites showed discrete regions of activation and inactivation during transient respiratory events. Imaged hippocampal activity increased 1-3 s before the enhanced inspiratory effort associated with sighs, and before resumption of breathing after apnea. State transitions lacking sighs and apnea did not elicit analogous optical activity patterns. The suprasylvian cortex, a control for site, showed no significant overall reflectance changes during phasic respiratory events, and no discrete regions of activation or inactivation. Spectral estimates of hippocampal electroencephalographic activity from 0-12 Hz showed significantly increased power at 3-4 Hz rhythmical slow activity before sighs and apnea, and increased 5-6 Hz rhythmical slow activity power during apnea, before resumption of breathing. Imaged activity and broadband hippocampal electroencephalogram power decreased during sighs. We propose that increased hippocampal activity before sigh onset and apnea termination indicates a role for the hippocampus in initiating inspiratory effort during transient respiratory events.

Non-invasive measurement of haemodynamics during sleep apnoea.

Sleep apnoeas are accompanied by large variations in heart rate (HR) and blood pressure (BP). This nocturnal variability in BP may be involved in the increased cardiovascular morbidity of these patients. Due to the complex interaction between asphyxia, intrathoracic pressure, cardiac function and autonomic activation, the exact haemodynamic mechanisms are unclear. To evaluate the components of the BP surges at resumption of breathing (RB) a non-invasive beat-to-beat measurement was taken of cardiac output (CO) by the pulse contour analysis of the Finapres signal. Six male normotensive patients, free of medication (37-60 y, BMI 26.5-43.0 kg m-2) were studied during polysomnography (apnoea index: 22-69 h-1). Systolic blood pressure rose from 126.5 +/- 1.3 mmHg at beginning apnoea (P1) to 140.4 +/- 1.3 at RB (P < 0.01, ANOVA). During sleep Stages 2 and 3, stroke volume decreased during RB to 96% of P1 value (NS). Due to an opposite change in HR, CO tended to rise at RB to 106% of P1. Computed total peripheral resistance rose during RB to 105% of P1 value (P < 0.011. Therefore, it is concluded that the surge in BP at RB after apnoea is due to concomitant increases in CO and in TPR. Both rises are presumably a consequence of sympathetic nervous activation by the arterial chemoreceptors.

Arterial blood pressure responses to graded transient arousal from sleep in normal humans.

During obstructive sleep apnea, transient arousal at the resumption of breathing is coincident with a substantial rise in blood pressure. To assess the hemodynamic effect of arousal alone, 149 transient stimuli were administered to five normal subjects. Two electroencephalograms (EEG), an electrooculogram, a submental electromyogram (EMG), and beat-to-beat blood pressure (Finapres, Ohmeda) were recorded in all subjects. Stimulus length was varied to produce a range of cortical EEG arousals that were graded as follows: 0, no increase in high-frequency EEG or EMG; 1, increased high-frequency EEG and/or EMG for < 10 s; 2, increased high-frequency EEG and/or EMG for > 10 s. Overall, compared with control values, average systolic pressure rose [nonrapid-eye-movement (NREM) sleep 10.0 +/- 7.69 (SD) mmHg; rapid-eye-movement (REM) sleep 6.0 +/- 6.73 mmHg] and average diastolic pressure rose (NREM sleep 6.1 +/- 4.43 mmHg; REM sleep 3.7 +/- 3.02 mmHg) over the 10 s following the stimulus (NREM sleep, P < 0.0001; REM sleep, P < 0.002). During NREM sleep, there was a trend toward larger blood pressure rises at larger grades of arousal (systolic: r = 0.22, 95% confidence interval 0.02-0.40; diastolic: r = 0.48, 95% confidence interval 0.31-0.62). The average blood pressure rise in response to the grade 2 arousals was approximately 75% of that during obstructive sleep apnea. Arousal stimuli that did not cause EEG arousal still produced a blood pressure rise (mean systolic rise 8.6 +/- 7.0 mmHg, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial chemoreceptor influences on the laryngeal chemoreflex.

