An Obstructive Sleep Apnea - A Novel Public Health Threat.

In patients with obstructive sleep apnea (OSA) during obstructive events, episodes of hypoxia and hypercapnia may modulate the autonomic nervous system (ANS) by increasing sympathetic tone and irritability, which contributes to sympathovagal imbalance and ultimately dysautonomia. Because OSA can alter ANS function through biochemical changes, we can assume that heart rate variability (HRV) will be altered in patients with OSA. Most studies show that in both the time and frequency domains, patients with OSA have higher sympathetic components and lower parasympathetic dominance than healthy controls. These results confirm autonomic dysfunction in these patients, but also provide new therapeutic directions. Respiratory methods that modulate ANS, e.g., cardiorespiratory biofeedback, could be beneficial for these patients. Heart rate variability assessment can be used as a tool to evaluate the effectiveness of OSA treatment due to its association with autonomic impairment.

Minute ventilation stabilization during all pressure-control / support mechanical ventilation modes.

The main goal of our prospective randomized study was comparing compare the effectiveness of ventilation control method "Automatic proportional minute ventilation (APMV) "versus manually set pressure control ventilation modes in relationship to lung mechanics and gas exchange. 80 patients undergoing coronary artery bypass grafting (CABG) were randomized into 2 groups. 40 patients in the first group No.1 (APMV group) were ventilated with pressure control (PCV) or pressure support ventilation (PSV) mode with APMV control. The other 40 patients (control group No.2) were ventilated with synchronized intermittent mandatory ventilation (SIMV-p) or pressure control modes (PCV) without APMV. Ventilation control with APMV was able to maintain minute ventilation more precisely in comparison with manual control (p<0.01), similarly deviations of ETCO(2) were significantly lower (p<0.01). The number of manual corrections of ventilation settings was significantly lower when APMV was used (p<0.01). The differences in lung mechanics and hemodynamics were not statistically significant. Ventilation using APMV is more precise in maintaining minute ventilation and gas exchange compared with manual settings. It required less staff intervention, while respiratory system mechanics and hemodynamics are comparable. APMV showed as effective and safe method applicable on top of all pressure control ventilation modes.

Strong coincidence between slow wave sleep and low AHI is explainable by the high instability of slow wave sleep to obstructive apnea exposure.

It is well known that in patients with obstructive sleep apnea syndrome (OSAS) the apnea-hypopnea index (AHI) is significantly decreased during slow wave sleep (SWS). It used to be explained by the ability of SWS to stabilize the upper airways against collapse. Another explanation, which is the focus of the current study, is that it is just a result of high instability of SWS to obstructive apnea exposure, i.e. high susceptibility of SWS to transition into lighter sleep stages during exposure to obstructive apneas. A retrospective chart review was performed on 560 males who underwent an overnight polysomnography. Two hundred and eighty-seven patients were eligible for the study. They were divided into 3 groups according to different AHI level. All three groups had a higher SWS occurrence in the lateral position than in the supine position. A special fourth group of patients was created with severe OSAS in the supine position but with very mild OSAS in the lateral position. This group had, in the lateral position, (A) higher AHI in NREM sleep (4.1+/-3.1/h vs. 0.7+/-1.2/h, p<0.001) as well as (B) higher SWS occurrence (27.7+/-15.0 % vs. 21.4+/-16.2 % of NREM sleep, p<0.05), than the group with the lowest AHI in the study, i.e. AHI<5/h in NREM sleep. These data suggest that strong coincidence between SWS and low AHI is the result of the high instability of SWS to obstructive apnea exposure. The data also support the presence of SWS-rebound in OSAS patients in the lateral body position.

Relationship between dynamic expiratory time constant tau(edyn) and parameters of breathing cycle in pressure support ventilation mode.

