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)

Serial assessments of respiratory function were performed over 1 to 8 years in 12 patients with myotonic dystrophy. Respiratory parameters included vital capacity (percentage of predicted value; %VC) and one-second forced expiratory volume (percentage of predicted value; FEV1.0%) on spirogram and arterial blood gases at rest. The patients who had no primary respiratory disease were ranged in age from 31 to 61 years, with an average age of 47 years, and their mean duration of illness was 20 years. All the subjects were severely disabled; only two patients were able to walk with assistance, but other ten patients were confined to a wheelchair. During the observation period, five patients died; 4 due to respiratory failure and one cardiac and respiratory failure. The following results were obtained: (1) almost all the patients showed a reduction in %VC, the severity of which was gradually progressed with advancing age. A significant negative correlation was observed between %VC and duration of illness. (2) PaCO2 was negatively correlated with %VC, while the relationship between PaO2 and %VC appeared to be a significant positive correlation. Chronic alveolar hypoventilation (hypercapnia and hypoxemia) was particularly likely when vital capacity (VC) was less than 40% of the predicted value in the patients. This study indicates that a reduction of VC plays an important role in development of respiratory failure in myotonic dystrophy and serial measurements of VC and arterial blood gases are useful in the detection of it.
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PMID:[Serial observations of respiratory function in disabled patients with myotonic dystrophy]. 826 95

Nasal intermittent positive-pressure ventilation (NIPPV) has been used for domiciliary ventilatory support, and to avoid intubation for acute respiratory failure in patients with chronic airflow limitation (CAL). Its role in weaning patients from assisted ventilation in intensive care has not been defined. We have used NIPPV to wean 14 patients with respiratory disease who were referred either because of predicted difficulty in weaning or failure to wean using standard techniques. Twelve patients were ventilated for acute respiratory failure; eight patients had CAL and four had chest wall or neuromuscular disease. Two further patients with chest disease were difficult to wean following surgery. Weaning was successful in 13 patients. NIPPV corrected hypoxia, reduced hypercapnia and was well tolerated. Weaning from NIPPV was achieved in all patients with CAL, although three patients with chest wall disease later required domiciliary ventilatory support. All but one of the patients survived to leave hospital. NIPPV may have an important role in weaning from assisted ventilation, particularly in patients with underlying chronic respiratory disease. This preliminary report needs to be followed by a controlled study comparing NIPPV with established weaning methods.
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PMID:Nasal intermittent positive-pressure ventilation in weaning intubated patients with chronic respiratory disease from assisted intermittent, positive-pressure ventilation. 849 99

We studied the relationship of sudden unexpected infant death/apparent life-threatening events (ALTE) to obstructive sleep apnea (OSA) in 74 index probands who had either sleep-laboratory-confirmed OSA or a clinical diagnosis of OSA requiring treatment, 62 matched control probands, and their spouses and first- and second-degree relatives. Sleep was monitored in the home overnight, and OSA was defined by respiratory disturbance indices (number of apneas/hypopneas per hour of sleep) corrected for normal increases with age. Information on sudden unexpected infant death/ALTE was obtained by questionnaire and was corroborated. For living relatives, data were obtained by questionnaire, examination, or study (cephalometric radiographs, ventilatory responsiveness to hypercapnia and hypoxia). Eight index families had 10 infants with sudden unexpected infant death/ALTE; two control families had three infants with sudden death (p = 0.11). All told, 91 of the 136 families (index plus control) included members with OSA, and all 10 infant death/ALTE families were among these (versus zero of 45 families with no OSA; p = 0.03). The sudden infant death/ALTE families had a greater frequency of two or more members with OSA (p = 0.06), reported more respiratory disease or allergy, were more frequently brachycephalic (p = 0.05), and had a smaller mean posterior nasal spine-basion distance (p = 0.0001) and ratio of anterior mandibular/anterior maxillary dental height (p < 0.05). Ventilatory responses to hypoxia were reduced in members of families with OSA (p = 0.008), with a trend toward the greatest blunting in subjects from families with OSA plus sudden unexpected infant death/ALTE. Thus, OSA in adults and sudden unexpected infant death/ALTE in their biologic relatives appear to be related. Familial factors influencing this association may include the degree of the predilection for OSA, liability for respiratory illness or allergy, dimensions of the oral-pharyngeal airway, and ventilatory response to hypoxia.
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PMID:The association of sudden unexpected infant death with obstructive sleep apnea. 866 46

