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Query: UMLS:C0020440 (hypercapnia)
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Nutritional assessment and management is an important therapeutic modality in patients with respiratory disease. Malnutrition adversely affects respiratory function. Nutritional therapy for the spontaneously breathing patient should include an appropriate diet plus the consideration of nutritional supplements. Complete nutritional support should be undertaken with enteral nutrition in critically ill patients with respiratory failure. Nutritional complications occur. Overfeeding can lead to nutritionally associated hypercapnia.
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PMID:Enteral nutrition in patients with respiratory disease. 877 78

Impaired pulmonary gas exchange can result from lung parenchymal failure inducing oxygenation deficiency and fatigue of the respiratory muscles, which is characterized by hypercapnia or a combination of both mechanisms. Contractility of and coordination between the diaphragm and the thoracoabdominal respiratory muscles predominantly determine the efficiency of spontaneous breathing. Sepsis, cardiac failure, malnutrition or acute changes of the load conditions may induce fatigue of the respiratory muscles. Augmentation of spontaneous breathing is not only achieved by the application of different technical principles or devices; it also has to improve perfusion, metabolism, load conditions and contractility of the respiratory muscles. Intermittent mandatory ventilation (IMV) allows spontaneous breathing of the patient and augments alveolar ventilation by periodically applying positive airway pressure tidal volumes, which are generated by the respirator. Potential advantages include lower mean airway pressure (PAW), as compared with controlled mechanical ventilation, and improved haemodynamics. Suboptimal IMV systems may impose increased work and oxygen cost of breathing, fatigue of the respiratory muscles and CO2 retention. During pressure support ventilation (PSV), inspiratory alterations of PAW or gas flow (trigger) are detected by the respirator, which delivers a gas flow to maintain PAW at a fixed value (usually 5-20 cm H2O) during inspiration. PSV may be combined with other modalities of respiratory therapy such as IMV or CPAP. Claimed advantages of PSV include decreased effort of breathing, reduced systemic and respiratory muscle consumption of oxygen, prophylaxis of diaphragmatic fatigue and an improved extubation rate after prolonged periods of mechanical ventilation. Minimum alveolar ventilation is not guaranteed during PSV; thus, close observation of the patient is mandatory to avoid serious respiratory complications. Continuous positive airway pressure breathing (CPAP) maintains PAW above atmospheric pressure throughout the respiratory cycle, which may increase functional residual capacity and decrease the effort of breathing. CPAP has been conceptually designed for the augmentation of spontaneous breathing and requires the intact central and peripheral regulation of the respiratory system. Airway pressure release ventilation (APRV) improves alveolar ventilation by intermittent release of PAW, which is kept above atmospheric pressure by means of a high-flow CPAP system. The opening of an expiratory valve for 1-2 s induces a decreased PAW and lung volume, which increases rapidly to pre-exhalation values after closure of the valve due to the high gas flow within the circuit (90-100 1/min). APRV may improve haemodynamics and VA/Q distribution as compared with conventional mechanical ventilation. Biphasic positive airway pressure (BIPAP) is characterized by the combination of spontaneous breathing and time-regulated, pressure-controlled mechanical ventilation. During the respiratory cycle the ventilator generates two alternating CPAP levels, which can be modified with regard to time and pressure. As with APRV, alveolar ventilation is maintained even if the spontaneous breathing efforts of the patient cease, which improves the safety of both modes of respiratory therapy. The contribution of spontaneous breathing to total minute ventilation may be important, since a decreased shunt and improved VA/Q relationship have been observed in experimental non-cardiogenic lung oedema. These data give support to the concept that spontaneous breathing should be maintained and augmented in the setting of acute respiratory failure.
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PMID:[Augmented spontaneous breathing]. 896 3

We previously reported that patients with spinal muscular atrophy do not lose muscle strength over time as measured quantitatively. However, we noted that many patients with spinal muscular atrophy suffer from what they call fatigue. We wondered if we could measure fatigue during a single maximal voluntary contraction, whether fatigue might increase with time, independent of muscle strength, and whether increasing fatigue might correlate with loss of function in some patients. We measured fatigue during a single maximal voluntary contraction in a cohort of patients having spinal muscular atrophy using quantitative strength testing. We included only patients with spinal muscular atrophy aged 5 years or older, so they could follow instructions regarding muscle contraction, and who were followed for at least 2 years. Seventy-six children with spinal muscular atrophy and 24 untrained individuals, aged 5 to 57 years (mean, 16.8 years), were studied. There was no discernible abnormal fatigue in patients with spinal muscular atrophy compared to untrained controls using our methodology. Thus, spinal muscular atrophy may not be associated with fatiguability. Moreover, spinal muscular atrophy does not appear to cause progressive muscle fatigue with age or loss of function. It is possible that fatigue was undetectable by our methods. An alternative explanation is that what patients describe as fatigue may be caused by factors outside the neuromuscular system. Such factors may include chronic respiratory insufficiency with hypoventilation and carbon dioxide retention as well as chronic malnutrition and negative nitrogen balance.
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PMID:Muscle fatigue in spinal muscular atrophy. 937

