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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Even if different mechanisms of various interactions during sleep are known, it is still unsolved by which mechanisms physiological reactions during sleep may start a pathophysiological course. Hypoxia, Hypercapnia and repetitive sympathetic elevations are well known elements in the control of the arterial resistance. Furthermore investigations in patients with sleep apnea showed changes of the pulsatile secretion pattern within the renin-angiotensin-system and the antinatriuretic peptides. These changes were reversible under nasal CPAP-therapy, nycturia as a frequent symptom disappeared. Nevertheless neither hypoxia nor intrathoracic pressure changes nor the arousals can assert the longterm influence on the blood pressure alone, a multifactorial confluence must be assumed. Further it is unclear how a tonic increase of the arterial blood pressure may occur in dependence of the REM- and NREM-sleep cycle changes as well as during daytime. First investigations in sleeping man seem to indicate, that a disturbance of the physiological coupling of breathing and circulation may present a pathogenetic element. Finally it remains open, whether the changes of the cardiorespiratory coupling during sleep of control persons and of patients with OSA are comparable, and whether they may be procured for an explanation of the pathogenesis of arterial and pulmonary hypertension. Further investigations in the control mechanisms of breathing and circulation related to the circuits of chemo- and baroreception, thresholds during wakefulness and sleep may be of decisive help to process the question, to what extent clinical states find a correlate in a disturbed cardiorespiratory coupling and, much more significantly, whether a disturbance in the physiological cardiorespiratory coupling appears already in early states of a disease. Sleep with ist complex physiology as well as with its characteristic pathophysiological phenomenon of sleep related breathing disorders has opened a new interdisciplinary field where tools like the polysomnography and electronic data analysis are used by physiologists, pathophysiologists as well as by physicians.
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PMID:[Cardiorespiratory coupling in obstructive sleep apnea (OSA)]. 924 90

Ventilation is under metabolic as well as under behavioural control. This causes a complex interaction between states of 'vigilance' and respiration. This paper briefly summarizes sleep-related changes of respiration and presents an experimental study on the course of respiratory CO2-sensitivity during a whole night's sleep in ten healthy volunteers. The feedback control of breathing was challenged by continuous step changes of inspired CO2 every 7 min, resulting in 60, 3-step steady-state hypercapnic ventilatory responses (HCVR) per night in each subject. We analysed the variability of baseline ventilation and the effects of hypercapnia on ventilation with respect to sleep stages. There were only small differences in baseline PCO2 and ventilation between sleep stages, but a high variability of the slope of the CO2-response curves in the course of the night, ranging from 0.5 to 3.0 L min(-1) Torr(-1). The HCVR was significantly lower during REM sleep than during all stages of NREM sleep. Due to a compensatory left shift of the flattened CO2-response curves, however, ventilation at baseline CO2 as well as during slight hypercapnia varied much less than would be expected from the high variability of slopes. We conclude that the characteristics of the CO2-sensitive feedback control system of respiration, are highly variable during sleep, but due to offsetting effects, PCO2 and ventilation remain quite stable in the physiological range.
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PMID:Variability of vigilance and ventilation: studies on the control of respiration during sleep. 985 49

A 64-year-old man with multiple system atrophy complained of daytime sleepiness, fatigue, and snoring. Neurological examination revealed severe autonomic failure, mild cerebellar ataxia and akinesia. Daytime blood gas analysis showed respiratory acidosis with hypoxia and hypercapnia. MR imaging of the brain showed atrophy of the pons, cerebellum and bilateral frontal lobes. Although paralysis of the vocal cord abduction was not found by laryngoscopy during daytime examination, polysomnography (PSG) showed heavy snoring with paradoxical respiration associated with severe desaturation during sleep as well as reduced slow wave sleep and REM sleep. He was diagnosed as having sleep-related upper airway obstructive breathing disorder probably due to Gerhardt syndrome. Tracheostomy was considered, but we performed nasal CPAP therapy during sleep because this therapy is non-invasive and would not impair his daily life. After nasal CPAP therapy, daytime sleepiness, fatigue, and snoring with desaturation improved, and PSG showed increased slow wave sleep. These results demonstrate that nasal CPAP therapy improves the quality of sleep and should be considered in patients with early stages of multiple system atrophy who exhibit sleep-related breathing disorders.
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PMID:[Effective nasal CPAP therapy for heavy snoring and paradoxical respiration during sleep in a case of multiple system atrophy]. 1034 49