There is intriguing evidence suggesting pathophysiologic relationships among dyspnea, hyperventilation, and panic anxiety. The symptoms of panic attacks and pulmonary disease overlap, so that panic anxiety can reflect underlying cardiopulmonary disease and dyspnea can reflect an underlying anxiety disorder. The pathogenesis of panic may be related to respiratory physiology by several mechanisms: the anxiogenic effects of hyperventilation, the catastrophic misinterpretation of respiratory symptoms, and/or a neurobiologic sensitivity to CO2, lactate, or other signals of suffocation. In a subset of patients with PD, incipient pulmonary dysfunction may also contribute to their anxiety symptoms. Patients with pulmonary disease, particularly those with obstructive lung disease, have a high rate of panic symptoms and PD. There is reason to believe that pulmonary disease constitutes a risk factor for the development of panic related to repeated experiences with dyspnea and life-threatening exacerbations of pulmonary dysfunction, repeated episodes of hypercapnia or hyperventilation, the use of anxiogenic medications, and the stress of coping with chronic disease. Panic in pulmonary patients may carry significant morbidity, including phobic avoidance of activity, overly aggressive treatment with anxiogenic medications, and more prolonged and frequent hospitalization. Successful treatment of panic in these patients can improve functional status and quality of life by relieving anxiety and dyspnea. Nonpharmacologic treatment of panic, including cognitive-behavioral approaches, can be useful in patients with concomitant respiratory disease. Sedating medications such as benzodiazepines should be used with caution in patients with pulmonary disease to avoid respiratory depression. Serotonergic antidepressants (SSRIs) and anxiolytics (buspirone) may be effective treatments for panic or generalized anxiety in pulmonary patients and have relatively little potential for significant adverse effects.
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PMID:Panic anxiety, dyspnea, and respiratory disease. Theoretical and clinical considerations. 868 Jul

This prospective study assessed, in 10 conscious patients without a history of chronic respiratory disease, the feasibility of mechanical pressure support ventilation with PEEP by face mask for the treatment of acute respiratory failure without hypercapnia. Pressure support level was determined to obtain a VT of 5 to 10 mL.kg-1 and a decrease of respiratory rate of more than 20%. FIO2 and PEEP levels were determined to obtain a SpO2 > 92% and a PaO2 > 70 mmHg. The efficiency of the technique was assessed through the time course of respiratory rate, PaO2, PaCO2 and SaO2. The technique was efficient in all patients and tracheal intubation was not required. During face mask ventilation, a significant decrease in respiratory rate and an increase in PaO2 and SaO2 were observed. Pressure support ventilation with PEEP by face mask is an efficient technique for the treatment of acute non hypercapnic respiratory failure in conscious and cooperative patients.
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PMID:[Inspiratory aid with facial masks during acute respiratory failure without hypercapnia]. 873 48

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

We investigated nocturnal oxygen desaturation (NOD) in 36 patients with stable chronic respiratory disease who were receiving home oxygen, therapy (HOT). Study data included medical history, chest roentgenograms, measurement of daytime arterial blood gases while awake, and spirometry. Each subject underwent full overnight oximetry monitoring. Three patients were excluded from further investigation because of periodic desaturation suggestive of sleep apnea. The remaining 33 subjects were divided into two groups: 21 patients with sequelae of pulmonary tuberculosis (TB-sequela) and 12 patients with chronic obstructive pulmonary disease (COPD). The COPD group was divided into two subgroups according to the Burrows classification (Am Rev Resp Dis. 90: 14-27, 1964): 5 patients with type A (Type A) and 7 patients with type B (Type B) COPD. The percentages of total sleep time with SaO2 < or = 85% (DST 85) and SaO2 < or = 90% (DST 90) were calculated for each subject. NOD was defined as DST 85 > or = 1%. Arterial oxygen partial pressure (PaO2) while awake was > or = 60 Torr in all subjects. No difference was observed in mean awake PaO2 values between the TB-sequela and COPD groups. NOD was detected in 8 TB-sequela patients but in none of the COPD patients. Mean DST 85 and DST 90 values were significantly (p < 0.05) higher for the TB-sequela group than for the COPD group. Of 15 TB-sequela patients who were able to complete spirometry tests, 6 had NOD. All 6 of these patients had hypercapnia while awake (PaCO2 > or = 50 Torr) and reduced vital capacity (< or = 50% predicted). No difference was observed in mean DST 90 or DST 85 values between the TypeA and TypeB COPD subgroups. We conclude that NOD is common in patients with chronic stable respiratory disease treated with HOT despite daytime euoxia. TB-sequela patients with hypercapnia and restrictive ventilatory impairment are at high risk for NOD.
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PMID:[Nocturnal oxygen desaturation during home oxygen therapy in patients with chronic respiratory disease]. 1072 46