In many patients with neuromuscular diseases, respiratory failure is mainly caused by alveolar hypoventilation in their terminal stages. Malnutrition is one of the common and serious problems in patients with chronic respiratory failure. Energy consumption for breathing is remarkably high in respiratory compromised patients, causing subsequent increase of total energy expenditure. However, most patients have limited capacity of oral intake. Nutritional depletion is associated with wasting of respiratory muscles, impairment of respiratory drive, alteration of respiratory pattern, and pathological change of pulmonary parenchyma. These indicate that nutritional and ventilatory support is very important in these patients. However, overfeeding also may have detrimental influence on respiratory failure. We experienced a Duchenne muscular dystrophy (DMD) patient on noninvasive positive pressure ventilation (NIPPV) who developed hypercapnia after total parenteral nutrition (TPN). Analysis of clinical course of this patient revealed that there is a significant correlation between PaCO2 and caloric intake. Excess carbohydrate intake can precipitate fat synthesis which induces over-production of carbon dioxide (CO2). Since NIPPV doesn't have a closed circuit, there are some difficulties in respiratory management, such as air leakage to stomach and mouth, and airway obstruction. Failure to optimize NIPPV setting against increased CO2 load might cause hypercapnia in this patient. These suggest that evaluation of energy expenditure and design of nutritional program are essential to avoid hypercapnia due to nutritional support.
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PMID:[Excess caloric intake induced severe hypercapnia in a patient with Duchenne muscular dystrophy on noninvansive positive pressure ventilation]. 1007 34

Malnutrition, hypoxia and energy deficit may affect protein metabolism. We wanted to evaluate the cross-sectional association between serum amino acids and fat-free mass in a group of hypoxic patients. We also wanted to explore, in the same group of patients, whether the blood amino-acid pattern could possibly be influenced by differences in lung function and energy intake. Serum amino acids were measured in 71 hypoxic underweight and normal-weight patients with advanced pulmonary disease and related to the fat-free-mass index, arterial oxygen (PaO2) and carbon dioxide tension (PaCO2), forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1) and energy intake. Only one amino acid (aspartic acid) remained significantly correlated to the fat-free-mass index after adjustments for age and sex (beta = -0.30, P=0.011). None of the amino acids were significantly correlated to PaO2 but alanine was significantly negatively correlated to PaCO2 (beta = -0.46, P<0.001), phenylalanine to FVC1 (beta = 0.52, P=0.001) and tyrosine to FVC (beta = 0.36, P=0.008). Citrulline and tryptophan were significantly correlated to energy intake (beta = 0.32, P=0.008; beta=0.37, P=0.009 respectively). In conclusion, there was no convincing association between fat free mass and serum amino acids. The negative effect of hypercapnia and reduced lung function on some serum amino acids was suggested and some amino acids were sensitive to reduced energy intake.
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PMID:Serum amino acids in relation to nutritional status, lung function and energy intake in patients with advanced pulmonary disease. 1100 Oct 78

The aim of this study was to analyse the correlates of reduced bone mineral density in patients with chronic obstructive pulmonary disease (COPD), with special regard to a possible protective role of hypercapnia. One hundred and four consecutive COPD inpatients in stabilized respiratory conditions underwent a comprehensive assessment of their health status. Bone mineral density was measured by X-ray absorptiometry at the lumbar site and at the femoral neck site. Differences in health-related variables between patients with (group O, n=62) and without (group N, n=42) lumbar and/or femoral neck osteoporosis were assessed first by univariate analysis and then by logistic regression analysis aimed to identify independent correlates of osteoporosis. Group O was characterized by worse nutritional status, as reflected by indices exploring either lean or fat mass, and by a trend towards lower forced expiratory volume in 1 sec/forced vital capacity ratio. Arterial tension of carbon dioxide lacked any correlation with bone mineral density. According to the logistic regression analysis, body mass index < or = 22 kg m(-2) qualified as the only and positive independent correlate of osteoporosis (odds ratio=4.18; 95% confidence intervals=1.19-14.71). In conclusion, malnutrition characterizes COPD patients with osteoporosis, while mild to moderate hypercapnia lacks either a positive or negative effect on bone mineral density. Longitudinal studies are needed to identify predictors rather than correlates of bone mineral density.
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PMID:Correlates of osteoporosis in chronic obstructive pulmonary disease. 1112 95

Nutritional management of patients with respiratory failure can be a model of nutritional management in chronically critically ill patients. This model requires recognition of the differing metabolic states of starvation and hypermetabolism. Starvation can result in malnutrition, with adverse effect on respiratory muscle strength, ventilatory drive, and immune defense mechanisms. General nutritional goals include preservation of lean body mass by providing adequate energy and positive nitrogen balance. General nutritional prescriptions for both states include a substrate mix of 20% protein, 60% to 70% carbohydrates, and 20% to 30% fat. Positive nitrogen balance is difficult to attain in hypermetabolic patients and energy requirements are increased compared with starved patients. Enteral nutrition should be the mode of initial nutrient delivery unless the gastrointestinal tract is nonfunctional. Monitoring of nutritional support is essential. Complications of nutritional support are multiple. Nutritional hypercapnia is an important complication in a chronically critically ill patient. Outcomes of selected long-term acute patients are poor, with only 8% of patients fully functional 1 year after discharge. Appropriate nutritional therapy is one aspect of management of these patients that has the possibility of optimizing function and survival.
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PMID:Nutrition in chronic critical illness. 1131 53

