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

The hypercapnic ventilation response (HCVR) is positively correlated with forced expired volume in 1 s (FEV1). Therefore, subjects of small stature or patients with lung disease have low values for HCVR. However, indexing the HCVR for the subject's predicted maximal voluntary ventilation (MVV) results in a corrected HCVR (CHCVR) which is not dependent on FEV1 in normal subjects [Respiration 1993;60:197-202]. We hypothesized that the CHCVR would also be useful in assessing chemosensitivity in patients with poor lung function. To obtain the predicted MVV, we used the linear regression for FEV1 vs. measured MVV obtained from 411 patients with a wide range of FEV1 values (MVV = 31.2 x FEV1 + 11.8, r = 0.90, p < 0.001). We compared HCVR and CHCVR to the occlusion pressure response to hypercapnia (OPRH) in 34 patients with chronic obstructive pulmonary disease (COPD) and in 19 patients with low FEV1 due to small stature. All patients had been referred for assessment of possible sleep apnea. The results for the two groups of patients were similar. For the COPD patients, the HCVR had high values for sensitivity (86%) and negative predictive value (94%), but specificity, positive predictive value and accuracy were low (59, 35 and 65%, respectively). In contrast, CHCVR had high values for all the foregoing (86, 96, 100, 100 and 97%, respectively). Our results suggest that the CHCVR is useful in assessing chemosensitivity in patients who are ventilation-limited.
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PMID:Hypercapnic ventilation response in patients with lung disease: improved accuracy by correcting for ventilation ability. 778 12

Human lung transplantation was successfully performed in the early eighties and is now an option for patients with endstage lung disease, which is associated with poor survival. Most frequent indications for lung transplantation are emphysema, cystic fibrosis, fibrosing alveolitis, primary pulmonary hypertension and Eisenmenger's syndrome. Single lung transplantation (SLT) is most often performed in emphysema, fibrosing alveolitis and other diseases which are not associated with chronic infection of the lung. Double lung transplantation was recently replaced by the technique of sequential single lung or bilateral lung transplantation (BLT). Cardiopulmonary bypass can often be avoided and problems of the airway anastomosis are less frequent using BLT. Main indications for this procedure are cystic fibrosis, bronchiectasis and primary pulmonary hypertension (PPH). In PPH often only SLT is performed. Cor pulmonale is reversible following SLT or BLT even if the heart is not replaced. Combined heart-lung transplantation (HLT) is reserved for some cases of Eisenmenger's syndrome and few centers still prefer HLT in patients with cystic fibrosis. Patients are usually accepted for transplantation when they are considered to have life expectancy of 12 to 24 months. Quality of life and physical working capacity are severely decreased and patients suffer dyspnea NYHA grade III or IV. Most of the patients are hypoxic and need continuous oxygen therapy. Hypercapnia is also a negative predictive factor for survival without transplantation. In PPH cardiac index of less than 2 litres/m2 is associated with poor outcome. Not only absolute values for FEV1 and pO2 have to be considered in finding the best moment for assessment for transplantation but the clinical course of the disease during previous months and years also has to be taken into account. Contraindications to transplantation include acute infection, concomitant diseases of other organs, bronchial carcinoma and psychiatric disorders if noncompliance is likely. To achieve good results after lung transplantation, proper donor and recipient selection, experienced surgery and careful postoperative management are essential. Complications must be diagnosed early to provide effective treatment. Most complications occur within the first months after surgery. Early complications include primary organ failure, pleural bleeding, problems at the site of the airway anastomosis, infection and acute rejection. Acute rejection is common but can be treated successfully if diagnosed early.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Lung transplantation]. 778 72

An experience of surgical non-thoracic emergencies in patients admitted for chronic lung disease is herein presented. Fifty-four patients out of 10457 admitted in the four Departments of Pneumology of the Binaghi Hospital (Cagliari) between 1-1-1985 and 31-3-1993, were referred to our Department of General Surgery due to non-thoracic surgical emergencies. There was a considerable delay in the referral (only 25% of patients within 12 hours from the onset of symptoms): indeed predominant respiratory symptoms, hypoxia and hypercapnia made these patients no responsive to symptoms of surgical emergency. Surgical emergencies in causal correlation with respiratory disease (intestinal occlusion due to abdominal metastases of lung carcinoma, complicated peptic ulcer) had the worst prognosis (mortality: 52.9%). Those in chance connection, such as acute limb ischemia and preexisting abdominal disease, had a less adverse outcome. Mortality, however, was 37.5%: this datum outlines the role of chronic lung disease in defining operative risk. The authors call attention to three groups of observed patients: 1) three patients were operated on for intestinal occlusion due to unrecognized abdominal neoplasia, that showed itself in the course of hospitalization in the Department of Pneumology for lung metastases; 2) in 3 cases symptoms and signs of acute abdomen were observed without abdominal disease. The cause of acute pseudoabdomen was diaphragmatic pleural or basal pulmonary inflammation; 3) the eight patients with pulmonary embolism were all admitted in the Department of Pneumology with a wrong diagnosis of bronchopneumonia.
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PMID:[Extrathoracic surgical emergencies in hospitalized patients with bronchopulmonary diseases. Analysis of the operative risk]. 780 66

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Assessment of ventilatory function in patients with neuromuscular disease. 786 89