Snoring, a leading symptom of the sleep apnoea syndrome (SAS), has been reported to be one of the risk factors for sleep-related cerebral strokes. Episodes of apnoea are accompanied by hypoxaemia as well as hypercapnia. As CO2 constitute a major regulatory factor controlling cerebral blood flow, it is likely that changes in cerebral perfusion are to be found in patients with SAS, which may be related to nocturnal stroke. A computer-assisted pulsed (2 mHz) Doppler ultrasonography system has been modified for continuous long-term and on-line recording of cerebral haemodynamics together with simultaneous polysomnography, continuous blood pressure recordings, and measurement of the end-expiratory CO2. The dynamics of cerebral blood flow velocity (CBFV) during sleep were measured in the right middle cerebral artery in 10 SAS patients. CBFV showed a characteristic nocturnal pattern with decreases during non-rapid eye movement (NREM) sleep and increases during REM sleep. Changes in sleep stage patterns as well as awakenings from NREM sleep were not regularly accompanied by corresponding changes in CBFV. Dramatic increases in CBFV could be observed during apnoeic episodes, with maximum increases during REM sleep. CO2 reactivity and changes in CBFV related to apnoea duration were markedly increased during sleep compared with the waking state in SAS patients. The dynamic feature of CBFV in relation to sleep patterns reflects quantitative uncoupling between cerebral electrical activity and cerebral perfusion during sleep in SAS patients as has been previously reported for normal subjects (Hajak et al. 1994). It supports a dissociation in the activity of central regulatory mechanisms during human sleep which might cause abnormal cerebral perfusion under certain circumstances. The increased CO2 reactivity during sleep in SAS suggests a 'hypersensitivity' of intracranial vasoactive receptors and/or disturbances in the central autonomic control of cerebrovascular functions. It may be concluded that, under certain conditions, the interaction of decreased cerebral perfusion in SAS patients with sleep-related cerebral perfusion patterns and haemodynamic changes during apnoeic episodes might lead to a critical reduction in cerebral perfusion.
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PMID:Cerebral perfusion during sleep-disordered breathing. 1060 90

Decrease of respiratory muscle capacities in neuromuscular disease can lead to chronic respiratory failure with permanent alveolar hypoventilation. Respiratory centers elaborate a strategy of breathing dedicated to prevent overt respiratory muscles fatigue. This strategy may worsen chronic hypercapnia. During sleep, ventilation decreases because a lessening in respiratory centers function. During NREM sleep hypoventilation is only an exacerbation of what is seen during wakefulness. During REM sleep, atonia worsens much more hypoventilation particularly when diaphragmatic function is impaired. The effects of atonia are amplified by a very low reactivity of respiratory centers. Nocturnal mechanical ventilation improves nocturnal hypoventilation and daytime arterial blood gases (ABG). Mechanism of improvement in ABG and how nocturnal hypoventilation and diurnal hypoventilation interact, are still a matter of debate.
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PMID:Nocturnal hypoventilation in chronic respiratory failure (CRF) due to neuromuscular disease. 1089 4

Patients with COPD who are hypoxaemic during wakefulness become more hypoxaemic during sleep. The most severe episodes of nocturnal desaturation generally occur during REM sleep. There is a strong relationship between nocturnal O2 saturation and the level of daytime PaO2: the more pronounced daytime hypoxaemia, the more severe nocturnal hypoxaemia. The worsening of hypoxaemia is due to a variable combination of alveolar hypoventilation and ventilation-perfusion mismatching, alveolar hypoventilation being the predominant mechanism, at least during REM sleep. The consequences of sleep-related hypoxaemia include peaks of pulmonary hypertension due to hypoxic pulmonary vasoconstriction, generally observed in patients with marked daytime hypoxaemia. Cardiac arrhythmias have been described but their clinical relevance has not been established. The prevalence of obstructive sleep apnoea syndrome (OSAS) is not greater in chronic obstructive pulmonary disease (COPD) patients than in the general population, but this association (Overlap Syndrome) is not rare since COPD and OSAS are both frequent diseases. Overlap patients are at a higher risk of developing respiratory insufficiency than are pure OSAS patients. Polysomnography is only indicated in COPD patients who are suspected of having OSAS. The treatment of nocturnal hypoxaemia is conventional O2 therapy (> or = 16/24 h) in COPD patients with marked daytime hypoxaemia (PaO2 < 55-60 mmHg) and conventional O2 therapy plus nocturnal non-invasive ventilation in some patients with marked hypercapnia. At present data are not sufficient for justifying the use of isolated nocturnal oxygen therapy in COPD patients with nocturnal desaturation but with mild daytime hypoxaemia (PaO2 > 60 mmHg).
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PMID:Sleep and chronic obstructive pulmonary disease. 1523 53

As the clinical signs of amyotrophic of lateral sclerosis (ALS) are late and not specific, spirometric measurements, study of respiratory strength muscles and analysis of night respiratory parameters are used to evaluate ventilatory functions. The prognostic value of vital capacity is well established, but with a poor sensitivity to detect the initial form of ALS. Gazometric parameters remain normal for a long time. Hypercapnia is late and due to a major reduction in the force of the inspiratory muscles. Level of diurnal venous bicarbonate could detect nighttime hypoventilation. Noninvasive techniques (Pimax, Pemax, snifftest) are available to explore the strength of respiratory muscles. Sleep is characterized by a long period of hypoventilation, essentially during REM-sleep. There are no guidelines concerning the appropriate mode, type and rhythm of explorations of diurnal and nocturnal respiratory functions.
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PMID:[Evaluation of ventilatory functions in amyotrophic lateral sclerosis]. 1712 10

