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

The underlying causes of acute severe or life threatening asthma are infections with respiratory viruses or Mycoplasma pneumoniae, rather than bacterial infections. In addition, exposure to various agents such as allergens, non-specific irritants or drugs, and inadequate long-term treatment may be responsible. High flow oxygen therapy, high dose topic beta(2)-agonists and systemic glucocorticosteroids should be used as baseline therapy in outpatients. In hospital, intravenous therapy-eventually including sedatives-can be administered under controlled or intensive care conditions. In patients with increasing respiratory pump weakness and alveolar hypoventilation, non-invasive and/or invasive mechanical ventilation may be required. In ventilated asthma patients permissive hypercarbia has been shown to reduce complications such as pneumothorax. Bronchoscopy and bronchial lavage are recommended for patients ventilated with increasing pressures or when atelectasis occurs.
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PMID:[Acute severe asthma in older adults]. 1505 78

Lung hyperinflation is a consequence of airway obstruction, increased airway resistance and compliance in patients with chronic obstructive pulmonary disease (COPD) which may result in respiratory muscle fatigue and deterioration of gas transfer. The aim of this study was to investigate the influence of hyperinflation on respiratory muscles, gas transfer and breathing pattern and compare the differences between mild and severe COPD. Twenty-eight COPD patients with radiological and tomographic evidence of emphysema were included in the study and they were divided into two groups according to the severity of COPD. Group I= FEV(1) < or = 49% (n= 16). Group II= FEV(1) > or = 50% (n= 12). Airflow rates were decreased and airway resistance was increased significantly in Group I. Maximal inspiratory pressure (MIP) was significantly reduced in Group I. FRC, RV and RV/TLC ratio were increased above 120% in both groups with more significant increase in Group I. Group I showed moderate hypoxemia (PaO(2) = 54.02 mmHg) with hypercapnia (PaCO(2)= 46.65 mmHg) whereas Group II patients were mildly hypoxemic (PaO(2)= 63.78 mmHg) with normocapnia. Parameters of breathing pattern were similar in both groups. Diaphragm height index (DHI) didn't showed significant difference between groups. But there were significant correlations between DHI and RV, FRC. MIP showed significant positive correlation with airflow rates and DLCO, negative correlation with lung volumes, positive correlation with PaO(2) and negative correlation with PaCO(2). FRC also negatively correlated with Ti and Ti/Ttot. In conclusion, hyperinflation present even in the mild forms of COPD causes inspiratory muscle weakness which in return results in impairment in gas transfer.
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PMID:[The effect of hyperinflation on respiratory muscles and breathing pattern in COPD]. 1514 1

Central sleep apnea syndrome (CSAS) is a disorder characterized by repeated apneic events during sleep with no associated ventilatory effort. CSAS is classified as either hypercapnic or non-hypercapnic. In the hypercapnic form of CSAS, increases in PaCO(2) generally result from reductions in ventilation or outright apneas due to an underlying depression of respiratory drive. Hypercapnic CSAS is common in central hypoventilation syndromes which may be primary (idiopathic) or secondary to other disorders that cause damage to the respiratory center. Non-hypercapnic CSAS is not associated with either a primary reduction in respiratory drive or respiratory muscle weakness. Non-hypercapnic CSAS can be a primary disorder or can occur secondary to high altitude, other medical illnesses such as congestive heart failure and central nervous system disease.
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PMID:[Central sleep apnea syndrome]. 1514 16

Diaphragmatic weakness in Charcot-Marie-Tooth (CMT) disease may be more common than generally acknowledged. Recognizing diaphragmatic weakness in a patient with CMT is important since recognition of this process may help explain the symptoms of breathlessness and orthopnea, as well as the development of hypercarbia. Although most patients with CMT have a normal lifespan, the subset of patients with diaphragmatic weakness may be at a higher risk of pulmonary morbidity and early mortality. Elevation of one or both hemidiaphragms on chest roentgenogram should raise the suspicion of diaphragmatic dysfunction and prompt further investigation.
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PMID:Phrenic nerve involvement in Charcot-Marie-Tooth disease. 1629 69