Study of the relationship between ventilation parameters: monitored expiratory time constant - tau(edyn) and breathing - trigger frequency (f(trig)) and time of breathing cycle (T(cy)) are main goals of this article. Parameters were analyzed during last 4+/-2 h before weaning from ventilation in 66 patients ventilated in pressure support mode (PSV). We have found out, that there exist mathematical relationships, observed during adequate gas exchange, yet not described. Monitored parameters are represented by tau(edyn), f(trig) and T(cy). The analysis showed close negative correlation between T(cy) and f(trig) (R(2)=0.903). This implies that each increasing of tau(edyn) causes decreasing of f(trig) and vice versa. The calculation of regression equation between tau(edyn) and T(cy) outlined that T(cy) = 5.2625 * tau(edyn) + 0.1242 (R(2)=0.85). Regulation of respiratory cycles by the respiratory center in the brain is probably based on evaluation of tau(edyn) as the tau(edyn) probably represents a regulatory element and T(cy) regulated element. It can be assumed, that respiratory center can optimize the work of breathing in order to minimize energy in system patient + ventilator. The unique relationship, described above could be useful in clinical practice for development of new ventilation modes.

Is ionized oxygen negatively or positively charged more effective for carboxyhemoglobin reduction compare to medical oxygen at atmospheric pressure?

Carbon monoxide (CO) reversibly binds to hemoglobin forming carboxyhemoglobin (COHb). CO competes with O(2) for binding place in hemoglobin leading to tissue hypoxia. Already 30 % saturation of COHb can be deadly. Medical oxygen at atmospheric pressure as a therapy is not enough effective. Therefore hyperbaric oxygen O(2) inhalation is recommended. There was a question if partially ionized oxygen can be a better treatment at atmospheric pressure. In present study we evaluated effect of partially ionized oxygen produced by device Oxygen Ion 3000 by Dr. Engler in elimination of COHb in vitro experiments and in smokers. Diluted blood with different content of CO was purged with 5 l/min of either medicinal oxygen O(2), negatively ionized O(2) or positively ionized O(2) for 15 min, then the COHb content was checked. In vivo study, 15 smokers inhaled of either medicinal oxygen O(2) or negatively ionized O(2), than we compared CO levels in expired air before and after inhalation. In both studies we found the highest elimination of CO when we used negatively ionized O(2). These results confirmed the benefit of short inhalation of negatively ionized O(2), in frame of Ionized Oxygen Therapy (I O(2)Th/Engler) which could be used in smokers for decreasing of COHb in blood.

Does obstructive sleep apnea worsen during REM sleep?

Although it is thought that obstructive sleep apnea (OSA) is worse during rapid eye movement (REM) sleep than in non-REM (NREM) sleep there are some uncertainties, especially about apnoe-hypopnoe-index (AHI). Several studies found no significant difference in AHI between both sleep stages. However, REM sleep is associated more with side sleeping compared to NREM sleep, which suggests that body position is a possible confounding factor. The main purpose of this study was to compare the AHI in REM and NREM sleep in both supine and lateral body position. A retrospective study was performed on 422 consecutive patients who underwent an overnight polysomnography. Women had higher AHI in REM sleep than NREM sleep in both supine (46.05+/-26.26 vs. 23.91+/-30.96, P<0.01) and lateral (18.16+/-27.68 vs. 11.30+/-21.09, P<0.01) body position. Men had higher AHI in REM sleep than NREM sleep in lateral body position (28.94+/-28.44 vs. 23.58+/-27.31, P<0.01), however, they did not reach statistical significance in supine position (49.12+/-32.03 in REM sleep vs. 45.78+/-34.02 in NREM sleep, P=0.50). In conclusion, our data suggest that REM sleep is a contributing factor for OSA in women as well as in men, at least in lateral position.

Severity of nocturnal cardiac arrhythmias correlates with intensity of sleep apnea in men.

