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

Normal children have a smaller upper airway than adults, but, nevertheless, snore less and have less apnea. We have previously shown that normal children have an upper airway that is resistant to collapse during sleep. We hypothesized that this resistance to collapse is due to preservation of upper airway neuromotor responses during sleep. Furthermore, we hypothesized that upper airway responses would be diminished in children with the obstructive sleep apnea syndrome (OSAS). We therefore compared the upper airway pressure-flow relationship during sleep between children with OSAS and controls. Measurements were made by correlating maximal inspiratory airflow with the level of nasal pressure applied via a mask. Neuromotor upper airway activation was assessed by evaluating the upper airway response to 1) hypercapnia and 2) intermittent, acute negative pressure. We found that children with OSAS had no significant response to either hypercapnia or negative pressure during sleep, compared with the normal children. After treatment of OSAS by tonsillectomy and adenoidectomy, there was a trend for normalization of upper airway responses. We conclude that upper airway dynamic responses are decreased in children with OSAS but recover after treatment. We speculate that the pharyngeal airway neuromotor responses present in normal children are a compensatory response for a relatively narrow upper airway. Further, we speculate that this compensatory response is lacking in children with OSAS, most likely due to either habituation to chronic respiratory abnormalities during sleep or to mechanical damage to the upper airway.
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PMID:Upper airway dynamic responses in children with the obstructive sleep apnea syndrome. 1555 13

It is clear that mechanical ventilation strategies influence the course of lung disease, and the choice of a ventilation strategy that avoids volutrauma and atelectrauma is firmly based on experimental literature and clinical experience. The application of a lung-protective strategy with reduced tidal volumes, effective lung recruitment, adequate PEEP to minimize alveolar collapse during expiration, and permissive hypercapnia has been shown to be advantageous in adult patients who have ARDS, although it has not been systematically studied in children. A significant body of literature confirms the beneficial effects of hypercapnic acidemia in the setting of acute lung injury. As a corollary, experimental evidence indicates that buffering hypercapnic acidosis abrogates its protective effects. The use of permissive hypercapnia as part of a lung-protective strategy in children should be accepted and perhaps even desired, provided it does not result in significant hemodynamic instability. This acceptance should be tempered with the recognition that a low-stretch, reduced-tidal volume strategy without hypercapnia has also been shown to improve outcomes in adults who have ARDS and that HFOV can generally provide lung-protective ventilation without necessarily inducing hypercapnia. Thus, a synthesis of the available clinical and research data strongly supports a graded approach to managing patients who have acute lung injury requiring intubation. The highest priority should be a mechanical ventilation strategy that limits the tidal volume, with the allowance of hypercapnia to a degree that does not compromise hemodynamic status.
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PMID:Is permissive hypercapnia a beneficial strategy for pediatric acute lung injury? 1695 99

Obstructive sleep apnea syndrome is caused by upper airway collapse during inspiration, causing intermittent hypoxemia, hypercapnia, acidosis, sympathetic nervous system activation, and arousal from sleep. Nighttime blood pressure is higher, but unexpectedly, daytime hypertension occurs. The prevalence of hypertension is very high and the incidence of hypertension increases as the number of apneic and hypopneic events per hour rises. Obesity is a major predisposing factor for the development of obstructive sleep apnea. Daytime sleepiness, snoring, and breathing pauses are important symptoms to elicit from the patient or sleep partner. Resistant hypertension is an important clue. Overnight polysomnography is required for diagnosis. Weight loss, avoidance of nocturnal sedatives, cessation of evening alcohol ingestion, and avoidance of the supine position during sleep are initial therapeutic actions in mild obstructive sleep apnea syndrome. Continuous positive airway pressure is the treatment of choice for patients unable to find relief from lifestyle changes. Blood pressure modestly improves with treatment.
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PMID:Obstructive sleep apnea syndrome. 1702 91

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

Lung injury in ventilated premature infants occurs primarily through the mechanism of volutrauma, often due to the combination of high tidal volumes in association with a high end-inspiratory volume and occasionally end-expiratory alveolar collapse. Tolerating a higher level of arterial partial pressure of carbon dioxide (PaCO2) is considered as 'permissive hypercapnia' and when combined with the use of low tidal volumes may reduce volutrauma and lead to improved pulmonary outcomes. Permissive hypercapnia may also protect against hypocapnia-induced brain hypoperfusion and subsequent periventricular leukomalacia. However, extreme hypercapnia may be associated with an increased risk of intracranial hemorrhage. It may therefore be important to avoid large fluctuations in PaCO2 values. Recent randomized clinical trials in preterm infants have demonstrated that mild permissive hypercapnia is safe, but clinical benefits are modest. The optimal PaCO2 goal in clinical practice has not been determined, and the available evidence does not currently support a general recommendation for permissive hypercapnia in preterm infants.
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PMID:Permissive hypercapnia to decrease lung injury in ventilated preterm neonates. 1897 27