The point mutation in the mitochondrial genome tRNA(Leu_ (A3243G) is associated with the syndrome of mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes (MELAS). We report a boy presenting with respiratory compromise and hypercarbia owing to severe muscle weakness. Historically, he demonstrated idiopathic growth hormone deficiency, retarded bone age, and exercise avoidance. Owing to severe respiratory compromise out of proportion to expected recovery, a metabolic work-up was performed. Muscle biopsy demonstrated abnormal mitochondria structure and heteroplasmic A3243G mutation. Idiopathic growth hormone deficiency and retarded bone age have not been previously reported in MELAS, and these findings delayed testing for mitochondrial disease. This case demonstrates that isolated muscle weakness in the context of other organ system abnormalities should make the investigator consider MELAS. (J Child Neurol 2006;21:77-79).
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PMID:A boy with muscle weakness, hypercarbia, and the mitochondrial DNA A3243G mutation. 1655 59

Involvement of respiratory muscles is a nearly constant feature of neuromuscular disorders, leading to respiratory failure. A careful respiratory follow up adapted to the variable time course of each disease is therefore mandatory. As the first step, a systematic clinical evaluation is essential to detect the subtle respiratory symptoms and signs related to respiratory muscle failure. Dyspnea and orthopnea are often late findings in patients with a usually severe functional impairment due to peripheral muscle weakness. Nocturnal respiratory events (obstructive sleep apnea syndrome and hypoventilation) are strongly suggested by daytime hypersomnolence and frequent morning headaches. Physical evaluation is essential to detect accessory muscle recruitment, supine abdominal paradox, and encumbrance of upper or lower airways. Vital capacity (VC) is the most classical lung function test. The major limitation of spirometry is its poor sensitivity to detect a moderate inspiratory muscle weakness. Supine VC may improve the detection of diaphragmatic involvement. Peak expiratory flow during cough (cough PEF) gives an overall evaluation of cough efficiency, values below 160 to 270 L/min suggesting poor airway clearance. Arterial blood gases are performed in case of clinical signs, significant deterioration of lung function tests, or sleep desaturations. Hypercapnia is weakly related to lung function results in patients with Steinert dystrophy and those with bulbar involvement. A specific evaluation of respiratory muscle strength is mandatory, as these tests are both sensitive and highly prognostic. Possible discrepancies (particularly in bulbar patients) between maximal inspiratory pressure (PImax) and sniff nasal inspiratory pressure (SNIP) justify to perform both measurements and to select the highest pressure. A maximal expiratory pressure (PEmax) below 45 cm H2O may indicate a compromised cough efficiency but the correlation with cough PEF may be poor. A screening nocturnal oxymetry is useful to detect sleep apneas and hypoventilation. Criteria defining significant desaturations remain however controversial. Suspicion of obstructive sleep apnea syndrome on clinical grounds or oxymetry findings should be confirmed by a conventional polysomnography.
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PMID:[Neuromuscular disorders - assessment of the respiratory muscles]. 1658 4

Metformin is a biguanide. Due to its effects in suppressing the hepatic production of endogenous glucose and in increasing insulin sensitivity in adipose tissue and skeletal muscle, the agent is used particularly in type 2 diabetes mellitus and metabolic syndrome, in which insulin resistance is especially pronounced. Lactic acidosis is one of the most important side effects of metformin. A male patient, born in 1923, was admitted to the emergency unit of our hospital for sudden vertigo, weakness, dyspnea, cyanosis, and lethargy. His history data showed that the patient had been suffering from type 2 diabetes mellitus for 10 years and taking Glargin (insulin), 12 U/kg, once daily and Glucophage (metformin), 850 mg thrice daily. The patient's general condition was fair; stupor, time and spatial orientation were absent. Analysis of arterial blood gases showed the presence of metabolic acidosis, hypokalemia, hypoxemia, and hypercapnia. Thereafter the patient was transferred to the intensive care unit of the hospital; intubated and connected to a T-bird ventilation apparatus. On the following day, an analysis of arterial blood gases indicated the proximity of the results to their physiological parameters. Ventilation was stopped; and monitoring of the patient continued by following the T-shape type of ventilation discontinuation. There were no X-ray signs of pneumonia or pulmonary edema. On the same day, the patient was extubated and oxygen inhalation in a dose of L/min was continued through a mask. On day 4 since therapy was initiated, the patient's vital signs, serum sugar and lactate levels became normal. By determining a new treatment regimen, the patient was discharged from the intensive care unit. Dyspnea, acidosis, and hypoxia developed in the patient resulted from lactic acidosis caused by the use of metformin. It should be remembered that dyspnea, acidosis, and hypoxia, which suddenly developed in metformin-treated patients with type 2 diabetes mellitus, may be caused by lactic acidosis.
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PMID:[A clinical case of development of lactic acid acidosis in a diabetic patient taking metformin]. 1675 49