Various cardiac arrhythmias frequently occur in patients with sleep apnea, but complex analysis of the relationship between their severity and the probable arrhythmogenic risk factors is conflicting. The question is what cardiovascular risk factors and how strongly they are associated with the severity of cardiac arrhythmias in sleep apnea. Adult males (33 with and 16 without sleep apnea), matched for cardiovascular co-morbidity were studied by polysomnography with simultaneous ECG monitoring. Arrhythmia severity was evaluated for each subject by a special 7-degree scoring system. Laboratory, clinical, echocardiographic, carotid ultrasonographic, ambulatory blood pressure, and baroreflex sensitivity values were also assessed. Moderate sleep apnea patients had benign, but more exaggerated cardiac arrhythmias than control subjects (2.53 ± 2.49 vs. 1.13 ± 1.64 degrees of cumulative severity, p < 0.05). We confirmed strong correlations between the arrhythmia severity and known arrhythmogenic risk factors (left ventricular ejection fraction and dimensions, right ventricular diameter, baroreflex sensitivity, carotid intima-media thickness, age, previous myocardial infarction, and also apnea-hypopnea index). In multivariate modelling only the apnea-hypopnea index indicating the sleep apnea intensity remained highly significantly correlated with the cumulative arrhythmia severity (beta = 0.548, p < 0.005). In conclusion, sleep apnea modifying cardiovascular risk factors and structures or functions provoked various nocturnal arrhythmias. The proposed scoring system allowed a complex analysis of the contribution of various triggers to arrhythmogenesis and confirmed the apnea-hypopnea index as an independent risk for nocturnal cardiac arrhythmia severity in sleep apnea.

Heart rate variability in hypertension caused by sleep disordered breathing and its modification by CPAP.

OBJECTIVES: 1) To analyze heart rate variability (HRV) changes, reflecting the sympathovagal balance with secondary hypertension caused by sleep disordered breathing (SDB), compared to healthy controls and essential hypertension without SDB; 2) to compare HRV changes between various degrees of SDB severity; and 3) to test the modification of HRV indices by continuous positive airway pressure (CPAP) in SDB patients. BACKGROUND: Differentiation of secondary hypertension caused by SDB from essential hypertension and healthy controls by ambulatory blood pressure measurement (ABPM) and its modification by CPAP, requires an analysis of HRV changes, as frequently used for the prediction of cardiovascular risk. METHODS: HRV changes were analyzed in 48 adults divided into six groups according to the apnoea/hypopnoea index (AHI), i.e. three groups with various degrees of SDB, a group with severe SDB after CPAP application, a group with essential hypertension without SDB, and a group of healthy controls. Night-time and daytime values of low frequency (LF) and high frequency (HF) bands and the LF/HF ratio were compared in the six groups. RESULTS: The night-time values of LF bands were higher in severe than in moderate and mild degrees of SDB, and the correlation of LF/HF ratio with AHI (r = 0.3511) suggests the gradual increase of sympathetic predominance with the severity of SDB. The high sympathetic activity substantially decreased after application of CPAP in severe SDB. CONCLUSION: The increased nocturnal values of the LF band and the LF/HF ratio, caused by frequent apnoea/ hypopnoea episodes, support the usefulness of HRV spectral analysis for the prediction of cardiovascular risk in patients with SDB (Tab. 1, Fig. 3, Ref. 36).

Management of obstructive sleep apnea in Europe.

OBJECTIVES: In Europe, the services provided for the investigation and management of obstructive sleep apnoea (OSA) varies from country to country. The aim of this questionnaire-based study was to investigate the current status of diagnostic pathways and therapeutic approaches applied in the treatment of OSA in Europe, qualification requirements of physicians involved in diagnosis and treatment of OSA, and reimbursement of these services. METHODS: Two questionnaires were sent to 39 physicians in 22 countries in Europe. In order to standardize the responses, the questionnaire was accompanied by an example. RESULTS: Sleep centers from 21 countries (38 physicians) participated. A broad consistency among countries with respect to the following was found: pathways included referral to sleep physicians/sleep laboratories, necessity for objective diagnosis (primarily by polysomnography), use of polygraphic methods, analysis of polysomnography (PSG), indications for positive airway pressure (PAP) therapy, application of standard continuous PAP (CPAP) therapy (100% with an CPAP/APAP ratio of 2.24:1), and the need (90.5%) and management of follow-up. Differences were apparent in reimbursement of the diagnostic procedures and follow-up, in the procedures for PAP titration from home APAP titration with portable sleep apnea monitoring (38.1%) up to hospital monitoring with PSG and APAP (85.7%), and in the qualification requirements of sleep physicians. CONCLUSIONS: Management of OSA in different European countries is similar except for reimbursement rules, qualification of sleep specialists and procedures for titration of the CPAP treatment. A European network (such as the one accomplished by the European Cooperation in Science and Technology [COST] B26 Action) could be helpful for implementing these findings into health-service research in order to standardize management in a cost effective perspective.

