Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-invasive positive pressure ventilation (NIV) is the provision of mechanical positive airway pressure ventilatory support through the patient's upper airway through mask interface. Conditions in which it has been shown to be effective are acute cardiogenic pulmonary oedema and acute hypercapnic exacerbations of chronic obstructive pulmonary disease. In such conditions, NIV is associated with reduced intensive care unit demands, a reduction in intubation rates, reduced health-care expenditure and improved survival. Other conditions, such as hypercapnia of other cause, hypoxaemic respiratory failure and acute asthma, have supportive, but less conclusive data. Indications, contraindications and guidelines for the use of NIV are discussed.
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PMID:Non-invasive positive pressure ventilation for acute respiratory failure: justified or just hot air? 1722 54

Charcot-Marie Tooth disease (CMT) encompasses several inherited peripheral motor-sensory neuropathies and is one of the most common inherited neuromuscular diseases. Charcot-Marie-Tooth disease can be associated with several disorders that may be encountered by the pulmonary physician, including restrictive pulmonary impairment, sleep apnea, restless legs, and vocal cord dysfunction. Restrictive pulmonary impairment has been described in association with phrenic nerve dysfunction, diaphragm dysfunction, or thoracic cage abnormalities. Central sleep apnea may be associated with diaphragm dysfunction and hypercapnia, whereas obstructive sleep apnea has been reported as possibly due to a pharyngeal neuropathy. Restless legs and periodic limb movement during sleep are found in a large proportion of patients with CMT2, a type of CMT associated with prominent axonal atrophy. Vocal cord dysfunction, possibly due to laryngeal nerve involvement, is found in association with several CMT types and can often mimic asthma. There may be special therapeutic considerations for the treatment of those conditions in individuals with CMT. For instance, bi-level positive airway pressure may be more appropriate than continuous positive airway pressure (CPAP) for the treatment of sleep apnea in the individual with concomitant restrictive pulmonary impairment. The prominence of peripheral neuropathy as a cause of the restless legs syndrome in CMT may justify treatment with neuropathic medications as opposed to the more commonly recommended dopaminergic agents. The risk of progression to bilateral vocal cord dysfunction in CMT and the risk of aspiration with laryngeal neuropathy may limit the therapeutic options available for vocal cord paralysis.
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PMID:Disorders of pulmonary function, sleep, and the upper airway in Charcot-Marie-Tooth disease. 1729 38

A 53-year-old woman visited a clinic for stridor and dyspnea, and was treated with steroid and heparin for bronchial asthma and pulmonary embolism. She was later admitted to our hospital for progressive dyspnea. Blood gas analysis showed severe hypoxemia with hypercapnia. Pulmonary funtion tests revealed severe obstractive pulmonary dysfunction. Chest computed tomography showed a mosaic perfusion pattern. Ventilation-perfusion scanning showed bilateral multiple matched defects, especially in the basal region. Since specimens of Video-assisted thoracoscopic surgical (VATS) lung biopsy showed lymphocytic infiltration in membranous bronchiole and occlusion of the membranous bronchiole lumen, bronchiolitis obliterans was diagnosed. We initiated treatment with steroids, macrolides and bronchodilators and her condition stabilized. Although these therapies did not cure the BO, they did retard its progression.
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PMID:[Case of idiopathic bronchiolitis obliterans successfully treated by medication]. 1831 52

A 39-year-old man presented to the emergency department (ED) in severe respiratory distress. He had a prior diagnosis of brittle asthma and had been admitted on several occasions but never previously ventilated. Therapy given in the first 3 hours of arrival included nebulized salbutamol (5 mg, x5), ipratropium bromide (0.5 mg), intravenous hydrocortisone (200 mg), and magnesium sulfate (2 g). His arterial blood gases continued to deteriorate. He was then given an intravenous bolus of salbutamol (250 microg) and heliox via facemask. His worsening status necessitated invasive ventilation. His hypercapnia and resultant respiratory acidosis improved rapidly, but there was a concurrent accumulation of lactic acid resulting in acidemia. This patient had lactic acidosis as a direct effect of administration of salbutamol. The development of hazardous salbutamol-induced toxicity in acute severe asthma is discussed.
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PMID:An under-recognized complication of treatment of acute severe asthma. 1841 Aug 27

Status asthmaticus requiring mechanical ventilation is an uncommon, life-threatening disorder in obstetric patients. The unique physiologic changes of pregnancy, impact of the fetus on the maternal condition, and concerns for fetal and maternal health and survival are particular concerns in critical illness. Furthermore, the issues of hypoxemia and hypercapnia, ventilator management and complications make this disease of respiratory failure an especially important area for review. There is abundant literature on the management of asthma during pregnancy; however the literature is very limited in those with status asthmaticus who require intensive care unit admission. We report our intensive care unit experience in the management of status asthmaticus in 5 pregnant patients and review the literature on management of status asthmaticus during pregnancy.
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PMID:Management of the obstetric patient with status asthmaticus. 1879 65

A 56-year-old woman presented to our hospital with acute severe asthma. As a consequence of severe refractory airflow limitation, moderate hypercapnia ensued for several days. Unexpectedly, the patient died as a result of brain stem herniation, in the absence of hypoxaemia, arterial hypotension or an intracranial mass lesion. We discuss the mechanisms that may have precipitated severe intracranial hypertension resulting in brain death, and the possible methods to detect and avoid such a devastating consequence.
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PMID:An unexpected ending: brain death following acute severe asthma. 1879 23