Complaints of poor sleep are very common in people with chronic respiratory disorders. In patients with chronic obstructive pulmonary disease (COPD), poor sleep may be due to many causes, including cough, excess mucous production, and frequent arousals from sleep caused by hypercapnia, as well as secondary to medications used to manage the lung disease. Patients with obstructive sleep apnea (OSA) also complain of excessive daytime sleepiness and fatigue due to poor-quality sleep, although the mechanism of sleep disruption is somewhat different from that in patients with COPD. Although benzodiazepines are often the drugs of choice for the management of insomnia, caution is suggested with the use of these agents in patients with chronic obstructive respiratory disease due to the reduction in upper airway muscle tone and blunting of the arousal response to hypercapnia. However, controlled trials with short-acting benzodiazepine receptor antagonists, including triazolam, zolpidem, and zaleplon, suggest that these agents may be safely used in selected patients who have mild to moderate COPD without daytime hypercapnia. Less data are available on the use of these agents for patients with OSA, but a preliminary trial using zaleplon suggests that respiratory function is not adversely affected in patients with mild to moderate OSA. Studies are needed to further define the benefit-risk ratio of the use of benzodiazepine receptor agonists for the management of insomnia in patients with chronic obstructive lung disease.
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PMID:Perspectives on the management of insomnia in patients with chronic respiratory disorders. 1075 6

Acute Respiratory Failure (ARF) results in an inability to maintain gas exchange at a rate commensurate with the demands of the body and results in hypoxemia and/or hypercarbia, the mechanisms of which may be different. Hypoxemia commonly occurs due to Ventilation Perfusion (V/Q) mismatching, intrapulmonary shunt, diffusion defect or hypoventilation. Hypercarpnic respiratory failure may also be multifactorial but is usually due to inhibited central respiratory drive or inefficient respiratory muscle pump. Hypercapnia may occur in upper and lower airways obstruction, respiratory muscle fatigue and occasionally due to excess CO2 production (burns and excessive glucose administration). Issues in management centre around assessment of severity, determining the need for intervention, establishing diagnosis and etiology and institution of specific treatment. Diagnosis of respiratory failure may be made clinically and confirmed by blood gas analysis. Calculation of oxygenation indices will delineate extent of hypoxemia. When evaluating a child with respiratory failure, one should be aware that a child with prominent respiratory symptoms may have non-respiratory disease (i.e. metabolic acidosis, DKA) and conversely, advanced respiratory failure may be present in a child with no respiratory distress (central hypoventilation secondary to drugs, infection) careful assessment of history, complete physical examination and evaluation of lab parameters may clarify the diagnosis. Serial assessment of sensorium, respiratory symptoms, ABG and response to treatment will provide valuable clues to determine the need for intervention. Oxygen, like any drug, must be administered in a prescribed dose, only when indicated with the potential risks borne in mind. A variety of oxygen delivery devices are available; which ever device is used, the resulting FiO2 and devisable end points must be clearly determined. Hazards of oxygen therapy range from retinal damage in premature infants, damage to the alveolar capillary membrane with resultant hypoxemia) atelectasis and decreased mucociliary activity.
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PMID:Acute respiratory failure and oxygen therapy. 1133 23

This prospective study of patients with acute respiratory illness or potential ventilatory compromise compared pCO(2) and pH on an arterial and a venous blood sample with the aims of determining whether venous pH and pCO(2) can replace arterial values in the management of patients with acute respiratory disease and to determine whether there is a cut-off level of venous pCO(2) that can accurately screen for significant hypercarbia (pCO(2) > 50 mm Hg). Data were analyzed using bias plot and receiver operator characteristic (ROC) curve methods. There were 196 sample-pairs analyzed; 56 (29%) had significant hypercarbia. For pH, there was very good agreement with venous samples being an average of 0.034 pH units lower than arterial samples. With respect to pCO(2), there was only fair agreement, with the pCO(2) on average 5.8 mm Hg higher in venous samples and 95% limits of agreement -8.8 to +20.5 mm Hg. The ROC curve analysis showed that a venous pCO(2) level of 45 mm Hg was a potential screening cutoff (sensitivity for the detection of hypercarbia of 100%, specificity 57%). This study shows that venous pH is an acceptable substitute for arterial measurement but there is not sufficient agreement for venous pCO(2) to be able to replace arterial pCO(2) in the clinical evaluation of ventilatory function. Venous pCO(2) may be able to be used as a screening test for hypercarbia using a screening cut-off of 45 mm Hg.
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PMID:Venous pCO(2) and pH can be used to screen for significant hypercarbia in emergency patients with acute respiratory disease. 1180 51


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