Severe nocturnal cardiac arrhythmias caused by sleep apnea-induced hypoxemia in males.

Nocturnal cardiac arrhythmias (NCA) were analyzed in patients with sleep apnea/hypopnea syndrome (SAHS) and controls. Occurrence and severity of NCA were compared in 33 SAHS patients and 16 control subjects, matched for cardiovascular risk factors. Continuous overnight polysomnography provided ECG, respiratory and sleep parameters for a comparative analysis. Various types and severity of NCA were detected already in moderate SAHS (apnea/hypopnea index = 26 ±15.6/h), reflecting the respiratory and atherosclerotic changes. Moderately severe arrhythmias, represented with benign and 2 complex types were caused by hypoxemia characterized by AHI, minimal SaO2, and lower values after desaturation. Three-time higher prevalence of complex arrhythmias in SAHS patients was not significantly different by usual statistical comparison, likely due to a low number of controls and a joint occurrence of various types and complex severity of arrhythmias in some patients. Therefore, a complex assessment of different types and varying severity of arrhythmias would require a scale specifically constructed for their evaluation.

Distinct generators for aspiration and expiration reflexes: localization, mechanisms and effects.

Re-evaluation of our earlier c-Fos-like immuno-reactive studies and brainstem transection/lesion experiments in over 40 anaesthetized, non-paralyzed cats allowed comparison of two distinct airway defensive reflexes with the distinct generators for inspiration (I) and expiration (E), described recently in juvenile rats. The spiration reflex (AspR) is characterized by solitary rapid and strong inspiratory effort with a reciprocal inhibition, preventing a subsequent active expiration, while the expiration reflex (ExpR) manifests by rapid and strong expiratory effort, starting without a preceding, inspiration, or reciprocal inhibition of occasional spontaneous inspiration. The retro-trapezoid nucleus/parafacial respiratory group neurones described as the distinct generator for active E in rats, are activated also during the ExpR in adult cats. Brainstem transection 5 mm above the obex eliminates the E generator and the ExpR, but preserves the I generator located in the pre-Bötzinger Complex, and also the AspR. This suggests the existence of a distinct I generator in cats as well as rats, and its contribution to the generation of the AspR. Persistence of the AspR in adult cats during asphyxic gasping, their similar character and the strong activation of I neurones at many places in the medulla and pons, suggest a common brainstem neuronal circuit contributing to generation of both the gasping and the gasp-like AspR. That the AspR and ExpR have distinct multilevel brainstem control mechanisms supports the dual theory of control and provides unique models for testing respiratory rhythm and pattern generation. The AspR may be compared with the powerful "auto-resuscitation effects of asphyxic gasping"; the ExpR may underly the effectiveness of the laryngeal chemoreflexes in prevention of lung diseases.

Provocation of aspiration reflexes and their effects on the pattern of cough and reflex apnea in cats.

Aspiration reflexes (AspRs) manifesting as reflex spasmodic inspirations and their effects on motor pattern of tracheobronchial cough and reflex apnea were studied on 22 spontaneously breathing pentobarbitone-anesthetized cats. AspRs induced during cough inspiration enhanced peak inspiratory (P<0.01) and expiratory (P<0.02) esophageal pressures, amplitudes of diaphragm (P<0.01) and abdominal muscles (P<0.05) EMG activity, and prolonged the entire expiratory period (P<0.01) and total cycle duration (P<0.05) of cough. Transient inhibitions and splits of cough expiration frequently occurred with AspR within active cough expiratory period; however, cough spatiotemporal characteristics were not altered significantly. Sub-threshold nasopharyngeal stimulation failing to provoke AspR had no significant effects on coughing. Hering-Breuer inflation apnea was moderately prolonged by AspRs (20%; P<0.05), unlike the apnea produced by continual mechanical laryngeal stimulation. AspRs are inducible during tested behaviors interacting with their motor pattern. Central mechanisms involving pulmonary stretch receptor stimulation is suggested for modulation of cough and inflation apnea by AspR.