In contrast to adults, newborn infants breathe from an elevated end-expiratory lung volume, determined by the interaction of airflow retardation (braking) by the diaphragm and larynx, and expiratory duration. To determine the effect of hypercapnia on this strategy, we examined changes in respiratory muscle activity and the ventilatory response to CO2 breathing in eight premature infants 33-34 wk gestational age in the first 3 postnatal days. We recorded tidal volume, airflow, and electromyograms (EMG) of the laryngeal abductor [posterior cricoarytenoid (PCA)], which abducts the vocal cords, and diaphragm during behaviorally determined quiet sleep in room air and during steady-state inhalation of 2% CO2 in air. As expected, tidal volume increased (P < 0.0005) without a change in inspiratory duration with hypercapnia. Unexpectedly, in all subjects, expiratory duration was longer during CO2 inhalation (P < 0.001), accompanied by marked changes in expiratory flow patterns consistent with increased expiratory braking. Diaphragm post-inspiratory EMG activity increased with hypercapnia (P < 0.005) with no change in baseline diaphragm or PCA EMG activity. Peak inspiratory EMG activity of the diaphragm and PCA increased with CO2 (10 and 37%, respectively; P < 0.05). We conclude that the mechanisms used to elevate end-expiratory lung volume are enhanced during hypercapnia in premature infants. This breathing strategy may be important in maintaining gas exchange in infants with lung disease.
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PMID:Hypercapnia increases expiratory braking in preterm infants. 812 87

The Bohr/Riley model of CO2 homeostasis describes the relationship between CO2 production, ventilation, and arterial PCO2 and assumes that ventilation and CO2 delivery to the lung are both anatomically and temporally well matched. In contrast to normal breathing, periodic patterns of ventilation show temporal mismatch of ventilation to CO2 delivery. We developed a computer model of lung CO2 clearance that uses CO2 transfer equations to generate iterative solutions for PCO2 in multiple body compartments as a function of time. During continuous ventilatory patterns our model predicts steady-state arterial PCO2 identical to that of the Bohr model. During periodic ventilation, we predict mean PCO2 will be elevated unless mean ventilation is increased above that required by the Bohr model. Waxing and waning tidal volumes, low functional residual capacity, and low capillary blood volume potentiate the hypercapnia. However, if cardiac output oscillates in phase with breathing, hypercapnia is minimized. This analysis suggests a new mechanism for the development of sustained hypercapnia, separate from absolute hypoventilation or the presence of lung disease.
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PMID:CO2 homeostasis during periodic breathing: predictions from a computer model. 830 89

We describe the clinical, radiologic, functional, and pulmonary hemodynamic characteristics of a group of 30 nonsmoking patients with a lung disease that may be related to intense, long-standing indoor wood-smoke exposure. The endoscopic and some of the pathologic findings are also presented. Intense and prolonged wood-smoke inhalation may produce a chronic pulmonary disease that is similar in many aspects to other forms of inorganic dust-exposure interstitial lung disease. It affects mostly country women in their 60s, and severe dyspnea and cough are the outstanding complaints. The chest roentgenograms show a diffuse, bilateral, reticulonodular pattern, combined with normalized or hyperinflated lungs, as well as indirect signs of pulmonary arterial hypertension (PAH). On the pulmonary function test the patients show a mixed restrictive-obstructive pattern with severe hypoxemia and variable degrees of hypercapnia. Endoscopic findings are those of acute and chronic bronchitis and intense anthracotic staining of the airways appears to be quite characteristic. Fibrous and inflammatory focal thickening of the alveolar septa as well as diffuse parenchymal anthracotic deposits are the most prominent pathologic findings, although inflammatory changes of the bronchial epithelium are also present. The patients had severe PAH in which, as in other chronic lung diseases, chronic alveolar hypoxia may play the main pathogenetic role. However, PAH in wood-smoke inhalation-associated lung disease (WSIALD) appears to be more severe than in other forms of interstitial lung disease and tobacco-related COPD. The patients we studied are a selected group and they may represent one end of the spectrum of the WSIALD.
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PMID:Pulmonary arterial hypertension and cor pulmonale associated with chronic domestic woodsmoke inhalation. 841 64

A 49-year-old woman was admitted to the hospital for hypercapnia. Pulmonary function testing showed small lung volumes without parenchymal lung disease. Muscle enzyme levels were normal and the EMG was nonspecific. Finally, muscle biopsy revealed abundant nemaline bodies characteristic of nemaline myopathy. Nasal intermittent pressure ventilation was started with a preset pressure ventilator during sleeping hours with a good response.
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PMID:Adult onset of nemaline myopathy presenting as respiratory insufficiency. 855 68

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

Artificial ventilation plays a key role in the treatment of acute respiratory distress syndrome (ARDS). Initially, the goal is to normalize gas exchange compromised by the lung disease. Positive pressure ventilation can however aggravate prior lesions of the pulmonary parenchyma, at least in areas of the lung accessible to ventilation. Computed tomography of the lung has given us a better understanding of the pathogenesis of these ventilation-induced lesions, leading to new ventilatory strategies aimed at assuring adequate oxygenation without damaging the parenchyma. These ventilatory modes may tolerate a certain degree of hypercapnia to avoid lung injury. Improved oxygenation relies on optimizing the ventilation/perfusion ratio, either with inhaled nitric oxide or a supine position to improve alveolar recruitment. In the most severe cases, extra-corporal gas exchange systems have shown their efficacy for patients whose lungs cannot be ventilated. Thus ventilation should be carefully adapted to each patient based on the severity of the ARDS and its clinical course. We present a practical protocol based on a hierarchy rationale for each ventilation mode and indicate the explorations required to adapt each mode to a specific patient.
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PMID:[Artificial ventilation in acute respiratory distress syndrome in adults. Towards an individual optimization]. 895 78


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