In neuromuscular disease (NMD) patients with progressive muscle weakness, respiratory muscles are also affected and hypercapnia can increase gradually as the disease progresses. The fundamental respiratory problems NMD patients experience are decreased alveolar ventilation and coughing ability. For these reasons, it is necessary to precisely evaluate pulmonary function to provide the proper inspiratory and expiratory muscle aids in order to maintain adequate respiratory function. As inspiratory muscle weakening progresses, NMD patients experience hypoventilation. At this point, respiratory support by mechanical ventilator should be initiated to relieve respiratory distress symptoms. Patients with adequate bulbar muscle strength and cognitive function who use a non-invasive ventilation aid, via a mouthpiece or a nasal mask, may have their hypercapnia and associated symptoms resolved. For a proper cough assist, it is necessary to provide additional insufflation to patients with inspiratory muscle weakness before using abdominal thrust. Another effective method for managing airway secretions is a device that performs mechanical insufflation-exsufflation. In conclusion, application of non-invasive respiratory aids, taking into consideration characterization of respiratory pathophysiology, have made it possible to maintain a better quality of life in addition to prolonging the life span of patients with NMD.
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PMID:Pulmonary rehabilitation in patients with neuromuscular disease. 1680 78

Amyotrophic lateral sclerosis (ALS) is a disease with progressive muscle weakness, also affecting respiratory muscles. In the terminal phase most patients experience a progression. Nutrition, speech and breathing capacity decrease. It is important to inform the patient and relatives in time and to give them a chance to decide. "Care Planning" and "Advance Directives" especially concerning ventilation reduces fear and helps the doctors and carers to decide, following the will of the patient. Nobody knows the speed of the progression. The patient in this case had few subjective symptoms at the time of the family conference. Progression till death lasted one month only. Treatment of his dyspnoe was not optimised, but during care all decisions were based on the actual will of the patient. Generally nocturnal hypoventilation, for instance non-invasive ventilation by BiPAP-mode, can relieve symptoms of dyspnoe in ALS patients. Low-dose morphine and/or benzodiazepine relieve respiratory discomfort and remove the negative spiral of dysnoe-fear-dyspnoe. Oxygen therapy is usually not needed (only in the very last stages of the disease) and is not recommended especially during the night. Hypercapnia can occur because of hypoventilation. This can cause growing unconsciousness and maybe death during sleep. Prolonging life is only possible by invasive long-term ventilation with all the problems of intensive care measures. The patient could have been given low dose morphine from the time of the family conference. Ventilation by CPAP-mode was insufficient for him.
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PMID:[Amyotrophic lateral sclerosis--when planning is almost too late]. 1683 Feb 50

Here we report two cases of congenital myopathy visited our hospital with respiratory failure. Case 1 was a 31-year-old woman, who had muscular weakness from birth but had never been diagnosed. She had an onset of pneumonia followed by severe type 2 respiratory failure. Even after the healing of pneumonia, hypercapnia remained. A diagnosis of nemaline myopathy was made after muscle biopsy. Case 2 is a 62-year-old man, who had slowly progressing respiratory failure accompanied with severe hypercapnea. His respiratory failure was improved by NIPPV. He also under went muscle biopsy and nemaline myopathy was diagnosed. Nemaline myopathy is one of congenital myopathy and is known to be a nonprogressive or slowly progressive disorder. However, some patients are diagnosed appropriately only when adult onset acute respiratory failure occurs.
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PMID:[Two cases of nemaline myopathy diagnosed after episodes of respiratory failure]. 1684 21


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