Medico-legal implications of sleep apnoea syndrome: driving license regulations in Europe.

BACKGROUND: Sleep apnoea syndrome (SAS), one of the main medical causes of excessive daytime sleepiness, has been shown to be a risk factor for traffic accidents. Treating SAS results in a normalized rate of traffic accidents. As part of the COST Action B-26, we looked at driving license regulations, and especially at its medical aspects in the European region. METHODS: We obtained data from Transport Authorities in 25 countries (Austria, AT; Belgium, BE; Czech Republic, CZ; Denmark, DK; Estonia, EE; Finland, FI; France, FR; Germany, DE; Greece, GR; Hungary, HU; Ireland, IE; Italy, IT; Lithuania, LT; Luxembourg, LU; Malta, MT; Netherlands, NL; Norway, EC; Poland, PL; Portugal, PT; Slovakia, SK; Slovenia, SI; Spain, ES; Sweden, SE; Switzerland, CH; United Kingdom, UK). RESULTS: Driving license regulations date from 1997 onwards. Excessive daytime sleepiness is mentioned in nine, whereas sleep apnoea syndrome is mentioned in 10 countries. A patient with untreated sleep apnoea is always considered unfit to drive. To recover the driving capacity, seven countries rely on a physician's medical certificate based on symptom control and compliance with therapy, whereas in two countries it is up to the patient to decide (on his doctor's advice) to drive again. Only FR requires a normalized electroencephalography (EEG)-based Maintenance of Wakefulness Test for professional drivers. Rare conditions (e.g., narcolepsy) are considered a driving safety risk more frequently than sleep apnoea syndrome. CONCLUSION: Despite the available scientific evidence, most countries in Europe do not include sleep apnoea syndrome or excessive daytime sleepiness among the specific medical conditions to be considered when judging whether or not a person is fit to drive. A unified European Directive seems desirable.

Sleep apnoea inducing hypoxemia is associated with early signs of carotid atherosclerosis in males.

The intima-media thickness (IMT) of carotid arteries as a marker of preclinical atherosclerosis was measured by ultrasonography in 49 subjects to determine, how strongly the obstructive sleep apnoea (OSA) syndrome is associated with atherosclerosis. Maximal IMT was higher in patients with cardiovascular diseases and with or without risk factors of atherosclerosis, presenting also OSA (apnoea-hypopnoea index=26.1+/-15.6/h) compared to controls without OSA (0.91+/-0.21 mm versus 0.77+/-0.18 mm, p<0.05). The prevalence of IMT > or = 0.85 mm was also higher in patients with cardiovascular pathology presenting OSA than without it (p<0.05). IMT(max) was increased in subjects with mild to moderate OSA alone (AHI=20.4+/-8.7/h) versus healthy controls (0.83+/-0.14 mm versus 0.63+/-0.08 mm, p<0.01). Regression analysis revealed a correlation of IMT(max) with the frequency, intensity and duration of intermittent hypoxemia reflected by AHI (p<0.01), minimal oxygen saturation (p<0.01) and time spent with Sa(O2) < 90% (p<0.05) in patients presenting OSA. The results indicate clear association between early signs of carotid atherosclerosis and moderate OSA in males with and without concomitant cardiovascular pathology.

[Regulation of respiration and its sleep-related disorders]. / Regulácia dýchania a jej a poruchy v spánku.

Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.

[Nocturnal cardiac dysrhythmias associated with obstructive sleep apnea]. / Výskyt nocných kardiálnych dysrytmií v súvislosti s obstrukcným spánkovým apnoe.

