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

Acute ventilatory insufficiency is characterized by hypercapnia, respiratory acidosis and secondary hypoxemia. The primary target of mechanical ventilation is improvement of alveolar ventilation, that means compensation of the ventilatory insufficiency. Noninvasive ventilation started as ventilatory support during the big polio epidemic, at that time in form of negative pressure ventilation. In the last two decades NIV is in form of positive pressure ventilation important for long-term ventilation at home, but there is also growing importance of NIV in the treatment of acute respiratory insufficiency in the intensive care unit. Main indication is the hypercapnic ventilatory failure in acute exacerbation of COPD. This paper will discuss ventilator therapy in general but also the data regarding the role of NIV in the treatment of hypercapnic failure. Specific points like interfaces, indications and contraindications of NIV are addressed.
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PMID:[Mechanical ventilation in acute ventilatory insufficiency]. 1760 89

The authors tested whether macrophage metalloelastase (MMP-12) and substance P (SP) were increased in the cigarette smoke (CS)-exposed female C3H/HeN mice with hypercapnic emphysema. The authors found that as compared to control (filtered air), 16 weeks of CS exposure significantly up-regulated mRNA and protein levels of MMP-12, the ratio of MMP-12/tissue inhibitor of matrix metalloproteinase-1, and SP/preprotachykinin-A (a precursor to SP) in the lungs. Importantly, a significant correlation was found between MMP-12 and SP, and between MMP-12/SP and the degrees of hypoxemia/hypercapnia denoted in CS-exposed mice. These data suggest a possible involvement of SP and MMP-12 in the pathogenesis of severe COPD.
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PMID:Cigarette smoke-induced hypercapnic emphysema in C3H mice is associated with increases of macrophage metalloelastase and substance P in the lungs. 1762 Jan 83

COPD is a frequent disease, affecting approximately one in four smokers. In older patients > 70 years of age, the proportion of individuals who never have smoked increases up to one in three individuals. Severe disease is present in 10%, and the limitation of performance is usually caused by airway obstruction, in a smaller portion of patients by the loss of alveolar surface (emphysema). After medical treatment with antiobstructive and anti-inflammatory drugs, oxygen remains a major therapy option. With it, hypercapnic patients benefit most from long-term therapy. Patients with predominant emphysema benefit most from high-flow (6-8 l/min) oxygen therapy during exercise. Permanent yellow or greenish sputum decoloration is suggestive of chronic bacterial colonization. This group of patients may benefit from a permanent inhalative therapy with antibiotics (mainly aminoglycosides). There is growing evidence from current literature to support this concept. If dyspnea is severe, especially during mild exercise, a subset of patients might benefit from the use of long-acting morphium. Goal of this therapy is to downregulate breathing control. Predominantly "pink puffers" seem to respond. A dose of 10-20 mg will usually be sufficient. Life-threatening hypercapnia is usually not observed with this form of therapy. Noninvasive ventilation is an option for patients with severe hypercapnia. Thereby, ventilatory pressure or inspiratory volume should be selected to effectively unload the respiratory muscles. This will increase quality of life. Life span is likely to be prolonged, however, comparative data where patients were effectively ventilated (as seen on the reduction of hypercapnia) are missing. A multicenter trial addressing this topic is currently being conducted in Germany. Independent of the severity of COPD, patients in general benefit from physical training with alternation of endurance and interval training being most effective. This will decrease the number of hospital admissions and probably mortality as well. Lung volume reduction surgery virtually treats lung hyperinflation. Bullectomy is still considered effective for isolated bullous emphysema as well as lobectomy, if this portion of the lung is without function. Shaving procedures are still associated with high rates of complications and should only be performed in selected cases. Effectiveness of endoscopic lung volume reduction surgery by implantation of plugs or valves cannot be assessed yet. First data are rather disappointing. Ultimate alternative remains lung transplantation with life expectancy ranging between 5-6 years independent of age. Indeed, consequent application of previously described measures might preserve a stable state over many years.
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PMID:[Clinical Year in Review - advanced COPD]. 1799 82

Hypoxia and endothelial dysfunction play a central role in the development of pulmonary hypertension. Cor pulmonale is a maladaptive response to pulmonary hypertension. The presence of peripheral edema in cor pulmonale is almost invariably associated with hypercapnia. Correction of abnormalities of gas exchange and ventilation can ameliorate pulmonary hypertension and improve survival. This review focuses on new information about the pathogenesis and treatment of pulmonary hypertension in COPD including information derived from lung volume reduction surgery, the role of brain natriuretic peptide, exhaled nitric oxide for diagnosis, and the treatment of cor pulmonale with recently available specific pulmonary vasodilators.
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PMID:Pulmonary hypertension and chronic cor pulmonale in COPD. 1822 65

Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) describe the phenomenon of sudden worsening in airway function and respiratory symptoms in patients with COPD. These exacerbations can range from self-limited diseases to episodes of florid respiratory failure requiring mechanical ventilation. The average patient with COPD experiences two such episodes annually, and they account for significant consumption of health care resources. Although bacterial infections are the most common causes of AECOPD, viral infections and environmental stresses are also implicated. AECOPD episodes can be triggered or complicated by other comorbidities, such as heart disease, other lung diseases (e.g., pulmonary emboli, aspiration, pneumothorax), or systemic processes. Pharmacologic management includes bronchodilators, corticosteroids, and antibiotics in most patients. Oxygen, physical therapy, mucolytics, and airway clearance devices may be useful in selected patients. In hypercapneic respiratory failure, noninvasive positive pressure ventilation may allow time for other therapies to work and thus avoid endotracheal intubation. If the patient requires invasive mechanical ventilation, the focus should be on avoiding ventilator-induced lung injury and minimizing intrinsic positive end-expiratory pressure. These may require limiting ventilation and "permissive hypercapnia." Although mild episodes of AECOPD are generally reversible, more severe forms of respiratory failure are associated with a substantial mortality and a prolonged period of disability in survivors.
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PMID:Acute exacerbations and respiratory failure in chronic obstructive pulmonary disease. 1845 67

COPD is a disease that is not confined to the airways and the lungs, but also produces systemic consequences. Muscle weakness is one of these. It is produced by a multitude of factors including deconditioning, systemic inflammation, oxidative stress, nutritional imbalance, reduced anabolic status, systemic corticosteroids, hypoxemia, hypercapnia, electrolyte disturbances, cardiac failure. The most important factors appear to be inactivity and systemic inflammation. Inactivity was shown to be present in patients with COPD from early in the course of the disease on. Systemic inflammation was shown to be predominantly present during COPD exacerbations. IL-6 has the propensity to reduce muscle function in experimental animals. At present there is no evidence of local production of cytokines in the muscle in patients with COPD. Muscle weakness is also important in the clinical course of the disease as it is associated with exercise intolerance, reduced quality of life, enhanced utilization of health care resources and reduced survival. Rehabilitation is the best treatment for muscle weakness and deconditioning in patients with COPD. Indeed, it is the intervention with the largest effect on health status and exercise capacity in these patients. Several factors that may enhance the effects of rehabilitation have been studied. These include: growth hormone/ IGF-I, anabolic steroids, clenbuterol, creatine, anti-cytokine treatment, erythropoietin, oxygen, non-invasive mechanical ventilation and electrical stimulation. Recently, the potential of protease-inhibitors in reversing deconditioning-induced muscle dysfunction was demonstrated. Adjuncts are potentially particularly useful in patients who do not respond to a rehabilitation programme. Analysis of large d-bases demonstrated that about one third of the patients does not respond to rehabilitation. A follow-up study suggests that decline in exercise capacity after a rehabilitation programme is particularly present in these patients and not in the patients with a clear initial response. A better understanding of the factors controlling the response to rehabilitation, may lead to significant advances in this field.
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PMID:Pulmonary rehabilitation 2007: from bench to practice and back. 1898 Jul 25

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

Hypercapnia (high CO(2) levels) occurs in a number of lung diseases and it is associated with worse outcomes in patients with chronic obstructive lung disease (COPD). However, it is largely unknown how hypercapnia is sensed and responds in nonneuronal cells. Here, we used C. elegans to study the response to nonanesthetic CO(2) levels and show that levels exceeding 9% induce aberrant motility that is accompanied by age-dependent deterioration of body muscle organization, slowed development, reduced fertility and increased life span. These effects occur independently of the IGF-R, dietary restriction, egg laying or mitochondrial-induced aging pathways. Transcriptional profiling analysis shows specific and dynamic changes in gene expression after 1, 6, or 72 h of exposure to 19% CO(2) including increased transcription of several 7-transmembrane domain and innate immunity genes and a reduction in transcription of many of the MSP genes. Together, these results suggest specific physiological and molecular responses to hypercapnia, which appear to be independent of early heat shock and HIF mediated pathways.
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PMID:Elevated CO2 levels affect development, motility, and fertility and extend life span in Caenorhabditis elegans. 1923 58

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 patients with severe COPD and chronic hypercapnic respiratory failure (CHRF) receiving non-invasive home ventilation has greatly increased. With regard to disease severity, a multidimensional assessment seems indicated. Base excess (BE), in particular, reflects the long-term metabolic response to chronic hypercapnia and thus constitutes a promising, easily accessible, integrative marker of CHRF. Infact, BE as well as nutritional status and lung hyperinflation have been identified as independent predictors of long-term survival. In addition and in a review with the literature, a broad panel of indices including frequent comorbidities are helpful for assessment and monitoring purposes of patients with CHRF. Accordingly, in view of the patients' individual risk profile, the decision about the initiation of NIV should probably not rely solely on symptoms and chronic persistent hypercapnia but include a spectrum of factors that specifically reflect disease severity. Owing to the physiologically positive effects of NIV and according to retrospective data, patients with COPD and recurrent hypercapnic respiratory decompensation and patients with prolonged mechanical ventilation and/or difficult weaning could also be considered for long-term non-invasive ventilation. This, however, has to be corroborated in future prospective trials.
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PMID:[Prognostic factors for COPD patients with chronic hypercapnic respiratory failure and home ventilation]. 1975 Apr 11


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