The histopathology of severe persistent asthma and chronic obstructive pulmonary disease is predominantly characterized by neutrophilic inflammation. It is posited that chronic hypoxia from hypoventilation in combination with hypoperfusion and hypercapnia are associated with induction of pulmonary tissue acidosis in SPA and COPD, which in turn provide ideal conditions to induce danger-associated molecular patterns, i.e., crystallized and calcium pyrophosphate. These stimuli in combination with other danger-related biochemical signals are capable of stimulating an innate immune receptor (cryopyrin inflammasome, NALP3) and cause interleukin-1beta secretion with subsequent neutrophilic inflammation. There is evidence to suggest that the mechanisms and pathobiology associated with chronic hypoxia, reduced perfusion and reoxygenation in SPA/COPD may exhibit similarities to the biphasic pathobiology involved in ischemia-reperfusion injury. A rationale is suggested for trials of IL-1beta targeted therapies as an adjunct strategy to control neutrophilic inflammation in these conditions.
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PMID:Interleukin-1beta targeted therapy in severe persistent asthma (SPA) and chronic obstructive pulmonary disease (COPD): proposed similarities between biphasic pathobiology of SPA/COPD and ischemia-reperfusion injury. 1916 Sep 37

Dyspnea is the unpleasant awareness of breathing while healthy persons will hardly sense their own breath at rest. Dyspnea is comparable to pain because both caution the organism that will activate protective mechanisms to avoid further damage. Dyspnea results from central nervous processing of respiratory feed back signals. Feed back from respiratory muscles, the chest wall, the airways and the lung reach the brain while partial pressure of oxygen and carbon dioxide is continuously monitored and arterial blood gases are permanently stabilized. Sensation of breathlessness depends on its origin. Main qualities of dyspnea include air hunger during hypercapnia, laboured breathing during increased minute ventilation and chest tightness in asthma. During chronic dyspnea, respiratory control aims for a new breathing pattern that will ease breathlessness. Since respiratory control includes both autonomic regulation and cortical modulation of breathing, voluntarily guided respiration can be employed to influence other autonomic regulated systems and pain perception.
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PMID:[Breathlessness: different causes and qualities of dyspnea]. 1955 55

Respiratory muscle fatigue in asthma and chronic obstructive lung disease (COPD) contributes to respiratory failure with hypercapnia, and subsequent respiratory acidosis. Therapeutic induction of acute metabolic acidosis further increases the respiratory drive and, therefore, may diminish ventilatory failure and hypercapnia. On the other hand, it is known that acute metabolic acidosis can also negatively affect (respiratory) muscle function and, therefore, could lead to a deterioration of respiratory failure. Moreover, we reasoned that the impact of metabolic acidosis on respiratory muscle strength and respiratory muscle endurance could be more pronounced in COPD patients as compared to asthma patients and healthy subjects, due to already impaired respiratory muscle function. In this study, the effect of metabolic acidosis was studied on peripheral muscle strength, peripheral muscle endurance, airway resistance, and on arterial carbon dioxide tension (PaCO(2)). Acute metabolic acidosis was induced by administration of ammonium chloride (NH(4)Cl). The effect of metabolic acidosis was studied on inspiratory and expiratory muscle strength and on respiratory muscle endurance. Effects were studied in a randomized, placebo-controlled cross-over design in 15 healthy subjects (4 male; age 33.2 +/- 11.5 years; FEV(1) 108.3 +/- 16.2% predicted), 14 asthma patients (5 male; age 48.1 +/- 16.1 years; FEV(1) 101.6 +/- 15.3% predicted), and 15 moderate to severe COPD patients (9 male; age 62.8 +/- 6.8 years; FEV(1) 50.0 +/- 11.8% predicted). An acute metabolic acidemia of BE -3.1 mmol x L(-1) was induced. Acute metabolic acidemia did not significantly affect strength or endurance of respiratory and peripheral muscles, respectively. In all subjects airway resistance was significantly decreased after induction of metabolic acidemia (mean difference -0.1 kPa x sec x L(-1) [95%-CI: -0.1 - -0.02]. In COPD patients PaCO(2) was significantly lowered during metabolic acidemia (mean difference -1.73 mmHg [-3.0 - -0.08]. In healthy subjects and in asthma patients no such effect was found. Acute metabolic acidemia did not significantly decrease respiratory or peripheral muscle strength, respectively muscle endurance in nomal subjects, asthma, or COPD patients. Metabolic acidemia significantly decreased airway resistance in asthma and COPD patients, as well as in healthy subjects. Moreover, acute metabolic acidemia slightly improved blood gas values in COPD patients. The results suggest that stimulation of ventilation in respiratory failure, by induction of metabolic acidemia will not lead to deterioration of the respiratory failure.
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PMID:Respiratory muscle strength and muscle endurance are not affected by acute metabolic acidemia. 1962 91

The prevalence of childhood obesity has more than tripled over the past five decades. Obesity results in low lung volumes, likely through increased loading of the chest wall and abdomen. The prevalence of asthma in children has paralleled the rise in obesity; obesity may increase the severity of asthma, but a direct link has been difficult to establish. Obesity is a risk factor for obstructive sleep apnea (OSA) in children as well as adults. Obese children may be at increased risk for persistent OSA following adenotonsillectomy treatment for OSA. Severe obesity and OSA may lead to the obesity-hypoventilation syndrome, with hypoxia, hypercapnia, and reduced ventilatory drive. Obesity can increase a child's risk for complications of anesthesia and recovery from surgery.
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PMID:Obesity and respiratory diseases in childhood. 1970 55


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