The occurrence of cardiac dysrhythmias have been analysed in 16 adult patients suffering from obstructive sleep apnea syndrome of various severity randomly selected from more than 300 persons examined in our sleep laboratory from 1996 with a complex polysomnography Alice 3 (Healthdyne). The number of apneic episodes emerging in the first, second and third part of sleep was practically the same although their duration prolonged during the night culminating with an average of 25 sec (p < 0.02). OSA episodes caused a decrease of oxyhaemoglobin saturation to lower values during REM compared to NREM sleep (76.1% versus 81.7%, p < 0.05). Cardiac dysrhythmias occurred more frequently during and immediately after, than before OSA episodes demonstrating their causal relations.

[Blood pressure and heart rate monitoring as a method of detection of sleep apnea]. / Monitorovanie TK a frekvencie srdca ako metóda zistovania výskytu spánkového apnoe.

UNLABELLED: Ambulatory blood pressure monitoring (ABPM) and heart rate variability measurement are frequently used by general practitioners for diagnostic of various cardiovascular diseases. Coincidence of hypertension, heart failure and sleep related breathing disorders are very common. Therefore we proposed to use ambulatory blood pressure monitoring device (ABPM), as a tool, for selection of proper patients for polysomnographic examination in sleep laboratory. METHODS: Power spectral analysis of heart rate (HR) monitored together with blood pressure (BP), was performed using a ABPM device (Cardiotens 01, Meditech Budapest) in 24 adults patients. Low frequency/high frequency ratio (LF/HF), which reflects the sympatho-vagal balance, was calculated for the period of sleep versus wakefulness (S/W). Our aim was to detect changes in sympatho-vagal tone during sleep in the following groups of patients: obstructive sleep apnea syndrome (OSAS, respiratory disturbance index RDI = 43.8, arousal index ArI = 17.1), upper airway resistance syndrome (UARS-RDI = 7.4, ArI = 18.3), CPAP treated group (RDI = 6.4, ArI = 8.1) and controls. RESULTS: S/W ratio reflecting sympathetic activation, was lower in controls (0.59), than in patients with OSAS (0.9; p < 0.025) or UARS (2.16, p < 0.01). S/W ratio in patients treated with CPAP (0.68) was similar to controls (p = 0.38). S/W ratio correlated moderately with arousal index (r = 0.94 in group of patients with OSAS). CONCLUSION: S/W ratio reflecting sympathetic activation upon arousal can be used for screening of patient with sleep related breathing disorders, as well as for assessment of CPAP treatment. ABPM with measurement of heart rate variability can detect also effectiveness of antihypertensive treatment with drugs influencing the autonomous nervous system.

Contribution of upper airway reflexes to apnoea reversal, arousal, and resuscitation.

Cardiorespiratory decompensation or even death may result from dysfunction of upper airway reflexes during sleep. This could manifest, for example, as a lack of pharyngeal dilation in obstructive sleep apnoea or failure of autoresuscitation by gasping in sudden infant death syndrome. Data obtained from experiments in anaesthetized cats suggest several clinicophysiological applications for upper airway reflexes possessing important pathogenetic and therapeutic potentials. Such reflex effects include: 1. Pharyngeal dilation as additional treatment in obstructive sleep apnoea. 2. Bronchodilation after deep nasal breathing in asthmatic attacks. 3. Oesophageal sphincter relaxation alleviating gastro-oesophageal reflux. 4. Provocation of sniff- and gasp-like aspiration for reversal of central apnoea. 5. Arousal from sleep increasing the general reactivity. 6. Increase in muscle tone underlying behavioural defence reactions. 7. Increase in sympathetic activity contributing to powerful cardiopulmonary-cerebral resuscitation. 8. Adrenergic reaction mediated by catecholamine secretion.

[Experience with polysomnography in the diagnosis of sleep apnea]. / Skúsenosti s polysomnografickou diagnostikou spánkového apnoe.

Whole-night recording of 9-30 parameters and calculation of various indices allow differentiation of various sleep related breathing disorders and estimation of their severity (Fig. 1, 2). Parallel monitoring of changes in ventilation, arterial oxygen saturation, ECG, EEG, EMG and others, give a possibility to appreciate the gradual development of cardiovascular, neuropsychic, endocrine-metabolic and other consequences of sleep related breathing disorders, their dependence on different phases and stages of sleep as well as their alterations by treatment.