Prolonged apnea and cardiovascular changes have been elicited in infant animals by the application of water to the laryngeal mucosa. Previous reports have produced conflicting evidence in regard to the possible role of arterial chemoreceptors in modulating this reflex. The present study was designed to determine the effect of carotid body stimulation or suppression on the duration of apnea and severity of cardiovascular changes in response to water in the larynx of piglets. The role of swallowing in terminating the apnea was also investigated. Hypoxia and isoproterenol, both carotid body stimuli, caused decreased apnea duration. Hyperoxia was associated with prolonged apnea duration; however, dopamine, which inhibits carotid body chemoreceptors, produced no significant change. Hypotension and bradycardia were only observed after prolonged apnea or chemoreceptor stimulation, supporting the concept that the cardiovascular component of the laryngeal chemoreflex is a result of changes in blood gas concentration rather than a direct response to laryngeal chemostimulation. The interval between water application and initiation of swallowing was not significantly affected by hypoxia or carotid body stimulation and swallowing did not always occur before resumption of breathing.

The influence of induced hypocapnia and sleep on the endogenous respiratory rhythm in humans.

1. Ventilation has been studied during hypocapnia produced by passive mechanical ventilation in ten normal human subjects. 2. During wakefulness, disconnection of the ventilator led to inconsistent apnoea of only brief duration. During sleep, at a similar degree of hypocapnia, disconnection of the ventilator led more consistently to apnoea which was also of much longer duration; the deeper the sleep stage, the longer the apnoea. 3. The resumption of breathing during sleep could precede or follow arousal or be unaccompanied by arousal; in the absence of prior arousal, the evidence suggests that a starting end-tidal CO2 pressure (PET, CO2) less than 41 mmHg could result in an apnoea during sleep stages I and II. 4. Subjects did not report any common sensation which led them to breathe following an apnoea whilst awake. 5. Prior hyperoxia in one subject prolonged the apnoea duration in both slow-wave sleep and rapid eye movement sleep. 6. The results are interpreted as showing that even during light sleep, the maintenance of the respiratory rhythm is critically dependent on the arterial CO2 and O2 tensions. During wakefulness, other behavioural drives, which may not reach consciousness, supervene.

Modifications of Cyclic Alternating Pattern in Sleep Apnea Syndrome

Within non-rapid eye movement sleep, two complementary modalities of arousal organization may be identified: (1) the cyclic alternating pattern (CAP), correlated with successive upward (phase A) and downward (phase B) fluctuations of arousal and arousal-related vegetative functions, and (2) non-CAP, corresponding to a relative stability of arousal and vegetative activities. In a 62-year-old overweight and heavily snoring man, complaining of excessive daytime sleepiness, three consecutive polysomnograms displayed a highly frequent occurrence of nocturnal apneas (apnea index: 15), mostly obstructive and mixed, limited to non-rapid eye movement sleep stages 1 and 2. The apneic episodes, that never occurred during non-CAP, exclusively appeared during the inhibitory phase B of CAP, whereas the following breathing resumption was mainly induced by an activating phase A pattern. The crucial effect of arousal instability on respiratory control is emphasized.

Transmural Pressure Measurements: Importance in the Assessment of Pulmonary Hypertension in Obstructive Sleep Apneas

Seven patients with OSAS were studied during nocturnal sleep in order to assess the trend of PAP throughout apneas and to identify factors possibly associated with such a trend. All patients underwent a polysomnography including the monitoring of PAP and esophageal pressure. While intravascular PAP decreased during apneas and increased at the resumption of breathing, transmural PAP values (ie, corrected for intrathoracic pressure swings) showed a trend toward a progressive increase throughout apneas and toward a decrease once ventilation had been resumed. The measurement of transmural values allowed a reliable assessment of PAP changes occurring during apneas, and different degrees of such changes shown by different patients may be related to a host of factors relevant to wakefulness and sleep, including individual responsivity to hypoxic stimulus.