Obstructive sleep apnea (OSA) is a common sleep-related disorder among the general population. This disorder occurs in all sleep stages, although is more intense during the REM sleep (rapid eye movement). In this stage appears generalized muscle atony, which includes the hypopharyngeal muscles; this causes narrowing of the upper airway lumen, difficult inside/outside air movement and mechanical obstruction. OSA is considered a risk for: a) difficult airway intubation/ventilation; b) increase of cardiovascular morbidity; c) development of hypoxia and hypercarbia during spontaneous or assisted ventilation techniques. For these reasons, it is possible to assume that OSA may increase the perioperative risk and should be timely and properly ascertained. The main objective of this paper is to review the effect of OSA in patients undergoing anesthetic and surgical procedures, whether it increases the perioperative risk, and the advantages of its timely identification and assessment when carrying out the pre-anesthetic evaluation.
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PMID:[Importance of the obstructive sleep apnea disorder for perioperative medicine]. 1794 75

Sleep-disordered breathing is a common and serious cause of metabolic, cardiovascular, and neurocognitive morbidity in children. The spectrum of obstructive sleep-disordered breathing ranges from habitual snoring to partial or complete airway obstruction, termed obstructive sleep apnea (OSA). Breathing patterns due to airway narrowing are highly variable, including obstructive cycling, increased respiratory effort, flow limitation, tachypnea, and/or gas exchange abnormalities. As a consequence, sleep homeostasis may be disturbed. Increased upper airway resistance is an essential component of OSA, including any combination of narrowing/retropositioning of the maxilla/mandible and/or adenotonsillar hypertrophy. However, in addition to anatomic factors, the stability of the upper airway is predicated on neuromuscular activation, ventilatory control, and arousal threshold. During sleep, most children with OSA intermittently attain a stable breathing pattern, indicating successful neuromuscular activation. At sleep onset, airway muscle activity is reduced, ventilatory variability increases, and an apneic threshold slightly below eupneic levels is observed in non-REM sleep. Airway collapse is offset by pharyngeal dilator activity in response to hypercapnia and negative lumenal pressure. Ventilatory overshoot results in sudden reduction in airway muscle activation, contributing to obstruction during non-REM sleep. Arousal from sleep exacerbates ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep. Understanding the pathophysiology of pediatric OSA may permit more precise clinical phenotyping, and therefore improve or target therapies related to anatomy, neuromuscular compensation, ventilatory control, and/or arousal threshold.
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PMID:Pathophysiology of pediatric obstructive sleep apnea. 1825 Feb 19

Hypercapnic respiratory failure is usually caused by an overload of the respiratory muscles (respiratory pump). After treatment of the underlying disease, mechanical ventilation will achieve optimal treatment success and higher degrees of respiratory muscle unloading will improve the outcome in terms of lower PaCO (2) levels and improved exercise performance. Routinely assisted modes are being used for ventilation, where the patient has to trigger the ventilator with his effort. Controlled ventilation is usually applied in sedated patients lacking spontaneous breathing efforts that are necessary to trigger the ventilator. Controlled ventilation, however, is feasible in awake patients but requires operator expertise. In this process, the respiratory pattern of the ventilator has to be adapted to the patient's own respiratory pattern. Changing conditions require a re-adaptation of parameters. In order to automatise this complex and time-consuming operation, a time-adaptive mode (TA-mode) has been developed. This programmed mode incorporates a self-learning algorithm, primarily detecting the patient's respiratory pattern. The software then calculates a matching flow profile using a motion equation that gives consideration to resistance and compliance. The operator has to pre-select allowed ranges of parameters (especially in- and expiratory pressures, IPAP and EPAP). After detection of a stable respiratory pattern (usually after 10 - 20 breaths), the ventilator will slowly increase the calculated flow profile and achieve controlled ventilation without irritating respiratory centres of the brain. Respiratory drive will cease usually within three to five minutes. Restart of the respiratory drive, for example, after coughing or during REM sleep with an altered respiratory pattern will be detected as ventilator fighting and the programme will return to the analysis algorithm again. After the respiratory pattern has become stable, the ventilator will take over ventilation again. The new mode has been validated in an accreditation study. For this purpose we selected 21 patients with stable hypercapnic respiratory failure, most of whom (20) had previously been ventilated with a controlled T-mode and only one patient had previously been ventilated with an assisted mode and adapted them to the new ventilator under polygraphic surveillance. Each time seven patients were adapted to a T-, ST- and TA-mode, respectively. Two patients, however, could not be adapted to ST-mode ventilation and were switched to TA-mode. PCO (2) values before and after ventilation were not significantly different between modes. Patient satisfaction was rated very good in 34 %, good in 45 % and non-gratifying in 21 % of cases ventilated with TA-mode. Consideration has to be given to the fact that patients previously had been receiving optimal ventilator treatment. The TA-mode is a self-learning system, capable of copying the patients own breathing pattern while awake, in order to achieve complete unloading of the respiratory muscles through controlled ventilation during a circumscribed period.
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PMID:[Time-adaptive mode, a new ventilation form for the treatment of respiratory insufficiency--a self-learning system]. 1843 1


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