The effects of the combination of a 'lowest' lung ventilation with extracorporeal elimination of carbon dioxide by interventional lung assist are described in a patient presenting with severe acute respiratory distress syndrome due to fulminant pneumonia. Reducing tidal volume to 3 ml.kg(-1) together with interventional lung assist resulted in a decrease in severe hypercapnia without alveolar collapse or hypoxaemia but with a decrease in serum levels of interleukin-6. This approach was applied for 12 days with recovery of the patient, without complications. Extracorporeal removal of carbon dioxide by interventional lung assist may be a useful tool to enable 'ultraprotective' ventilation in severe acute respiratory distress syndrome.
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PMID:Pumpless extracorporeal removal of carbon dioxide combined with ventilation using low tidal volume and high positive end-expiratory pressure in a patient with severe acute respiratory distress syndrome. 1914 99

Venous gas embolism (VGE) is a rare but potentially lethal complication of many forms of surgery, especially posterior fossa neurosurgery where the incidence is reported to be up to 80% - it can also occur in laparoscopic surgery. It usually occurs early in the procedure during insufflation of the abdomen. Rapid entry or large volumes of gas entering the venous circulation initiate a predictable chain of pathophysiological events which may continue to cardiovascular collapse. Arterial hypoxaemia, hypercapnia, decreased end-tidal CO(2), arrhythmias, myocardial ischaemia and elevated central venous and pulmonary arterial pressures can occur. The management of VGE relies on a high index of suspicion and close liaison between anaesthetist, surgeon and theatre staff. The authors present a case of venous gas embolism (VGE) during laparoscopic cholecystectomy (LC) which presented without many of the usual clinical features and was diagnosed by auscultation of a millwheel murmur.
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PMID:Venous gas embolism: An unusual complication of laparoscopic cholecystectomy. 1972 76

Obstructive sleep apnoea (OSA) is a common disorder characterized by the repetitive complete or partial collapse of the upper airway during sleep. It results in intermittent hypoxaemia and hypercapnia, cortical arousals and surges of sympathetic activity. The occurrence of OSA has also been linked to serious long-term adverse health consequences; such as hypertension, metabolic dysfunction, cardiovascular disease, neurocognitive deficits and motor vehicle accidents. There have been several advances in the field of particular clinical importance: (i) the development of portable monitoring as part of a simplified clinical algorithm for the diagnosis of OSA in selected patients; (ii) growing awareness of the cardio-metabolic health consequences of OSA and (iii) emerging evidence to support a range of non-continuous positive airway pressure (CPAP) treatment modalities, such as oral appliances.
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PMID:Obstructive sleep apnoea--an update. 1981 52

Central sleep apnea (CSA) describes a group of conditions in which cessations in air flow occur without respiratory effort. In contrast, obstructive sleep apnea patients have ongoing respiratory effort during respiratory events. However, considerable overlap exists in the pathogenesis and clinical presentation of obstructive sleep apnea and CSA. A good working knowledge of the mechanisms underlying CSA is important for optimal clinical care. In general, CSA can be classified into those with excessive drive (eg, Cheyne-Stokes breathing) versus those with inadequate drive (eg, sleep hypoventilation syndrome). One critical factor contributing to the cessation of air flow during sleep is the concept of the apnea threshold, such that a P(aCO(2)) value below a certain level will lead to cessations in breathing. P(aCO(2)) can fall below the chemical apnea threshold when drive is excessive (eg, robust chemosensitivity) or when hyperventilation is occurring (eg, following arousal). Another important factor is the loss of the so-called wakefulness drive to breathe, such that some rise in P(aCO(2)) is likely to occur at the onset of sleep. A variety of factors contribute to this rise, including upper-airway collapse and diminished chemosensitivity (particularly during rapid-eye-movement sleep). In patients with low central drive, this further loss of drive at sleep onset can lead to marked hypercapnia in some cases. The treatment of CSA is also reviewed in some detail, including a role for positive airway pressure (eg, bi-level positive airway pressure in hypoventilation patients) and optimization of medical therapy (eg, in Cheyne-Stokes breathing). A paucity of research exists in this area, emphasizing the opportunities for young investigators who are interested in this field.
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PMID:What is central sleep apnea? 2079 99

The most distinctive functional abnormality in asthma is increased airway resistance (Raw), especially in those airways located peripherically (< 2 mm diameter). Smooth muscle contraction, mucous hypersecretion and swelling of the airway wall due to inflammation and/or remodeling are major factors originating airway lumen diminution. However, two other factors also favoring airway closure in asthma are surfactant alterations produced by the inflammatory process and decrement of transpulmonary pressure (PL), also known as elastic recoil pressure. In normal conditions, at the end of a passive expiration there is equilibrium between the lung tendency to collapse and of the chest wall tendency to expansion. During an asthma exacerbation lungs loss elasticity, i.e., the already decreased PL is accentuated, making that equilibrium between lungs and chest wall is achieved at higher volumes (increment of functional residual capacity [FRC]), which implies that the patient breaths maybe the same tidal volume but with more inflated lungs. During a forceful expiration the premature airway closure originates air trapping (increased residual volume). If asthma exacerbation is severe enough, abnormal regional ventilation might be in disequilibrium with respect to blood perfusion and cause hypoxemia, and the enhanced respiratory work load might lead to respiratory muscle fatigue, hypoventilation and hypercapnia.
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PMID:[Physiopathology of asthma]. 2087 50


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