Respiratory failure as a result of overload and/or reduced capacity of the respiratory muscles is the most common cause of unsuccessful weaning and the need for long term mechanical ventilation. Chronic obstructive pulmonary disease (COPD) is the most common underlying cause leading into long term mechanical ventilation. The most important clinical parameter for fatigue of the respiratory muscles is the rapid shallow breathing index. Other essential factors which impact weaning failure, are the underlying diseases (e. g. neuromuscular disease or heart failure), micro- and macro aspiration, malnutrition, anemia and obesity. A protocol based strategy to discontinue mechanical ventilation and the use of weaning predictors are helpful. Nonetheless the experienced physician is irreplacable in the weaning process. Reconditioning of the respiratory muscles is the main focus during weaning after long term mechanical ventilation and all therapeutic measures should be targeted to unload the fatiguing respiratory muscles. With the widely used assisted ventilation modes, the inspiratory work of breathing is still significantly increased. Only controlled mechanical ventilation (pressure- or volume controlled), which may also be applied to unsedated patients when individually adapted, offers the best possible relief and recovery of the respiratory muscles. Additional strategies, such as the balancing of anemia, reduction of the respiratory drive with i. e. morphine derivates, oxygen therapy during spontaneous-breathing trials and supine position for patients with obesity contribute to the recovery. Particularly patients with chronic lung diseases with hypercapnia benefit from the use of non invasive ventilation (NIV) after extubation to prevent postextubation failure and even after tracheostomy. However, NIV should only be applied under close monitoring and in cooperative patients, always considering the limits of the method. Dying under mechanical ventilation in the end stage illness is still a challenge for all involved persons. In the end stage of their disease for some patients it is possible to discontinue mechanical ventilation so they can spend the last period of their lives on a normal ward or even at home.
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PMID:[Difficult weaning]. 1704 78

Advanced age, smoking habit, obesity or malnutrition, the coexistence of hypercapnia, bronchospasm or bronchial hypersecretion, the lack of pre-operative preparation and/or a prolonged duration of anaesthesia can negatively influence respiratory function in patients undergoing abdominal or thoracic surgery. Spirometric testing of pulmonary function is recommended in patients with a history of tobacco use or dyspnoea who are considered for cardiac or upper abdominal surgery and for all patients who are candidated for lung resection. Spirometry can provide cut-off values of acceptable risk in patients that are candidated for abdominal and thoracic surgery. At-risk patients having resective lung surgery should undergo a split lung function study with quantitative lung scanning or computed tomography in order to estimate the function of residual parenchyma after surgery. In patients with borderline estimated values, a cardiopulmonary exercise test is useful to further stratify surgical risk.(www.actabiomedica.it)
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PMID:Respiratory effects of surgery and pulmonary function testing in the preoperative evaluation. 1717 84

Acid-sensitive K+ channels of the tandem P-domain K+-channel family (TASK-1 and TASK-3) have been implicated in peripheral and central respiratory chemosensitivity; however, because of the lack of decisive pharmacological agents, the final proof of the role of the TASK channel in the chemosensory control of breathing has been missing. In the mouse, TASK-1 and TASK-3 channels are dispensable for central respiratory chemosensitivity (Mulkey et al., 2007). Here, we have used knock-out animals to determine whether TASK-1 and TASK-3 channels play a role in the carotid body function and chemosensory control of breathing exerted by the carotid body chemoreceptors. Ventilatory responses to hypoxia (10% O2 in inspired air) and moderate normoxic hypercapnia (3-6% CO2 in inspired air) were significantly reduced in TASK-1 knock-out mice. In contrast, TASK-3-deficient mice showed responses to both stimuli that were similar to those developed by their wild-type counterparts. TASK-1 channel deficiency resulted in a marked reduction of the hypoxia (by 49%)- and CO2 (by 68%)-evoked increases in the carotid sinus nerve chemoafferent discharge recorded in the in vitro superfused carotid body/carotid sinus nerve preparations. Deficiency in both TASK-1 and TASK-3 channels increased baseline chemoafferent activity but did not cause a further reduction of the carotid body chemosensory responses. These observations provide direct evidence that TASK-1 channels contribute significantly to the increases in the carotid body chemoafferent discharge in response to a decrease in arterial P(O2) or an increase in P(CO2)/[H+]. TASK-1 channels therefore play a key role in the control of ventilation by peripheral chemoreceptors.
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PMID:A role for TASK-1 (KCNK3) channels in the chemosensory control of breathing. 1875 86


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